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\n \n 2020\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n Dur3 and nrt2 genes in the bloom-forming dinoflagellate Prorocentrum minimum: Transcriptional responses to available nitrogen sources.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Chemosphere, 241. 2020.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Dur3$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n 2019\n \n \n (9)\n \n \n

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\n \n\n \n \n \n \n \n \n Trichophyton mentagrophytes and T interdigitale genotypes are associated with particular geographic areas and clinical manifestations.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Mycoses, 62(11): 1084-1091. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Trichophyton$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n PDXK mutations cause polyneuropathy responsive to pyridoxal 5′-phosphate supplementation.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Annals of Neurology, 86(2): 225-240. 2019.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"PDXK$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n Objective: To identify disease-causing variants in autosomal recessive axonal polyneuropathy with optic atrophy and provide targeted replacement therapy. Methods: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of variants on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on recombinant protein, patient-derived fibroblasts, plasma, and erythrocytes. Response to supplementation was measured with clinical validated rating scales, electrophysiology, and biochemical quantification. Results: We identified biallelic mutations in PDXK in 5 individuals from 2 unrelated families with primary axonal polyneuropathy and optic atrophy. The natural history of this disorder suggests that untreated, affected individuals become wheelchair-bound and blind. We identified conformational rearrangement in the mutant enzyme around the ATP-binding pocket. Low PDXK ATP binding resulted in decreased erythrocyte PDXK activity and low pyridoxal 5′-phosphate (PLP) concentrations. We rescued the clinical and biochemical profile with PLP supplementation in 1 family, improvement in power, pain, and fatigue contributing to patients regaining their ability to walk independently during the first year of PLP normalization. Interpretation: We show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP. We show that the biochemical profile can be rescued with PLP supplementation associated with clinical improvement. As B6 is a cofactor in diverse essential biological pathways, our findings may have direct implications for neuropathies of unknown etiology characterized by reduced PLP levels. ANN NEUROL 2019;86:225–240. © 2019 The Authors. Annals of Neurology published by Wiley Periodicals, Inc. on behalf of American Neurological Association.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Prion Properties of Alpha-Synuclein.\n \n \n \n \n\n\n \n Schwarzman, A.; Senkevich, K.; Emelyanov, A.; and Pchelina, S.\n\n\n \n\n\n\n Molekuliarnaia biologiia, 53(3): 380-387. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Prion$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman2019380,\r\nauthor={Schwarzman, A.L. and Senkevich, K.A. and Emelyanov, A.K. and Pchelina, S.N.},\r\ntitle={Prion Properties of Alpha-Synuclein},\r\njournal={Molekuliarnaia biologiia},\r\nyear={2019},\r\nvolume={53},\r\nnumber={3},\r\npages={380-387},\r\ndoi={10.1134/S0026898419030182},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85067784888&doi=10.1134%2fS0026898419030182&partnerID=40&md5=1c4766834f9977c5a70302dc3b04748d},\r\naffiliation={Konstantinov St. Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Leningrad oblast, Gatchina, 188300, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, 197022, Russian Federation},\r\nabstract={The prion properties of alpha-synuclein, a key aggregating protein involved in the pathogenesis of so-called synucleinopathies, including Parkinson's disease (PD), dementia with Lewy bodies, multiple system atrophy, and its various conformers are discussed. It is shown that alpha-synuclein may be transferred between cells by prion-like propagation. Similarly to other prions, alpha-synuclein aggregation develops from the initial lag-phase (nucleation) to the subsequent growth phase (elongation), and to the stationary phase where the aggregates and monomers exist in equilibrium. Similarly to prions, alpha-synuclein undergoes conformational changes from an alpha-helix to its beta-folded structure. However, there is currently no evidence that alpha-synuclein-dependent PD can be transmitted from person-to-person. This review describes the prion properties of alpha-synuclein, possible ways of its intercellular propagation, and novel approaches to PD diagnostics.},\r\nauthor_keywords={alpha-synuclein;  alpha-synuclein transmission;  Parkinson's disease;  prions},\r\npublisher={NLM (Medline)},\r\nissn={00268984},\r\npubmed_id={31184602},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Biol. (Mosk.)},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Prion Properties of Alpha-Synuclein.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Molecular Biology, 53(3): 335-341. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Prion$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n Human Peripheral Blood Macrophages As a Model for Studying Glucocerebrosidase Dysfunction.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 13(2): 100-106. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Human$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n Mononuclear Cells of Peripheral Blood in vitro. A Model of Antipsychotic Therapy Personalization.\n \n \n \n \n\n\n \n Grunina, M.; Zabotina, A.; Pchelina, M.; Nasyrova, R.; Sosin, D.; Ershov, E.; Taraskina, A.; and Krupitskiy, E.\n\n\n \n\n\n\n Cell and Tissue Biology, 13(1): 64-69. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Mononuclear$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Grunina201964,\r\nauthor={Grunina, M.N. and Zabotina, A.M. and Pchelina, M.M. and Nasyrova, R.F. and Sosin, D.N. and Ershov, E.E. and Taraskina, A.E. and Krupitskiy, E.M.},\r\ntitle={Mononuclear Cells of Peripheral Blood in vitro. A Model of Antipsychotic Therapy Personalization},\r\njournal={Cell and Tissue Biology},\r\nyear={2019},\r\nvolume={13},\r\nnumber={1},\r\npages={64-69},\r\ndoi={10.1134/S1990519X1901005X},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85065664184&doi=10.1134%2fS1990519X1901005X&partnerID=40&md5=88ab86e61eec3bdce943a294537fe0fc},\r\naffiliation={Petersburg Nuclear Physics Institute named by B. P. Konstantinov of National Research Center “Kurchatov Institute”, Gatchina, Leningrad oblast  188300, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, 197022, Russian Federation; National Medical Psychoneurological Research Institute named by V. M. Bekhterev, St. Petersburg, 192019, Russian Federation; Kashchenko Psychiatric Hospital No. 1, GatchinaNikolskoe, Leningrad oblast  188357, Russian Federation},\r\nabstract={Abstract: The implementation of a unified strategy for prescribing antipsychotics has proved to be an ineffective approach to the treatment of mentally ill patients. The study of the efficiency of pharmacological drugs on models mimicking the individual pathophysiology of the patient is one means of personalized (predictive) therapy. We evaluated the mRNA level for the genes of the neurotransmitters’ receptors (ADR1B, HRH1, HTR2А, DRD1, DRD2, DRD4, and DRD5). These are targets of antipsychotic drugs; therefore, they can be used as the probable biomarkers of the success of the treatment of mental illnesses of schizophrenic spectrum. We used peripheral blood mononuclear cells (PBMC) in vitro as the therapeutic model. The study included 108 patients with a proved diagnosis of schizophrenia spectrum disorders, receiving a haloperidol or olanzapine as a monotherapy. The patients were divided into two groups based on their response to the pharmacotherapy (effective or ineffective). The response was estimated with psychometric analysis performed on 28 ± 2 days of the treatment. In the group with ineffective therapy, the level of expression of the studied genes in PBMC in vitro had increased with the presence of the antipsychotic drug, while, in the group of patients with positive dynamics of mental status normalization, the analyzed level of expression remained virtually unchanged. The highest significant differences for patients with different responses on the pharmacological treatment were observed for the ADR1B and HRH1 genes in the case of olanzapine therapy (Р = 0.004 and 0.038, respectively) and for the HTR2A gene in the case of haloperidol therapy (Р = 0.039). At the same time, basic levels of gene expression in non-cultivated PBMC were not associated with the patient’s response to therapy. Thus, the mRNA level for genes of neurotransmission in PBMC in vitro in the presence of antipsychotics can be proposed as a biomarker for predicting the pharmacotherapy outcome for mentally ill patients. © 2019, Pleiades Publishing, Ltd.},\r\nauthor_keywords={antipsychotic drugs;  mRNA level;  neurotransmission receptors;  peripheral blood mononuclear cells;  schizophrenia spectrum disorders;  therapy efficiency predictors},\r\n}

\n\n\n

\n Abstract: The implementation of a unified strategy for prescribing antipsychotics has proved to be an ineffective approach to the treatment of mentally ill patients. The study of the efficiency of pharmacological drugs on models mimicking the individual pathophysiology of the patient is one means of personalized (predictive) therapy. We evaluated the mRNA level for the genes of the neurotransmitters’ receptors (ADR1B, HRH1, HTR2А, DRD1, DRD2, DRD4, and DRD5). These are targets of antipsychotic drugs; therefore, they can be used as the probable biomarkers of the success of the treatment of mental illnesses of schizophrenic spectrum. We used peripheral blood mononuclear cells (PBMC) in vitro as the therapeutic model. The study included 108 patients with a proved diagnosis of schizophrenia spectrum disorders, receiving a haloperidol or olanzapine as a monotherapy. The patients were divided into two groups based on their response to the pharmacotherapy (effective or ineffective). The response was estimated with psychometric analysis performed on 28 ± 2 days of the treatment. In the group with ineffective therapy, the level of expression of the studied genes in PBMC in vitro had increased with the presence of the antipsychotic drug, while, in the group of patients with positive dynamics of mental status normalization, the analyzed level of expression remained virtually unchanged. The highest significant differences for patients with different responses on the pharmacological treatment were observed for the ADR1B and HRH1 genes in the case of olanzapine therapy (Р = 0.004 and 0.038, respectively) and for the HTR2A gene in the case of haloperidol therapy (Р = 0.039). At the same time, basic levels of gene expression in non-cultivated PBMC were not associated with the patient’s response to therapy. Thus, the mRNA level for genes of neurotransmission in PBMC in vitro in the presence of antipsychotics can be proposed as a biomarker for predicting the pharmacotherapy outcome for mentally ill patients. © 2019, Pleiades Publishing, Ltd.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Possible Involvement of Genes Related to Lysosomal Storage Disorders in the Pathogenesis of Parkinson’s Disease.\n \n \n \n \n\n\n \n Rudenok, M.; Alieva, A.; Nikolaev, M.; Kolacheva, A.; Ugryumov, M.; Pchelina, S.; Slominsky, P.; and Shadrina, M.\n\n\n \n\n\n\n Molecular Biology, 53(1): 24-31. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Possible$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Rudenok201924,\r\nauthor={Rudenok, M.M. and Alieva, A.K. and Nikolaev, M.A. and Kolacheva, A.A. and Ugryumov, M.V. and Pchelina, S.N. and Slominsky, P.A. and Shadrina, M.I.},\r\ntitle={Possible Involvement of Genes Related to Lysosomal Storage Disorders in the Pathogenesis of Parkinson’s Disease},\r\njournal={Molecular Biology},\r\nyear={2019},\r\nvolume={53},\r\nnumber={1},\r\npages={24-31},\r\ndoi={10.1134/S002689331901014X},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064542511&doi=10.1134%2fS002689331901014X&partnerID=40&md5=bda7c18981d23de885e11507498d37d1},\r\naffiliation={Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russian Federation; St. Petersburg National Research Academic University of the Russian Academy of Sciences, St. Petersburg, 194021, Russian Federation; Koltsov Institute of Developmental Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation},\r\nabstract={Abstract—: Parkinson’s disease (PD) characterized with slow continuous degeneration of dopaminergic neurons in the substantia nigra is one of the most common neurodegenerative diseases, but its etiology and pathogenesis are not fully understood. The pathogenesis of PD involves the impairment of lysosomal autophagy, which also contributes to lysosomal storage disorders (LSDs). In this work, the expression of genes related to lysosomal autophagy: Hspa8, Lamp2, Tfam, Slc18a2, and Vps35, was analyzed in the brain tissues of mice with the earliest stage of MPTP-induced PD. The detected decrease in Hspa8 and Lamp2 mRNA levels suggests that dysfunction of lysosomal autophagy may be involved in the earliest stages of PD pathogenesis. A decrease in the rate of lysosomal autophagy may affect the accumulation of damaged proteins and the formation of protein inclusions in PD. Genes related to the lysosome function may be involved in development of both LSD and PD at the earliest stages of these pathophysiological processes. © 2019, Pleiades Publishing, Inc.},\r\nauthor_keywords={chaperone-mediated autophagy;  gene expression;  lysosome;  MPTP;  Parkinson’s disease},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)17-315-50003 mol_nr},\r\n}

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Possible Involvement of Genes Related to Lysosomal Storage Disorders in the Pathogenesis of Parkinson's Disease.\n \n \n \n \n\n\n \n Rudenok, M.; Alieva, A.; Nikolaev, M.; Kolacheva, A.; Ugryumov, M.; Pchelina, S.; Slominsky, P.; and Shadrina, M.\n\n\n \n\n\n\n Molekuliarnaia biologiia, 53(1): 28-36. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Possible$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Rudenok201928,\r\nauthor={Rudenok, M.M. and Alieva, A.K. and Nikolaev, M.A. and Kolacheva, A.A. and Ugryumov, M.V. and Pchelina, S.N. and Slominsky, P.A. and Shadrina, M.I.},\r\ntitle={Possible Involvement of Genes Related to Lysosomal Storage Disorders in the Pathogenesis of Parkinson's Disease},\r\njournal={Molekuliarnaia biologiia},\r\nyear={2019},\r\nvolume={53},\r\nnumber={1},\r\npages={28-36},\r\ndoi={10.1134/S0026898419010142},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85063643050&doi=10.1134%2fS0026898419010142&partnerID=40&md5=f67f9d12c0d875b9eae1788504d5cc61},\r\naffiliation={Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182, Russian Federation; St. Petersburg National Research Academic University of the Russian Academy of Sciences, St. Petersburg, 194021, Russian Federation; Koltsov Institute of Developmental Biology, Russian Academy of Sciences, Moscow, 119334, Russian Federation},\r\nabstract={Parkinson's disease (PD) characterized with slow continuous degeneration of dopaminergic neurons in the substantia nigra is one of the most common neurodegenerative diseases, but its etiology and pathogenesis are not fully understood. The pathogenesis of PD involves the impairment of lysosomal autophagy, which also contributes to lysosomal storage disorders (LSDs). In this work, the expression of genes related to lysosomal autophagy: Hspa8, Lamp2, Tfam, Slc18a2, and Vps35, was analyzed in the brain tissues of mice with the earliest stage of MPTP-induced PD. The detected decrease in Hspa8 and Lamp2 mRNA levels suggests that dysfunction of lysosomal autophagy maybe involved in the earliest stages of PD pathogenesis. A decrease in the rate of lysosomal autophagy may affect the accumulation of damaged proteins and the formation of protein inclusions in PD. Genes related to the lysosome function may be involved in development of both LSD and PD at the earliest stages of these pathophysiological processes.},\r\nauthor_keywords={chaperone-mediated autophagy;  gene expression;  lysosome;  MPTP;  Parkinson's disease},\r\npublisher={NLM (Medline)},\r\nissn={00268984},\r\npubmed_id={30895950},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Biol. (Mosk.)},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n Application of high-sensitivity flow cytometry in combination with low-voltage scanning electron microscopy for characterization of nanosized objects during platelet concentrate storage.\n \n \n \n \n\n\n \n Fedorov, A.; Kondratov, K.; Kishenko, V.; Mikhailovskii, V.; Kudryavtsev, I.; Belyakova, M.; Sidorkevich, S.; Vavilova, T.; Kostareva, A.; Sirotkina, O.; and Golovkin, A.\n\n\n \n\n\n\n Platelets. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Application$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Fedorov2019,\r\nauthor={Fedorov, A. and Kondratov, K. and Kishenko, V. and Mikhailovskii, V. and Kudryavtsev, I. and Belyakova, M. and Sidorkevich, S. and Vavilova, T. and Kostareva, A. and Sirotkina, O. and Golovkin, A.},\r\ntitle={Application of high-sensitivity flow cytometry in combination with low-voltage scanning electron microscopy for characterization of nanosized objects during platelet concentrate storage},\r\njournal={Platelets},\r\nyear={2019},\r\ndoi={10.1080/09537104.2019.1599337},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064479543&doi=10.1080%2f09537104.2019.1599337&partnerID=40&md5=bda69acb2e1d912cefe14c332aef0cec},\r\naffiliation={Institute of molecular biology and genetics, Almazov National Medical Research Centre, St. Petersburg, Russian Federation; Department of Laboratory Medicine and Genetics, Institute of Medical Education, Almazov National Medical Research Centre, St. Petersburg, Russian Federation; Interdisciplinary Resource Center for Nanotechnology, Saint-Petersburg State University, St. Petersburg, Russian Federation; Department of Fundamental Medicine, Far Eastern Federal University, Vladivostok, Russian Federation; Department of Immunology, Institute of Experimental Medicine, St. Petersburg, Russian Federation; Department of blood transfusion, Almazov National Medical Research Centre, St. Petersburg, Russian Federation; Petersburg Nuclear Physics Institute named by B.P. Konstantinov of National Research Centre «Kurchatov Institute», Gatchina, Leningradskaya oblast, Russian Federation},\r\nabstract={Platelet concentrates are used in clinic for therapy and prophylaxis of conditions associated with platelet deficiency or malfunction. The characteristics of platelet concentrates gradually change during pretransfusion storage, affecting their clinical effectiveness and the risk of adverse transfusion reactions. The presence of platelet-derived membrane vesicles is an important characteristic of platelet concentrates. Due to their functionality, changes in the number and molecular compositions of platelet-derived vesicles have major effects on the clinical properties of platelet preparations. The existence of different subpopulations of membrane vesicles requires analytical methods capable of providing information at the individual vesicle level. Such methods include flow cytometry and electron microscopy. However, conventional flow cytometry has certain limitations, since the diameters of many platelet-derived membrane vesicles are smaller than its detection limit. The use of classical scanning electron microscopy is also limited due to the requirement for coating with a layer of conductive material, which impedes the detection of small extracellular vesicles. Here, a combination of high-sensitivity flow cytometry and low-voltage scanning electron microscopy was used to increase sensitivity and resolution in the detection of nanosized objects present in platelet concentrates during storage. Apheresis platelet concentrates from eight healthy adult donors were investigated on days 2 and 7 of storage. Fractions of nanosized objects were obtained by differential centrifugation. Fluorophore-conjugated antibodies were used to detect marker-positive vesicles derived from platelets (CD41), red blood cells (CD235a), leukocytes (CD45), and endothelial cells (VEGFR2). Near-spherical objects with diameters ranging from 25 to 700 nm were observed by low-voltage scanning electron microscopy in platelet concentrates and its fractions. On day 7 of storage, objects with diameters of less than 100 nm were attached to and clustered near the terminal ends of pseudopod-like projections. High-sensitivity flow cytometry showed that during storage numbers of CD41(pos) vesicles elevated more than fivefold and numbers of marker-negative nanosized objects, which did not carry any of the investigated cell type-specific markers elevated more than twofold. Major changes in both CD41(pos) vesicles and marker-negative nanosized objects abundances were observed for objects with diameters around 100 nm bead equivalents. Overall, these results emphasized the importance of application of high-sensitivity methods for monitoring the characteristics of cell-derived nanosized objects during platelet concentrate storage. © 2019, © 2019 Taylor & Francis Group, LLC.},\r\nauthor_keywords={High-sensitivity flow cytometry;  low-voltage scanning electron microscopy;  membrane vesicles;  nanosized objects;  storage of platelet concentrate},\r\ncorrespondence_address1={Golovkin, A.; Institution of molecular biology and genetics, National Almazov Medical Research CentreRussian Federation; email: golovkin_a@mail.ru},\r\npublisher={Taylor and Francis Ltd},\r\nissn={09537104},\r\ncoden={PLTEE},\r\nlanguage={English},\r\nabbrev_source_title={Platelets},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n Platelet concentrates are used in clinic for therapy and prophylaxis of conditions associated with platelet deficiency or malfunction. The characteristics of platelet concentrates gradually change during pretransfusion storage, affecting their clinical effectiveness and the risk of adverse transfusion reactions. The presence of platelet-derived membrane vesicles is an important characteristic of platelet concentrates. Due to their functionality, changes in the number and molecular compositions of platelet-derived vesicles have major effects on the clinical properties of platelet preparations. The existence of different subpopulations of membrane vesicles requires analytical methods capable of providing information at the individual vesicle level. Such methods include flow cytometry and electron microscopy. However, conventional flow cytometry has certain limitations, since the diameters of many platelet-derived membrane vesicles are smaller than its detection limit. The use of classical scanning electron microscopy is also limited due to the requirement for coating with a layer of conductive material, which impedes the detection of small extracellular vesicles. Here, a combination of high-sensitivity flow cytometry and low-voltage scanning electron microscopy was used to increase sensitivity and resolution in the detection of nanosized objects present in platelet concentrates during storage. Apheresis platelet concentrates from eight healthy adult donors were investigated on days 2 and 7 of storage. Fractions of nanosized objects were obtained by differential centrifugation. Fluorophore-conjugated antibodies were used to detect marker-positive vesicles derived from platelets (CD41), red blood cells (CD235a), leukocytes (CD45), and endothelial cells (VEGFR2). Near-spherical objects with diameters ranging from 25 to 700 nm were observed by low-voltage scanning electron microscopy in platelet concentrates and its fractions. On day 7 of storage, objects with diameters of less than 100 nm were attached to and clustered near the terminal ends of pseudopod-like projections. High-sensitivity flow cytometry showed that during storage numbers of CD41(pos) vesicles elevated more than fivefold and numbers of marker-negative nanosized objects, which did not carry any of the investigated cell type-specific markers elevated more than twofold. Major changes in both CD41(pos) vesicles and marker-negative nanosized objects abundances were observed for objects with diameters around 100 nm bead equivalents. Overall, these results emphasized the importance of application of high-sensitivity methods for monitoring the characteristics of cell-derived nanosized objects during platelet concentrate storage. © 2019, © 2019 Taylor & Francis Group, LLC.\n

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\n \n 2018\n \n \n (31)\n \n \n

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\n \n\n \n \n \n \n \n \n SNCA variants and alpha-synuclein level in CD45+ blood cells in Parkinson's disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Journal of the Neurological Sciences, 395: 135-140. 2018.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"SNCA$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Mutation analysis of Parkinson's disease genes in a Russian data set.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Neurobiology of Aging, 71: 267.e7-267.e10. 2018.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Mutation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n The Release of Membrane Vesicles with Mature MicroRNA-221 and Activated Caspase-3 by Platelets during Storage of Platelet Concentrate.\n \n \n \n \n\n\n \n Kishenko, V.; Kondratov, K.; Mikhailovsky, V.; Sidorkevich, S.; Vavilova, T.; Sirotkina, O.; and Fedorov, A.\n\n\n \n\n\n\n Cell and Tissue Biology, 12(6): 506-509. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Kishenko2018506,\r\nauthor={Kishenko, V.V. and Kondratov, K.A. and Mikhailovsky, V.Y. and Sidorkevich, S.V. and Vavilova, T.V. and Sirotkina, O.V. and Fedorov, A.V.},\r\ntitle={The Release of Membrane Vesicles with Mature MicroRNA-221 and Activated Caspase-3 by Platelets during Storage of Platelet Concentrate},\r\njournal={Cell and Tissue Biology},\r\nyear={2018},\r\nvolume={12},\r\nnumber={6},\r\npages={506-509},\r\ndoi={10.1134/S1990519X18060056},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85059347486&doi=10.1134%2fS1990519X18060056&partnerID=40&md5=2cfffd56087e89418a1efdbe5ccd2955},\r\naffiliation={Almazov National Medical Research Center of the Ministry of Health of the Russian Federation, St. Petersburg, 197341, Russian Federation; St. Petersburg State University, Interdisciplinary Resource Center for Nanotechnology, St. Petersburg, 199034, Russian Federation; Petersburg Nuclear Physics Institute Named after Konstantinov, National Research Center Kurchatov Institute, Gatchina, Leningrad oblast  188300, Russian Federation; Pavlov First St. Petersburg State Medical University of the Ministry of Healthcare of the Russian Federation, St. Petersburg, 197022, Russian Federation},\r\nabstract={Abstract—: The preparation and storage of platelet concentrate can be accompanied by activation of platelets and triggering of apoptosis, increasing the formation of platelet membrane vesicles and worsening the therapeutic properties of such preparations. However, the mechanisms for the regulation of apoptosis in platelets and the molecular composition of platelet membrane vesicles associated with this process have so far remained poorly understood. The aim of the work was to study proapoptotic caspase-3 and antiapoptotic microRNA-221 levels in platelets and platelet membrane vesicles during the storage of platelet concentrate preparations. The object of the study was samples of the pooled platelet concentrates (n = 6), taken from the containers on the second and seventh days of storage. Full length and activated caspase-3 were found in platelets and in fractions of membrane vesicles. The proportion of activated caspase-3 in platelets increased during storage. MicroRNA-221 was found in platelets, fractions of membrane vesicles, as well as in the extravesicular fraction. During storage, levels of microRNA-221 increased 8-fold (P = 0.004) in the fraction of membrane vesicles pelleted at 100 000 g. The results of the study indicate that the membrane vesicles released by platelets during storage contain mature microRNA-221 and the activated form of caspase-3. © 2018, Pleiades Publishing, Ltd.},\r\nauthor_keywords={caspase-3;  exosomes;  membrane vesicles;  microRNA-221;  platelet concentrate},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)16-04-01142},\r\n}

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\n \n\n \n \n \n \n \n \n A low blood copper concentration is a co-morbidity burden factor in Parkinson's disease development.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Neuroscience Research, 135: 54-62. 2018.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n The Influence of Rs6311 and Rs6313 Polymorphisms of Serotonin 2a Receptor Gene (HTR2A) on Its mRNA and Protein Levels in Peripheral Blood Leukocytes in Treatment with Antipsychotics.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 12(5): 382-390. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n Abstract—: The 5-hydroxytrypamine (serotonin) 2A receptor (5-HTR2A) is the key receptor involved in the monoaminergic regulation of the body, which determines the biological functions and behavior of a person, and the target of the action of atypical antipsychotics. Polymorphic variants of the HTR2А gene rs6311 (-1438 A>G) and rs6313 (102 T>C)), potentially associated with impairment of the effectiveness of posttranscriptional processes, are considered to be risk factors for neuropsychiatric and cognitive pathologies. In the present study, we performed genotyping of these allelic variants among patients with schizophrenia spectrum disorders on antipsychotic therapy (haloperidol or olanzapine) (n = 60) and in the control group (n = 106). High linkage disequilibrium of allelic variants rs6311 and rs6313 (D' = 0.98) was found, and significant differences between the distribution of control group genotypes and patients with schizophrenia spectrum disorders were not detected. The contribution of the carriage of homozygous genotype GG (CC) into the efficacy of haloperidol therapy (р = 0.048) was shown. The effect of single nucleotide polymorphic variants rs6311 and rs6313 of the HTR2A gene on the mRNA level of the gene and the amount of 5-HTR2A in patients with mental disorders on the antipsychotic therapy was estimated for the first time. Before treatment, the level of the mRNA of the HTR2A gene was not different between the genotypes, whereas the amount of the 5-HTR2A protein was significantly higher in carriers of the AA (TT) genotype (р = 0.004). While mRNA level of HTR2A gene (р = 0.034) was increased in carriers of the GG (CC) genotype on haloperidol therapy. Olanzapine therapy reduced the amount of 5-HTR2A in the carriers of the wild-type “A” allele, apparently due to the pharmacological effect of the drug. Thus, the obtained data suggest that antipsychotic drugs, regardless of their affinity, modulate the transcription and/or translation of the HTR2A gene in the rs6311 (rs6313) genotype-dependent manner, and may affect the effectiveness of therapy. © 2018, Pleiades Publishing, Ltd.\n

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\n \n\n \n \n \n \n \n \n The Effect of Dopamine on Gene Expression of Alpha-synuclein and Transcription Factors GATA-1, GATA-2, and ZSCAN21 in Parkinson’s Disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 12(5): 410-418. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n Abstract: At present, it is believed that disregulation of alpha-synuclein (SNCA) metabolism and its aggregation is associated with the pathogenesis of Parkinson’s disease (PD). It is thought that the death of dopaminergic neurons in PD can be mediated by the effect of dopamine on the process of alpha-synuclein oligomerization, primarily by direct oxidation of the protein. At the same time, the effect of dopamine on the regulation mechanism of the SNCA gene expression is not excluded. It is known that transcription factors GATA-1, GATA-2, and ZSCAN21 can participate in the regulation of SNCA expression. In the present study, we evaluated the effect of exogenous dopamine (100 μM) on the mRNA level of the SNCA, GATA-1, GATA-2, and ZSCAN21 genes and the level of total alpha-synuclein in cultured peripheral blood lymphocytes (PBL) of patients with PD (n = 18) and individuals of the control group (n = 14) using real-time PCR and ELISA, subsecuently. A decrease in the SNCA expression level under the action of dopamine was first found in PBL of patients with PD (P = 0.013), of the control group (P = 0.004), and of the combined group that included patients with PD and control individuals (P = 0.001). When assessing alpha-synuclein level, a tendency toward its decrease in PBL of individuals from the control group (P = 0.068), as well as of the combined group of PD patients and control individuals (P = 0.059), was revealed by comparing the cells treated and untreated with dopamine. An increase in the mRNA level of the ZSCAN21 gene in PBL of control group individuals (P = 0.022), as well as of the GATA-1 gene in PBL of the group of patients with PD (P = 0.019) cultured in the presence of dopamine, was shown. An increase in the mRNA levels of the genes GATA-1, GATA-2, and ZSCAN21 in PBL under the treatment with dopamine was also observed in the combined group of patients with PD and control individuals (P = 0.027, 0.029, and 0.002 for GATA-1, GATA-2, and ZSCAN21, respectively). Thus, the obtained data show the effect of dopamine on the mRNA level of the SNCA, GATA-1, GATA-2, and ZSCAN21 genes in cultured PBL of PD patients and control group individuals, suggesting a possible effect of dopamine on the regulation of SNCA expression. © 2018, Pleiades Publishing, Ltd.\n

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\n \n\n \n \n \n \n \n \n Blood lysosphingolipids accumulation in patients with parkinson's disease with glucocerebrosidase 1 mutations.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Movement Disorders, 33(8): 1325-1330. 2018.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Blood$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Inhibition of Taq polymerase activity by singlet oxygen generation at photodynamic therapy.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n 2018.\n cited By 0; Conference of International Conference PhysicA.SPb 2017 ; Conference Date: 24 October 2017 Through 26 October 2017; Conference Code:137476\n\n\n\n
\n\n\n\n \n \n $\"Inhibition$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n \n \n 1 download\n \n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Whole-exome sequencing in searching for new variants associated with the development of Parkinson's disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Frontiers in Aging Neuroscience, 10(MAY). 2018.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Whole-exome$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Dielectric Properties of Oligonucleotides on the Surface of Si Nanosandwich Structures.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Semiconductors, 52(5): 612-614. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Dielectric$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Etiology of invasive candidosis agents in Russia: a multicenter epidemiological survey.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Frontiers of Medicine, 12(1): 84-91. 2018.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Etiology$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Plasma dopamine and SNCA gene expression in CD45+ peripheral blood cells in Parkinson’s desease.\n \n \n \n \n\n\n \n Emelyanov, À.; Lavrinova, A.; Litusova, E.; Kulabukhova, D.; Miliukhina, I.; Berkovich, O.; and Pchelina, S.\n\n\n \n\n\n\n Tsitologiya, 60(7): 540-543. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Plasma$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Emelyanov2018540,\r\nauthor={Emelyanov, À.K. and Lavrinova, A.O. and Litusova, E.M. and Kulabukhova, D.G. and Miliukhina, I.V. and Berkovich, O.A. and Pchelina, S.N.},\r\ntitle={Plasma dopamine and SNCA gene expression in CD45+ peripheral blood cells in Parkinson’s desease},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={7},\r\npages={540-543},\r\ndoi={10.31116/tsitol.2018.07.10},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064659934&doi=10.31116%2ftsitol.2018.07.10&partnerID=40&md5=3724faf39843d0a654ad7a3fec550f37},\r\naffiliation={Petersburg Nuclear Physics Institute, National Research Centre Kurchatov Institute, Gatchina, Leningrad Region, 188300, Russian Federation; I. P. Pavlov First St. Petersburg State Medical University, Ministry of Healtheare of Russian Federation, St. Petersburg, 197022, Russian Federation; St. Petersburg National Research Academic University RAS, St. Petersburg, 194021, Russian Federation; Institute of Experimental Medicine, St. Petersburg, 197376, Russian Federation},\r\nabstract={Alpha-synuclein (SNCA) aggregation is implicated in the pathogenesis of Parkinson’s disease (PD). In numerous studies an effect of dopamine on alpha-synuclein oligomerization was shown. In this study we evaluated plasma dopamine level in drug-naive sporadic PD (sPD) patients (n = 50) and controls (n = 31). The correlation between plasma dopamine level and gene expression, total and oligomeric alpha-synuclein levels in CD45 + peripheral blood cells was assessed. We found no difference in plasma dopamine level betweens sPD patients and controls. No correlation between plasma dopamine level and SNCA gene expression, total and oligomeric alpha-synuclein levels in CD45 + peripheral blood cells was observed. Thus, our data suggest that there is no link between alpha-synuclein gene expression in CD45+ cells and plasma dopamine level. © 2018 Sankt Peterburg. All rights reserved.},\r\nauthor_keywords={Alpha-synuclein;  CD45+ peripheral blood cells;  Dopamine;  Parkinson’s disease;  SNCA gene},\r\ncorrespondence_address1={Emelyanov, À.K.; Petersburg Nuclear Physics Institute, National Research Centre Kurchatov InstituteRussian Federation; email: e_anton_gen@mail.ru},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Macrophages from peripheral human blood as a model for studying glucocerebrosidase dysfunction.\n \n \n \n \n\n\n \n Nikolaev, M.; Kopytova, A.; Baydakova, G.; Emelyanov, A.; Salogub, G.; Senkevich, K.; Usenko, T.; Gorchakova, M.; Kovalchuk, Y.; Berkovich, O.; Zakharova, E.; and Pchelina, S.\n\n\n \n\n\n\n Tsitologiya, 60(12): 1022-1028. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Macrophages$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Nikolaev20181022,\r\nauthor={Nikolaev, M.A. and Kopytova, A.E. and Baydakova, G.V. and Emelyanov, A.K. and Salogub, G.N. and Senkevich, K.A. and Usenko, T.S. and Gorchakova, M.V. and Kovalchuk, Yu.P. and Berkovich, O.A. and Zakharova, E.Yu. and Pchelina, S.N.},\r\ntitle={Macrophages from peripheral human blood as a model for studying glucocerebrosidase dysfunction},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={12},\r\npages={1022-1028},\r\ndoi={10.1134/S004137711812009X},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064648002&doi=10.1134%2fS004137711812009X&partnerID=40&md5=308f8d6a0360bbdbfce4121557db70c3},\r\naffiliation={B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Centre Kurchatov Institute, Gatchina, Leningrad Region, 188300, Russian Federation; I. P. Pavlov First St. Petersburg State Medical University, St. Petersburg, 197022, Russian Federation; Medical-Genetics Scientific Center, Moscow, 115522, Russian Federation; Almazov National Medical Research Centre, St. Petersburg, 197341, Russian Federation},\r\nabstract={Mutations of the GBA gene cause Gaucher disease (GD), a lysosomal storage disease (LSD), connected with decreased activity of the lysosomal enzyme glucocerebrosidase (GCase). Both, homozygous and heterozygous states of GBA mutations implicate an increased risk of Parkinson’s disease (PD). Cell-based model in vitro from patients with mutations in the GBA gene is crucial for the new approaches of GD and PD treatment by increasing the GCase enzymatic activity, in particular, using pharmacological chaperones. The current study is based on the use of homogeneous populations of primary human macrophages for investigation of GCase disfunc-tions. The efficiency of different methods for macrophages culturing was compared with subsequent evaluation of GCase enzymatic activity and lysosphingolipids concentration in the dry spots of macrophages by means of LC-MS/MS. The efficiency of pharmacological chaperones isofagomine and ambroxol in restoring GCase enzymatic activity in the macrophages from GD patients was tested. The following research allowed to propose an approach in vitro to screening the potential drugs increases the activity of GCase. © 2018 Sankt Peterburg. All rights reserved.},\r\nauthor_keywords={Glucocerebrosidase;  Lysosphingolipids;  Macrophages;  Parkinson’s disease},\r\ncorrespondence_address1={Nikolaev, M.A.; B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Centre Kurchatov InstituteRussian Federation; email: Nikolaev_MA@pnpi.nrcki.ru},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Dopamine effect on the SNCA and GATA-1, GATA-2, ZSCAN21 genes expression in Parkinson’S disease.\n \n \n \n \n\n\n \n Emelyanov, A.; Lavrinova, A.; Litusova, E.; Knyazev, N.; Kulabukhova, D.; Garaeva, L.; Miliukhina, I.; Berkovich, O.; and Pchelina, S.\n\n\n \n\n\n\n Tsitologiya, 60(5): 365-372. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Dopamine$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Emelyanov2018365,\r\nauthor={Emelyanov, A.K. and Lavrinova, A.O. and Litusova, E.M. and Knyazev, N.A. and Kulabukhova, D.G. and Garaeva, L.A. and Miliukhina, I.V. and Berkovich, O.A. and Pchelina, S.N.},\r\ntitle={Dopamine effect on the SNCA and GATA-1, GATA-2, ZSCAN21 genes expression in Parkinson’S disease},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={5},\r\npages={365-372},\r\ndoi={10.31116/tsitol.2018.05.06},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064620903&doi=10.31116%2ftsitol.2018.05.06&partnerID=40&md5=febc42440d598538d667e49120df46f2},\r\naffiliation={Petersburg Nucleae Physics Institute named by B. P. Konstantinov of National Research Centre «Kurchatov Institute», Gatchina, Leningrad Region, 188300, Russian Federation; I. P. Pavlov First St. Petersburg State Medical University, St. Petersburg, 197022, Russian Federation; Federal State Budgetary Institution of Higher Education and Science St. Petersburg National Research Academic University RAS, St. Petersburg, 194021, Russian Federation; Institute of Experimental Medicine, St. Petersburg, 194064, Russian Federation; Institute of Cytology RAS, St. Petersburg, 194064, Russian Federation},\r\nabstract={Impaired metabolism of alpha-synuclein and its aggregation are implicated with the pathogenesis of Parkinson’s disease (PD). Alpha-synuclein oligomerization leading to neurodegeneration was suggested to be influenced by dopamine induced oxidation. At the same time, dopamine mediated regulation of SNCA gene expression is not excluded. The transcription factors GATA-1, GATA-2, ZSCAN21 were shown to regulate SNCA expression. We evaluated the effect of exogenous dopamine on the SNCA, GATA-1, GATA-2, ZSCAN21 genes expression and alpha-synuclein levels in cultured peripheral blood lymphocytes (PBL) from PD patients (n = 18) and controls (n = 14). Dopamine caused a decrease in SNCA gene expression in the PBL from PD patients (P = 0.013), controls (P = 0.004) and in combined group (P = 0.001). Also we revealed the tendency to decrease alpha-synuclein level in dopamine treated PBL from controls (P = 0.068) and in combined group (P = 0.059). An increased the mRNA levels of the ZSCAN21 and GATA-1 genes in the cultured dopamine-treated PBL from controls (P = 0.022) and PD patients (P = 0.019) were shown. Also it was found that dopamine increase mRNA levels of the GATA-1, GATA-2, and controls (P = 0.027, 0.029 and 0.002, respectively). Thus, our data suggest that dopamine might influence on the SNCA, GATA-1, GATA-2, and ZSCAN21 genes expression in cultured peripheral blood lymphocytes from PD patients and controls. © 2018 Sankt Peterburg.All rights reserved.},\r\nauthor_keywords={Alpha-synuclein;  Dopamine;  GATA-2;  Genes of GATA-1;  Parkinson’s disease;  SNCA gene;  ZSCAN21 transcription factors peripheral blood lymphocytes},\r\ncorrespondence_address1={Emelyanov, A.K.; Petersburg Nucleae Physics Institute named by B. P. Konstantinov of National Research Centre «Kurchatov Institute»Russian Federation; email: e_anton_gen@mail.ru},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The genetic predictors of cognitive impairment in Parkinson’s disease.\n \n \n \n \n\n\n \n Senkevich, K.; Miliukhina, I.; and Pchelina, S.\n\n\n \n\n\n\n Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova, 118(8): 109-117. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Senkevich2018109,\r\nauthor={Senkevich, K.A. and Miliukhina, I.V. and Pchelina, S.N.},\r\ntitle={The genetic predictors of cognitive impairment in Parkinson’s disease},\r\njournal={Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova},\r\nyear={2018},\r\nvolume={118},\r\nnumber={8},\r\npages={109-117},\r\ndoi={10.17116/jnevro2018118081109},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85057107287&doi=10.17116%2fjnevro2018118081109&partnerID=40&md5=4ad83ad29d8ca83ed912973534e875d0},\r\naffiliation={Institute of Experimental Medicine, St. Petersburg, Russian Federation; Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russian Federation; St. Petersburg Nuclear Physics Institute named by Konstantinov of NRC «Kurchatov Institute», Gatchina, Russian Federation},\r\nabstract={Parkinson’s disease (PD) is a common neurodegenerative disorder that can be both sporadic and familial. A number of studies are devoted to the study of non-motor symptoms in PD today. Cognitive deficits, and especially dementia, are one of the most severe and disabling non-motor symptoms of PD. More than a quarter of patients in the early stages of PD have a moderate cognitive impairment, more than half of patients with PD develop dementia within 10 years from the date of diagnosis. Using genome-wide association studies (GWAS), a number of genes associated with cognitive impairment have been identified based on a comparison of genetic and clinical phenotypes. These genes can be divided into three groups: genes that lead to the development of PD and are inherited according to the laws of Mendel (SNCA), genes that are risk factors for PD development (GBA, MAPT) and genes associated with the development of cognitive impairment, but not with PD (COMT, APOE, BDNF). This review examines the effect of genetic variants in the above-mentioned genes on cognitive functions in patients with PD. The elucidation of the genetic basis of cognitive deficits in PD could help in choice of treatment tactics and in development of new therapeutic strategies. © 2018, Media Sphera Publishing Group. All rights reserved.},\r\nauthor_keywords={Cognitive impairment;  Dementia;  Mutations;  Parkinson’s disease},\r\ncorrespondence_address1={Senkevich, K.A.; Institute of Experimental MedicineRussian Federation; email: senkon@gmail.com},\r\npublisher={Media Sphera Publishing Group},\r\nissn={19977298},\r\npubmed_id={30251988},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh. Nevrologii Psihiatrii im. S.S. Korsakova},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Peripheral blood mononuclear cells in vitro — Personalization model of antipsychotic therapy.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Tsitologiya, 60(7): 549-554. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Peripheral$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Serotonin 2A receptor (HTR2A) gene polymorphisms RS6311 and RS6313 modulate mRNA and protein expression in peripheral blood leukocytes during antipsychotic administration.\n \n \n \n \n\n\n \n Zabotina, À.; Belinskaya, M.; Zhuravlev, A.; Nasyrova, R.; Sosin, D.; Ershov, Å.; Taraskina, À.; and Krupitsky, Å.\n\n\n \n\n\n\n Tsitologiya, 60(5): 381-389. 2018.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Serotonin$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Zabotina2018381,\r\nauthor={Zabotina, À.Ì. and Belinskaya, M.A. and Zhuravlev, A.S. and Nasyrova, R.F. and Sosin, D.N. and Ershov, Å.Å. and Taraskina, À.Å. and Krupitsky, Å.Ì.},\r\ntitle={Serotonin 2A receptor (HTR2A) gene polymorphisms RS6311 and RS6313 modulate mRNA and protein expression in peripheral blood leukocytes during antipsychotic administration},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={5},\r\npages={381-389},\r\ndoi={10.31116/tsitol.2018.05.08},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85059475152&doi=10.31116%2ftsitol.2018.05.08&partnerID=40&md5=5a1110312960b53167a808303deec248},\r\naffiliation={Petersburg Nuclear Physics Institute named by B. P. Konstantinov of National Research Centre Kurchatov Institute, Gatchina, 188300, Russian Federation; I. P. Pavlov First S. Petersburg State Medical University, S. Petersburg, 197022, Russian Federation; V. M. Bekhterev National Medical Research Center Psychiatry and Neurology, S. Petersburg, 192019, Russian Federation; S. Petersburg Psychiatric Hospital N 1 named after P. P. Kashchenko, Leningrad Region, Gatchina district, v. Nikolskoe, 188357, Russian Federation},\r\nabstract={5-hydroxytryptamine (serotonin) 2À receptor (5-HTR 2A ) plays the key role in monoaminergic regulation of the human organism. It determines the biological functions and the behavior of a human, also being a target for atypical antipsychotics. Polymorphic variants of the gene HTR2À (rs6311 (-1438 A&gt;G) è rs6313 (102 T&gt;C)) are considered as risk factors for various pathologies, mainly affecting neuropsychiatric and cognitive functions, potentially associated with impaired efficiency of post-transcriptional procceses and protein processing. In the current study, our research team genotyped the afformentioned allelic variants in group of patients with schizophrenic disorders treated by haloperidol or olanzapine (n = 60) and in control group of volunteers in the North-West region of Russia. Disequilibrium linkage of allelic variants rs6311 and rs6313 (DR = 0.98) has been detected, but there was not significant difference in the distribution of genotypes between the control group and the patients with schizophrenia. The contribution of the carrier of the homozygous genotype GG (CC) to the efficiency of therapy with haloperidol has been shown (p = 0.048). For the first time the effect of rs6311 and rs6313 of the HTR2A gene on the relative level of mRNA of the gene and the amount of 5-HTR 2A in mentally ill patients with antipsychotic therapy have been estimated. Before the treatment there were no differences in mRNA levels between the two groups, whereas the amount of the 5-HTR 2A protein was significantly higher in AA (TT) genotype carriers (ð = 0.004). During haloperidol treatment mRNA level was increased in patients with GG (ÑÑ) genotype (ð = 0.034). The therapy with olanzapine decreased the amount of the 5-HTR 2A protein in the group of patients with wild type allele A, likely due to the pharmacological effect of the drug. Thus, the data suggest that antipsychotic drugs regardless of their affinity, modulate the process of transcription and/or translation of the HTR2A gene in a genotype rs6311 (rs6313) dependent manner and might affect the efficiency of the therapy. © 2018 Sankt Peterburg.All rights reserved.},\r\nauthor_keywords={Antipsychotic therapy;  HTR2A gene;  Peripheral blood leukocytes;  Schizophrenic disorders;  Serotonin receptor 2A (5-HTR2A)},\r\ncorrespondence_address1={Zabotina, À.Ì.; Petersburg Nuclear Physics Institute named by B. P. Konstantinov of National Research Centre Kurchatov InstituteRussian Federation; email: a.zabotina@gmail.com},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n 5-hydroxytryptamine (serotonin) 2À receptor (5-HTR 2A ) plays the key role in monoaminergic regulation of the human organism. It determines the biological functions and the behavior of a human, also being a target for atypical antipsychotics. Polymorphic variants of the gene HTR2À (rs6311 (-1438 A>G) è rs6313 (102 T>C)) are considered as risk factors for various pathologies, mainly affecting neuropsychiatric and cognitive functions, potentially associated with impaired efficiency of post-transcriptional procceses and protein processing. In the current study, our research team genotyped the afformentioned allelic variants in group of patients with schizophrenic disorders treated by haloperidol or olanzapine (n = 60) and in control group of volunteers in the North-West region of Russia. Disequilibrium linkage of allelic variants rs6311 and rs6313 (DR = 0.98) has been detected, but there was not significant difference in the distribution of genotypes between the control group and the patients with schizophrenia. The contribution of the carrier of the homozygous genotype GG (CC) to the efficiency of therapy with haloperidol has been shown (p = 0.048). For the first time the effect of rs6311 and rs6313 of the HTR2A gene on the relative level of mRNA of the gene and the amount of 5-HTR 2A in mentally ill patients with antipsychotic therapy have been estimated. Before the treatment there were no differences in mRNA levels between the two groups, whereas the amount of the 5-HTR 2A protein was significantly higher in AA (TT) genotype carriers (ð = 0.004). During haloperidol treatment mRNA level was increased in patients with GG (ÑÑ) genotype (ð = 0.034). The therapy with olanzapine decreased the amount of the 5-HTR 2A protein in the group of patients with wild type allele A, likely due to the pharmacological effect of the drug. Thus, the data suggest that antipsychotic drugs regardless of their affinity, modulate the process of transcription and/or translation of the HTR2A gene in a genotype rs6311 (rs6313) dependent manner and might affect the efficiency of the therapy. © 2018 Sankt Peterburg.All rights reserved.\n

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\n \n\n \n \n \n \n \n \n Investigation of Paraoxonase 1 Activity in Factory Workers Having Long-Term Contact with Organophosphorus Compounds.\n \n \n \n \n\n\n \n Razgildina, N.; Miroshnikova, V.; Fomichev, A.; Malysheva, E.; Panteleeva, A.; and Pchelina, S.\n\n\n \n\n\n\n Russian Journal of Genetics: Applied Research, 8(1): 96-100. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Investigation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Razgildina201896,\r\nauthor={Razgildina, N.D. and Miroshnikova, V.V. and Fomichev, A.V. and Malysheva, E.V. and Panteleeva, A.A. and Pchelina, S.N.},\r\ntitle={Investigation of Paraoxonase 1 Activity in Factory Workers Having Long-Term Contact with Organophosphorus Compounds},\r\njournal={Russian Journal of Genetics: Applied Research},\r\nyear={2018},\r\nvolume={8},\r\nnumber={1},\r\npages={96-100},\r\ndoi={10.1134/S2079059718010124},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85043677586&doi=10.1134%2fS2079059718010124&partnerID=40&md5=f84e25e1efdcf8259df7780e92169032},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, NRC Kurchatov Institute, Gatchina, 188300, Russian Federation; First Pavlov St. Petersburg State Medical University, Ministry of Health of Russia, St. Petersburg, 197022, Russian Federation; Kirov Military Medical Academy, Ministry of Defense of Russia, St. Petersburg, 194044, Russian Federation},\r\nabstract={The liver enzyme paraoxonase 1 (PON1) plays an important role in protecting the body from the toxic effects of organophosphorus compounds (OPs) through their hydrolysis. PON1 activity is determined by the polymorphic loci of the PON1 gene. In this work, the polymerase chain reaction followed by restriction analysis was used to type the polymorphic loci Q191R, L54M, and C(–108)T of the PON1 gene, and PON1 activity was measured in 68 male factory workers having long-term contact with OPs and in the control group (N = 37). PON1 activity among factory workers relative to the substrate of paraoxone was increased in comparison with the control group (p < 0.05). It is shown that the increase in PON1 activity in factory workers having long-term contact with OPs is modulated by genotypes of the PON1 gene. © 2018, Pleiades Publishing, Ltd.},\r\nauthor_keywords={C(–108)T;  L54M;  organophosphorus compounds (OPs);  paraoxonase 1 (PON1);  polymorphic loci Q191R;  PON1 gene},\r\n}

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\n \n\n \n \n \n \n \n \n Single-nucleotide polymorphism in a local population of Trichophyton rubrum.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Medical Mycology, 56(1): 125-128. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Single-nucleotide$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Modern views on gait impairment in parkinson`s disease and its correction.\n \n \n \n \n\n\n \n Miliukhina, I.; and Gracheva, E.\n\n\n \n\n\n\n Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova, 118(6): 96-101. 2018.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Modern$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Miliukhina201896,\r\nauthor={Miliukhina, I.V. and Gracheva, E.V.},\r\ntitle={Modern views on gait impairment in parkinson`s disease and its correction},\r\njournal={Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova},\r\nyear={2018},\r\nvolume={118},\r\nnumber={6},\r\npages={96-101},\r\ndoi={10.17116/jnevro20181186196},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85050779813&doi=10.17116%2fjnevro20181186196&partnerID=40&md5=1c42165b255aff4ac4b35b56beff5192},\r\naffiliation={Institute of Experimental Medicine, St-Petersburg, Russian Federation; Pavlov First St-Petersburg State Medical University, St-Petersburg, Russian Federation},\r\nabstract={The article reviews the causes of gait impairment in patients with Parkinson’s disease (PD). The emphasis is made on modern ideas, according to which gait impairment in PD is caused by a multisystem lesion and non-dopaminergic dependent mechanisms play the leading role. It is highlighted that gait impairment in PD is associated with the disruption of frontal/subcortical neural pathways which requires a special approach to pharmacological and non-pharmacological therapy. Based on pathogenetic mechanisms, much attention is paid to anti-dementia medications. Attention is drawn to the fact that the use of memantine hydrochloride (akatinol memantine) is a promising direction for gait impairment correction in the advanced and late stages of PD due to the improvement of glutamatergic transfer from the striatum to the specific areas of the cerebral cortex involved in gait control. The results of the latest clinical trials are analyzed. © Team of authors, 2018.},\r\nauthor_keywords={Akatinol memantine;  Cognitive gait control;  Cortical gait control;  Gait impairment;  Memantine hydrochloride;  Parkinson’s disease},\r\npublisher={Media Sphera Publishing Group},\r\nissn={19977298},\r\npubmed_id={30040809},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh. Nevrologii Psihiatrii im. S.S. Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Adiponectine gene expression in subcutaneous and intra-abdominal adipose tissue in women with varying degrees of obesity.\n \n \n \n \n\n\n \n Razgildina, N.; Brovin, D.; Pobozheva, I.; Panteleeva, A.; Miroshnikova, V.; Belyaeva, O.; Baranova, E.; Polyakova, E.; Berkovich, O.; and Pchelina, S.\n\n\n \n\n\n\n Tsitologiya, 60(7): 531-535. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Adiponectine$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Razgildina2018531,\r\nauthor={Razgildina, N.D. and Brovin, D.L. and Pobozheva, I.A. and Panteleeva, A.A. and Miroshnikova, V.V. and Belyaeva, O.D. and Baranova, E.I. and Polyakova, E.A. and Berkovich, O.A. and Pchelina, S.N.},\r\ntitle={Adiponectine gene expression in subcutaneous and intra-abdominal adipose tissue in women with varying degrees of obesity},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={7},\r\npages={531-535},\r\ndoi={10.31116/tsitol.2018.07.08},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064640282&doi=10.31116%2ftsitol.2018.07.08&partnerID=40&md5=2e9eff2bc5bcca5a6a1945cee55390cf},\r\naffiliation={B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Centre, Gatchina, Leningrad Region, 188300, Russian Federation; I. P. Pavlov First St. Petersburg State Medical University, Ministry of Healthcare of Russian Federation197022, Russian Federation},\r\nabstract={Adiponectin being one of the most important adipokines secreted by adipose tissue regulates energy homeostasis and demonstrates anti-inflammatory and anti-atherogenic effects. In this study the ADIPOQ gene expression in subcutaneous adipose tissue (SAT) and intra-abdominal visceral adipose tissue (VAT) was investigated concerning to its association of with body mass index (BMI) and waist circumference (WC), as well as total serum adiponectin in women. Samples of SAT and VAT were obtained from 50 women who underwent abdominal surgery (BMI > 25, n = 34, BMI < 25, n = 16). It was demonstrated that SAT differs from VAT by increased levels of ADIPOQ gene expression (P < 0.05). The mRNA level of the ADIPOQ gene was negatively correlated with BMI and WC and was reduced in overweight women (P < 0.05). These results suggest that SAT is more active in the synthesis and secretion of adiponectin in the bloodstream and makes the main contribution to the positive effects of this adipokine. © 2018 Sankt Peterburg. All rights reserved.},\r\nauthor_keywords={Adiponectin;  ADIPOQ gene;  Subcutaneous adipose tissue;  Visceral adipose tissue},\r\ncorrespondence_address1={Razgildina, N.D.; B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research CentreRussian Federation; email: razgnata@mail.ru},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Role of gut microbiota in pathogenesis of Parkinson's disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Nevrologicheskii Zhurnal, 22(6): 280-286. 2018.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Role$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n «Brain-gut-microbiota axis» includes central, neuroendocrine and neuroimmunological nervous systems, sympathetic and parasympathetic parts of autonomic nervous system and gut microbiota. In the present article are discussed the mechanisms of mutual impact of gut microbiota and nervous and immune systems during PD, rôle of gut microbiota in the launch of process of neurodegeneration. Gastrointestinal tract dysfunction during PD uncludes constipation, hypotrophy, periodontitis and gingivitis, dysphagy, gastric emptying troubles, defecation difficulties, infections, caused by helicobacteriosis and intestinal dysbiosis. Gut microbiota's composition during PD has its own particularitites: there have been observed increase of Enterobacteriaceae type of bacteria, decrease in quantity of Faecalibacterium prausnitzii, bacteria belonging to the families Lactobacillaceae and Prevotellaceae. There have been several discriptions of relations between gut microbiota composition and motor and non-motor manifestations of the disease. «Brain-gut-microbiota axis» works in two directions and participates in modulations of pro and antiinflammatory reactions, there has been discovered an impact of gut microbiota on the immune mechanisms of PD development, neuroinflammation and balance of pro- and antiinflammatory cytokines. Inflammation related to the changes in intestine microbiocenosis can contribute to Alpha-Synuclein development, further developments lead to peripheral inflammation, immunosypressive; also, autoimmune processes lead to degradation of dopaminergic neurons. Further research related of the «Brain-gut-microbiota axis» during PD can lead to discover new aspects of pathophysiology of the disease, discovery of peripheral biomarkers in enteric nervous system, development of new therapeutic methods based on corrections of gut microbiocenosis disfunction with help of probiotics, autoprobiotics or even fecal microbiota transplantation. © 2018 Izdatel'stvo Meditsina. All rights reserved.\n

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\n \n\n \n \n \n \n \n \n Investigation of Na+/K+-ATPase role in cancer cells' functioning.\n \n \n \n \n\n\n \n Perkov, S.; Emelyanov, A.; Shmakov, S.; and Bogdanov, A.\n\n\n \n\n\n\n 2018.\n cited By 0; Conference of 5th International School and Conference on Optoelectronics, Photonics, Engineering and Nanostructures, Saint Petersburg OPEN 2018 ; Conference Date: 2 April 2018 Through 5 April 2018; Conference Code:144220\n\n\n\n
\n\n\n\n \n \n $\"Investigation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@CONFERENCE{Perkov2018,\r\nauthor={Perkov, S.A. and Emelyanov, A.K. and Shmakov, S.V. and Bogdanov, A.A.},\r\ntitle={Investigation of Na+/K+-ATPase role in cancer cells' functioning},\r\njournal={Journal of Physics: Conference Series},\r\nyear={2018},\r\nvolume={1124},\r\nnumber={3},\r\ndoi={10.1088/1742-6596/1124/3/031023},\r\nart_number={031023},\r\nnote={cited By 0; Conference of 5th International School and Conference on Optoelectronics, Photonics, Engineering and Nanostructures, Saint Petersburg OPEN 2018 ; Conference Date: 2 April 2018 Through 5 April 2018;  Conference Code:144220},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85060998468&doi=10.1088%2f1742-6596%2f1124%2f3%2f031023&partnerID=40&md5=deeb90251a6f923112c8094934898cc1},\r\naffiliation={Nanobiotech Lab, St. Petersburg Academic University, St.-Petersburg, 194021, Russian Federation; Saint Petersburg Clinical Scientific and Practical Center for Special Types of Medical Care, Russian Federation; Bionics Lab, ITMO University, St.-Petersburg, Russian Federation; Petersburg Nuclear Physics Institute, Gatchina, Russian Federation; Pavlov First Saint-Petersburg State Medical University, St.-Petersburg, Russian Federation},\r\nabstract={Na+/K+-ATPase is an essential protein for cell functioning which has a great impact on osmotic stabilization, electrochemical potential and volume of the cell. According to the research of A Bogdanov and co-authors there is an overexpression of ATP1A1 and down-regulation of ATP1A2 in breast cancer cells [1]. Therefore, we assumed an existence of correlation between cancer cells proliferation and ATPase expression, which gives a possibility to regulate cancer cells proliferation via ATPase inhibition. In this research we have found a down-regulation of ATP1A1 in K562 cells after its processing with AgNO 3 . We expect that our research could help in investigating Na+/K+-ATPase role in cancer cells' functioning. © Published under licence by IOP Publishing Ltd.},\r\npublisher={Institute of Physics Publishing},\r\nissn={17426588},\r\nlanguage={English},\r\nabbrev_source_title={J. Phys. Conf. Ser.},\r\ndocument_type={Conference Paper},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Circulating endothelial cells and endothelial progenitor cells as a marker of endothelial dysfunction in hypertensive patients survived after ischemic stroke (review).\n \n \n \n \n\n\n \n Topuzova, M.; Alekseeva, T.; Vavilova, T.; Sirotkina, O.; and Klocheva, E.\n\n\n \n\n\n\n Arterial Hypertension (Russian Federation), 24(1): 57-64. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Circulating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Topuzova201857,\r\nauthor={Topuzova, M.P. and Alekseeva, T.M. and Vavilova, T.V. and Sirotkina, O.V. and Klocheva, E.G.},\r\ntitle={Circulating endothelial cells and endothelial progenitor cells as a marker of endothelial dysfunction in hypertensive patients survived after ischemic stroke (review)},\r\njournal={Arterial Hypertension (Russian Federation)},\r\nyear={2018},\r\nvolume={24},\r\nnumber={1},\r\npages={57-64},\r\ndoi={10.18705/1607-419X-2018-24-1-57-64},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85044506939&doi=10.18705%2f1607-419X-2018-24-1-57-64&partnerID=40&md5=a4f53a6328dbb9260009f9a1f65d7de5},\r\naffiliation={Almazov National Medical Research Centre, 2 Akkuratov street, St-Petersburg, 197341, Russian Federation; Petersburg Nuclear Physics Institute named after Konstantinov, National Research Center, Kurchatov Institute, Gatchina, Russian Federation; North-West State Medical University named after Mechnikov, St-Petersburg, Russian Federation},\r\nabstract={The main causes of ischemic stroke (IS) include arterial hypertension (HTN) and cerebral atherosclerosis. Based on the recent evidence, vascular endothelium is considered a target organ in patients with HTN and atherosclerosis, as well as an effector in their pathogenesis. The concept of endothelial dysfunction includes structural and functional changes in the endothelium. The level of circulating endothelial cells (CECs) and endothelial progenitor cells (EPCs) in the blood allows us to judge about degree of endothelial damage and its reparative activity. The article presents data on the diagnostic value of assessment of CECs and EPCs by flow cytometry for predicting the course and outcomes of IS in hypertensive patients. © 2018 All-Russian Public Organization Antihypertensive League. All rights reserved.},\r\nauthor_keywords={Circulating endothelial cells;  Endothelial dysfunction;  Ischemic stroke;  Lacunar stroke;  Progenitor endothelial cells},\r\ncorrespondence_address1={Topuzova, M.P.; Almazov National Medical Research Centre, 2 Akkuratov street, Russian Federation; email: marcun@rambler.ru},\r\npublisher={All-Russian Public Organization Antihypertensive League},\r\nissn={1607419X},\r\nlanguage={Russian},\r\nabbrev_source_title={Arter. Hypertens.},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Investigating the effect of singlet oxygen on polymerase activity during modulated irradiation at photodynamic treatment.\n \n \n \n \n\n\n \n Kaydanov, N.; Klimenko, V.; Emelyanov, A.; Knyazev, N.; and Bogdanov, A.\n\n\n \n\n\n\n 2018.\n cited By 0; Conference of Biophotonics: Photonic Solutions for Better Health Care VI 2018 ; Conference Date: 23 April 2018 Through 26 April 2018; Conference Code:137213\n\n\n\n
\n\n\n\n \n \n $\"Investigating$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@CONFERENCE{Kaydanov2018,\r\nauthor={Kaydanov, N.E. and Klimenko, V.V. and Emelyanov, A.K. and Knyazev, N.A. and Bogdanov, A.A.},\r\ntitle={Investigating the effect of singlet oxygen on polymerase activity during modulated irradiation at photodynamic treatment},\r\njournal={Proceedings of SPIE - The International Society for Optical Engineering},\r\nyear={2018},\r\nvolume={10685},\r\ndoi={10.1117/12.2318952},\r\nart_number={106854T},\r\nnote={cited By 0; Conference of Biophotonics: Photonic Solutions for Better Health Care VI 2018 ; Conference Date: 23 April 2018 Through 26 April 2018;  Conference Code:137213},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85049159716&doi=10.1117%2f12.2318952&partnerID=40&md5=656a24463c36ba41f7623af97930d444},\r\naffiliation={St. Petersburg Academic University, St Petersburg, Russian Federation; St. Petersburg Clinical Scientific and Practical Center for Special Types of Medical Care, St. Petersburg, Russian Federation; Petersburg Nuclear Physics Institute NRC Kurchatov Institute, Gatchina, Russian Federation; Institute of Cytology, St Petersburg, Russian Federation; ITMO University, St. Petersburg, Russian Federation},\r\nabstract={The goal of this study was to assess the ability of singlet oxygen generated at photodynamic treatment using different irradiation modes to inhibit the enzyme TAQ polymerase activity. Experimentally were determined the laser irradiation dose and the singlet oxygen concentration that results to complete inhibition of TAQ polymerase activity. The results show that using pulse mode irradiation is 1.5x more efficient then continuous wave. TAQ polymerase damage was also assessed by fluorescence spectrometry - tryptophan residues fluorescence is decreased if damaged by singlet oxygen during photodynamic treatment. It was observed that on doses, where TAQ polymerase looses its enzymatic activity the fluorescence decreases only by 7%. The fluorescence decrement of tryptophan correlates with damage to the enzyme. © 2018 SPIE.},\r\neditor={Popp J., Tuchin V.V., Pavone F.S.},\r\nsponsors={CNRS; iCube; Investissements d'Avenvir; Strasbourg the Europtimist; The Society of Photo-Optical Instrumentation Engineers (SPIE); Universite de Strasbourg},\r\npublisher={SPIE},\r\nissn={0277786X},\r\nisbn={9781510618961},\r\ncoden={PSISD},\r\nlanguage={English},\r\nabbrev_source_title={Proc SPIE Int Soc Opt Eng},\r\ndocument_type={Conference Paper},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Platelets release membrane vesicles carrying the mature MicroRNA-221 and activated caspase-3 during the platelet concentrate storage.\n \n \n \n \n\n\n \n Kishenko, V.; Kondratov, K.; Mikhailovskii, V.; Sidorkevich, S.; Vavilova, T.; Sirotkina, O.; and Fedorov, A.\n\n\n \n\n\n\n Tsitologiya, 60(7): 563-566. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Platelets$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Kishenko2018563,\r\nauthor={Kishenko, V.V. and Kondratov, K.A. and Mikhailovskii, V.Yu. and Sidorkevich, S.V. and Vavilova, T.V. and Sirotkina, O.V. and Fedorov, A.V.},\r\ntitle={Platelets release membrane vesicles carrying the mature MicroRNA-221 and activated caspase-3 during the platelet concentrate storage},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={7},\r\npages={563-566},\r\ndoi={10.31116/tsitol.2018.07.15},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064593358&doi=10.31116%2ftsitol.2018.07.15&partnerID=40&md5=10e4c7ca212a0a470fbc992a6ce4dfcd},\r\naffiliation={V. A. Almazov National Medical Research Centre, St. Petersburg, 197341, Russian Federation; St. Petersburg State University, Interdisciplinary Resource Centre for Nanotechnology, St. Petersburg, 199034, Russian Federation; Konstantinov Petersburg Nuclear Physics Institute, National Research Centre Kurchatov Institute, Gatchina, Leningrad Region, 188300, Russian Federation; I. P. Pavlov First St. Petersburg State Medical University, Ministry of Healthcare of Russian Federation, St. Petersburg, 197022, Russian Federation},\r\nabstract={The isolation and storage of platelet concentrates can be accompanied by platelets activation and apoptosis, which cause membrane vesicles release and decline in therapeutic properties of concentrates. However, the mechanisms for the regulation of platelet apoptosis as well as the molecular composition of platelet membrane vesicles remain poorly understood. The aim of the study was to analyze the levels of pro-apoptotic caspase-3 and anti-apoptotic microRNA-221 in platelets and platelet membrane vesicles during storage of platelet concentrates. The object of the study was samples of the pooled platelet concentrates (n = 6), collected from the containers on the 2nd and the 7th day of storage. Full length and activated caspase-3 were found in platelets and in fractions of membrane vesicles. The proportion of activated caspase-3 in platelets increased during storage. MicroRNA-221 was found in platelets, fractions of membrane vesicles, as well as in the extravesicular fraction. During storage, levels of microRNA-221 increased 8-fold (Ð = 0.004) in the fraction of membrane vesicles pelleted at 100 000 g. The results of the work indicate that the membrane vesicles, released by platelets during storage, carry the mature microRNA-221 and the activated form of caspase-3. © 2018 Sankt Peterburg. All rights reserved.},\r\nauthor_keywords={Caspase-3;  Exsomes;  Membrane vesicles;  MicroRNA-221;  Platelet concentrate},\r\ncorrespondence_address1={Sirotkina, O.V.; V. A. Almazov National Medical Research CentreRussian Federation; email: olga_sirotkina@mail.ru},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Expression of the glucocorticoid receptor alpha and beta isoforms in obstructive lung disease.\n \n \n \n \n\n\n \n Ulitina, A.; Vsevolodskaia, E.; Mironova, Z.; Gorbunkov, S.; Akopov, A.; Pchelina, S.; and Trofimov, V.\n\n\n \n\n\n\n Tsitologiya, 60(7): 536-539. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Expression$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Ulitina2018536,\r\nauthor={Ulitina, A.S. and Vsevolodskaia, E.I. and Mironova, Zh.A. and Gorbunkov, S.D. and Akopov, A.L. and Pchelina, S.N. and Trofimov, V.I.},\r\ntitle={Expression of the glucocorticoid receptor alpha and beta isoforms in obstructive lung disease},\r\njournal={Tsitologiya},\r\nyear={2018},\r\nvolume={60},\r\nnumber={7},\r\npages={536-539},\r\ndoi={10.31116/tsitol.2018.07.09},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064674739&doi=10.31116%2ftsitol.2018.07.09&partnerID=40&md5=9de943af61d0430e48570831c530b858},\r\naffiliation={Department of Molecular, Genetic and Nanobiological Technologies, I. P. Pavlov First St. Petersburg State Medical University, Ministry of Healthcare of Russian Federation, St. Petersburg, 197022, Russian Federation; Department of Hospital Therapy, I. P. Pavlov First St. Petersburg State Medical University, Ministry of Healthcare of Russian Federation, St. Petersburg, 197022, Russian Federation; Department of Thoracic Surgery, I. P. Pavlov First St. Petersburg State Medical University, Ministry of Healthcare of Russian Federation, St. Petersburg, 197022, Russian Federation; B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Centre Kurchatov Institute, Gatchina, Leningrad Region, 188300, Russian Federation},\r\nabstract={Glucocorticosteroids are widely used in chronic obstructive lung pathology, and they act via glucocorticoid receptor (GR). GRa and GRb are antagonists, and GRa is a main functional isoform. The purposes of our study were to assess mRNA levels of Gra and GRb in subjects with chronic obstructive lung pathology (asthma (BA), chronic obstructive pulmonary disease (COPD), and BA+COPD overlap). We have also compared mRNA levels in the peripheral blood and the lung bioptates and searched for relationship between mRNA levels and the clinical examination data. 72 patients and control group (n = 32) were included in the study. We showed the decrease of GRa and GRb expression in patients with BA compared to both BA+COPD overlap and control group. In BA+COPD overlap, GRa mRNA level was negatively correlated with the exacerbation rate, and the expression of GRb was associated with the lung hypertension and industrial pollutants in anamne-sis; GRa/bratio was correlated with blood eosinophils count, and it was decreased in subjects with severe Bron-chospasm. In COPD patients, we showed a positive correlation between isoforms expression in the peripheral blood and the lung tissue for both GRa and GRb. We may conclude that the change in the Gra and GRb expression in BA group is greater than in BA+COPD group. In BA+COPD group the decrease in the GRa expression, as well as the increase in the GRb expression, are associated with the more severe disease course. GRa and GRb expression in the peripheral blood reflects their organ-specific expression in the lung tissue. © 2018 Sankt Peterburg. All rights reserved.},\r\nauthor_keywords={Expression;  Glucocorticoid receptor;  Glucocorticosteroids;  NR3C1 gene;  Obstructive lung pathology},\r\ncorrespondence_address1={Ulitina, A.S.; Department of Molecular, Genetic and Nanobiological Technologies, I. P. Pavlov First St. Petersburg State Medical University, Ministry of Healthcare of Russian FederationRussian Federation; email: anna.s.ulitina@yandex.ru},\r\npublisher={Sankt Peterburg},\r\nissn={00413771},\r\ncoden={TSITA},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Influence of electrostatic interactions on cell-penetrating peptide-small interfering RNA complex formation and intracellular delivery efficiency.\n \n \n \n \n\n\n \n Svirina, A.; Terterov, I.; Klimenko, V.; Shmakov, S.; Knyazev, N.; Emelyanov, A.; Vysochinskaya, V.; and Bogdanov, A.\n\n\n \n\n\n\n 2018.\n cited By 0; Conference of 5th International School and Conference on Optoelectronics, Photonics, Engineering and Nanostructures, Saint Petersburg OPEN 2018 ; Conference Date: 2 April 2018 Through 5 April 2018; Conference Code:144220\n\n\n\n
\n\n\n\n \n \n $\"Influence$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@CONFERENCE{Svirina2018,\r\nauthor={Svirina, A. and Terterov, I. and Klimenko, V. and Shmakov, S. and Knyazev, N. and Emelyanov, A. and Vysochinskaya, V. and Bogdanov, A.},\r\ntitle={Influence of electrostatic interactions on cell-penetrating peptide-small interfering RNA complex formation and intracellular delivery efficiency},\r\njournal={Journal of Physics: Conference Series},\r\nyear={2018},\r\nvolume={1124},\r\nnumber={3},\r\ndoi={10.1088/1742-6596/1124/3/031005},\r\nart_number={031005},\r\nnote={cited By 0; Conference of 5th International School and Conference on Optoelectronics, Photonics, Engineering and Nanostructures, Saint Petersburg OPEN 2018 ; Conference Date: 2 April 2018 Through 5 April 2018;  Conference Code:144220},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85060968519&doi=10.1088%2f1742-6596%2f1124%2f3%2f031005&partnerID=40&md5=63b9a460a60a5f2460032ddc4084aa51},\r\naffiliation={Nanobiotech Lab, St. Petersburg Academic University, St.-Petersburg, 194021, Russian Federation; Saint Petersburg Clinical Scientific and Practical Center of Specialized Types of Medical Care, St.-Petersburg, 197758, Russian Federation; Institute of Cytology, RAS, St.-Petersburg, 194064, Russian Federation; Saint Petersburg Nuclear Physics Institute, National Research Center, Kurchatov Institute, Lenoblast, 188300, Russian Federation; Research Institute of Influenza, St.-Petersburg, 197376, Russian Federation; Bionics Lab, ITMO University, St.-Petersburg, 197101, Russian Federation},\r\nabstract={Cell-penetrating peptides (CPP) are short positively charged biopolymers that can translocate through lipid membranes. Due to their unique properties CPPs are promising agents for intracellular drug delivery. In this work we studied potency of intracellular delivery of small interfering RNA (siRNA) by means of two CPPs, namely primary amphipathic MPG-ΔNLS peptide and secondary amphipathic EB1 peptide. Optimal concentration conditions and peptide-to-siRNA ratios have been found for stable peptide-siRNA complex formation and delivery efficiency has been shown. © Published under licence by IOP Publishing Ltd.},\r\n}

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\n \n\n \n \n \n \n \n \n Predictors of adverse clinical course of coronary heart disease: The results from dynamical observation.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Cardiology, 23(7): 60-66. 2018.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Predictors$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Polymorphic variants of G/C+915 transforming growth factor beta 1 and atrial fibrillation in patients with metabolic syndrome.\n \n \n \n \n\n\n \n Ma, Y.; Ionin, V.; Zaslavskaya, E.; Ulitina, A.; Panteleeva, A.; Belyaeva, O.; Pchelina, S.; and Baranova, E.\n\n\n \n\n\n\n Arterial Hypertension (Russian Federation), 24(1): 93-100. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Polymorphic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Ma201893,\r\nauthor={Ma, Y. and Ionin, V.A. and Zaslavskaya, E.L. and Ulitina, A.S. and Panteleeva, A. and Belyaeva, O.D. and Pchelina, S.N. and Baranova, E.I.},\r\ntitle={Polymorphic variants of G/C+915 transforming growth factor beta 1 and atrial fibrillation in patients with metabolic syndrome},\r\njournal={Arterial Hypertension (Russian Federation)},\r\nyear={2018},\r\nvolume={24},\r\nnumber={1},\r\npages={93-100},\r\ndoi={10.18705/1607-419X-2018-24-1-93-100},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85044519133&doi=10.18705%2f1607-419X-2018-24-1-93-100&partnerID=40&md5=92e076e797ad2d29cd19fabb4b5815d8},\r\naffiliation={First Pavlov State Medical University of St. Petersburg, 6-8 Lev Tolstoy street, St-Petersburg, 197022, Russian Federation; Almazov National Medical Research Center, St-Petersburg, Russian Federation; B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Center, Kurchatov Institute, Gatchina, Russian Federation},\r\nabstract={Objective. Metabolic syndrome (MS) increases the risk of atrial fibrillation (AF). The probability of the incident AF increases in case of atrial fibrosis and remodeling. Transforming growth factor beta 1 (TGF-ß1, encoding gene TGFB1) induces myocardial fibrosis, in particular, in the atria. We analyzed the distribution of CC, CG and GG genotypes G/C+915 polymorphism of TGFB1 gene in patients with MS and AF. Design and methods. We included 426 subjects (30-65 years old): 222 patients with MS, including 115 patients with paroxysmal and permanent AF. The control group included 209 healthy individuals without cardiovascular disease and metabolic disorders. Genomic DNA was isolated from the venous blood. Allelic variants were identified by polymerase chain reaction followed by restriction analysis with endonucleases BglI. Results. GG genotype G/C (+915) TGFB1 gene in patients with MS and AF is more frequent than in MS patients without AF (97,4 and 87,9 %, respectively; ? 2 = 6,19, p = 0,013) and in healthy individuals (97,4 and 86,6 %, respectively; ? 2 = 8,77, p = 0,003). GG genotype is associated with an increased the risk of AF in patients with MS (odds ratio (OR): 5,74, 95 % confidence interval (CI): 1,71-19,33, p = 0,012). There were no differences in GG genotype G/C (+915) TGFB1 gene in MS patients without AF and healthy individuals. GC genotype G/C (+915) TGFB1 gene in healthy individuals was found more frequently than in MS with AF (12,4 and 2,6 %, respectively; ? 2 = 7,63, p = 0,006) and more frequently in MS patients without AF (12,1 and 2,6 %, respectively; X2 = 6,19, p = 0,013). C allele (genotype GC+CC) gene TGFB1 is associated with the decreased risk of AF in patients with MS (OR = 0,19, 95 % CI 0,05-0,70, ? = 0,001). Conclusions. We found an association of G/C (+915) TGFB1 gene with the risk of AF in patients with MS. C allele (CC and CG genotypes) seems to be protective and is associated with the 5,3-fold reduction in the risk of AF in patients with MS. We suggest that increased expression of gene TGFB1 causes heterogeneity of conduction and contributes to the AF in patients with MS. © 2018 All-Russian Public Organization Antihypertensive League. All rights reserved.},\r\nauthor_keywords={Atrial fibrillation;  G/C (+ 915) polymorphism of the TGFB1 gene;  Metabolic syndrome;  Transforming growth factor beta 1},\r\ncorrespondence_address1={Ionin, V.A.; First Pavlov State Medical University of St. Petersburg, 6-8 Lev Tolstoy street, Russian Federation; email: ionin.v.a@gmail.com},\r\npublisher={All-Russian Public Organization Antihypertensive League},\r\nissn={1607419X},\r\nlanguage={Russian},\r\nabbrev_source_title={Arter. Hypertens.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n

\n Objective. Metabolic syndrome (MS) increases the risk of atrial fibrillation (AF). The probability of the incident AF increases in case of atrial fibrosis and remodeling. Transforming growth factor beta 1 (TGF-ß1, encoding gene TGFB1) induces myocardial fibrosis, in particular, in the atria. We analyzed the distribution of CC, CG and GG genotypes G/C+915 polymorphism of TGFB1 gene in patients with MS and AF. Design and methods. We included 426 subjects (30-65 years old): 222 patients with MS, including 115 patients with paroxysmal and permanent AF. The control group included 209 healthy individuals without cardiovascular disease and metabolic disorders. Genomic DNA was isolated from the venous blood. Allelic variants were identified by polymerase chain reaction followed by restriction analysis with endonucleases BglI. Results. GG genotype G/C (+915) TGFB1 gene in patients with MS and AF is more frequent than in MS patients without AF (97,4 and 87,9 %, respectively; ? 2 = 6,19, p = 0,013) and in healthy individuals (97,4 and 86,6 %, respectively; ? 2 = 8,77, p = 0,003). GG genotype is associated with an increased the risk of AF in patients with MS (odds ratio (OR): 5,74, 95 % confidence interval (CI): 1,71-19,33, p = 0,012). There were no differences in GG genotype G/C (+915) TGFB1 gene in MS patients without AF and healthy individuals. GC genotype G/C (+915) TGFB1 gene in healthy individuals was found more frequently than in MS with AF (12,4 and 2,6 %, respectively; ? 2 = 7,63, p = 0,006) and more frequently in MS patients without AF (12,1 and 2,6 %, respectively; X2 = 6,19, p = 0,013). C allele (genotype GC+CC) gene TGFB1 is associated with the decreased risk of AF in patients with MS (OR = 0,19, 95 % CI 0,05-0,70, ? = 0,001). Conclusions. We found an association of G/C (+915) TGFB1 gene with the risk of AF in patients with MS. C allele (CC and CG genotypes) seems to be protective and is associated with the 5,3-fold reduction in the risk of AF in patients with MS. We suggest that increased expression of gene TGFB1 causes heterogeneity of conduction and contributes to the AF in patients with MS. © 2018 All-Russian Public Organization Antihypertensive League. All rights reserved.\n

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\n \n\n \n \n \n \n \n \n Common carotid intima-media thickness, levels of total and high-molecular weight adiponectin in women with abdominal obesity.\n \n \n \n \n\n\n \n Brovin, D.; Belyaeva, O.; Pchelina, S.; Berezina, A.; Karonova, T.; Bazhenova, E.; Kolodina, D.; Bakulina, A.; Polyakova, E.; Listopad, O.; Nikolaichuk, E.; Berkovich, O.; Baranova, E.; and Shlyakhto, E.\n\n\n \n\n\n\n Kardiologiya, 58(6): 29-36. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Common$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Brovin201829,\r\nauthor={Brovin, D.L. and Belyaeva, O.D. and Pchelina, S.N. and Berezina, A.V. and Karonova, T.L. and Bazhenova, E.A. and Kolodina, D.A. and Bakulina, A.S. and Polyakova, E.A. and Listopad, O.V. and Nikolaichuk, E.I. and Berkovich, O.A. and Baranova, E.I. and Shlyakhto, E.V.},\r\ntitle={Common carotid intima-media thickness, levels of total and high-molecular weight adiponectin in women with abdominal obesity},\r\njournal={Kardiologiya},\r\nyear={2018},\r\nvolume={58},\r\nnumber={6},\r\npages={29-36},\r\ndoi={10.18087/cardio.2018.6.10122},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85055616251&doi=10.18087%2fcardio.2018.6.10122&partnerID=40&md5=6cff4c3876a29e9a6efb3f2cbca910b4},\r\naffiliation={Acad. I. P. Pavlov First St.-Petersburg State Medical University, St.-Petersburg, Russian Federation; Almazov National Medical Research Centre, St.-Petersburg, Russian Federation},\r\nabstract={To investigate influence of different forms of adiponectin on carotid intima-media thickness (CIMT) in women with abdominal obesity (AO) in St.-Petersburg. It has been recognized before that AO is associated with cardiovascular diseases, including atherosclerosis, but mechanism of this association remains unclear. AO leads to imbalance of adipokines, in particularly decrease to investigate influence of different forms of adiponectin on carotid intima-media thickness (CIMT) in women with abdominal obesity (AO) in St.-Petersburg. It has been recognized before that AO is associated with cardiovascular diseases, including atherosclerosis, but mechanism of this association remains unclear. AO leads to imbalance of adipokines, in particularly decrease. © 2018 Media Sphera Publishing Group. All rights reserved.},\r\nauthor_keywords={Abdominal obesity;  Common carotid arteries;  High molecular weight adiponectin;  Intima-media thickness;  Total adiponectin},\r\ncorrespondence_address1={Brovin, D.L.; Acad. I. P. Pavlov First St.-Petersburg State Medical UniversityRussian Federation; email: dlbrovin@mail.ru},\r\npublisher={Media Sphera Publishing Group},\r\nissn={00229040},\r\npubmed_id={30362434},\r\nlanguage={Russian},\r\nabbrev_source_title={Kardiologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2017\n \n \n (17)\n \n \n

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\n \n\n \n \n \n \n \n \n Potential diagnostic markers of olanzapine efficiency for acute psychosis: A focus on peripheral biogenic amines.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n BMC Psychiatry, 17(1). 2017.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Potential$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n Background: Biomarkers are now widely used in many fields of medicine, and the identification of biomarkers that predict antipsychotic efficacy and adverse reactions is a growing area of psychiatric research. Monoamine molecules of the peripheral bloodstream are possible prospective biomarkers based on a growing body of evidence indicating that they may reflect specific changes in neurotransmitters in the brain. The aim of this study was to detect peripheral biogenic amine indicators of patients with acute psychosis and to test the correlations between the biological measures studied and the psychopathological status of the patients. Methods: This research included 60 patients with acute psychosis treated with olanzapine (n=30) or haloperidol (n=30). Here, we measured biogenic amine indicators, including mRNA levels of dopamine receptor D4 (DRD4) and the serotonin 2A receptor (5HTR2A), in peripheral blood mononuclear cells (PBMCs) using quantitative real-time polymerase chain reaction and serum dopamine concentrations by enzyme linked immunosorbent assay (ELISA). Psychopathological status was evaluated using psychometric scales. The assessments were conducted prior to and after 14 and 28 days of treatment. Results: The administration of haloperidol, but not olanzapine, up-regulated 5HTR2A mRNA in a linear manner, albeit without statistical significance (p=0.052). Both drugs had non-significant effects on DRD4 mRNA levels. Nevertheless, a positive correlation was found between DRD4 and 5HTR2A mRNA levels over a longitudinal trajectory, suggesting co-expression of the two genes. A significant positive correlation was observed between 5HTR2A mRNA levels and total Positive and Negative Syndrome Scale (PANSS) scores in both groups of patients before treatment. A significant correlation between baseline 5HTR2A mRNA levels and PANSS scores on days 14 and 28 of treatment remained for patients treated with olanzapine only. Moreover, a significant positive correlation was observed between blood serum dopamine levels and scores on extrapyramidal symptom scales in the olanzapine group. Conclusions: The DRD4 and 5HTR2A genes are co-expressed in PBMCs during antipsychotic administration. Despite a correlation between the studied biogenic amine indicators and the psychopathological status of patients, reliable biomarkers of treatment response could not be determined. © 2017 The Author(s).\n

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\n \n\n \n \n \n \n \n \n SsDNA damage dependence from singlet oxygen concentration at photodynamic interaction.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n 2017.\n cited By 1; Conference of 4th International School and Conference \"\"Saint Petersburg OPEN 2017\"\" on Optoelectronics, Photonics, Engineering and Nanostructures ; Conference Date: 3 April 2017 Through 6 April 2017; Conference Code:132151\n\n\n\n
\n\n\n\n \n \n $\"SsDNA$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Differential expression of CD42b and CD9 proteins in platelets and extracellular membrane vesicles during platelet-concentrate storage.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 11(6): 440-446. 2017.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Differential$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Links of gut microbiota composition with alcohol dependence syndrome and alcoholic liver disease.\n \n \n \n \n\n\n \n Dubinkina, V.; Tyakht, A.; Odintsova, V.; Yarygin, K.; Kovarsky, B.; Pavlenko, A.; Ischenko, D.; Popenko, A.; Alexeev, D.; Taraskina, A.; Nasyrova, R.; Krupitsky, E.; Shalikiani, N.; Bakulin, I.; Shcherbakov, P.; Skorodumova, L.; Larin, A.; Kostryukova, E.; Abdulkhakov, R.; Abdulkhakov, S.; Malanin, S.; Ismagilova, R.; Grigoryeva, T.; Ilina, E.; and Govorun, V.\n\n\n \n\n\n\n Microbiome, 5(1): 141. 2017.\n cited By 29\n\n\n\n
\n\n\n\n \n \n $\"Links$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Dubinkina2017141,\r\nauthor={Dubinkina, V.B. and Tyakht, A.V. and Odintsova, V.Y. and Yarygin, K.S. and Kovarsky, B.A. and Pavlenko, A.V. and Ischenko, D.S. and Popenko, A.S. and Alexeev, D.G. and Taraskina, A.Y. and Nasyrova, R.F. and Krupitsky, E.M. and Shalikiani, N.V. and Bakulin, I.G. and Shcherbakov, P.L. and Skorodumova, L.O. and Larin, A.K. and Kostryukova, E.S. and Abdulkhakov, R.A. and Abdulkhakov, S.R. and Malanin, S.Y. and Ismagilova, R.K. and Grigoryeva, T.V. and Ilina, E.N. and Govorun, V.M.},\r\ntitle={Links of gut microbiota composition with alcohol dependence syndrome and alcoholic liver disease},\r\njournal={Microbiome},\r\nyear={2017},\r\nvolume={5},\r\nnumber={1},\r\npages={141},\r\ndoi={10.1186/s40168-017-0359-2},\r\nnote={cited By 29},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85040805631&doi=10.1186%2fs40168-017-0359-2&partnerID=40&md5=6e91ddbdcc79c5730c8c502027691a1e},\r\naffiliation={Moscow Institute of Physics and Technology, Institutskiy per. 9, Dolgoprudny, Moscow Region, 141700, Russia; Federal Research and Clinical Center of Physical-Chemical Medicine, Malaya Pirogovskaya 1a, Moscow, 119435, Russia; Department of Bioengineering, University of Illinois at Urbana-Champaign, 1304 W. Springfield Avenue Urbana, Champaign, IL, 61801, USA; Carl R. Woese Institute for Genomic Biology, 1206 West Gregory Drive, Urbana, IL, 61801, USA; ITMO University, Kronverkskiy pr. 49, Saint-Petersburg, 197101, Russia; Saint-Petersburg Bekhterev Psychoneurological Research Institute, Bekhtereva 3, Saint-Petersburg, 192019, Russia; Moscow Clinical Scientific Center, Shosse Entuziastov 86, Moscow, 111123, Russia; Kazan State Medical University, Butlerova 49, Kazan, 420012, Russia; Kazan Federal University, Kremlyovskaya 18, Kazan, 420008, Russia},\r\nabstract={BACKGROUND: Alcohol abuse has deleterious effects on human health by disrupting the functions of many organs and systems. Gut microbiota has been implicated in the pathogenesis of alcohol-related liver diseases, with its composition manifesting expressed dysbiosis in patients suffering from alcoholic dependence. Due to its inherent plasticity, gut microbiota is an important target for prevention and treatment of these diseases. Identification of the impact of alcohol abuse with associated psychiatric symptoms on the gut community structure is confounded by the liver dysfunction. In order to differentiate the effects of these two factors, we conducted a comparative "shotgun" metagenomic survey of 99 patients with the alcohol dependence syndrome represented by two cohorts-with and without liver cirrhosis. The taxonomic and functional composition of the gut microbiota was subjected to a multifactor analysis including comparison with the external control group.\r\nRESULTS: Alcoholic dependence and liver cirrhosis were associated with profound shifts in gut community structures and metabolic potential across the patients. The specific effects on species-level community composition were remarkably different between cohorts with and without liver cirrhosis. In both cases, the commensal microbiota was found to be depleted. Alcoholic dependence was inversely associated with the levels of butyrate-producing species from the Clostridiales order, while the cirrhosis-with multiple members of the Bacteroidales order. The opportunist pathogens linked to alcoholic dependence included pro-inflammatory Enterobacteriaceae, while the hallmarks of cirrhosis included an increase of oral microbes in the gut and more frequent occurrence of abnormal community structures. Interestingly, each of the two factors was associated with the expressed enrichment in many Bifidobacterium and Lactobacillus-but the exact set of the species was different between alcoholic dependence and liver cirrhosis. At the level of functional potential, the patients showed different patterns of increase in functions related to alcohol metabolism and virulence factors, as well as pathways related to inflammation.\r\nCONCLUSIONS: Multiple shifts in the community structure and metabolic potential suggest strong negative influence of alcohol dependence and associated liver dysfunction on gut microbiota. The identified differences in patterns of impact between these two factors are important for planning of personalized treatment and prevention of these pathologies via microbiota modulation. Particularly, the expansion of Bifidobacterium and Lactobacillus suggests that probiotic interventions for patients with alcohol-related disorders using representatives of the same taxa should be considered with caution. Taxonomic and functional analysis shows an increased propensity of the gut microbiota to synthesis of the toxic acetaldehyde, suggesting higher risk of colorectal cancer and other pathologies in alcoholics.},\r\nauthor_keywords={Acetaldehyde;  Alcoholic dependence syndrome;  Alcoholic liver cirrhosis;  Bifidobacterium;  Gut-brain axis;  Human gut microbiota;  Lactobacillus;  Metagenome;  Virulence factors},\r\nissn={20492618},\r\npubmed_id={29041989},\r\nlanguage={English},\r\nabbrev_source_title={Microbiome},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n BACKGROUND: Alcohol abuse has deleterious effects on human health by disrupting the functions of many organs and systems. Gut microbiota has been implicated in the pathogenesis of alcohol-related liver diseases, with its composition manifesting expressed dysbiosis in patients suffering from alcoholic dependence. Due to its inherent plasticity, gut microbiota is an important target for prevention and treatment of these diseases. Identification of the impact of alcohol abuse with associated psychiatric symptoms on the gut community structure is confounded by the liver dysfunction. In order to differentiate the effects of these two factors, we conducted a comparative \"shotgun\" metagenomic survey of 99 patients with the alcohol dependence syndrome represented by two cohorts-with and without liver cirrhosis. The taxonomic and functional composition of the gut microbiota was subjected to a multifactor analysis including comparison with the external control group. RESULTS: Alcoholic dependence and liver cirrhosis were associated with profound shifts in gut community structures and metabolic potential across the patients. The specific effects on species-level community composition were remarkably different between cohorts with and without liver cirrhosis. In both cases, the commensal microbiota was found to be depleted. Alcoholic dependence was inversely associated with the levels of butyrate-producing species from the Clostridiales order, while the cirrhosis-with multiple members of the Bacteroidales order. The opportunist pathogens linked to alcoholic dependence included pro-inflammatory Enterobacteriaceae, while the hallmarks of cirrhosis included an increase of oral microbes in the gut and more frequent occurrence of abnormal community structures. Interestingly, each of the two factors was associated with the expressed enrichment in many Bifidobacterium and Lactobacillus-but the exact set of the species was different between alcoholic dependence and liver cirrhosis. At the level of functional potential, the patients showed different patterns of increase in functions related to alcohol metabolism and virulence factors, as well as pathways related to inflammation. CONCLUSIONS: Multiple shifts in the community structure and metabolic potential suggest strong negative influence of alcohol dependence and associated liver dysfunction on gut microbiota. The identified differences in patterns of impact between these two factors are important for planning of personalized treatment and prevention of these pathologies via microbiota modulation. Particularly, the expansion of Bifidobacterium and Lactobacillus suggests that probiotic interventions for patients with alcohol-related disorders using representatives of the same taxa should be considered with caution. Taxonomic and functional analysis shows an increased propensity of the gut microbiota to synthesis of the toxic acetaldehyde, suggesting higher risk of colorectal cancer and other pathologies in alcoholics.\n

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\n \n\n \n \n \n \n \n \n THZ emission and detection by quantum faraday effect in silicon nanosandwich-structures.\n \n \n \n \n\n\n \n Chernev, A.; Bagraev, N.; Chromov, V.; Klyachkin, L.; Malyarenko, A.; Rul, N.; Emelyanov, A.; and Dubina, M.\n\n\n \n\n\n\n 2017.\n cited By 0; Conference of 42nd International Conference on Infrared, Millimeter, and Terahertz Waves, IRMMW-THz 2017 ; Conference Date: 27 August 2017 Through 1 September 2017; Conference Code:131126\n\n\n\n
\n\n\n\n \n \n $\"THZ$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@CONFERENCE{Chernev2017,\r\nauthor={Chernev, A.L. and Bagraev, N.T. and Chromov, V.S. and Klyachkin, L.E. and Malyarenko, A.M. and Rul, N.I. and Emelyanov, A.K. and Dubina, M.V.},\r\ntitle={THZ emission and detection by quantum faraday effect in silicon nanosandwich-structures},\r\njournal={International Conference on Infrared, Millimeter, and Terahertz Waves, IRMMW-THz},\r\nyear={2017},\r\ndoi={10.1109/IRMMW-THz.2017.8067224},\r\nart_number={8067224},\r\nnote={cited By 0; Conference of 42nd International Conference on Infrared, Millimeter, and Terahertz Waves, IRMMW-THz 2017 ; Conference Date: 27 August 2017 Through 1 September 2017;  Conference Code:131126},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85033687278&doi=10.1109%2fIRMMW-THz.2017.8067224&partnerID=40&md5=747e4fb2f5bffe833a38581ceebb9b2c},\r\naffiliation={St Petersburg Academic University, St Petersburg, 194021, Russian Federation; Ioffe Institute, St Petersburg, 194021, Russian Federation},\r\nabstract={We demonstrate a novel approach to the problem of THz emission and detection by quantum Faraday effect that manifests itself in conductance of topological edge channels of silicon nanosandwich-structures. © 2017 IEEE.},\r\nsponsors={Centro de Investigaciones en Optica, A.C. (CIO); Consejo Nacional de Ciencia y Tecnologia's (CONACYT); et al.; IEEE; IRMMW-THz Society; Laboratorio Nacional de Ciencia y Tecnologia de Terahertz (LANCYTT)},\r\npublisher={IEEE Computer Society},\r\nissn={21622027},\r\nisbn={9781509060481},\r\nlanguage={English},\r\nabbrev_source_title={Int. Conf. Infrared, Millim., Terahertz Waves, IRMMW-THz},\r\ndocument_type={Conference Paper},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic association study of exfoliation syndrome identifies a protective rare variant at LOXL1 and five new susceptibility loci.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Nature Genetics, 49(7): 993-1004. 2017.\n cited By 26\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Transmission of pathogenic protein aggregates in Alzheimer's disease.\n \n \n \n \n\n\n \n Schwarzman, A.; and Sarantseva, S.\n\n\n \n\n\n\n Molekuliarnaia biologiia, 51(3): 418-422. 2017.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Transmission$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman2017418,\r\nauthor={Schwarzman, A.L. and Sarantseva, S.V.},\r\ntitle={Transmission of pathogenic protein aggregates in Alzheimer's disease},\r\njournal={Molekuliarnaia biologiia},\r\nyear={2017},\r\nvolume={51},\r\nnumber={3},\r\npages={418-422},\r\ndoi={10.7868/S0026898417030144},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85032626865&doi=10.7868%2fS0026898417030144&partnerID=40&md5=8e2becc485276d87487bf549fbf4c4ac},\r\naffiliation={Konstantinov St. Petersburg Nuclear Physics Institute Kurchatov Institute National Research Center Gatchina, Leningrad oblast Russia; Konstantinov St. Petersburg Nuclear Physics Institute Kurchatov Institute National Research Center Gatchina, Leningrad oblast Russia},\r\nabstract={Deposits of amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein in the brain of patients are major neuropathological features of Alzheimer's disease (AD). For a long time, the possibility of horizontal transmission of Aβ aggregates from cell to cell and from person to person remained hypothetical, since there was no experimental evidence. However, in 1993, the formation of senile plaques was confirmed in the brains of animals after intracerebral injections of AD patient brain homogenates or homogenates of the brain of transgenic mice enriched with Aβ aggregates. Other experiments indicate that amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein may be transferred from cell to cell like prions. In 2015 and 2016, it was reported that AD could be transmitted to humans during medical procedures, i.e., that this disease might be iatrogenic. This review discusses the mechanisms by which pathogenic Aβ protein can be transmitted between cells and analyzes the current evidence concerning the possibility of horizontal Aβ transmission from person to person.},\r\nauthor_keywords={Alzheimer's disease;  amyloid peptide (Aβ);  Aβ transmission;  prions},\r\nissn={00268984},\r\npubmed_id={28707657},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Biol. (Mosk.)},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Transmission of pathogenic protein aggregates in Alzheimer’s disease.\n \n \n \n \n\n\n \n Schwarzman, A.; and Sarantseva, S.\n\n\n \n\n\n\n Molecular Biology, 51(3): 368-371. 2017.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Transmission$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman2017368,\r\nauthor={Schwarzman, A.L. and Sarantseva, S.V.},\r\ntitle={Transmission of pathogenic protein aggregates in Alzheimer’s disease},\r\njournal={Molecular Biology},\r\nyear={2017},\r\nvolume={51},\r\nnumber={3},\r\npages={368-371},\r\ndoi={10.1134/S0026893317030141},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85021271494&doi=10.1134%2fS0026893317030141&partnerID=40&md5=f69dbfecac3c1dec31ab554ffa036c6b},\r\naffiliation={Konstantinov St. Petersburg Nuclear Physics Institute, Kurchatov Institute National Research Center, Gatchina, Leningrad oblast, 188300, Russian Federation},\r\nabstract={Deposits of amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein in the brain of patients are major neuropathological features of Alzheimer’s disease (AD). For a long time, the possibility of horizontal transmission of Aβ aggregates from cell to cell and from person to person remained hypothetical, since there was no experimental evidence. However, in 1993, the formation of senile plaques was confirmed in the brains of animals after intracerebral injections of AD patient brain homogenates. or homogenates of the brain of transgenic mice enriched with Aβ aggregates Other experiments indicate that amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein may be transferred from cell to cell like prions. In 2015 and 2016, it was reported that AD could be transmitted to humans during medical procedures, i.e., that this disease might be iatrogenic. This review discusses the mechanisms by which pathogenic Aβ protein can be transmitted between cells and analyzes the current evidence concerning the possibility of horizontal Aβ transmission from person to person. © 2017, Pleiades Publishing, Inc.},\r\nauthor_keywords={Alzheimer’s disease;  amyloid peptide (Aβ);  Aβ transmission;  prions},\r\ncorrespondence_address1={Schwarzman, A.L.; Konstantinov St. Petersburg Nuclear Physics Institute, Kurchatov Institute National Research CenterRussian Federation; email: aschwart1@yandex.ru},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={00268933},\r\nlanguage={English},\r\nabbrev_source_title={Mol. Biol.},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Data on gut metagenomes of the patients with alcoholic dependence syndrome and alcoholic liver cirrhosis.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Data in Brief, 11: 98-102. 2017.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Data$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Dataset of total, oligomeric alpha-synuclein and hemoglobin levels in plasma in Parkinson׳s disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Data in Brief, 10: 182-185. 2017.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Dataset$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Oligomeric α-synuclein and glucocerebrosidase activity levels in GBA-associated Parkinson's disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Neuroscience Letters, 636: 70-76. 2017.\n cited By 15\n\n\n\n
\n\n\n\n \n \n $\"Oligomeric$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n The clinical features of parkinson’s disease in patients with mutations and polymorphic variants of GBA gene.\n \n \n \n \n\n\n \n Senkevich, K.; Miliukhina, I.; Beletskaia, M.; Gracheva, E.; Kudrevatykh, A.; Nikolaev, M.; Emelyanov, A.; Kopytova, A.; Timofeeva, A.; Yakimovskii, A.; and Pchelina, S.\n\n\n \n\n\n\n Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova, 117(10): 81-86. 2017.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Senkevich201781,\r\nauthor={Senkevich, K.A. and Miliukhina, I.V. and Beletskaia, M.V. and Gracheva, E.V. and Kudrevatykh, A.V. and Nikolaev, M.A. and Emelyanov, A.K. and Kopytova, A.E. and Timofeeva, A.A. and Yakimovskii, A.F. and Pchelina, S.N.},\r\ntitle={The clinical features of parkinson’s disease in patients with mutations and polymorphic variants of GBA gene},\r\njournal={Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova},\r\nyear={2017},\r\nvolume={117},\r\nnumber={10},\r\npages={81-86},\r\ndoi={10.17116/jnevro201711710181-86},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85034811306&doi=10.17116%2fjnevro201711710181-86&partnerID=40&md5=287f4340ecb9c709dd9d661c0b0f9c46},\r\naffiliation={Institute of Experimental Medicine, St. Petersburg, Russian Federation; Pavlov First Saint Petersburg State Medical University, St. Petersburg, Russian Federation; National Research Center, «Kurchatov Institute», Konstantinov Petersburg Nuclear Physics Institute, St. Petersburg, Russian Federation},\r\nabstract={Background. Mutations in the glucocerebrosidase gene (GBA) increase the risk of Parkinson’s disease (PD) by 6—10 times in all populations and are associated with the early-onset of PD, development of cognitive impairment and presence of psychotic disorders. At the same time, polymorphic variants associated with the twofold increase in the risk of PD were also described in the GBA gene. Objective. To estimate the clinical features of PD in patients with mutations and polymorphic variants of the GBA gene. Material and methods. Evaluation of motor, cognitive, emotional, psychotic and autonomic dysfunctions in patients with mutations (N370S, L444P) and polymorphic variants (E326K, T369M) in the GBA gene was performed using clinical scales. Results. Patients with mutations (mGBA-PD), and with polymorphic variants (pGBA-PD) in the GBA gene were compared with the group of patients with sporadic PD (sPD). Compared to sPD, affective disorders (depression and anxiety) were more expressed in the mGBA-PD group (p=0.001) and the general GBA-PD group (p=0.001) assessed with Sheehan anxiety rating scale, in the pGBA-PD group (p=0.012) and the general GBA-PD group (p=0.05) assessed with the NPI, in the mGBA-PD (p=0.003), pGBA-PD (p=0.022), and general GBA-PD groups (p=0.001) assessed with the Hospital Anxiety and Depression scale (HADS ≪A≫), and in the pGBA-PD group (p=0.005) assessed with the HADS ≪D≫. Non-motor symptoms assessed with the PD-NMS were more expressed in the pGBA-PD patients (p=0.007) and in the total group with GBA-PD (p=0,014) compared to sPD. Cognitive impairment measured with MMSE was more marked in mGBA-PD patients (p=0.022). Differences in motor and non-motor clinical symptoms between pGBA-PD and mGBA-PD groups were not found. Conclusion. Thus, clinical features of non-motor symptoms were described both in carriers of GBA mutations and polymorphisms. Identification of the specific clinical phenotype of PD in carriers of GBA polymorphic variants is important due to their relatively high prevalence in PD patients. © 2017, Media Sphera Publishing Group. All rights reserved.},\r\nauthor_keywords={GBA;  Glucocerebrosidase;  Non-motor symptoms;  Parkinson’s disease},\r\npublisher={Media Sphera Publishing Group},\r\nissn={19977298},\r\npubmed_id={29171494},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh. Nevrologii Psihiatrii im. S.S. Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n Background. Mutations in the glucocerebrosidase gene (GBA) increase the risk of Parkinson’s disease (PD) by 6—10 times in all populations and are associated with the early-onset of PD, development of cognitive impairment and presence of psychotic disorders. At the same time, polymorphic variants associated with the twofold increase in the risk of PD were also described in the GBA gene. Objective. To estimate the clinical features of PD in patients with mutations and polymorphic variants of the GBA gene. Material and methods. Evaluation of motor, cognitive, emotional, psychotic and autonomic dysfunctions in patients with mutations (N370S, L444P) and polymorphic variants (E326K, T369M) in the GBA gene was performed using clinical scales. Results. Patients with mutations (mGBA-PD), and with polymorphic variants (pGBA-PD) in the GBA gene were compared with the group of patients with sporadic PD (sPD). Compared to sPD, affective disorders (depression and anxiety) were more expressed in the mGBA-PD group (p=0.001) and the general GBA-PD group (p=0.001) assessed with Sheehan anxiety rating scale, in the pGBA-PD group (p=0.012) and the general GBA-PD group (p=0.05) assessed with the NPI, in the mGBA-PD (p=0.003), pGBA-PD (p=0.022), and general GBA-PD groups (p=0.001) assessed with the Hospital Anxiety and Depression scale (HADS ≪A≫), and in the pGBA-PD group (p=0.005) assessed with the HADS ≪D≫. Non-motor symptoms assessed with the PD-NMS were more expressed in the pGBA-PD patients (p=0.007) and in the total group with GBA-PD (p=0,014) compared to sPD. Cognitive impairment measured with MMSE was more marked in mGBA-PD patients (p=0.022). Differences in motor and non-motor clinical symptoms between pGBA-PD and mGBA-PD groups were not found. Conclusion. Thus, clinical features of non-motor symptoms were described both in carriers of GBA mutations and polymorphisms. Identification of the specific clinical phenotype of PD in carriers of GBA polymorphic variants is important due to their relatively high prevalence in PD patients. © 2017, Media Sphera Publishing Group. All rights reserved.\n

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\n \n\n \n \n \n \n \n \n Molecular genetic and immunological aspects of invasive aspergillosis.\n \n \n \n \n\n\n \n Shadrivova, O.; Frolova, E.; Taraskina, A.; and Klimko, N.\n\n\n \n\n\n\n Jurnal Infektologii, 9(1): 47-54. 2017.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Shadrivova201747,\r\nauthor={Shadrivova, O.V. and Frolova, E.V. and Taraskina, A.E. and Klimko, N.N.},\r\ntitle={Molecular genetic and immunological aspects of invasive aspergillosis},\r\njournal={Jurnal Infektologii},\r\nyear={2017},\r\nvolume={9},\r\nnumber={1},\r\npages={47-54},\r\ndoi={10.22625/2072-6732-2017-9-1-47-54},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85018435059&doi=10.22625%2f2072-6732-2017-9-1-47-54&partnerID=40&md5=4434389ebb7262c48e08765d3f9362f9},\r\naffiliation={North-Western State Medical University Named after I.I. Mechnikov, Saint-Petersburg, Russian Federation},\r\nabstract={Aspergillus is very widely spread in nature. Daily people inhale to several thousand spores of micromycetes, however, an effective immune response prevents to development of the disease. In case of violation the mechanisms of innate and adaptive immune response as a result of genetic defects or iatrogenic immunosuppression Aspergillus spp. become pathogenic and can cause severe invasive infections in immunocompromised patients. Until now there are no reliable biomarkers for the risk prediction of invasive aspergillosis and monitoring the effectiveness of treatment of infectious process. In our review, we are considering the most important genetic and immunological factors affecting susceptibility to Aspergillus spp., The analysis of which can provide an individual approach to antifungal therapy / prevention in immunocompromised patients.},\r\nauthor_keywords={Antifungal therapy;  Aspergillus spp.;  Genetic predisposition;  Immune response;  Immunologic biomarkers},\r\npublisher={Interregional public organization Association of infectious disease specialists of Saint-Petersburg and Leningrad region (IPO AIDSSPbR)},\r\nissn={20726732},\r\nlanguage={Russian},\r\nabbrev_source_title={J. Infektol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Investigation of paraoxonase 1 activity of the workers at the plant, who have long-term contact with organophosphorus compounds.\n \n \n \n \n\n\n \n Razgildina, N.; Miroshnikova, V.; Fomichev, A.; Malysheva, E.; Panteleeva, A.; and Pchelina, S.\n\n\n \n\n\n\n Ecological Genetics, 15(1): 57-63. 2017.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Investigation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Razgildina201757,\r\nauthor={Razgildina, N.D. and Miroshnikova, V.V. and Fomichev, A.V. and Malysheva, E.V. and Panteleeva, A.A. and Pchelina, S.N.},\r\ntitle={Investigation of paraoxonase 1 activity of the workers at the plant, who have long-term contact with organophosphorus compounds},\r\njournal={Ecological Genetics},\r\nyear={2017},\r\nvolume={15},\r\nnumber={1},\r\npages={57-63},\r\ndoi={10.17816/ecogen15157-63},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85036646299&doi=10.17816%2fecogen15157-63&partnerID=40&md5=362cb2e8dd3fce80f201d3d5bf177802},\r\naffiliation={Molecular and Radiation Biophysics Department, B.P. Konstantinov Nuclear Physics Institute in Saint Petersburg, Gatchina, Russian Federation; Department of Military Field Therapy, S.M. Kirov Military Medical Academy, Saint Petersburg, Russian Federation},\r\nabstract={Liver enzyme paraoxonase 1 (PON1) plays an important role in protection the organism from toxic effects of organophosphorus compounds (OPs) via their hydrolysis whose rate and efficiency depend on PON1 serum level activity. PON1 activity is largely determined by the polymorphic variants of the PON1 gene. Effect of long-term work with exposure to the toxic OPs on the PON1 activity is almost unknown. The aim of the present work was to study the effect of long-term work with exposure to the toxic OPs on PON1 serumen zymatic activity dependi n g on polymor phisms Q191R, L54M, C(-108)T PON1 gene. Materials and methods: PON1 serum enzymatic activity and PON1 polymorphisms were determined in men, who were categorized in 2 groups: workers of companies providing storage and disposal of the OPs (68) and control group (37). The PON1 191, PON1 55 and PON1 108 polymorphisms were studied by polymerase chain reaction/restriction fragment length polymorphism. PON1 serum enzymatic activity was measured by a spectrophotometric method using paraoxon. Results: PON1 activity in workers with exposure to the toxic OPs relative was increased compared to the control group (p = 0,027). Differences in serum PON1 activity was shown for the car riers of cer tain genot ypes of the P O N1 gene: PON1 serum activity was higher in workers compared to controls only for LL genotype (L54M polymorphism) and C allele (C(-108)T polymorphism) car riers (p < 0,001 and p = 0,002, correspondently). Conclusion: We suggest that the increase in serum PON1 activity in workers providing storage and disposal of OPs could be modulated with the polymorphic variants of the PON1 gene.},\r\nauthor_keywords={Organophosphorus com pounds (ops);  Paraoxonase 1 (PON1);  Paraoxonase-1 gene;  Polymorphisms},\r\npublisher={LLC Eco-Vector},\r\nissn={18110932},\r\nlanguage={Russian},\r\nabbrev_source_title={Ecol. Genet.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genetic risk factors of macrovascular complications in patients with type 2 diabetes.\n \n \n \n \n\n\n \n Bystrova, A.; Ulitina, A.; Kim, M.; Skoryukova, S.; Miroshnikova, V.; Panteleeva, A.; Korelskaya, N.; He, Z.; Nikolaev, M.; Pchelina, S.; Baranova, E.; and Krasilnikova, E.\n\n\n \n\n\n\n Kardiologiya, 57(2): 17-22. 2017.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Bystrova201717,\r\nauthor={Bystrova, A.A. and Ulitina, A.S. and Kim, M.V. and Skoryukova, S.A. and Miroshnikova, V.V. and Panteleeva, A.A. and Korelskaya, N.A. and He, Z. and Nikolaev, M.A. and Pchelina, S.N. and Baranova, E.I. and Krasilnikova, E.I.},\r\ntitle={Genetic risk factors of macrovascular complications in patients with type 2 diabetes},\r\njournal={Kardiologiya},\r\nyear={2017},\r\nvolume={57},\r\nnumber={2},\r\npages={17-22},\r\ndoi={10.18565/cardio.2017.2.17-22},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85020789640&doi=10.18565%2fcardio.2017.2.17-22&partnerID=40&md5=4b65520c9a24f736b53c658130bdc386},\r\naffiliation={I.P. Pavlov St.-Petersburg State Medical University, St.-Petersburg, Russian Federation; B.P.Konstantinov Petersburg Nuclear Physics Institute National Research Centre Kurchatov Institute, St.-Petersburg, Russian Federation; Federal Almazov North-West Medical Research Centre, St.-Petersburg, Russian Federation},\r\nabstract={High risk of macrovascular complications in patients with type 2 diabetes mellitus (T2DM) is caused by insulin resistance and atherogenic dyslipidemia that may be genetically determined. The aim of this study was to assess the association of polymorphic genetic variants APOA5 (S19W/rs3135506), CETP (Taq1B/rs708272), PONI (Q192R/rs662) and PPARG (Pro12Ala/rs1801282) with T2DM and macrovascular complications in patients with T2DM resident in Northwestern Russia. We examined 386 patients with T2DM and 199 healthy controls. Genotyping was performed by polymerase chain reaction followed by restriction analysis. The study revealed the protective role of allele 12Ala of PPARG gene against T2DM development (odds ratio [OR]=0.58; 95% confidence interval [CI] 0.39-0.85). B1B1 genotype of CETP was associated with increased risk of stroke in T2DM patients (OR=1.85; 95% CI 1.07-3.21). RR genotype of PONI was associated with increased risk of T2DM with stroke (OR=2.98; 95% CI 1.01-8.84). According to study results Pro12Ala (rs1801282) variant of PPARG affected the risk of T2DM; polymorphic variants of CETP CTaq1B/rs708272) and PONI (Q192R/rs662) contributed to the risk of macrovascular complications of T2DM.},\r\nauthor_keywords={Complications;  Genetic factors;  Macrovascular;  Type 2 diabetes},\r\ncorrespondence_address1={Bystrova, A.A.; I.P. Pavlov St.-Petersburg State Medical UniversityRussian Federation; email: abystrova@inbox.ru},\r\npublisher={Media Sphera Publishing Group},\r\nissn={00229040},\r\npubmed_id={28290785},\r\nlanguage={Russian},\r\nabbrev_source_title={Kardiologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Leptin gene expression in epicardial adipose tissue in males with coronary heart disease.\n \n \n \n \n\n\n \n Polyakova, E.; Draganova, A.; Kolodina, D.; Nifontov, S.; Alekseeva, G.; Kolesnik, O.; Miroshnikova, V.; Panteleeva, A.; Pobozheva, I.; Razgildina, N.; Novikov, V.; Nemkov, A.; Maslevtsov, D.; Gavrilenkov, V.; Galkina, O.; Belyaeva, O.; Pchelina, S.; Berkovich, O.; and Baranova, E.\n\n\n \n\n\n\n Arterial Hypertension (Russian Federation), 23(6): 488-497. 2017.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Leptin$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Polyakova2017488,\r\nauthor={Polyakova, E.A. and Draganova, A.S. and Kolodina, D.A. and Nifontov, S.E. and Alekseeva, G.V. and Kolesnik, O.S. and Miroshnikova, V.V. and Panteleeva, A.A. and Pobozheva, I.A. and Razgildina, N.D. and Novikov, V.K. and Nemkov, A.S. and Maslevtsov, D.V. and Gavrilenkov, V.I. and Galkina, O.V. and Belyaeva, O.D. and Pchelina, S.N. and Berkovich, O.A. and Baranova, E.I.},\r\ntitle={Leptin gene expression in epicardial adipose tissue in males with coronary heart disease},\r\njournal={Arterial Hypertension (Russian Federation)},\r\nyear={2017},\r\nvolume={23},\r\nnumber={6},\r\npages={488-497},\r\ndoi={10.18705/1607-419X-2017-23-6-488-497},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85041098516&doi=10.18705%2f1607-419X-2017-23-6-488-497&partnerID=40&md5=672fa660e8f200320a48840859c5fc86},\r\naffiliation={First Pavlov State Medical University of St. Petersburg, 6-8 Lev Tolstoy street, St Petersburg, 197022, Russian Federation; B. P. Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Gatchina, Russian Federation; Almazov National Medical Research Centre, St Petersburg, Russian Federation},\r\nabstract={Objective. Evaluate leptin gene expression in epicardial adipose tissue in males with coronary heart disease (CHD). Design and methods. We enrolled 106 males: 57 males with CHD aged 61,3 ± 1,1 years old and 49 males without CHD aged 57,3 ± 1,3 years old (p > 0,05). Epicardial adipose tissue (EAT) specimens were obtained in 65 males (57 males with CHD and 8 males with valvular heart disease without CHD) undergoing cardiac surgery. Serum leptin was measured by immune enzyme assay (IEA). Leptin mRNA (messenger ribonucleic acid) level in EAT was assessed by real-time polymerase chain reaction. All patients underwent coronaroangiography and echocardiography. Results. Leptin mRNA level in EAT was significantly higher in males with CHD and atherosclerosis of main coronary arteries. Patients with multivessel (3 and more coronary arteries) atherosclerotic lesions showed higher leptin mRNA level in EAT than in subjects with lesions of 1-2 coronary artery and in patients without CHD: 2,84 ± 0,04 (RU), 1,91 ± 0,03 RU and 1,41 ± 0,02 RU, respectively (p < 0,05). Conclusions. Paracrine activity of epicardial adipose tissue plays a role in the pathogenesis of coronary atherosclerotic lesions in males.},\r\nauthor_keywords={Atherosclerosis;  Cardiovascular risk;  Coronary heart disease;  Epicardial adipose tissue;  Leptin;  Leptin gene expression},\r\ncorrespondence_address1={Polyakova, E.A.; First Pavlov State Medical University of St. Petersburg, 6-8 Lev Tolstoy street, Russian Federation; email: polyakova-ea@yahoo.com},\r\npublisher={All-Russian Public Organization Antihypertensive League},\r\nissn={1607419X},\r\nlanguage={Russian},\r\nabbrev_source_title={Arter. Hypertens.},\r\ndocument_type={Editorial},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Pharmacogenetic and epigenetic features of asthma3COPD overlap syndrome.\n \n \n \n \n\n\n \n Mironova, Z.; Vsevolodskaya, E.; Trofimov, V.; Ulitina, A.; Pchelina, S.; Dubina, M.; Gorbunkov, S.; and Akopov, A.\n\n\n \n\n\n\n Pulmonologiya, 27(1): 7-11. 2017.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Pharmacogenetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Mironova20177,\r\nauthor={Mironova, Z.A. and Vsevolodskaya, E.I. and Trofimov, V.I. and Ulitina, A.S. and Pchelina, S.N. and Dubina, M.V. and Gorbunkov, S.D. and Akopov, A.L.},\r\ntitle={Pharmacogenetic and epigenetic features of asthma3COPD overlap syndrome},\r\njournal={Pulmonologiya},\r\nyear={2017},\r\nvolume={27},\r\nnumber={1},\r\npages={7-11},\r\ndoi={10.18093/0869-0189-2017-27-1-7-11},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85046054446&doi=10.18093%2f0869-0189-2017-27-1-7-11&partnerID=40&md5=5fb14107d34e4b70da68d8ddea90e6ce},\r\naffiliation={Department of Hospital Internal Medicine, Healthcare Ministry of Russia, Academician I.P.Pavlov Federal First Saint-Petersburg State Medical University, ul. L'va Tolstogo 6 - 8, Saint-Petersburg, 197089, Russian Federation; Division of Molecular and Nanobiological Technology, Healthcare Ministry of Russia, Academician I.P.Pavlov Federal First Saint-Petersburg State Medical University, Russian Federation; Division of Thoracic Surgery, Research Institute of Surgery and Urgent Medicine, Healthcare Ministry of Russia, Academician I.P.Pavlov Federal First Saint-Petersburg State Medical University, Academician I.P.Pavlov Federal First Saint-Petersburg State Medical University, Russian Federation},\r\nabstract={Recently, investigation of asthma-COPD overlap syndrome (ACOS) is an actual topic due to difficulties in diagnosis and treatment. The aim of our study was to investigate HDAC2, PI3K-δ, GR-α, and GR-β relative expressions in order to found markers of steroid sensitivity in ACOS patients. Methods. We examined 31 ACOS patients and 32 control patients. Blood levels of HDAC2, PI3K-δ, GR-α, and GR-β mRNAs were measured by the real-time polymerase chain reaction. Results. Reduced expressions of HDAC2 and GR-α, as well as increased expressions of PI3K-δ and GR-β could result in lower steroid sensitivity and more severe ACOS course. Conclusion. Investigation of pharmacogenetic and epigenetic mecha- nisms of steroid sensitivity in patients with ACOS could predict the efficacy of steroids and personalize the choice of the targeted treatment.},\r\nauthor_keywords={Bronchial asthma;  Chronic obstructive pulmonary disease;  Epigenetics;  Overlap syndrome;  Pharmacogenetics},\r\npublisher={Medical Education},\r\nissn={08690189},\r\nlanguage={Russian},\r\nabbrev_source_title={Pulmonologiya},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2016\n \n \n (17)\n \n \n

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\n \n\n \n \n \n \n \n \n Regulation of ABCA1 and ABCG1 transporter gene expression in the intraabdominal adipose tissue.\n \n \n \n \n\n\n \n Miroshnikova, V.; Panteleeva, A.; Bazhenova, E.; Demina, E.; Usenko, T.; Nikolaev, M.; Semenova, I.; Neimark, A.; He, J.; Belyaeva, O.; Berkovich, O.; Baranova, E.; and Pchelina, S.\n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 10(4): 327-334. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Regulation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Miroshnikova2016327,\r\nauthor={Miroshnikova, V.V. and Panteleeva, A.A. and Bazhenova, E.A. and Demina, E.P. and Usenko, T.S. and Nikolaev, M.A. and Semenova, I.A. and Neimark, A.E. and He, J. and Belyaeva, O.D. and Berkovich, O.A. and Baranova, E.I. and Pchelina, S.N.},\r\ntitle={Regulation of ABCA1 and ABCG1 transporter gene expression in the intraabdominal adipose tissue},\r\njournal={Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry},\r\nyear={2016},\r\nvolume={10},\r\nnumber={4},\r\npages={327-334},\r\ndoi={10.1134/S199075081604003X},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84996562226&doi=10.1134%2fS199075081604003X&partnerID=40&md5=6b3dd567ae39cc86ce7512870773bc56},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, National Research Center “Kurchatov Institute,” Orlova Roshcha, Gatchina, 188300, Russian Federation; Pavlov First Saint Petersburg State Medical University, Saint Petersburg, Russian Federation},\r\nabstract={Tissue specific expression of genes encoding the cholesterol transporters ABCA1 and ABCG1 as well as genes encoding the most important transcriptional regulators of adipogenesis (LXRα, LXRβ, PPARγ and RORα) has been investigated in intraabdominal adipose tissue (IAT) samples from obese patients and patients without overweight. A direct correlation between the content of ABCA1 and ABCG1 proteins and the RORα protein level (r = 0.480, p < 0.05; r = 0.435, p < 0.05, respectively) suggests involvement of the transcription factor RORα in the regulation of ABCA1 and ABCG1 protein levels in IAT. ABCA1 and ABCG1 gene expression positively correlated with such obesity indicators as body mass index (BMI) (r = 0.522, p = 0.004; r = 0.594, p = 0.001, respectively) and waist circumference (r = 0.403, p = 0.033; r = 0.474, p = 0.013, respectively). The development of obesity is also associated with decreased IAT levels of RORα and LXRβ mRNA (p = 0.016 and p = 0.002, respectively). This suggest that the nuclear factor RORα can play a significant role in the regulation of cholesterol metabolism and control IAT expression of ABCA1 and ABCG1 genes, while the level of IAT LXRβ gene expression may be an important factor associated with the development of obesity. © 2016, Pleiades Publishing, Ltd.},\r\nauthor_keywords={ABCA1 and ABCG1 transporters;  gene expression;  intraabdominal adipose tissue;  transcriptional regulators},\r\ncorrespondence_address1={Miroshnikova, V.V.; Konstantinov Petersburg Nuclear Physics Institute, National Research Center “Kurchatov Institute,” Orlova RoshchaRussian Federation; email: mutantropol@mail.ru},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={19907508},\r\nlanguage={English},\r\nabbrev_source_title={Biochem. (Moscow) Suppl. Ser. B Biomed. Chem.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Dielectric properties of DNA oligonucleotides on the surface of silicon nanostructures.\n \n \n \n \n\n\n \n Bagraev, N.; Chernev, A.; Klyachkin, L.; Malyarenko, A.; Emel’yanov, A.; and Dubina, M.\n\n\n \n\n\n\n Semiconductors, 50(10): 1333-1337. 2016.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Dielectric$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Bagraev20161333,\r\nauthor={Bagraev, N.T. and Chernev, A.L. and Klyachkin, L.E. and Malyarenko, A.M. and Emel’yanov, A.K. and Dubina, M.V.},\r\ntitle={Dielectric properties of DNA oligonucleotides on the surface of silicon nanostructures},\r\njournal={Semiconductors},\r\nyear={2016},\r\nvolume={50},\r\nnumber={10},\r\npages={1333-1337},\r\ndoi={10.1134/S1063782616100079},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84990889343&doi=10.1134%2fS1063782616100079&partnerID=40&md5=45dc680dc94519022d8a8e8b50b2fcd5},\r\naffiliation={St. Petersburg Polytechnic University, St. Petersburg, 195251, Russian Federation; Ioffe Physical–Technical Institute, Russian Academy of Sciences, St. Petersburg, 194021, Russian Federation; St. Petersburg Academic University—Nanotechnology Research and Education Center, Russian Academy of Sciences, St. Petersburg, 194021, Russian Federation},\r\nabstract={Planar silicon nanostructures that are formed as a very narrow silicon quantum well confined by δ barriers heavily doped with boron are used to study the dielectric properties of DNA oligonucleotides deposited onto the surface of the nanostructures. The capacitance characteristics of the silicon nanostructures with oligonucleotides deposited onto their surface are determined by recording the local tunneling current–voltage characteristics by means of scanning tunneling microscopy. The results show the possibility of identifying the local dielectric properties of DNA oligonucleotide segments consisting of repeating G–C pairs. These properties apparently give grounds to correlate the segments with polymer molecules exhibiting the properties of multiferroics. © 2016, Pleiades Publishing, Ltd.},\r\ncorrespondence_address1={Bagraev, N.T.; St. Petersburg Polytechnic UniversityRussian Federation; email: bagraev@mail.ioffe.ru},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={10637826},\r\nlanguage={English},\r\nabbrev_source_title={Semiconductors},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Reconstruction of phylogenetic relationships in dermatomycete genus Trichophyton Malmsten 1848 based on ribosomal internal transcribed spacer region, partial 28S rRNA and beta-tubulin genes sequences.\n \n \n \n \n\n\n \n Pchelin, I.; Zlatogursky, V.; Rudneva, M.; Chilina, G.; Rezaei-Matehkolaei, A.; Lavnikevich, D.; Vasilyeva, N.; and Taraskina, A.\n\n\n \n\n\n\n Mycoses, 59(9): 566-575. 2016.\n cited By 8\n\n\n\n
\n\n\n\n \n \n $\"Reconstruction$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pchelin2016566,\r\nauthor={Pchelin, I.M. and Zlatogursky, V.V. and Rudneva, M.V. and Chilina, G.A. and Rezaei-Matehkolaei, A. and Lavnikevich, D.M. and Vasilyeva, N.V. and Taraskina, A.E.},\r\ntitle={Reconstruction of phylogenetic relationships in dermatomycete genus Trichophyton Malmsten 1848 based on ribosomal internal transcribed spacer region, partial 28S rRNA and beta-tubulin genes sequences},\r\njournal={Mycoses},\r\nyear={2016},\r\nvolume={59},\r\nnumber={9},\r\npages={566-575},\r\ndoi={10.1111/myc.12505},\r\nnote={cited By 8},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84983567910&doi=10.1111%2fmyc.12505&partnerID=40&md5=df6814e41d72496a3231348c9650bb86},\r\naffiliation={Kashkin Research Institute of Medical Mycology, I.I. Mechnikov North-Western State Medical University, St. Petersburg, Russian Federation; Department of Invertebrate Zoology, Faculty of Biology, St. Petersburg State University, St. Petersburg, Russian Federation; Health Research Institute, Infectious and Tropical Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran; Department of Medical Mycology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran},\r\nabstract={Trichophyton spp. are important causative agents of superficial mycoses. The phylogeny of the genus and accurate strain identification, based on the ribosomal ITS region sequencing, are still under development. The present work is aimed at (i) inferring the genus phylogeny from partial ITS, LSU and BT2 sequences (ii) description of ribosomal ITS region polymorphism in 15 strains of Trichophyton interdigitale. We performed DNA sequence-based species identification and phylogenetic analysis on 48 strains belonging to the genus Trichophyton. Phylogenetic relationships were inferred by maximum likelihood and Bayesian methods on concatenated ITS, LSU and BT2 sequences. Ribosomal ITS region polymorphisms were assessed directly on the alignment. By phylogenetic reconstruction, we reveal major anthropophilic and zoophilic species clusters in the genus Trichophyton. We describe several sequences of the ITS region of T. interdigitale, which do not fit in the traditional polymorphism scheme and propose emendations in this scheme for discrimination between ITS sequence types in T. interdigitale. The new polymorphism scheme will allow inclusion of a wider spectrum of isolates while retaining its explanatory power. This scheme was also found to be partially congruent with NTS typing technique. © 2016 Blackwell Verlag GmbH},\r\nauthor_keywords={28S rRNA;  beta-tubulin;  Dermatophyte;  internal transcribed spacer;  phylogeny;  Trichophyton},\r\ncorrespondence_address1={Pchelin, I.M.; Kashkin Research Institute of Medical Mycology, I.I. Mechnikov North-Western State Medical UniversityRussian Federation; email: arcella.oraia@gmail.com},\r\npublisher={Blackwell Publishing Ltd},\r\nissn={09337407},\r\ncoden={MYCSE},\r\npubmed_id={27071492},\r\nlanguage={English},\r\nabbrev_source_title={Mycoses},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Terahertz response of DNA oligonucleotides on the surface of silicon nanostructures.\n \n \n \n \n\n\n \n Bagraev, N.; Chernev, A.; Klyachkin, L.; Malyarenko, A.; Emel’yanov, A.; and Dubina, M.\n\n\n \n\n\n\n Semiconductors, 50(9): 1208-1215. 2016.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Terahertz$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Bagraev20161208,\r\nauthor={Bagraev, N.T. and Chernev, A.L. and Klyachkin, L.E. and Malyarenko, A.M. and Emel’yanov, A.K. and Dubina, M.V.},\r\ntitle={Terahertz response of DNA oligonucleotides on the surface of silicon nanostructures},\r\njournal={Semiconductors},\r\nyear={2016},\r\nvolume={50},\r\nnumber={9},\r\npages={1208-1215},\r\ndoi={10.1134/S1063782616090037},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84986236356&doi=10.1134%2fS1063782616090037&partnerID=40&md5=32804343541ca314d41778a7c72f98a8},\r\naffiliation={Peter the Great Saint-Petersburg Polytechnic University, ul. Polytekhnicheskaya 29, St. Petersburg, 195251, Russian Federation; Ioffe Physical–Technical Institute, Russian Academy of Sciences, ul. Politekhnicheskaya 26, St. Petersburg, 194021, Russian Federation; Saint Petersburg Academic University—Nanotechnology Research and Education Center, Russian Academy of Sciences, ul. Khlopina 8/3, St. Petersburg, 194021, Russian Federation},\r\nabstract={The possibility of identifying DNA oligonucleotides deposited onto the region of the edge channels of silicon nanostructures is considered. The role of various THz (terahertz) radiation harmonics of silicon nanostructures in the resonance response of oligonucleotides is analyzed. In particular, this makes it possible to compare single-stranded 100_ and 50_mer DNA oligonucleotides. A technique for the rapid identification of different oligonucleotides by measuring changes in the conductance and transverse potential difference of silicon nanostructures with microcavities, embedded in the edge channels for selecting THz radiation characteristics, is proposed. © 2016, Pleiades Publishing, Ltd.},\r\ncorrespondence_address1={Bagraev, N.T.; Peter the Great Saint-Petersburg Polytechnic University, ul. Polytekhnicheskaya 29, Russian Federation; email: bagraev@mail.ioffe.ru},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={10637826},\r\nlanguage={English},\r\nabbrev_source_title={Semiconductors},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n SNCA alleles rs356219 and rs356165 are associated with Parkinson’s disease and increased α-synuclein gene expression in CD45+ blood cells.\n \n \n \n \n\n\n \n Emelyanov, A.; Andoskin, P.; Miliukhina, I.; Timofeeva, A.; Yakimovskii, A.; Senkevich, K.; Nikolaev, M.; and Pchelina, S.\n\n\n \n\n\n\n Cell and Tissue Biology, 10(4): 277-283. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"SNCA$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Emelyanov2016277,\r\nauthor={Emelyanov, A.K. and Andoskin, P.A. and Miliukhina, I.V. and Timofeeva, A.A. and Yakimovskii, A.F. and Senkevich, K.A. and Nikolaev, M.A. and Pchelina, S.N.},\r\ntitle={SNCA alleles rs356219 and rs356165 are associated with Parkinson’s disease and increased α-synuclein gene expression in CD45+ blood cells},\r\njournal={Cell and Tissue Biology},\r\nyear={2016},\r\nvolume={10},\r\nnumber={4},\r\npages={277-283},\r\ndoi={10.1134/S1990519X16040064},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84981742485&doi=10.1134%2fS1990519X16040064&partnerID=40&md5=47a755d84d0618d65d910b0e1851abe0},\r\naffiliation={Russian Research Centre Kurchatov Institute, Konstantinov St. Petersburg Nuclear Physics Institute, Gatchina, 188300, Russian Federation; Pavlov First State Medical University of St. Petersburg, St. Petersburg, 197022, Russian Federation; St. Petersburg Academic University, Nanotechnology Research and Education Center of the Russian Academy of Sciences (Academic University), St. Petersburg, 194021, Russian Federation; Federal State Budgetary Scientific Institution Institute of Experimental Medicine, St. Petersburg, 197376, Russian Federation},\r\nabstract={Impaired metabolism of α-synuclein (SNCA) and its aggregation are key molecular events underlying Parkinson’s disease (PD). Emerging data show that there is a connection between PD and the gene locus containing the SNCA gene. Meta-analyses have demonstrated a highly significant PD connection with single nucleotide polymorphisms (SNPs) rs356165 (A/G) and rs356219 (A/G) in the SNCA gene. We conducted SNP genotyping in 260 PD patients (n = 260) and 262 healthy people (n = 262) from northwestern regions of Russia. Linkage disequilibrium was registered between rs356219 and rs356165 alleles (D' = 0.926). It was confirmed that G alleles (rs356165 and rs356219) are associated with increased risk of PD development. For the first time, we have evaluated the relationship between rs356165 and rs356219 and levels of SNCA mRNA and α-synuclein protein in CD45+ peripheral blood cells in drug-naïve PD patients (n = 43) and controls (n = 39). Both the level of mRNA SNCA gene and that of α-synuclein protein were increased in carriers of rs356219 and rs356165 compared to carriers with AA genotype in control group (in the group of healthy people) (p = 0.046 and p = 0.039, respectively). Linkage disequilibrium was shown between associated marker alleles. Our data suggest that rs356165 and rs356219 allele variants may affect the PD development by up-regulation of SNCA expression. © 2016, Pleiades Publishing, Ltd.},\r\nauthor_keywords={CD45+ cells;  gene expression;  Parkinson’s disease;  risk factors;  α-synuclein},\r\ncorrespondence_address1={Emelyanov, A.K.; Russian Research Centre Kurchatov Institute, Konstantinov St. Petersburg Nuclear Physics InstituteRussian Federation; email: sopchelina@hotmail.com},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={1990519X},\r\nlanguage={English},\r\nabbrev_source_title={Cell Tissue Biol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Metagenomic analysis of taxonomic and functional changes in gut microbiota of patients with the alcohol dependence syndrome.\n \n \n \n \n\n\n \n Dubinkina, V.; Tyakht, A.; Ilina, E.; Ischenko, D.; Kovarsky, B.; Yarygin, K.; Pavlenko, A.; Popenko, A.; Alexeev, D.; Taraskina, A.; Nasyrova, R.; Krupitski, E.; Skorodumova, L.; Larin, A.; Kostryukova, E.; and Govorun, V.\n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 10(2): 184-190. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Metagenomic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Dubinkina2016184,\r\nauthor={Dubinkina, V.B. and Tyakht, A.V. and Ilina, E.N. and Ischenko, D.S. and Kovarsky, B.A. and Yarygin, K.S. and Pavlenko, A.V. and Popenko, A.S. and Alexeev, D.G. and Taraskina, A.E. and Nasyrova, R.F. and Krupitski, E.M. and Skorodumova, L.O. and Larin, A.K. and Kostryukova, E.S. and Govorun, V.M.},\r\ntitle={Metagenomic analysis of taxonomic and functional changes in gut microbiota of patients with the alcohol dependence syndrome},\r\njournal={Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry},\r\nyear={2016},\r\nvolume={10},\r\nnumber={2},\r\npages={184-190},\r\ndoi={10.1134/S1990750816020037},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84971657661&doi=10.1134%2fS1990750816020037&partnerID=40&md5=1944c3b91289be9ee47e374d33cd24cf},\r\naffiliation={Moscow Institute of Physics and Technology (State University), Institutskii per. 9, Dolgoprudny, Moscow region, 141700, Russian Federation; Department of Molecular Biology and Genetics, Scientific Research Institute of Physico-Chemical Medicine, ul. Malaya Pirogovskaya 1a, Moscow, 119435, Russian Federation; Saint-Petersburg Bekhterev Psychoneurological Research Institute, ul. Bekhtereva 3, Saint-Petersburg, 192019, Russian Federation},\r\nabstract={The first metagenomic study of gut microbiota in patients with the alcohol dependence syndrome (ADS) has been performed in the whole-genome sequencing (“shotgun”) format. Taxonomic analysis revealed changes in the relative abundance of the predominant bacteria associated with inflammatioln (including increased levels of Ruminococcus gnavus and R. torques, and decreased levels of Faecalibacterium and Akkermansia genera). The microbiota of ADS patients was characterized by the presence of opportunistic pathogens rarely detected in metagenomes of healthy individuals from different countries. Comparative analysis of total metabolic potential revealed increased relative abundance of KEGG pathways associated with the response to oxidative stress. ADS patients also had increased levels of two specific groups of genes encoding enzymes involved in the metabolism of alcohol, as well as virulence factors. It is possible that gut microbiota of ADS patients demonstrating changes in both taxonomic and functional composition plays a role in modulating the effects of alcohol on the host body © 2016, Pleiades Publishing, Ltd.},\r\nauthor_keywords={alcohol dependence syndrome;  gut microbiota;  metabolic potential;  metagenome;  microbial alcohol metabolism;  virulence factors},\r\ncorrespondence_address1={Dubinkina, V.B.; Moscow Institute of Physics and Technology (State University), Institutskii per. 9, Russian Federation; email: dubinkina@phystech.edu},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={19907508},\r\nlanguage={English},\r\nabbrev_source_title={Biochem. (Moscow) Suppl. Ser. B Biomed. Chem.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Loss of VPS13C Function in Autosomal-Recessive Parkinsonism Causes Mitochondrial Dysfunction and Increases PINK1/Parkin-Dependent Mitophagy.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n American Journal of Human Genetics, 98(3): 500-513. 2016.\n cited By 92\n\n\n\n
\n\n\n\n \n \n $\"Loss$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Role of the ABC transporters A1 and G1, key reverse cholesterol transport proteins, in atherosclerosis.\n \n \n \n \n\n\n \n Demina, E.; Miroshnikova, V.; and Schwarzman, A.\n\n\n \n\n\n\n Molekuliarnaia biologiia, 50(2): 223-230. 2016.\n cited By 9\n\n\n\n
\n\n\n\n \n \n $\"Role$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Demina2016223,\r\nauthor={Demina, E.P. and Miroshnikova, V.V. and Schwarzman, A.L.},\r\ntitle={Role of the ABC transporters A1 and G1, key reverse cholesterol transport proteins, in atherosclerosis},\r\njournal={Molekuliarnaia biologiia},\r\nyear={2016},\r\nvolume={50},\r\nnumber={2},\r\npages={223-230},\r\ndoi={10.7868/S002689841602004X},\r\nnote={cited By 9},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84976527615&doi=10.7868%2fS002689841602004X&partnerID=40&md5=82c9e3f77722c2af728d376d5123f8d2},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Leningrad oblast, Gatchina, 188300, Russian Federation; Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Leningrad oblast, Gatchina, 188300, Russian Federation; Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Leningrad oblast, Gatchina, 188300, Russian Federation; Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Leningrad oblast, Gatchina, 188300, Russian Federation; Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Leningrad oblast, Gatchina, 188300, Russian Federation},\r\nabstract={Atherosclerosis is one of the most common causes of death worldwide. Epidemiology studies firmly established an inverse relationship between atherogenesis and distorted lipid metabolism, in particular, higher levels of total cholesterol, an accumulation of CH-laden macrophages (foam cells), and lower plasma levels of antiatherogenic high density lipoprotein (HDL). It is believed that the reverse cholesterol transport, a process that removes excess cholesterol from peripheral tissues/cells including macrophages to circulating HDL, is one of the main mechanisms responsible for anti-atherogenic properties of HDL. The key proteins of reverse cholesterol transport-ATP-binding cassette transporters A1 (ABCA1) and G1 (ABCG1)-mediate the cholesterol efflux from macrophages and prevent their transformation into foam cells. This review focuses on the role of ABC transporters A1 and G1 in the pathogenesis of atherosclerosis.},\r\nauthor_keywords={ABCA1;  ABCG1;  Atherosclerosis;  reverse cholesterol transport},\r\nissn={00268984},\r\npubmed_id={27239842},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Biol. (Mosk.)},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Role of the ABC transporters A1 and G1, key reverse cholesterol transport proteins, in atherosclerosis.\n \n \n \n \n\n\n \n Demina, E.; Miroshnikova, V.; and Schwarzman, A.\n\n\n \n\n\n\n Molecular Biology, 50(2): 193-199. 2016.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"Role$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Demina2016193,\r\nauthor={Demina, E.P. and Miroshnikova, V.V. and Schwarzman, A.L.},\r\ntitle={Role of the ABC transporters A1 and G1, key reverse cholesterol transport proteins, in atherosclerosis},\r\njournal={Molecular Biology},\r\nyear={2016},\r\nvolume={50},\r\nnumber={2},\r\npages={193-199},\r\ndoi={10.1134/S0026893316020047},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84969504837&doi=10.1134%2fS0026893316020047&partnerID=40&md5=e3f0b4691d54b1a3c6af2c014effe056},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Gatchina, Leningrad oblast  188300, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, 197022, Russian Federation},\r\nabstract={Atherosclerosis is one of the most common causes of death worldwide. Epidemiology studies firmly established an inverse relationship between atherogenesis and distorted lipid metabolism, in particular, higher levels of total cholesterol, an accumulation of CH-laden macrophages (foam cells), and lower plasma levels of antiatherogenic high density lipoprotein (HDL). It is believed that the reverse cholesterol transport, a process that removes excess cholesterol from peripheral tissues/cells including macrophages to circulating HDL, is one of the main mechanisms responsible for anti-atherogenic properties of HDL. The key proteins of reverse cholesterol transport—ATP-binding cassette transporters A1 (ABCA1) and G1 (ABCG1)—mediate the cholesterol efflux from macrophages and prevent their transformation into foam cells. This review focuses on the role of ABC transporters A1 and G1 in the pathogenesis of atherosclerosis. © 2016, Pleiades Publishing, Inc.},\r\nauthor_keywords={ABCA1;  ABCG1;  atherosclerosis;  reverse cholesterol transport},\r\ncorrespondence_address1={Demina, E.P.; Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov InstituteRussian Federation; email: citritt@gmail.com},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={00268933},\r\nlanguage={English},\r\nabbrev_source_title={Mol. Biol.},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n A Novel Nonsense Mutation in DNAJC6 Expands the Phenotype of Autosomal-Recessive Juvenile-Onset Parkinson's Disease.\n \n \n \n \n\n\n \n Elsayed, L.; Drouet, V.; Usenko, T.; Mohammed, I.; Hamed, A.; Elseed, M.; Salih, M.; Koko, M.; Mohamed, A.; Siddig, R.; Elbashir, M.; Ibrahim, M.; Durr, A.; Stevanin, G.; Lesage, S.; Ahmed, A.; and Brice, A.\n\n\n \n\n\n\n Annals of Neurology, 79(2): 335-337. 2016.\n cited By 19\n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Elsayed2016335,\r\nauthor={Elsayed, L.E.O. and Drouet, V. and Usenko, T. and Mohammed, I.N. and Hamed, A.A.A. and Elseed, M.A. and Salih, M.A.M. and Koko, M.E. and Mohamed, A.Y.O. and Siddig, R.A. and Elbashir, M.I. and Ibrahim, M.E. and Durr, A. and Stevanin, G. and Lesage, S. and Ahmed, A.E. and Brice, A.},\r\ntitle={A Novel Nonsense Mutation in DNAJC6 Expands the Phenotype of Autosomal-Recessive Juvenile-Onset Parkinson's Disease},\r\njournal={Annals of Neurology},\r\nyear={2016},\r\nvolume={79},\r\nnumber={2},\r\npages={335-337},\r\ndoi={10.1002/ana.24591},\r\nnote={cited By 19},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84958122839&doi=10.1002%2fana.24591&partnerID=40&md5=66df274c0dc0508983d766ec9176ef30},\r\naffiliation={Inserm U1127, CNRS UMR7225, Sorbonne Universités, UPMC Université Paris 06, UMR-S1127, Institut du Cerveau et de la Moelle Épinière, Paris, France; Ecole Pratique des Hautes Etudes, Pitié-Salpêtrière Hospital, ICM, Paris, France; Faculty of Medicine, University of Khartoum, Khartoum, Sudan; Division of Pediatric Neurology, Department of Pediatrics, College of Medicine, King Saud University, Riyadh, Saudi Arabia; Department of Biochemistry, Faculty of Medicine, National University, Khartoum, Sudan; Faculty of Science, University of Elneelen, Khartoum, Sudan; Department of Molecular Biology, Institute of Endemic Diseases, University of Khartoum, Khartoum, Sudan; APHP, Department of Genetics, Pitié-Salpêtrière Hospital, Paris, France},\r\npublisher={John Wiley and Sons Inc.},\r\nissn={03645134},\r\ncoden={ANNED},\r\npubmed_id={26703368},\r\nlanguage={English},\r\nabbrev_source_title={Ann. Neurol.},\r\ndocument_type={Letter},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n SNCA rs356219 AND rs356165 VARIANTS ARE ASSOCIATED WITH PARKINSON'S DISEASE AND INCREASED ALPHA-SYNUCLEIN GENE EXPRESSION IN THE CD45(+)-BLOOD CELLS.\n \n \n \n \n\n\n \n Emelyanov, A.; Andoskin, P.; Miliukhina, I.; Timofeeva, A.; Yakimovskii, A.; Senkevich, K.; Nikolaev, M.; and Pchelina, S.\n\n\n \n\n\n\n Tsitologiia, 58(2): 99-104. 2016.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"SNCA$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Emelyanov201699,\r\nauthor={Emelyanov, A.K. and Andoskin, P.A. and Miliukhina, I.V. and Timofeeva, A.A. and Yakimovskii, A.F. and Senkevich, K.A. and Nikolaev, M.A. and Pchelina, S.N.},\r\ntitle={SNCA rs356219 AND rs356165 VARIANTS ARE ASSOCIATED WITH PARKINSON'S DISEASE AND INCREASED ALPHA-SYNUCLEIN GENE EXPRESSION IN THE CD45(+)-BLOOD CELLS},\r\njournal={Tsitologiia},\r\nyear={2016},\r\nvolume={58},\r\nnumber={2},\r\npages={99-104},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84974688139&partnerID=40&md5=f3f95cf078314bd8293e24042800c491},\r\nabstract={Impaired metabolism of alpha-synuclein (SNCA) and its aggregation are now implicated in the pathogenesis of Parkinson's disease (PD). Previous studies have found association between PD and gene locus, containing the SNCA gene. Meta-analysis have shown high significant association of single nucleotide polymorphisms (SNPs) rs356165 (A/G) and rs356219 (A/G) in the SNCA gene with PD. We genotyped these SNPs in 260 PD patients and 262 controls from north-western region of Russia. Alleles "G" of rs356165 and rs356219 were associated with increased risk of PD development. Linkage disequilibrium was shown between associated marker alleles. We studied the relationship between rs356165 and rs356219 and levels of mRNA SNCA and alpha-synuclein in CD45+ peripheral blood cells in drug-naive PD patients (n = 43) and controls (n = 39). Alleles "G" of rs356165 and rs356219 were associated with increased levels of SNCA expression (p = 0.046) and high alpha-synuclein levels (p = 0.039) in controls. Our data suggest that rs356165 and rs356219 variants might influence on PD development by upregulating SNCA expression.},\r\nissn={00413771},\r\npubmed_id={27228655},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiia},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Increase in GP IIb-IIIa and P2Y12 Receptors in Activated Platelets as the Possible Indicator of de novo Protein Synthesis.\n \n \n \n \n\n\n \n Sirotkina, O.; Laskovets, A.; Andoskin, P.; Emelyanov, A.; Zabotina, A.; and Vavilova, T.\n\n\n \n\n\n\n Molekuliarnaia biologiia, 50(1): 128-135. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Increase$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina2016128,\r\nauthor={Sirotkina, O.V. and Laskovets, A.B. and Andoskin, P.A. and Emelyanov, A.K. and Zabotina, A.M. and Vavilova, T.V.},\r\ntitle={Increase in GP IIb-IIIa and P2Y12 Receptors in Activated Platelets as the Possible Indicator of de novo Protein Synthesis},\r\njournal={Molekuliarnaia biologiia},\r\nyear={2016},\r\nvolume={50},\r\nnumber={1},\r\npages={128-135},\r\ndoi={10.7868/S0026898416010183},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85055602054&doi=10.7868%2fS0026898416010183&partnerID=40&md5=ae14335457a954fa3b581caf966c26f2},\r\naffiliation={Konstantinov St. Petersburg Institute of Nuclear Physics, Kurchatov Institute Scientific Research Center, Leningrad oblast, Gatchina, 188300, Russian Federation; Almazov North-West Federal Medical Research Center, St. Petersburg, 197341, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, 197022, Russian Federation; Mechnikov North-West State Medical University, St. Petersburg, 191015, Russian Federation},\r\nabstract={Although platelets lack nuclei, they are capable of de novo protein synthesis. We speculate that key platelet receptors are involved in the regulation of this process, and the changes in their number indicate the de novo protein synthesis in platelets. The object of our study was native platelets obtained from healthy donors. Using flow cytometry and Western blot, we determined the number of GP IIb-IIIa receptors (fibrinogen receptor) and P2Y12 receptors (ADP receptor) on the surface of platelets upon their activation with ADP and collagen. To verify the approaches and techniques used, we studied IL-1β protein, which was previously shown to be synthesized de novo in activated platelets. GP IIb-IIIa receptor numbers correlate with the number of P2Y12 receptors on the cell surface (R = 0.45, p = 0.03). It was demonstrated that the platelet receptor numbers are higher on the surface of the cells with high functional activity. According to the data obtained by Western blot, upon the cell activation with ADP, the number of GP IIb-IIIa and P2Y12 receptors increases, which may serve as evidence of these proteins being synthesized in the activated platelets. It was observed that the level of P2Y12 and IL-1β was lower in the samples where GP IIb-IIIa receptor was blocked by the selective inhibitor, i.e., the Fab fragment of the antibodies that specifically recognizes the GP IIb-IIIa complex. This suggests the important role of GP IIb-IIIa receptor in the regulation of protein synthesis.},\r\nauthor_keywords={de novo protein synthesis;  flow cytometry;  in vitro platelet activation;  platelet receptor GP IIb-IIIa;  platelet receptor P2Y12;  platelets;  Western blott},\r\nissn={00268984},\r\npubmed_id={27028818},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Biol. (Mosk.)},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Increase in GP IIb-IIIa and P2Y12 receptors in activated platelets as the possible indicator of de novo protein synthesis.\n \n \n \n \n\n\n \n Sirotkina, O.; Laskovets, A.; Andoskin, P.; Emelyanov, A.; Zabotina, A.; and Vavilova, T.\n\n\n \n\n\n\n Molecular Biology, 50(1): 111-117. 2016.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Increase$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina2016111,\r\nauthor={Sirotkina, O.V. and Laskovets, A.B. and Andoskin, P.A. and Emelyanov, A.K. and Zabotina, A.M. and Vavilova, T.V.},\r\ntitle={Increase in GP IIb-IIIa and P2Y12 receptors in activated platelets as the possible indicator of de novo protein synthesis},\r\njournal={Molecular Biology},\r\nyear={2016},\r\nvolume={50},\r\nnumber={1},\r\npages={111-117},\r\ndoi={10.1134/S0026893316010180},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84961923087&doi=10.1134%2fS0026893316010180&partnerID=40&md5=bfcf8f06743688712dfe4b5723a3b8ac},\r\naffiliation={Konstantinov St. Petersburg Institute of Nuclear Physics, Kurchatov Institute Scientific Research Center, Gatchina, Leningrad oblast, 188300, Russian Federation; Almazov North-West Federal Medical Research Center, St. Petersburg, 197341, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, 197022, Russian Federation; Mechnikov North-West State Medical University, St. Petersburg, 191015, Russian Federation},\r\nabstract={Although platelets lack nuclei, they are capable of de novo protein synthesis. We speculate that key platelet receptors are involved in the regulation of this process, and the changes in their number indicate the de novo protein synthesis in platelets. The object of our study was native platelets obtained from healthy donors. Using flow cytometry and Western blot, we determined the number of GP IIb-IIIa receptors (fibrinogen receptor) and P2Y12 receptors (ADP receptor) on the surface of platelets upon their activation with ADP and collagen. To verify the approaches and techniques used, we studied IL-1β protein, which was previously shown to be synthesized de novo in activated platelets. GP IIb-IIIa receptor numbers correlate with the number of P2Y12 receptors on the cell surface (R = 0.45, p = 0.03). It was demonstrated that the platelet receptor numbers are higher on the surface of the cells with high functional activity. According to the data obtained by Western blot, upon the cell activation with ADP, the number of GP IIb-IIIa and P2Y12 receptors increases, which may serve as evidence of these proteins being synthesized in the activated platelets. It was observed that the level of P2Y12 and IL-1β was lower in the samples where GP IIb-IIIa receptor was blocked by the selective inhibitor, i.e., the Fab fragment of the antibodies that specifically recognizes the GP IIb-IIIa complex. This suggests the important role of GP IIb-IIIa receptor in the regulation of protein synthesis. © 2016, Pleiades Publishing, Inc.},\r\nauthor_keywords={de novo protein synthesis;  flow cytometry;  in vitro platelet activation;  platelet receptor GP IIb-IIIa;  platelet receptor P2Y12;  platelets;  Western blott},\r\ncorrespondence_address1={Sirotkina, O.V.; Konstantinov St. Petersburg Institute of Nuclear Physics, Kurchatov Institute Scientific Research CenterRussian Federation; email: olga_sirotkina@mail.ru},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={00268933},\r\nlanguage={English},\r\nabbrev_source_title={Mol. Biol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Mutation del 1,02kb in the CLN3 gene and extrapyramidal syndrome.\n \n \n \n \n\n\n \n Nuzhnyi, E.; Yakimovskii, A.; Timofeeva, A.; Usenko, T.; Nikolaev, M.; Emelyanov, A.; Amosov, V.; Bubnova, E.; Boukina, A.; Zakharova, E.; and Pchelina, S.\n\n\n \n\n\n\n Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova, 116(8): 50-53. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Mutation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Nuzhnyi201650,\r\nauthor={Nuzhnyi, E.P. and Yakimovskii, A.F. and Timofeeva, A.A. and Usenko, T.S. and Nikolaev, M.A. and Emelyanov, A.K. and Amosov, V.I. and Bubnova, E.V. and Boukina, A.M. and Zakharova, E.Y. and Pchelina, S.N.},\r\ntitle={Mutation del 1,02kb in the CLN3 gene and extrapyramidal syndrome},\r\njournal={Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova},\r\nyear={2016},\r\nvolume={116},\r\nnumber={8},\r\npages={50-53},\r\ndoi={10.17116/jnevro20161168150-53},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84989220463&doi=10.17116%2fjnevro20161168150-53&partnerID=40&md5=c811a8296a8f6eb547e86911773bddf5},\r\naffiliation={Pavlov First St. Petersburg State Medical University, St. Petersburg, Russian Federation; Konstantinov St. Petersburg Institute of Nuclear Physics, National Research «Kurchatov Center», St. Petersburg, Russian Federation; Medical Genetics Center, Moscow, Russian Federation},\r\nabstract={Mutations in the GBA and SMPD1 genes, which lead to the development of lysosomal storage diseases, are high risk factors for Parkinson’s disease and dementia with Lewy bodies. We screened the mutations in the GALC and CLN3 genes in patients with Parkinson’s disease and control subjects. A heterozygous CLN3 mutation (del 1.02 kb) carrier with clinical features of the unusual extrapyramidal syndrome was identified. A role of CLN3 mutations in the development of neurodegenerative disorders is discussed. © 2016, Media Sphera. All Rights Reserved.},\r\nauthor_keywords={Lysosomal storage diseases;  Neurodegeneration;  Neuronal ceroid lipofuscinosis;  Parkinson’s disease},\r\ncorrespondence_address1={Pchelina, S.N.; Pavlov First St. Petersburg State Medical UniversityRussian Federation; email: sopchelina@hotmail.com},\r\npublisher={Media Sphera},\r\nissn={19977298},\r\npubmed_id={27635612},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh. Nevrologii Psihiatrii im. S.S. Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Regulation of ABCA1 and ABCG1 gene expression in the intraabdominal adipose tissue.\n \n \n \n \n\n\n \n Miroshnikova, V.; Panteleeva, A.; Bazhenova, E.; Demina, E.; Usenko, T.; Nikolaev, M.; Semenova, I.; Neimark, A.; He, J.; Belyaeva, O.; Berkovich, O.; Baranova, E.; and Pchelina, S.\n\n\n \n\n\n\n Biomeditsinskaya Khimiya, 62(3): 283-289. 2016.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Regulation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Miroshnikova2016283,\r\nauthor={Miroshnikova, V.V. and Panteleeva, A.A. and Bazhenova, E.A. and Demina, E.P. and Usenko, T.S. and Nikolaev, M.A. and Semenova, I.A. and Neimark, A.E. and He, J. and Belyaeva, O.D. and Berkovich, O.A. and Baranova, E.I. and Pchelina, S.N.},\r\ntitle={Regulation of ABCA1 and ABCG1 gene expression in the intraabdominal adipose tissue},\r\njournal={Biomeditsinskaya Khimiya},\r\nyear={2016},\r\nvolume={62},\r\nnumber={3},\r\npages={283-289},\r\ndoi={10.18097/PBMC20166203283},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84997522653&doi=10.18097%2fPBMC20166203283&partnerID=40&md5=382b318bc8e14efb995e61db60f754e0},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, National Research Center Kurchatov Institute, Orlova Roshcha, Gatchina, 188300, Russian Federation; Pavlov First Saint Petersburg State Medical University, St.-Petersburg, Russian Federation},\r\nabstract={Tissue specific expression of genes encoding cholesterol transporters ABCA1 and ABCG1 as well as genes encoding the most important transcriptional regulators of adipogenesis - LXRa, LXRp, PPARy and RORa has been investigated in intraabdominal adipose tissue (IAT) samples. A direct correlation between the content of ABCA1 and ABCG1 proteins with RORa protein level (r=0.480, p<0.05; r=0.435, p<0.05, respectively) suggests the role of the transcription factor RORa in the regulation of IAT ABCA1 and ABCG1 protein levels. ABCA1 and ABCG1 gene expression positively correlated with obesity indicators such as body mass index (BMI) (r=0.522, p=0.004; r=0.594, p=0.001, respectively) and waist circumference (r=0.403, p=0.033; r=0.474, p=0.013, respectively). The development of obesity is associated with decreased IAT levels of RORa and LXRp mRNA (p=0.016 and p=0.002, respectively). These data suggest that the nuclear factor RORa can play a significant role in the regulation of cholesterol metabolism and control IAT expression of ABCA1 and ABCG1, while the level of IAT LXRp gene expression may be an important factor associated with the development of obesity.},\r\nauthor_keywords={ABCA1 and ABCG1 transporters;  Gene expression;  Intraabdominal adipose tissue;  Transcriptional regulators},\r\npublisher={Russian Academy of Medical Sciences},\r\nissn={23106905},\r\npubmed_id={27420620},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomeditsinskaya Khim.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Issues of medical specialists education. Foundation of institute of independent professional experts.\n \n \n \n \n\n\n \n Sirotkina, O.; Ishchuk, T.; Parmon, E.; and Shlyakhto, E.\n\n\n \n\n\n\n Russian Journal of Cardiology, 137(9): 41-45. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Issues$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina201641,\r\nauthor={Sirotkina, O.V. and Ishchuk, T.N. and Parmon, E.V. and Shlyakhto, E.V.},\r\ntitle={Issues of medical specialists education. Foundation of institute of independent professional experts},\r\njournal={Russian Journal of Cardiology},\r\nyear={2016},\r\nvolume={137},\r\nnumber={9},\r\npages={41-45},\r\ndoi={10.15829/1560-4071-2016-9-41-45},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85042370635&doi=10.15829%2f1560-4071-2016-9-41-45&partnerID=40&md5=8393c72e66bec324e4898b118396539e},\r\naffiliation={Federal Almazov North-West Medical Research Centre of the Ministry of Health, Saint Petersburg, Russian Federation},\r\nabstract={Medical care improvement in Russan Federation directly depends upon implementation to broad practice of professionally-public accreditation of professional educational programs of medical profile. Important role in the evaluation of professional education and specialists preparing, including physicians, for the labour market and professional standards, play a personality of expert participating in accreditation procedure. Under the realization of Russian Society of Cardiology project “Professional-public accreditation of educational programs as an element of medical education improvement” and with involvement of the Central expert board of Russian Unity of medical association “National medical board” in FSBI “North-Western Federal Medical Research Centre n. a. V. A. Almazov” of the Ministry of Health, experts training is go for professional-public accreditation of the programs of medical profile. © 2016, Silicea-Poligraf. All rights reserved.},\r\nauthor_keywords={Educational programs of medical profile;  Experts training;  Professional-public accreditation},\r\ncorrespondence_address1={Sirotkina, O.V.; Federal Almazov North-West Medical Research Centre of the Ministry of HealthRussian Federation; email: olga_sirotkina@mail.ru},\r\npublisher={Silicea-Poligraf},\r\nissn={15604071},\r\nlanguage={Russian},\r\nabbrev_source_title={Russ. J. Cardiol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Genome technologies in pulmonology: A role of microRNA in asthma and COPD development.\n \n \n \n \n\n\n \n Mironova, Z.; D'Yachenko, N.; Ulitina, A.; Trofimov, V.; Pchelina, S.; and Dubina, M.\n\n\n \n\n\n\n Pulmonologiya, 26(1): 5-11. 2016.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genome$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Mironova20165,\r\nauthor={Mironova, Zh.A. and D'Yachenko, N.A. and Ulitina, A.S. and Trofimov, V.I. and Pchelina, S.N. and Dubina, M.V.},\r\ntitle={Genome technologies in pulmonology: A role of microRNA in asthma and COPD development},\r\njournal={Pulmonologiya},\r\nyear={2016},\r\nvolume={26},\r\nnumber={1},\r\npages={5-11},\r\ndoi={10.18093/0869-0189-2016-26-1-5-11},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85046242372&doi=10.18093%2f0869-0189-2016-26-1-5-11&partnerID=40&md5=94dc10f1680b964748b362aa9bd83cab},\r\naffiliation={Academician I.P.Pavlov First Saint-Petersburg State Medical University, Healthcare Ministry of Russia, 6 / 8, L'va Tolstogo str, Saint-Petersburg, 197089, Russian Federation; Saint-Petersburg Federal National Research Academic University of Russian Science Academy, Ministry of Education and Science of Russia: 8 / 3, Khlopina str, Saint-Petersburg, 194021, Russian Federation},\r\nabstract={MicroRNAs (miRNAs) are small noncoding RNA molecules that affect gene expression and thus take part in the epigenetic regulation of almost all physiological and pathological processes. About 1,800 human miRNAs have been discovered to date; however, biological functions and protein tar-gets for the majority remain to be unknown. Within the respiratory system, miRNAs contribute to the lung growth and lifelong maintenance of pul-monary homeostasis. Recently, the leading role of miRNAs in pathogenesis of various pulmonary diseases has been found, including asthma, chron-ic obstructive pulmonary disease (COPD) and lung cancer. Due to a significant progress in studying interactions between genes and their products and environmental factors, a great role of epigenetic variability, which is gene expression change not related to DNA damage, but could be inherited con-sistently, became apparent. There are three levels of epigenetic regulation corresponding to three main mechanisms: genomic (DNA methylation), proteomic (histone modification) and transcriptomic (regulation through RNA, primarily miRNA). Extending our knowledge on a role of miRNAs for the respiratory system could open new therapeutic targets and diagnostic markers for respiratory diseases, particularly asthma and COPD.},\r\nauthor_keywords={Asthma;  Chronic Obstructive Pulmonary Disease;  Cigarette Smoke;  Environment;  Epigenetic regulation;  Immune Response;  Micrornas},\r\npublisher={Medical Education},\r\nissn={08690189},\r\nlanguage={Russian},\r\nabbrev_source_title={Pulmonologiya},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2015\n \n \n (14)\n \n \n

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\n \n\n \n \n \n \n \n \n The Key Proteins of Dopaminergic Neurotransmission of Human Peripheral Blood Lymphocytes: Changed mRNA Level in Alcohol Dependence Syndrome.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 160(2): 271-274. 2015.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Specifics of lipid metabolism and atorvastatin efficacy in type 2 diabetes with carriage of various polymorphisms of cholesterol ether carrying protein TaqIB gene.\n \n \n \n \n\n\n \n Kim, M.; Skoryukova, S.; Bystrova, A.; Baranova, E.; Pchelina, S.; and Shlyakhto, E.\n\n\n \n\n\n\n Russian Journal of Cardiology, 126(10): 24-29. 2015.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Specifics$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Kim201524,\r\nauthor={Kim, M.V. and Skoryukova, S.A. and Bystrova, A.A. and Baranova, E.I. and Pchelina, S.N. and Shlyakhto, E.V.},\r\ntitle={Specifics of lipid metabolism and atorvastatin efficacy in type 2 diabetes with carriage of various polymorphisms of cholesterol ether carrying protein TaqIB gene},\r\njournal={Russian Journal of Cardiology},\r\nyear={2015},\r\nvolume={126},\r\nnumber={10},\r\npages={24-29},\r\ndoi={10.15829/1560-4071-2015-10-24-29},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84973606570&doi=10.15829%2f1560-4071-2015-10-24-29&partnerID=40&md5=80369ab8f95f0cff896d97bd3cf36507},\r\naffiliation={SBEI HPE First Saint-Petersburg State Medical University n. a. Pavlov I. P. of the Healthcare Ministry, Saint-Petersburg, Russian Federation; FSBI North-Western Federal Medical Research Center of the Healthcare Ministry, Saint-Petersburg, Russian Federation},\r\nabstract={Aim. To assess the specifics of lipid metabolism and efficacy of atorvastatin therapy in Saint-Petersburg citizens, having 2 type diabetes (DM2) — the carriers of various TaqIB gene polymorphisms, the cholesterol ethers transporting protein (CETP). Material and methods. Totally 382 patients studied, with DM2, native for statins, and 187 almost healthy individuals. All participants underwent blood sampling with lipids test and molecular-genetic testing. Into atorvastatin group we included 164 patients with DM2 and dyslipidemia. Lipid profile parameters were assessed at baseline and in 3 months of atorvastatin therapy. Results. In almost healthy individuals the carriage of B1B2 genotype of TaqIB polymorphism of CETP gene is associated with higher levels of triglycerides, low density lipoproteides cholesterol, very low density cholesterol and atherogenity coefficient, comparing to these values in B2B2 carriers. DM2 patients had higher triglycerides level if B1B1 comparing to B2B2. In DM2 type, triglycerides level also was higher in B1B1 than in B2B2 (p=0,044), other lipid spectrum parameters did not differ between two groups. While comparing the efficacy of atorvastatin therapy in various genotypes carriers of TaqIB polymorphism gene CETP, there were no differences of the studied parameters within treatment. While evaluating the target levels reach of lipid spectrum on the atrovastatin therapy it was found, that only B1B1 carriers reached target triglycerides level (p=0,017). Conclusion. In DM2 patients the arrangement of genotypes and alleles of TaqIB polymorphism of CETP gene did not differ of this in healthy individuals, in carriers of different genotypes of this gene lipidogram parameters at baseline and on treatment by atorvastatin for 3 months did not differ, in B1B1 carriers the levels of triglycerides reached target values on atorvastatin. © 2015, Silicea-Poligraf. All rights reserved.},\r\nauthor_keywords={Atorvastatin;  Cholesterol ether transfer protein gene;  Diabetes mellitus;  Dyslipidemia},\r\ncorrespondence_address1={Kim, M.V.; SBEI HPE First Saint-Petersburg State Medical University n. a. Pavlov I. P. of the Healthcare MinistryRussian Federation; email: marykim86@mail.ru},\r\npublisher={Silicea-Poligraf},\r\nissn={15604071},\r\nlanguage={Russian},\r\nabbrev_source_title={Russ. J. Cardiol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Expression of human amyloid precursor protein in Drosophila melanogaster nerve cells causes a decrease in presynaptic gene mRNA levels.\n \n \n \n \n\n\n \n Rodin, D.; Schwarzman, A.; and Sarantseva, S.\n\n\n \n\n\n\n Genetics and Molecular Research, 14(3): 9225-9232. 2015.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Expression$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Rodin20159225,\r\nauthor={Rodin, D.I. and Schwarzman, A.L. and Sarantseva, S.V.},\r\ntitle={Expression of human amyloid precursor protein in Drosophila melanogaster nerve cells causes a decrease in presynaptic gene mRNA levels},\r\njournal={Genetics and Molecular Research},\r\nyear={2015},\r\nvolume={14},\r\nnumber={3},\r\npages={9225-9232},\r\ndoi={10.4238/2015.August.10.2},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84939159597&doi=10.4238%2f2015.August.10.2&partnerID=40&md5=20620a489bff9a4f4919f73e30a9b10d},\r\naffiliation={Molecular and Radiation Biophysics Division, National Research Centre ‘Kurchatov Institute’ B.P. Konstantinov Petersburg Nuclear Physics Institute, Gatchina, Russian Federation; Molecular Genetics Department, Institute of Experimental Medicine of The North-West Branch of the Russian Academy of Medical Sciences, Saint-Petersburg, Russian Federation},\r\nabstract={Amyloid precursor protein (APP) is a key player in Alzheimer’s disease. The proteolytic cleavage of APP results in various short peptide fragments including the toxic amyloid-beta peptide, which is a main component of senile plaques. However, the functions of APP and its processed fragments are not yet well understood. Here, using real-time polymerase chain reaction, we demonstrate that exogenous expression of APP, its mutant form APP-Swedish, or two truncated forms in Drosophila melanogaster causes a significant (P ≤ 0.05) drop in the mRNA levels of the presynaptic proteins synaptotagmin-1 and neuronal synaptobrevin. The results obtained from this study suggest a potential role of APP or its fragments in the regulation of synaptic gene transcription. © FUNPEC-RP.},\r\nauthor_keywords={Alzheimer’s disease;  Amyloid precursor protein;  Drosophila;  Synaptic protein},\r\ncorrespondence_address1={Rodin, D.I.; Molecular and Radiation Biophysics Division, National Research Centre ‘Kurchatov Institute’ B.P. Konstantinov Petersburg Nuclear Physics InstituteRussian Federation; email: rodin.dmitry@icloud.com},\r\npublisher={Fundacao de Pesquisas Cientificas de Ribeirao Preto},\r\nissn={16765680},\r\npubmed_id={26345855},\r\nlanguage={English},\r\nabbrev_source_title={Genet. Mol. Res.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n DNA detection by THz pumping.\n \n \n \n \n\n\n \n Chernev, A.; Bagraev, N.; Klyachkin, L.; Emelyanov, A.; and Dubina, M.\n\n\n \n\n\n\n Semiconductors, 49(7): 944-948. 2015.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"DNA$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Chernev2015944,\r\nauthor={Chernev, A.L. and Bagraev, N.T. and Klyachkin, L.E. and Emelyanov, A.K. and Dubina, M.V.},\r\ntitle={DNA detection by THz pumping},\r\njournal={Semiconductors},\r\nyear={2015},\r\nvolume={49},\r\nnumber={7},\r\npages={944-948},\r\ndoi={10.1134/S1063782615070064},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84937405681&doi=10.1134%2fS1063782615070064&partnerID=40&md5=dc20e76df9c2f9be4fa06bb6a7fa1084},\r\naffiliation={St. Petersburg Academic University—Nanotechnology Research and Education Centre, Russian Academy of Sciences, St. Petersburg, 194021, Russian Federation; Ioffe Physicotechnical Institute, Russian Academy of Sciences, St. Petersburg, 194021, Russian Federation},\r\nabstract={DNA semiconductor detection and sequencing is considered to be the most promising approach for future discoveries in genome and proteome research which is dramatically dependent on the challenges faced by semiconductor nanotechnologies. DNA pH-sensing with ion-sensitive field effect transistor (ISFET) is well-known to be a successfully applied electronic platform for genetic research. However this method lacks fundamentally in chemical specificity. Here we develop the first ever silicon nanosandwich pump device, which provides both the excitation of DNA fragments’ self-resonant modes and the feedback for current-voltage measurements at room temperature. This device allows direct detection of singlestranded label-free oligonucleotides by measuring their THz frequency response in aqueous solution. These results provide a new insight into the nanobioelectronics for the future real-time technologies of direct gene observations. © 2015, Pleiades Publishing, Ltd.},\r\nfunding_details={Russian Foundation for Basic Research13-0012055 ofi-m},\r\ncorrespondence_address1={Chernev, A.L.; St. Petersburg Academic University—Nanotechnology Research and Education Centre, Russian Academy of SciencesRussian Federation},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={10637826},\r\nlanguage={English},\r\nabbrev_source_title={Semiconductors},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Reduction of the level of LXRβ mRNA and PPARγ mRNA in macrophages stimulated with a macrophage colony-stimulating factor in patients with atherosclerosis.\n \n \n \n \n\n\n \n Demina, Y.; Miroshnikova, V.; Mayorov, N.; Davydenko, V.; and Schvartzman, A.\n\n\n \n\n\n\n Russian Journal of Genetics: Applied Research, 5(2): 155-158. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Reduction$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Demina2015155,\r\nauthor={Demina, Y.P. and Miroshnikova, V.V. and Mayorov, N.V. and Davydenko, V.V. and Schvartzman, A.L.},\r\ntitle={Reduction of the level of LXRβ mRNA and PPARγ mRNA in macrophages stimulated with a macrophage colony-stimulating factor in patients with atherosclerosis},\r\njournal={Russian Journal of Genetics: Applied Research},\r\nyear={2015},\r\nvolume={5},\r\nnumber={2},\r\npages={155-158},\r\ndoi={10.1134/S2079059715020021},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84928600296&doi=10.1134%2fS2079059715020021&partnerID=40&md5=624d9bb7a8479da15fb164ec4fa72f91},\r\naffiliation={Petersburg Nuclear Physics Institute, Gatchina, 188300, Russian Federation; First Pavlov State Medical University, St. Petersburg, 197089, Russian Federation; Institute of Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg, 197376, Russian Federation},\r\nabstract={Nuclear receptors LXRα/β and PPARγ play an important role in the regulation of lipid metabolism and reverse cholesterol transport. However, the effect of the expression of LXRα/β and PPARγ genes in macrophages on the development of atherosclerosis remains poorly studied. We determined the levels of LXRα mRNA, LXRβ mRNA, and PPARγ mRNA by a real-time polymerase chain reaction in macrophages cultivated for 5 days with macrophage colony-stimulating factor (M-CSF). The levels of LXRβ mRNA and PPARγ mRNA were lower in patients with coronary artery stenosis than in the control group, p < 0.001. The groups did not differ in the content of LXRα mRNA (p = 0.17). We suggest that the level of expression of LXRβ and PPARγ genes in macrophages may be a significant factor associated with the development of atherosclerosis. © 2015, Pleiades Publishing, Ltd.},\r\nauthor_keywords={atherosclerosis;  coronary artery stenosis;  LXRα/β genes;  macrophages;  PPARγ gene},\r\ncorrespondence_address1={Demina, Y.P.; Petersburg Nuclear Physics InstituteRussian Federation},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={20790597},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Genet. Appl. Res.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Plasma Oligomeric Alpha-Synuclein Is Associated With Glucocerebrosidase Activity in Gaucher Disease.\n \n \n \n \n\n\n \n Nuzhnyi, E.; Emelyanov, A.; Boukina, T.; Usenko, T.; Yakimovskii, A.; Zakharova, E.; and Pchelina, S.\n\n\n \n\n\n\n Movement Disorders, 30(7): 989-991. 2015.\n cited By 12\n\n\n\n
\n\n\n\n \n \n $\"Plasma$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Nuzhnyi2015989,\r\nauthor={Nuzhnyi, E. and Emelyanov, A. and Boukina, T. and Usenko, T. and Yakimovskii, A. and Zakharova, E. and Pchelina, S.},\r\ntitle={Plasma Oligomeric Alpha-Synuclein Is Associated With Glucocerebrosidase Activity in Gaucher Disease},\r\njournal={Movement Disorders},\r\nyear={2015},\r\nvolume={30},\r\nnumber={7},\r\npages={989-991},\r\ndoi={10.1002/mds.26200},\r\nnote={cited By 12},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84931956998&doi=10.1002%2fmds.26200&partnerID=40&md5=0ebbc550df16f2fa1a82a7914d064fd3},\r\naffiliation={First Pavlov's State Medical University of Saint-Petersburg, St. Petersburg, Russian Federation; Petersburg Nuclear Physics Institute, St. Petersburg, Russian Federation; Medical-genetics Scientific Center, Moscow, Russian Federation; St. Petersburg Academic University-Nanothecnology Research and Education Centre, RAS, St. Petersburg, Russian Federation},\r\nabstract={Background: The link between Parkinson's disease (PD) and Gaucher disease (GD), the most common lysosomal storage disease associated with loss of glucocerebrosidase (GBA) activity, can be explained by abnormal accumulation of oligomeric alpha-synuclein (α-Syn) species resulting from mutations in the GBA gene. However, in GD, the relationship between GBA activity and α-Syn accumulation in biological fluids has not been investigated. Methods: We analyzed plasma oligomeric α-Syn levels, leucocyte GBA activity, and plasma chitotriosidase activity in 21 patients with GD. Results: Negative correlation between plasma oligomeric α-Syn levels, and leucocyte GBA activity was observed in patients with GD (R2=0.487; P<0.001). Conclusion: The decrease in GBA activity may influence α-Syn oligomerization, explaining the high risk of PD development in GD patients. © 2015 International Parkinson and Movement Disorder Society.},\r\nauthor_keywords={Alpha-synuclein;  Gaucher disease;  Glucocerebrosidase;  Oligomerization;  Parkinson's disease},\r\ncorrespondence_address1={Pchelina, S.; St. Petersburg Nuclear Physics Institute, Human Molecular Genetics, Leningrad area, Russian Federation},\r\npublisher={John Wiley and Sons Inc.},\r\nissn={08853185},\r\ncoden={MOVDE},\r\npubmed_id={25962734},\r\nlanguage={English},\r\nabbrev_source_title={Mov. Disord.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

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\n \n\n \n \n \n \n \n \n Dopamine neurotransmission of peripheral blood lymphocytes is a potential biomarker of psychiatric and neurological disorders.\n \n \n \n \n\n\n \n Taraskina, A.; Nasyrova, R.; Grunina, M.; Zabotina, A.; Ivashchenko, D.; Ershov, E.; Sosin, D.; Kirnichnaya, K.; Ivanov, M.; and Krupitsky, E.\n\n\n \n\n\n\n Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova, 2015(9): 65-69. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Dopamine$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Taraskina201565,\r\nauthor={Taraskina, A.E. and Nasyrova, R.F. and Grunina, M.N. and Zabotina, A.M. and Ivashchenko, D.V. and Ershov, E.E. and Sosin, D.N. and Kirnichnaya, K.A. and Ivanov, M.V. and Krupitsky, E.M.},\r\ntitle={Dopamine neurotransmission of peripheral blood lymphocytes is a potential biomarker of psychiatric and neurological disorders},\r\njournal={Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova},\r\nyear={2015},\r\nvolume={2015},\r\nnumber={9},\r\npages={65-69},\r\ndoi={10.17116/jnevro20151159165-69},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84955734585&doi=10.17116%2fjnevro20151159165-69&partnerID=40&md5=080bbc0af73895c028def897cb95c666},\r\naffiliation={Bekhterev St. Petersburg Psychoneurological Research Institute, St. Petersburg, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, Russian Federation; Konstantinov Petersburg Nuclear Physics Institute, National Research Centre »Kurchatov Institutes, St. Petersburg, Russian Federation; Kashchenko St. Petersburg City Psychiatric Hospital №1, St. Petersburg, Russian Federation; Mechnikov North-Western State Medical University, St. Petersburg, Russian Federation},\r\nabstract={Current literature on a role of dopamine in the development of mental and neurological disorders suggests that the discovery of endogenous dopamine in peripheral blood lymphocytes gave rise to a new line of research. Dopamine receptors are not only found on cells of the innate immune response (nonspecific), but also on cells of adaptive immune response (specific): T and B lymphocytes. These facts bring a new evidence of interrelationships between the peripheral immune system, neuroinflammation and neurodegeneration and suggest new ways for investigation of the pathogenesis of different mental and neurological disorders, in particular Parkinson's disease, Alzheimer's disease and schizophrenia. There is strong evidence that ligands of dopamine receptors can change the expression of coding genes both in central neurons and in peripheral cells. Thus, peripheral blood lymphocytes may prove a cellular tool to identify dopamine transmission disturbances in neuropsychiatric diseases, as well as to monitor the effects of pharmacological treatment. © 2015, Media Sphera. All rights reserved.},\r\nauthor_keywords={Dopamine;  Dopamine receptors;  Neuropsychiatric disorders;  Peripheral blood lymphocytes},\r\npublisher={Media Sphera},\r\nissn={19977298},\r\npubmed_id={26569007},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh. Nevrologii Psihiatrii im. S.S. Korsakova},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n

\n \n\n \n \n \n \n \n \n Pharmacogenetic-based risk assessment of antipsychotic-induced extrapyramidal symptoms.\n \n \n \n \n\n\n \n Kirnichnaya, K.; Sosin, D.; Ivanov, M.; Mikhaylov, V.; Ivashchenko, D.; Ershov, E.; Taraskina, A.; Nasyrova, R.; and Krupitsky, E.\n\n\n \n\n\n\n Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova, 2015(4): 113-125. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Pharmacogenetic-based$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Kirnichnaya2015113,\r\nauthor={Kirnichnaya, K.A. and Sosin, D.N. and Ivanov, M.V. and Mikhaylov, V.A. and Ivashchenko, D.V. and Ershov, E.E. and Taraskina, A.E. and Nasyrova, R.F. and Krupitsky, E.M.},\r\ntitle={Pharmacogenetic-based risk assessment of antipsychotic-induced extrapyramidal symptoms},\r\njournal={Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova},\r\nyear={2015},\r\nvolume={2015},\r\nnumber={4},\r\npages={113-125},\r\ndoi={10.17116/jnevro201511541113-125},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84962016539&doi=10.17116%2fjnevro201511541113-125&partnerID=40&md5=0328955e6d7e130763c4b2894b28ad6c},\r\naffiliation={Bekhterev St. Petersburg Psychoneurological Research Institute, St. Petersburg, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, Russian Federation; Kashchenko St. Petersburg City Psychiatric Hospital No1, St. Petersburg, Russian Federation},\r\nabstract={«Typical» antipsychotics remain the wide-prescribed drugs in modern psychiatry. But these drugs are associated with development of extrapyramidal symptoms (EPS). Preventive methods of EPS are actively developed and they concentrate on personalized approach. The method of taking into account genetic characteristics of patient for prescribing of treatment was proven as effective in cardiology, oncology, HIV-medicine. In this review the modern state of pharmacogenetic research of antipsychotic-induced EPS are considered. There are pharmacokinetic and pharmacodynamic factors which impact on adverse effects. Pharmacokinetic factors are the most well-studied to date, these include genetic polymorphisms of genes of cytochrome P450. However, evidence base while does not allow to do the significant prognosis of development of EPS based on genetic testing of CYP2D6 and CYP1A2 polymorphisms. Genes of pharmacodynamics factors, which realize the EPS during antipsychotic treatment, are the wide field for research. In separate part of review research of such systems as dopaminergic, serotonergic, adrenergic, glutamatergic, GABAergic, BDNF were analyzed. The role of oxidative stress factors in the pathogenesis of antipsychotic-induced EPS was enough detailed considered. The system of those factors may be used for personalized risk assessment of antipsychotics’ safety in the future. Although there were numerous studies, the pharmacogenetic-based prevention of EPS before prescribing of antipsychotics was not introduced. However, it is possible to distinguish the most perspectives markers for further research. Furthermore, brief review of new candidate genes provides here, but only preliminary results were published. The main problem of the field is the lack of highquality studies. Moreover, the several results were not replicated in repeat studies. The pharmacogenetic-based research must be standardized by ethnicity of patients. But there is the ethnical misbalance in world literature. These facts explain why the introduction of pharmacogenetic testing for risk assessment of antipsychotic-induced EPS is so difficult to achieve. © 2015, Media Sphera. All rights reserved.},\r\nauthor_keywords={Adverse effects;  Antipsychotics;  Extrapyramidal symptoms;  Pharmacogenetics;  Pharmacogenomics;  Risk assessment},\r\npublisher={Media Sphera Publishing Group},\r\nissn={19977298},\r\npubmed_id={26322366},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh. Nevrologii Psihiatrii im. S.S. Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n

\n «Typical» antipsychotics remain the wide-prescribed drugs in modern psychiatry. But these drugs are associated with development of extrapyramidal symptoms (EPS). Preventive methods of EPS are actively developed and they concentrate on personalized approach. The method of taking into account genetic characteristics of patient for prescribing of treatment was proven as effective in cardiology, oncology, HIV-medicine. In this review the modern state of pharmacogenetic research of antipsychotic-induced EPS are considered. There are pharmacokinetic and pharmacodynamic factors which impact on adverse effects. Pharmacokinetic factors are the most well-studied to date, these include genetic polymorphisms of genes of cytochrome P450. However, evidence base while does not allow to do the significant prognosis of development of EPS based on genetic testing of CYP2D6 and CYP1A2 polymorphisms. Genes of pharmacodynamics factors, which realize the EPS during antipsychotic treatment, are the wide field for research. In separate part of review research of such systems as dopaminergic, serotonergic, adrenergic, glutamatergic, GABAergic, BDNF were analyzed. The role of oxidative stress factors in the pathogenesis of antipsychotic-induced EPS was enough detailed considered. The system of those factors may be used for personalized risk assessment of antipsychotics’ safety in the future. Although there were numerous studies, the pharmacogenetic-based prevention of EPS before prescribing of antipsychotics was not introduced. However, it is possible to distinguish the most perspectives markers for further research. Furthermore, brief review of new candidate genes provides here, but only preliminary results were published. The main problem of the field is the lack of highquality studies. Moreover, the several results were not replicated in repeat studies. The pharmacogenetic-based research must be standardized by ethnicity of patients. But there is the ethnical misbalance in world literature. These facts explain why the introduction of pharmacogenetic testing for risk assessment of antipsychotic-induced EPS is so difficult to achieve. © 2015, Media Sphera. All rights reserved.\n

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\n \n\n \n \n \n \n \n \n Complete genome sequence of an enterotoxigenic Bacteroides fragilis clinical isolate.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Genome Announcements, 3(3). 2015.\n cited By 8\n\n\n\n
\n\n\n\n \n \n $\"Complete$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Specific features of the enteric microbiota composition in patients with alcoholic liver cirrhosis.\n \n \n \n \n\n\n \n Shalikiani, N.; Bakulin, I.; Dubinkina, V.; Ishchenko, D.; Alexeev, D.; Tyakht, A.; Pavlenko, A.; Ilyina, E.; Kostryukova, E.; Taraskina, A.; Skorodumova, L.; Maev, I.; and Govorun, V.\n\n\n \n\n\n\n Terapevticheskii Arkhiv, 87(12): 59-65. 2015.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Specific$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Shalikiani201559,\r\nauthor={Shalikiani, N.V. and Bakulin, I.G. and Dubinkina, V.B. and Ishchenko, D.S. and Alexeev, D.G. and Tyakht, A.V. and Pavlenko, A.V. and Ilyina, E.N. and Kostryukova, E.S. and Taraskina, A.E. and Skorodumova, L.O. and Maev, I.V. and Govorun, V.M.},\r\ntitle={Specific features of the enteric microbiota composition in patients with alcoholic liver cirrhosis},\r\njournal={Terapevticheskii Arkhiv},\r\nyear={2015},\r\nvolume={87},\r\nnumber={12},\r\npages={59-65},\r\ndoi={10.17116/terarkh2015871259-65},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84974623247&doi=10.17116%2fterarkh2015871259-65&partnerID=40&md5=5c3ac5c96c56973ff9e898f45a773143},\r\naffiliation={Moscow Clinical Research and Practical Center, Moscow Healthcare Department, Moscow, Russian Federation; Moscow Institute of Physics and Technology, Dolgoprudnyi, Russian Federation; Research Institute of Physicochemical Medicine, Federal Biomedical Agency of Russia, Moscow, Russian Federation; Kazan (Volga) Federal University, Kazan, Russian Federation; A.I. Evdokimov Moscow State University of Medicine and Dentistry, Ministry of Health of Russia, Moscow, Russian Federation},\r\nabstract={Aim. To establish the specific features of the taxonomic and functional composition of the enteric microbiota in patients with alcoholic liver cirrhosis (LC). Subjects and methods. Metagenomic analysis was used to study the taxonomic composition and functional potential of the enteric microbiota in 20 patients with alcoholic LC. Total DNA was isolated from the patients' fecal samples; thereafter full genome sequencing was carried out. The metagenomic analysis yielded the results of the relative taxonomic and functional abundance of microbial species in the test samples. These were comparatively analyzed with the previously published metagenomic datasets of healthy population cohorts in the Russian Federation, as well as in Denmark, China, and the USA. Results. In the majority of patients, the dominant part of the intestinal community represented bacterial species constituting the normal human intestinal flora. At the same time, abnormal gut microbiota composition, which was suggestive of marked dysbacteriosis, was identified in a number of patients. In addition, pooled analysis of the data could identify a number of species with a statistically significantly increase and decrease in the relative abundance as compared to the control groups. Thus, the enteric microbiota of the patients with alcoholic LC showed a high proportion of bacteria characteristic of the oral cavity. Analysis of the pooled metabolic potential of the microbiota in these patients demonstrated the higher abundance of enzyme genes involved in alcohol metabolism. Conclusion. In the patients with alcoholic LC, the microbiota composition changes identified in individual bacterial species may be associated with gastrointestinal comorbidities, such as chronic erosive gastritis, chronic pancreatitis, and gastric ulcer. The alterations occurring in alcoholic cirrhosis promote the penetration and generation of oral cavity-specific microorganisms in the human intestine. This may a potential biomarker for the diagnosis of liver diseases. The bacterial enzyme genes involved in alcohol metabolism have an increased abundance in patients with alcoholic LC and healthy volunteers from the Russian Federation.},\r\nauthor_keywords={Alcoholic cirrhosis;  Enteric microbiota;  Intestinal microbial community;  Metagenome;  Microbiome},\r\ncorrespondence_address1={Shalikiani, N.V.; Moscow Clinical Research and Practical Center, Moscow Healthcare DepartmentRussian Federation; email: nino_shalikiani@yahoo.com},\r\npublisher={Media Sphera},\r\nissn={00403660},\r\ncoden={TEARA},\r\npubmed_id={26978420},\r\nlanguage={Russian},\r\nabbrev_source_title={Ter. Arkh.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n

\n Aim. To establish the specific features of the taxonomic and functional composition of the enteric microbiota in patients with alcoholic liver cirrhosis (LC). Subjects and methods. Metagenomic analysis was used to study the taxonomic composition and functional potential of the enteric microbiota in 20 patients with alcoholic LC. Total DNA was isolated from the patients' fecal samples; thereafter full genome sequencing was carried out. The metagenomic analysis yielded the results of the relative taxonomic and functional abundance of microbial species in the test samples. These were comparatively analyzed with the previously published metagenomic datasets of healthy population cohorts in the Russian Federation, as well as in Denmark, China, and the USA. Results. In the majority of patients, the dominant part of the intestinal community represented bacterial species constituting the normal human intestinal flora. At the same time, abnormal gut microbiota composition, which was suggestive of marked dysbacteriosis, was identified in a number of patients. In addition, pooled analysis of the data could identify a number of species with a statistically significantly increase and decrease in the relative abundance as compared to the control groups. Thus, the enteric microbiota of the patients with alcoholic LC showed a high proportion of bacteria characteristic of the oral cavity. Analysis of the pooled metabolic potential of the microbiota in these patients demonstrated the higher abundance of enzyme genes involved in alcohol metabolism. Conclusion. In the patients with alcoholic LC, the microbiota composition changes identified in individual bacterial species may be associated with gastrointestinal comorbidities, such as chronic erosive gastritis, chronic pancreatitis, and gastric ulcer. The alterations occurring in alcoholic cirrhosis promote the penetration and generation of oral cavity-specific microorganisms in the human intestine. This may a potential biomarker for the diagnosis of liver diseases. The bacterial enzyme genes involved in alcohol metabolism have an increased abundance in patients with alcoholic LC and healthy volunteers from the Russian Federation.\n

\n\n\n

\n \n\n \n \n \n \n \n \n Metagenomic analysis of taxonomic and functional changes in gut microbiota of patients with alcoholic dependence syndrome.\n \n \n \n \n\n\n \n Dubinkina, V.; Tyakht, A.; Ilina, E.; Ischenko, D.; Kovarsky, B.; Yarygin, K.; Pavlenko, A.; Popenko, A.; Alexeev, D.; Taraskina, A.; Nasyrova, R.; Krupitski, E.; Skorodumova, L.; Larin, A.; Kostryukova, E.; and Govorun, V.\n\n\n \n\n\n\n Biomeditsinskaya Khimiya, 61(6): 742-749. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Metagenomic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Dubinkina2015742,\r\nauthor={Dubinkina, V.B. and Tyakht, A.V. and Ilina, E.N. and Ischenko, D.S. and Kovarsky, B.A. and Yarygin, K.S. and Pavlenko, A.V. and Popenko, A.S. and Alexeev, D.G. and Taraskina, A.E. and Nasyrova, R.F. and Krupitski, E.M. and Skorodumova, L.O. and Larin, A.K. and Kostryukova, E.S. and Govorun, V.M.},\r\ntitle={Metagenomic analysis of taxonomic and functional changes in gut microbiota of patients with alcoholic dependence syndrome},\r\njournal={Biomeditsinskaya Khimiya},\r\nyear={2015},\r\nvolume={61},\r\nnumber={6},\r\npages={742-749},\r\ndoi={10.18097/PBMC20156106742},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84965185519&doi=10.18097%2fPBMC20156106742&partnerID=40&md5=f70a0e102fe446d91e1d6b081f401024},\r\naffiliation={Moscow Institute of Physics and Technology, State University, 9 Institutskii Per., Moscow Region, Dolgoprudny, 141700, Russian Federation; Scientific Research Institute of Physico-Chemical Medicine, Department of Molecular Biology and Genetics, 1a Malaya Pirogovskaya str., Moscow, 119435, Russian Federation; Saint-Petersburg Bekhterev Psychoneurological Research Institute, 3 Bekhterev str., Saint-Petersburg, 192019, Russian Federation},\r\nabstract={Here we present the first metagenomic study of gut microbiota in patients with alcohol dependence syndrome (ADS) performed in the whole-genome ("shotgun") format. Taxonomic analysis highlighted changes in community "drivers" abundance previously associated with inflammatory processes (including increase in Ruminococcus gnavus and torques, as well as decrease in Faecalibacterium and Akkermansia). Microbiota of alcoholics manifested presence of specific opportunistic pathogens rarely detected in healthy control subjects of the world. Differential analysis of metabolic potential basing on changes in KEGG Orthology groups abundance revealed increase in pathways associated with response to oxidative stress. Analysis of two specific gene groups - alcohol metabolism and virulence factors - also showed increase in comparison with the control groups. We suggest that gut microbiota distinct in alcoholics by both taxonomic and functional composition plays role in modulating the effect of alcohol on host organism.},\r\nauthor_keywords={Alcohol dependence syndrome;  Gut microbiota;  Metabolic potential;  Metagenome;  Microbial alcohol metabolism;  Virulence factors},\r\npublisher={Russian Academy of Medical Sciences},\r\nissn={23106905},\r\npubmed_id={26716747},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomeditsinskaya Khim.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The molecular mechanisms of platelets activation in patients with cerebrovascular disease.\n \n \n \n \n\n\n \n Sirotkina, O.; Laskovets, A.; Goldobin, V.; Topanova, A.; Karelov, D.; and Vavilova, T.\n\n\n \n\n\n\n Biomeditsinskaya Khimiya, 61(5): 606-612. 2015.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina2015606,\r\nauthor={Sirotkina, O.V. and Laskovets, A.B. and Goldobin, V.V. and Topanova, A.A. and Karelov, D.V. and Vavilova, T.V.},\r\ntitle={The molecular mechanisms of platelets activation in patients with cerebrovascular disease},\r\njournal={Biomeditsinskaya Khimiya},\r\nyear={2015},\r\nvolume={61},\r\nnumber={5},\r\npages={606-612},\r\ndoi={10.18097/PBMC20156105606},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84983142929&doi=10.18097%2fPBMC20156105606&partnerID=40&md5=e680a36af4e9f594592ec51a9537f367},\r\naffiliation={National Research Centre Kurchatov Institute, B.P. Konstantinov Petersburg Nuclear Physics Institute, Orlova Roshcha str. Leningrad District, Gatchina, 188300, Russian Federation; Federal Almazov North-West Medical Research Centre, 2 Akkuratova str, St.-Petersburg, 197341, Russian Federation; Mechnikov North-Western State Medical University, 41, Kirochnaya str., St.-Petersburg, 191015, Russian Federation; St. Petersburg State Polytechnical University, 29 Politehnicheskaya str., St.-Petersburg, 195251, Russian Federation},\r\nabstract={Cerebrovascular disease is a main cause of mortality and one of the big medical problems. After the vascular wall's damage the endothelial cells secrete the von Willebrand factor which then connects with its platelet's receptor GP Ib-V-IX. There are two polymorphisms Thrl45Met and T(-5)C of the GP Iba gene associated with arterial thrombosis development. Also the difference in platelets' genes expressions was shown in patients with various clinical course of ischemic heart disease. The aim of this study was to investigate the role of platelet's receptor for von Willebrand factor in platelets' activation in patients with cerebrovascular disease. 123 patients with cerebrovascular disease and 97 healthy donors were included into the study. We analyzed the level of receptor for von Willebrand factor on platelet's membrane by flow cytometry, Thrl45Met and T(-5)C GP Iba polymorphiams by PCR-RFLP, the GP Iba gene expression by RT-PCR and ADP-induced platelet aggregation by Bom method. We have shown: 1) the 145Met GP Iba allele prevalence in patients with atherotrombotic stroke development due to macroangiopathy; 2) the pre-mRNA transform into the mature mRNA in activated platelets and this process may be stopped by the antiplatelet therapy by acetylsalicylic acid.},\r\nauthor_keywords={GP Iba gene;  Mature mRNA Iba;  Pre-mRNA Iba;  Receptor for von Willebrand factor;  Thrl45Met and T(-5)C GP Iba gene polymorphisms},\r\npublisher={Russian Academy of Medical Sciences},\r\nissn={23106905},\r\npubmed_id={26539867},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomeditsinskaya Khim.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The molecular mechanisms of platelet activation in patients with cerebrovascular disease.\n \n \n \n \n\n\n \n Sirotkina, O.; Laskovets, A.; Goldobin, V.; Topanova, A.; Karelov, D.; and Vavilova, T.\n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 9(1): 79-85. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina201579,\r\nauthor={Sirotkina, O.V. and Laskovets, A.B. and Goldobin, V.V. and Topanova, A.A. and Karelov, D.V. and Vavilova, T.V.},\r\ntitle={The molecular mechanisms of platelet activation in patients with cerebrovascular disease},\r\njournal={Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry},\r\nyear={2015},\r\nvolume={9},\r\nnumber={1},\r\npages={79-85},\r\ndoi={10.1134/S1990750815010102},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84923818210&doi=10.1134%2fS1990750815010102&partnerID=40&md5=0e285f4519058c66622bf99591c6dce7},\r\naffiliation={National Research Centre Kurchatov Institute, Konstantinov Petersburg Nuclear Physics Institute, Orlova Roshcha, Gatchina, Leningrad district, 188300, Russian Federation; Almazov Federal Medical Research Centre, ul. Akkuratova 2, St. Petersburg, 197341, Russian Federation; Mechnikov North-Western State Medical University, ul. Kirochnaya 41, St. Petersburg, 191015, Russian Federation; St. Petersburg State Polytechnical University, ul. Politehnicheskaya 29, St. Petersburg, 195251, Russian Federation},\r\nabstract={Cerebrovascular diseases are the second leading cause of mortality and are one of the most important medical and social problems. After the damage of the vascular wall endothelial cells secrete von Willebrand factor that binds to its receptor, glycoprotein GP Ib-V-IX, on the platelet surface. There are two known GP Ibα gene polymorphisms, Thr145Met and T(−5)C, associated with the risk of the development of arterial thrombosis and there are differences in the expression profile of platelets from patients with various courses of coronary heart disease. The aim of this study was to determine the role of the platelet receptor for von Willebrand factor in platelet activation in patients with cerebrovascular disease. The study included 123 patients with cerebrovascular disease and 97 healthy volunteers; in their platelets the following parameters were analyzed: the level of von Willebrand factor receptor by flow cytometry, the presence of GP Ibα polymorphisms Thr145Met and T(-5)C by PCR followed by subsequent restriction analysis, the level of GP Ibα gene expression by real-time PCR, and ADP-induced aggregation according to Born. We have shown that: (1) the polymorphic allele 145Met GP Ibα is more common in patients with ischemic stroke followed on macroangiopathy of cerebral vessels; (2) in activated platelets GP Ibα pre-mRNA is converted into mature mRNA, and this process is blocked by administration antiplatelet agents (e.g. acetylsalicylic acid). © 2015, Pleiades Publishing, Ltd.},\r\nauthor_keywords={GP Ibα gene;  GP Ibα mRNA;  GP Ibα polymorphisms Thr145Met and T(−5)C;  GP Ibα pre-mRNA;  von Willebrand factor receptor},\r\nfunding_details={Russian Foundation for Basic Research12-04-01296-a},\r\ncorrespondence_address1={Sirotkina, O.V.; National Research Centre Kurchatov Institute, Konstantinov Petersburg Nuclear Physics Institute, Orlova Roshcha, Russian Federation},\r\npublisher={Maik Nauka-Interperiodica Publishing},\r\nissn={19907508},\r\nlanguage={English},\r\nabbrev_source_title={Biochem. (Moscow) Suppl. Ser. B Biomed. Chem.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The new approach to evaluation of endothelium dysfunction: Detection of number of circulating endothelium cells using flow cytometry technique.\n \n \n \n \n\n\n \n Feoklistova, V.; Vavilkova, T.; Sirotkina, O.; Boldueva, S.; Gaikovaia, L.; Leonova, I.; Laskovets, A.; and Ermakov, A.\n\n\n \n\n\n\n Klinichescheskaya Laboratornaya Diagnostika, 2015-January(4): 23-26. 2015.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Feoklistova201523,\r\nauthor={Feoklistova, V.S. and Vavilkova, T.V. and Sirotkina, O.V.I. and Boldueva, S.A. and Gaikovaia, L.B. and Leonova, I.A. and Laskovets, A.B. and Ermakov, A.I.},\r\ntitle={The new approach to evaluation of endothelium dysfunction: Detection of number of circulating endothelium cells using flow cytometry technique},\r\njournal={Klinichescheskaya Laboratornaya Diagnostika},\r\nyear={2015},\r\nvolume={2015-January},\r\nnumber={4},\r\npages={23-26},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84938916243&partnerID=40&md5=3c68eb426c732e81966b1d731ec96742},\r\naffiliation={I.I. Mechnikov North-Western State Medical, University of Minzdrav of Russia, St. Petersburg, 191015, Russian Federation; V.A. Almazov Federal Medical Research Center of Minzdrav of Russia, St. Petersburg, 197341, Russian Federation; B.P. Konstantinov St. Petersburg Institute of Nuclear Physics, Gatchina, Leningradskaia Oblast, 188350, Russian Federation},\r\nabstract={The endothelium dysfunction takes leading place in pathogenesis of development of cardiovascular diseases. The circulating endothelium cells of peripheral blood can act as a direct cell marker of damage and remodeling of endothelium. The study was carried out to develop a new approach to diagnose of endothelium dysfunction by force of determination of number of circulating endothelium cells using flow cytometry technique and to apply determination of circulating endothelium cells for evaluation of risk of development of ischemic heart disease in women of young and middle age. The study embraced 62 female patients with angiography confirmed ischemic heart disease, exertional angina pectoris at the level of functional class I-11 (mean age 51±6 years) and 49 women without anamnesis of ischemic heart disease (mean age 52±9 years). The occurrence of more than three circulating endothelium cells by 3x105 leukocytes in peripheral blood increases relative risk of development of ischemic heart disease up to 4 times in women of young and middle age and risk of development of acute myocardial infarction up to 8 times in women with ischemic heart disease. The study demonstrated possibility to apply flow cytometry technique to quantitatively specify circulating endothelium cells in peripheral blood and forecast risk of development of ischemic heart disease in women of young and middle age depending on level of circulating endothelium cells.},\r\nauthor_keywords={Circulating endothelium cells: flow cytometry;  Endothelium dysfunction;  Ischemic heart disease},\r\npublisher={Izdatel'stvo Meditsina},\r\nissn={08692084},\r\npubmed_id={26189287},\r\nlanguage={Russian},\r\nabbrev_source_title={Klin. Lab. Diagn.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2014\n \n \n (11)\n \n \n

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\n \n\n \n \n \n \n \n \n Relationships of glycoproteins IIb-IIIa and Ib content with mean platelet volume and their genetic polymorphisms.\n \n \n \n \n\n\n \n Khaspekova, S.; Zyuryaev, I.; Yakushkin, V.; Sirotkina, O.; Zaytseva, N.; Ruda, M.; Panteleev, M.; and Mazurov, A.\n\n\n \n\n\n\n Blood Coagulation and Fibrinolysis, 25(2): 128-134. 2014.\n cited By 9\n\n\n\n
\n\n\n\n \n \n $\"Relationships$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Khaspekova2014128,\r\nauthor={Khaspekova, S.G. and Zyuryaev, I.T. and Yakushkin, V.V. and Sirotkina, O.V. and Zaytseva, N.O. and Ruda, M.Y. and Panteleev, M.A. and Mazurov, A.V.},\r\ntitle={Relationships of glycoproteins IIb-IIIa and Ib content with mean platelet volume and their genetic polymorphisms},\r\njournal={Blood Coagulation and Fibrinolysis},\r\nyear={2014},\r\nvolume={25},\r\nnumber={2},\r\npages={128-134},\r\ndoi={10.1097/MBC.0b013e328364b025},\r\nnote={cited By 9},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84894090437&doi=10.1097%2fMBC.0b013e328364b025&partnerID=40&md5=9df5c571835b2e7c18e5289c65355493},\r\naffiliation={Russian Cardiology Research and Production Complex, Russian Ministry of Health, 3rd Cherepkovskaya, 15a, Moscow 121552, Russian Federation; Petersburg Nuclear Physics Institute, Russian Federation; North-Western State Medical University, Russian Ministry of Health, Saint-Petersburg, Russian Federation; Faculty of Physics, Moscow State University, Russian Federation; Center for Theoretical Problems of Physicochemical Pharmacology, Moscow, Russian Federation},\r\nabstract={Quantity of platelet adhesion molecules significantly varies in normal donors and cardiovascular patients and might be affected by platelet size and genetic variations. In this study, we assessed relationships of the content of glycoprotein (GP) IIb-IIIa and GPIb with mean platelet volume (MPV) and their genetic polymorphisms. MPV and GPIIb-IIIa and GPIb numbers were measured in 116 patients with acute coronary syndrome (ACS) at days 1, 3-5 and 8-12 after disease onset and in 32 healthy volunteers. GPIIb-IIIa and GPIb allelic variants were determined in ACS patients. Strong interactions of GPIIb-IIIa and GPIb numbers and MPV were observed in ACS patients and healthy volunteers. In patients, coefficients of correlation (r) were 0.642 and 0.510 (analysis of individual mean values) and in volunteers - 0.594 and 0.508 for GPIIb-IIIa and GPIb, respectively (everywhere P<0.005). In ACS patients, correlations were highly significant at each tested time point. GPIIb-IIIa and GPIb genetic polymorphisms [GPIIIa Leu33Pro, GPIbα Thr145Met and GPIbα (-5)T/C (Kozak)] determined in ACS patients had no significant impact on their expression. Modest correlation was revealed between MPV and plasma thrombopoietin (TPO) measured at the first day of ACS (r=0.279, P=0.005). The data obtained indicated that GPIIb-IIIa and GPIb levels are mainly affected by platelet size (MPV) but not by their genetic variations. In some ACS patients, production of large platelets with high GPIIb-IIIa and GPIb contents might be stimulated by elevated TPO. © 2014 Wolters Kluwer Health.},\r\nauthor_keywords={acute coronary syndrome;  glycoprotein Ib;  glycoprotein IIb-IIIa;  mean platelet volume;  platelets;  thrombopo},\r\ncorrespondence_address1={Mazurov, A.V.; Russian Cardiology Research and Production Complex, Russian Ministry of Health, 3rd Cherepkovskaya, 15a, Moscow 121552, Russian Federation; email: avmazurov@list.ru},\r\nissn={09575235},\r\ncoden={BLFIE},\r\npubmed_id={23941967},\r\nlanguage={English},\r\nabbrev_source_title={Blood Coagul. Fibrinolysis},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Molecular basis of Parkinson's disease linked with mutations in the LRRK2 gene.\n \n \n \n \n\n\n \n Pchelina, S.; emel'ianov , A.; and Usenko, T.\n\n\n \n\n\n\n Molekuliarnaia biologiia, 48(1): 3-14. 2014.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pchelina20143,\r\nauthor={Pchelina, S.N. and emel'ianov, A.K. and Usenko, T.S.},\r\ntitle={Molecular basis of Parkinson's disease linked with mutations in the LRRK2 gene},\r\njournal={Molekuliarnaia biologiia},\r\nyear={2014},\r\nvolume={48},\r\nnumber={1},\r\npages={3-14},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84927783605&partnerID=40&md5=aacf6fe538e155cb28c97d4050b70150},\r\nabstract={Parkinson's disease (PD) is a common neurodegenerative disorder. Disease symptoms correlate with the degeneration of dopaminergic neurons in substantia nigra pars compacta. A number of factors are supposed to take part in PD pathogenesis including alpha-synuclein aggregation, oxidative stress, mitochondrial dysfunction and apoptosis, although the precise molecular mechanism of neudegeneration remains unknown. PD is generally a sporadic neuro- logical disorder, however, rare monogenic forms have been described during previous 15 years. Despite of the fact that mutations in the leucine-rich repeat kinase (LRRK2) gene are the most common cause of inherited forms of PD known today, the mechanisms by which mutations in the LRRK2 gene lead to disease remain unclear. It's difficult to understand the signaling pathways, regulated by LRRK2 in the absence of its clear physiological substrates. The G2019S substitution was shown to be the most common in mutations' spectrum of the LRRK2 gene in different populations which makes it easier to reveal patients with LRRK2-associated PD. In this review LRRK2 influence on protein aggregation, cytoskeletal dynamics, apoptosis rate and inflammatory response is discussed. Groups of patients with inherited forms of PD with known etiology are worth to be included into investigations. It could promote our un- derstanding of the mechanisms of neurodegeneration in more common sporadic cases.},\r\nissn={00268984},\r\npubmed_id={25842821},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Biol. (Mosk.)},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Molecular basis of Parkinsons's disease linked to LRRK2 mutations.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Molecular Biology, 48(1): 1-10. 2014.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Increased plasma oligomeric alpha-synuclein in patients with lysosomal storage diseases.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Neuroscience Letters, 583: 188-193. 2014.\n cited By 18\n\n\n\n
\n\n\n\n \n \n $\"Increased$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n The expression of ABCG1 transporter gene in peripheral blood mononuclear cells of patients with atherosclerosis.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 8(4): 337-343. 2014.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Abcg1 transporter gene expression in peripheral blood mononuclear cells of patients with atherosclerosis.\n \n \n \n \n\n\n \n Miroshnikova, V.; Demina, E.; Mayorov, N.; Davydenko, V.; Kurjanov, P.; Vavilov, V.; Vinogradov, A.; Denisenko, A.; and Schwarzman, A.\n\n\n \n\n\n\n Tsitologiya, 56(3): 234-240. 2014.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"Abcg1$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Miroshnikova2014234,\r\nauthor={Miroshnikova, V.V. and Demina, E.P. and Mayorov, N.V. and Davydenko, V.V. and Kurjanov, P.S. and Vavilov, V.N. and Vinogradov, A.G. and Denisenko, A.D. and Schwarzman, A.L.},\r\ntitle={Abcg1 transporter gene expression in peripheral blood mononuclear cells of patients with atherosclerosis},\r\njournal={Tsitologiya},\r\nyear={2014},\r\nvolume={56},\r\nnumber={3},\r\npages={234-240},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84904622167&partnerID=40&md5=b19c0896c5b96bfd805037891409af80},\r\naffiliation={Petersburg Nuclear Physics Institute, Gatchina, Russian Federation; St. Retersburg I. P. Pavlov State Medical University, Russian Federation; Institute of Experimental Medicine RAMS, St.-Petersburg, Russian Federation},\r\nabstract={Accumulation of cholesterol in arterial wall macrophages is a main hallmark of atherosclerosis. The ABCG1 transporter mediates cholesterol efflux to high density lipoproteins (HDL) and plays an important role in macrophage foam cell formation. The goal of our study was to investigate the potential role of ABCG1 in atherosclerosis development in humans. ABCG1 gene expression has been examined in leukocytes, monocytes and monocyte-derived macrophages of patients with atherosclerosis and in the control group. Real time PCR and Western blotting were used to determine ABCG1 mRNA and ABCG1 protein levels. Monocyte ABCG1 mRNA level was inversely correlated with the rate of artery occlusion (r =0.45, P = 0.016). Patients with 100 % artery occlusions had decreased monocyte ABCG1 mRNA levels compared to patients who had smaller plaques and controls (P < 0.05). ABCG1 mRNA (P < 0.001) and ABCG1 protein (P < 0.05) levels in macrophages of patients with coronary artery stenosis were significantly reduced compared to the control group. No significant correlation between the ABCG1 gene expression in mononuclear cells and HDL cholesterol concentration has been found. Our study suggests that decrease in the ABCG1 gene expression in macrophages is associated with atherosclerosis.},\r\nauthor_keywords={ABCG1;  Atherosclerosis;  Macrophages;  Monocytes},\r\ncorrespondence_address1={Miroshnikova, V.V.; Petersburg Nuclear Physics Institute, Gatchina, Russian Federation; email: mutantropol@mail.ru},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={00413771},\r\ncoden={TSITA},\r\npubmed_id={25509420},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The clinical heterogenity of Parkinson’s disease.\n \n \n \n \n\n\n \n Miliukhina, I.; Karpenko, M.; Timofeeva, A.; and Skorometz, A.\n\n\n \n\n\n\n Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova, 2014(8): 13-18. 2014.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Miliukhina201413,\r\nauthor={Miliukhina, I.V. and Karpenko, M.N. and Timofeeva, A.A. and Skorometz, A.A.},\r\ntitle={The clinical heterogenity of Parkinson’s disease},\r\njournal={Zhurnal Nevrologii i Psihiatrii imeni S.S. Korsakova},\r\nyear={2014},\r\nvolume={2014},\r\nnumber={8},\r\npages={13-18},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84962030361&partnerID=40&md5=5f2265100285a3462fc473740c5252a3},\r\naffiliation={Research Institute of Experimental Medicine, North-West Branch of the Russian Academy of Sciences, St. Petersburg, Russian Federation; St. Petersburg State Polytechnical University, St. Petersburg, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, Russian Federation},\r\nabstract={Objective. To identify clinical signs that determine a phenotypic heterogeneity of idiopathic Parkinson’s disease (PD) using cluster analysis. Material and methods. Cluster analysis was applied to main clinical signs characteristic of disease course and to the results of examination of 72 PD patients based on 5 scales. Results. Clinical signs that determine a phenotypic heterogeneity of PD were identified. The most significant variables were a form of disease, predominance of akinetic/rigid syndrome or tremor syndrome as well as the age at disease onset, severity of motor deficit and autonomic symptoms. Conclusion. The definition «a form of PD» has a wider meaning compared to established one. To determine a form of disease, we recommend to consider both the predominance of a definite motor symptom and a set of additional clinical parameters. © 2014, Media Sphera. All rights reserved.},\r\nauthor_keywords={Akinetic/rigid form;  Clinical heterogeneity;  Cluster analysis;  Parkinson’s disease;  Tremor form},\r\npublisher={Media Sphera},\r\nissn={19977298},\r\npubmed_id={25345625},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh. Nevrologii Psihiatrii im. S.S. Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Factors influencing platelet aggregation in patients with acute coronary syndrome.\n \n \n \n \n\n\n \n Mazurov, A.; Zyuryaev, I.; Khaspekova, S.; Yakushkin, V.; Sirotkina, O.; and Ruda, M.\n\n\n \n\n\n\n Terapevticheskii Arkhiv, 86(9): 83-89. 2014.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Factors$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Mazurov201483,\r\nauthor={Mazurov, A.V. and Zyuryaev, I.T. and Khaspekova, S.G. and Yakushkin, V.V. and Sirotkina, O.V. and Ruda, M.Ya.},\r\ntitle={Factors influencing platelet aggregation in patients with acute coronary syndrome},\r\njournal={Terapevticheskii Arkhiv},\r\nyear={2014},\r\nvolume={86},\r\nnumber={9},\r\npages={83-89},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84923429951&partnerID=40&md5=6c5d41d824ba7fc3507c4e9de2fe3bee},\r\naffiliation={Russian Cardiology Research-and-Production Complex, Russian Ministry of Health, Moscow, Russian Federation; B.P. Konstantinov Saint Petersburg Nuclear Physics Institute, Gatchina, Leningrad Region, Russian Federation; V.A. Almazov Federal Medical Research Centre, Saint Petersburg, United States},\r\nabstract={Aim. To study factors influencing platelet aggregation in patients with acute coronary syndrome (ACS). Subjects and methods. The investigation enrolled 147 patients with ACS. Their blood was sampled on days 1, 3-5, and 8-12 days after the onset of ACS. All the patients received acetylsalicylic acid (ASA) 300 mg on day 1, then 100 mg/day and Clopidogrel 300-600 mg on day 1, then 75-150 mg/day. Platelet aggregation was analyzed in 65 patients on day 1 after ASA intake, but prior to Clopidogrel therapy. The aggregation was induced by 5 and 20 μmol of ADP. Results. With the use of Clopidogrel 75 mg/day on day 3-5, platelet aggregation was reduced by 2.1 and 1.7 times for 5 and 20 umol of ADP, respectively, as compared to day 1 (ASA without Clopidogrel) and remained unchanged on days 8-12. Increasing the dose of Clopidogrel up to 150 mg/day potentiated its antiaggregatory effect. On day 1 (ASA without Clopidogrel), there was a direct correlation between platelet aggregation levels and mean platelet volume (MPV) (correlation coefficients (r), 0.526 (p<0.001) and 0.368 (p=0.015) for 5 and 20 umol of ADP, and between platelet aggregation levels and glycoprotein (GP) IIb-IIIa (r=0.387; p=0.002 and r=0.411 (p<0.001) for 5 and 20 pmol of ADP. No similar correlations were found on days 3-5 and 8-12 of administration of ASA and Clopidogrel. The genetic polymorphism of GP IIb-IIIa (GP IIIa Leu33Pro) was not noted to affect platelet aggregation. Examining the effects of genetic variations in cytochrome P450 isoform CYP2C19 (a Clopidogrel metabolizer) revealed the enhanced aggregation stimulated with 20 pmol of ADP in the carriers of slowly clopidogrel-metabolizing haplotype of CYP2C19 (differences were found on days 3-5 as compared to rapidly and routinely metabolizing haplotypes). Conclusion. In the patients with ACS, platelet aggregation is influenced by MPV, GP lib-Ilia levels, and CYP2C19 polymorphism and is not by GP IIb-IIIa polymorphism.},\r\nauthor_keywords={Acute coronary syndrome;  Aspirin;  Clopidogrel;  Glycoprotein IIb-IIIa;  Mean platelet volume;  Platelet aggregation;  Platelets},\r\npublisher={Media Sphera},\r\nissn={00403660},\r\ncoden={TEARA},\r\npubmed_id={25518511},\r\nlanguage={Russian},\r\nabbrev_source_title={Ter. Arkh.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The study of the neuroprotective activity of the apolipoprotein e peptide mimetic Cog1410 in transgenic strains of Drosophila melanogaster.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 8(1): 37-42. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Mean platelet volume: Interrelation with platelet aggregation activity and glycoprotein IIb-IIIa and Ib expression levels.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 8(2): 134-142. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Mean$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n\n\n

\n Increased mean platelet volume (MPV) is an independent risk factor of thrombotic events in patients with cardiovascular diseases. Interactions of MPV with platelet aggregation activity and contents of glycoprotein (GP) IIb-IIIa (αIIb/β3 integrin, fibrinogen receptor) and GP Ib (von Willebrand factor recep- tor) have been investigated in this study. The study was performed in a group of healthy volunteers (n = 38) and a group of patients with acute coronary syndrome (ACS, n = 116). Patient's blood was collected at days 1, 3-5 and 8-12 after ACS development. All patients received acetylsalicylic acid (ASA, inhibitor of thrombox-ane A2 synthesis) as the antiaggregant therapy and most of them also received clopidogrel (ADP receptor antagonist), except 44 patients who had not taken clopidogrel at day 1 before first blood collection. Aggrega-tion of volunteers' platelets was stimulated by 1.25, 2.5, 5 and 20 μM ADP, while aggregation of patients' platelets was stimulated by 5 and 20 μM ADP. GP IIb-IIIa and GP Ib content on the platelet surface was measured using 125I-labelled monoclonal antibodies. GP IIb-IIIa and GP Ib genetic polymorphisms were determined in ACS patients. In healthy donors significant correlations between MPV and aggregation levels have been recognized at 1.25 μM and 2.5 μM ADP (correlation coefficient (r) values of 0.396 and 0.373, p < 0.05), while at 5 μM and 20 μM ADP these interactions did not reach the level of statistical significance (r values of 0.279 and 0.205, p > 0.05). Correlations between MPV and aggregation levels were observed at day 1 of ACS in a subgroup of patients receiving ASA but before the beginning of clopidogrel treatment (r values of 0.526, p < 0.001 and 0.368, p < 0.05 for 5 and 20 μM ADP, respectively). Correlations between these parameters were not found during combined treatment of patients with ASA and clopidogrel. Strong direct correlations between MPV and GP IIb-IIIa and GP Ib contents were detected in both healthy donors and ACS patients (at all time points): the r values ranged from 0.439 to 0.647 (p ≤ 0.001 for all correlations). Genetic polymorphisms of GP IIb-IIIa (GP IIIa Leu33Pro) and GP Ib ((-5)T/C (Kozak) and Thr145Met) identified in ACS patients did not affect expression levels of corresponding glycoproteins. The data obtained indicate that increased MPV values correlate with increased platelet aggregation activity and enhanced GP IIb-IIIa and GP Ib expression. © Pleiades Publishing, Ltd., 2014.\n

\n\n\n

\n \n\n \n \n \n \n \n \n [Mean platelet volume: interactions with platelet aggregation activity and glycoprotein IIb-IIIa and Ib expression levels].\n \n \n \n \n\n\n \n Khaspekova, S.; Ziuriaev, I.; Iakushkin, V.; Naǐmushin, I.; Sirotkina, O.; Zaǐtseva, N.; Ruda, M.; and Mazurov, A.\n\n\n \n\n\n\n Biomeditcombining double inverted brevesinskaicombining double inverted brevea khimiicombining double inverted brevea, 60(1): 94-108. 2014.\n cited By 9\n\n\n\n
\n\n\n\n \n \n $\"[Mean$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Khaspekova201494,\r\nauthor={Khaspekova, S.G. and Ziuriaev, I.T. and Iakushkin, V.V. and Naǐmushin, I.A. and Sirotkina, O.V. and Zaǐtseva, N.O. and Ruda, M.I. and Mazurov, A.V.},\r\ntitle={[Mean platelet volume: interactions with platelet aggregation activity and glycoprotein IIb-IIIa and Ib expression levels].},\r\njournal={Biomedit{combining double inverted breve}sinskai{combining double inverted breve}a khimii{combining double inverted breve}a},\r\nyear={2014},\r\nvolume={60},\r\nnumber={1},\r\npages={94-108},\r\ndoi={10.18097/pbmc20146001094},\r\nnote={cited By 9},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84900003923&doi=10.18097%2fpbmc20146001094&partnerID=40&md5=9b3a298b6848c1f812ac9bf13087dda5},\r\nabstract={Increased mean platelet volume (MPV) is an independent risk factor of thrombotic events in patients with cardiovascular diseases. Interactions of MPV with platelet aggregation activity and contents of glycoprotein (GP) IIb-IIIa (alphaIIb/beta3 integrin, fibrinogen receptor) and GP Ib (von Willebrand factor receptor) were investigated in this study. Investigation was performed in a group of healthy volunteers (n = 38) and in a group of patients with acute coronary syndrome (ACS). In patients blood was collected at days 1, 3-5 and 8-12 after ACS development. As an antiaggregant therapy all patients received acetylsalicylic acid (ASA, inhibitor of thromboxane A2 synthesis) and most of them--clopidogrel (ADP receptor antagonist) with the exception of part of the patients (n = 44) at day 1 who had not taken clopidogrel before first blood collection. In volunteers platelet aggregation was stimulated by 1.25, 2.5, 5 and 20 M ADP, and in patients--by 5 and 20 M ADP. GP IIb-IIIa and GP Ib content on platelet surface was measured using 125I-labelled monoclonal antibodies. GP IIb-IIIa and GP Ib genetic polymorphisms were determined in ACS patients. In healthy donors significant correlations between MPV and aggregation levels were revealed at 1.25 and 2.5 M ADP (coefficients of correlation (r)--0.396 and 0.373, p < 0.05) and at 5 and 20 those interactions did not reach significant level (r--0.279 and 0.205, p > 0.05). Correlations between MPV and aggregation levels were observed at day 1 of ACS in a subgroup of patients who received ASA but had not started clopidogrel treatment (r--0.526, p < 0.01 and 0.368, p < 0.05 for 5 and 20 M ADP respectively). Interactions between these parameters were not registered upon combined treatment with ASA and clopidogrel. Strong direct correlations between MPV and GP IIb-IIIa and GP Ib contents were detected in healthy donors and ACS patients (at all time points) -r from 0.439 to 0.647 (p < or = 0.001 for all correlations). Genetic polymorphisms of GP IIb-IIIa (GP IIIa Leu33Pro) and GP Ib ((-5)T/C (Kozak) and Thr145Met) identified in ACS patients did not affect expression levels of corresponding glycoproteins. The data obtained indicated that increased MPV values correlate with increased platelet aggregation activity and enhanced GP IIb-IIIa and GP Ib expression.},\r\ncorrespondence_address1={Khaspekova, S.G.},\r\nissn={23106972},\r\npubmed_id={24749250},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomed Khim},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n

\n Increased mean platelet volume (MPV) is an independent risk factor of thrombotic events in patients with cardiovascular diseases. Interactions of MPV with platelet aggregation activity and contents of glycoprotein (GP) IIb-IIIa (alphaIIb/beta3 integrin, fibrinogen receptor) and GP Ib (von Willebrand factor receptor) were investigated in this study. Investigation was performed in a group of healthy volunteers (n = 38) and in a group of patients with acute coronary syndrome (ACS). In patients blood was collected at days 1, 3-5 and 8-12 after ACS development. As an antiaggregant therapy all patients received acetylsalicylic acid (ASA, inhibitor of thromboxane A2 synthesis) and most of them–clopidogrel (ADP receptor antagonist) with the exception of part of the patients (n = 44) at day 1 who had not taken clopidogrel before first blood collection. In volunteers platelet aggregation was stimulated by 1.25, 2.5, 5 and 20 M ADP, and in patients–by 5 and 20 M ADP. GP IIb-IIIa and GP Ib content on platelet surface was measured using 125I-labelled monoclonal antibodies. GP IIb-IIIa and GP Ib genetic polymorphisms were determined in ACS patients. In healthy donors significant correlations between MPV and aggregation levels were revealed at 1.25 and 2.5 M ADP (coefficients of correlation (r)–0.396 and 0.373, p < 0.05) and at 5 and 20 those interactions did not reach significant level (r–0.279 and 0.205, p > 0.05). Correlations between MPV and aggregation levels were observed at day 1 of ACS in a subgroup of patients who received ASA but had not started clopidogrel treatment (r–0.526, p < 0.01 and 0.368, p < 0.05 for 5 and 20 M ADP respectively). Interactions between these parameters were not registered upon combined treatment with ASA and clopidogrel. Strong direct correlations between MPV and GP IIb-IIIa and GP Ib contents were detected in healthy donors and ACS patients (at all time points) -r from 0.439 to 0.647 (p < or = 0.001 for all correlations). Genetic polymorphisms of GP IIb-IIIa (GP IIIa Leu33Pro) and GP Ib ((-5)T/C (Kozak) and Thr145Met) identified in ACS patients did not affect expression levels of corresponding glycoproteins. The data obtained indicated that increased MPV values correlate with increased platelet aggregation activity and enhanced GP IIb-IIIa and GP Ib expression.\n

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\n \n 2013\n \n \n (5)\n \n \n

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\n \n\n \n \n \n \n \n \n SNCA, LRRK2, MAPT polymorphisms and Parkinson's disease in Russia.\n \n \n \n \n\n\n \n Emelyanov, A.; Andoskin, P.; Yakimovskii, A.; Usenko, T.; Nuzhnyi, E.; Nikolaev, M.; and Pchelina, S.\n\n\n \n\n\n\n Parkinsonism and Related Disorders, 19(11): 1064-1065. 2013.\n cited By 11\n\n\n\n
\n\n\n\n \n \n $\"SNCA,$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Emelyanov20131064,\r\nauthor={Emelyanov, A. and Andoskin, P. and Yakimovskii, A. and Usenko, T. and Nuzhnyi, E. and Nikolaev, M. and Pchelina, S.},\r\ntitle={SNCA, LRRK2, MAPT polymorphisms and Parkinson's disease in Russia},\r\njournal={Parkinsonism and Related Disorders},\r\nyear={2013},\r\nvolume={19},\r\nnumber={11},\r\npages={1064-1065},\r\ndoi={10.1016/j.parkreldis.2013.06.003},\r\nnote={cited By 11},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84886582121&doi=10.1016%2fj.parkreldis.2013.06.003&partnerID=40&md5=5666b1b7a28b61bae448fbbb798aa42f},\r\naffiliation={Petersburg Nuclear Physics Institute, St. Petersburg, Russian Federation; Pavlov First St. Petersburg State Medical University, St. Petersburg, Russian Federation; St. Petersburg Academic Univ. - Nanotechnology Research and Education Centre, RAS, St. Petersburg, Russian Federation},\r\nauthor_keywords={Genetic association;  LRRK2;  MAPT;  Parkinson's disease;  Risk factor;  SNCA},\r\ncorrespondence_address1={Pchelina, S.; Department of Molecular and Gene Technologies, Pavlov's State Medical University of Saint-Petersburg, L. Tolstogo Str. 6/8, Russian Federation; email: sopchelina@hotmail.com},\r\npublisher={Elsevier Ltd},\r\nissn={13538020},\r\ncoden={PRDIF},\r\npubmed_id={23830801},\r\nlanguage={English},\r\nabbrev_source_title={Parkinsonism Relat. Disord.},\r\ndocument_type={Letter},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n ABCA1 mRNA and protein levels in M-CSF-activated macrophages from patients with arterial stenosis.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 7(6): 522-527. 2013.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"ABCA1$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n [Gender differences in clinical and hemoreologic disorders in elderly patients with non-cardioembolic ischemic stroke].\n \n \n \n \n\n\n \n Goldobin, V.; Klocheva, E.; Vavilova, T.; Sirotkina, O.; and Laskovets, A.\n\n\n \n\n\n\n Advances in gerontology = Uspekhi gerontologii / Rossiǐskaicombining double inverted brevea akademiicombining double inverted brevea nauk, Gerontologicheskoe obshchestvo, 26(1): 137-142. 2013.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"[Gender$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Goldobin2013137,\r\nauthor={Goldobin, V.V. and Klocheva, E.G. and Vavilova, T.V. and Sirotkina, O.V. and Laskovets, A.B.},\r\ntitle={[Gender differences in clinical and hemoreologic disorders in elderly patients with non-cardioembolic ischemic stroke].},\r\njournal={Advances in gerontology = Uspekhi gerontologii / Rossiǐskai{combining double inverted breve}a akademii{combining double inverted breve}a nauk, Gerontologicheskoe obshchestvo},\r\nyear={2013},\r\nvolume={26},\r\nnumber={1},\r\npages={137-142},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84886894202&partnerID=40&md5=4289f5fa9be636198b9a8ce2309d3b6e},\r\nabstract={Clinical manifestation and platelet homeostasis parameter results in elderly patients with atherothrombotic and lacunar strokes are presented. There is platelet activation in these patients manifested by increasing of P-selectin expression in response to adenosindiphosphate induction on flow-cytometry. Agregometry method was not informative for platelet activity estimation in these patients. Von Willebrand factor receptor expression on the platelet may have prognostic value for acute period. The fibrinogen receptor expression on the platelet was increased in women with stroke comparing with men.},\r\ncorrespondence_address1={Goldobin, V.V.},\r\nissn={15619125},\r\npubmed_id={24003740},\r\nlanguage={Russian},\r\nabbrev_source_title={Adv Gerontol},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n ABCA1 mRNA and protein levels in M-CSF macrophages from patients with arterial stenosis.\n \n \n \n \n\n\n \n Demina, E.; Miroshnikova, V.; Majorov, N.; Davydenko, V.; and Schwarzman, A.\n\n\n \n\n\n\n Tsitologiya, 55(8): 580-585. 2013.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"ABCA1$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Demina2013580,\r\nauthor={Demina, E.P. and Miroshnikova, V.V. and Majorov, N.V. and Davydenko, V.V. and Schwarzman, A.L.},\r\ntitle={ABCA1 mRNA and protein levels in M-CSF macrophages from patients with arterial stenosis},\r\njournal={Tsitologiya},\r\nyear={2013},\r\nvolume={55},\r\nnumber={8},\r\npages={580-585},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84904469780&partnerID=40&md5=3f2ae52120186f8a5c97026fc84774c7},\r\naffiliation={B.P. Konstantinov Petersburg Nuclear Physics Institute, Gatchina, Mexico; St-Petersburg I.P. Pavlov State Medical University, Russian Federation; Inst. of Exp. Med. of the N. W. Br. of the Russ. Acad. of Med. Sci., St-Petersburg, Russian Federation},\r\nabstract={ABCA1 transporter is one of the key factors defining the level of antiatherogenic HDL in plasma. It is actively involved in the removal of cholesterol from peripheral tissues by reverse cholesterol transport. However, the influence of the level of ABCA1 mRNA and the level of ABCA1 protein 1 in macrophages in atherosclerosis remains unexplored. Using real time PCR we determined ABCA1 mRNA level in macrophages cultured for 5 days with macrophage colony-stimulating factor (M-CSF). ABCA1 mRNA levels in macrophages from patients with arterial stenosis were increased when compared with the control group, P = 0.04. According to a Western blot analysis ABCA1 protein level in macrophages from patients was significantly lower than in the control group, P = 0.01. Our results suggest that the level of ABCA1 mRNA and level of ABCA1 protein in macrophages may be important factors in the development of atherosclerosis.},\r\nauthor_keywords={ABCA1;  Artery stenosis;  Atherosclerosis;  Macrophages;  Reverse cholesterol transport},\r\npublisher={Maik Nauka Publishing / Springer SBM},\r\nissn={00413771},\r\ncoden={TSITA},\r\npubmed_id={25486791},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Possibilities of clinical laboratory evaluation of antiplatelet therapy effectiveness in patients with ischemic heart disease.\n \n \n \n \n\n\n \n Sirotkina, O.; Laskovets, A.; Lipunova, A.; Gaykovaya, L.; Boldueva, S.; and Vavilova, T.\n\n\n \n\n\n\n Rational Pharmacotherapy in Cardiology, 9(1): 31-34. 2013.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Possibilities$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina201331,\r\nauthor={Sirotkina, O.V. and Laskovets, A.B. and Lipunova, A.S. and Gaykovaya, L.B. and Boldueva, S.A. and Vavilova, T.V.},\r\ntitle={Possibilities of clinical laboratory evaluation of antiplatelet therapy effectiveness in patients with ischemic heart disease},\r\njournal={Rational Pharmacotherapy in Cardiology},\r\nyear={2013},\r\nvolume={9},\r\nnumber={1},\r\npages={31-34},\r\ndoi={10.20996/1819-6446-2013-9-1-31-34},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85029744967&doi=10.20996%2f1819-6446-2013-9-1-31-34&partnerID=40&md5=05c3d636e9dd5e8010849aa067ed9ff8},\r\naffiliation={North-Western State Medical University named after I.I. Mechnikov, Kirochnaya ul. 41, St. Petersburg, 191015, Russian Federation; Petersburg Nuclear Physics Institute named after B.P. Konstantinov, Orlova Roshcha, Gatchina, Leningrad region, 188350, Russian Federation},\r\nabstract={Aim. To evaluate the functional activity of platelets by the optical standard aggregatometry and induced flow cytofluorometry during antiplatelet therapy with clopidogrel and acetylsalicylic acid (ASA). Material and methods. The evaluation of platelet function in 30 patients with ischemic heart disease treated with dual antiplatelet therapy (ASA and clopidogrel) was performed by two methods: the standard photometric method with the assessment of degree of light transmission at the maximum point and by the original method of induced flow cytofluorometry with the platelet activity evaluation by changing of glycoprotein (GP) IIb/IIIa receptor level and the expression of P-selectin before and after ADP induction. Results. Increase in platelet functional activity was detected in patients with ASA monotherapy at initial evaluation by both induced flow cytofluorometry and standard photometric method. After one month dual antiplatelet therapy platelet function significantly decreased according to standard photometric method (from 61.4±3.6 to 45.9±3.7; p < 0.05; the induction of 2.5 mM ADP), as well as according to flow cytofluorometry with changing of GP IIb/IIIa receptor level (from 12.2±0.8% to 5.2±0.8%; p < 0.05) and the expression of P-selectin (from 70.5±5.9% to 57.4±5.9%; p < 0.05). Conclusion. The combined use of laboratory methods to assess platelet function (traditional and high-tech) provides cardiologist with additional tool for assessing the effectiveness of antiplatelet therapy in patients with ischemic heart disease. © 2013 by the American College of Cardiology Foundation.},\r\nauthor_keywords={Antiplatelet therapy;  Clopidogrel;  GP IIb/IIIa receptor;  Induced flow cytofluorometry;  P-selectin},\r\ncorrespondence_address1={Sirotkina, O.V.; North-Western State Medical University named after I.I. Mechnikov, Kirochnaya ul. 41, Russian Federation; email: olgasirotkina@list.ru},\r\npublisher={Stolichnaya Izdatelskaya Kompaniya},\r\nissn={18196446},\r\nlanguage={Russian},\r\nabbrev_source_title={Ration. Pharmacother. Cardiol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2012\n \n \n (7)\n \n \n

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\n \n\n \n \n \n \n \n \n Apoptosis of peripheral blood lymphocytes in patients with lrrk2-assoctated parkinson's disease.\n \n \n \n \n\n\n \n Usenko, T.; Emelyanov, A.; Yakimovskii, A.; Bogankova, N.; Vavilova, T.; Schwarzman, A.; and Pchelina, S.\n\n\n \n\n\n\n Tsitologiya, 54(1): 44-48. 2012.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Apoptosis$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Usenko201244,\r\nauthor={Usenko, T.S. and Emelyanov, A.K. and Yakimovskii, A.F. and Bogankova, N.A. and Vavilova, T.V. and Schwarzman, A.L. and Pchelina, S.N.},\r\ntitle={Apoptosis of peripheral blood lymphocytes in patients with lrrk2-assoctated parkinson's disease},\r\njournal={Tsitologiya},\r\nyear={2012},\r\nvolume={54},\r\nnumber={1},\r\npages={44-48},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84862256335&partnerID=40&md5=ef55c46a2fc775ad5bf62c4970ea0c86},\r\naffiliation={Petersburg Nuclear Physics Institute RAS, Russian Federation; St. Petersburg State I. P. Pavlov Medical University, Russian Federation; St. Petersburg State Medical Academy, Russian Federation},\r\nabstract={Mutations in the Leucine Reach Repeat Kinase 2 (LRRK2) gene are the most frequent cause of familial Parkinson's disease (PD). Although the precise physiological and pathological role of LRRK2 is unclear, a direct lin between mutant LRRK2 and apoptosis has been suggested. Using How cytometric analysis (PI+Annexin V(FITC)) we showed increased spontaneous apoptosis of peripheral blood lymphocytes in patients with LRRK.2-associated PD compared to controls after 24 (P &lt; 0.016) and 48 (P &lt; 0.031 ) h of incubation (5% CO 2, 37 °C). We found the increased FAS mRNA level in peripheral blood lymphocytes of patients with LRRK2-associated PD compared to controls (P &lt; 0.05) and to sporadic PD (sPD) (P &lt; 0.002). Significant difference in FAS expression between patients with LRRK2-associated PD and controls remained after three years and was detected after 1 and 24 h during lymphocyte incubation (P &lt; 0.03 and 0.05, respectively). Increased spontaneous lymphocytes apoptosis along to increased FAS expression in patients with LRRK2-associated PD suggest that LRRK2 mutations may lead to the activation of extrinsic apoptotic way.},\r\nauthor_keywords={Apoptosis;  BCL-2;  FAS;  LRRK2;  Lymphocytes;  Parkinson's disease},\r\ncorrespondence_address1={Usenko, T.S.; Petersburg Nuclear Physics Institute RASRussian Federation},\r\nissn={00413771},\r\ncoden={TSITA},\r\npubmed_id={22567899},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Morphological and functional abnormalities in neuromuscular junctions of drosoph1la melanogaster induced by the expression of human app gene.\n \n \n \n \n\n\n \n Sarantseva, S.; Kislik, G.; Tkacheno, N.; Vasiliev, A.; and Schwarzman, A.\n\n\n \n\n\n\n Tsitologiya, 54(5): 421-429. 2012.\n cited By 3\n\n\n\n
\n\n\n\n \n \n $\"Morphological$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva2012421,\r\nauthor={Sarantseva, S.V. and Kislik, G.A. and Tkacheno, N.A. and Vasiliev, A.N. and Schwarzman, A.L.},\r\ntitle={Morphological and functional abnormalities in neuromuscular junctions of drosoph1la melanogaster induced by the expression of human app gene},\r\njournal={Tsitologiya},\r\nyear={2012},\r\nvolume={54},\r\nnumber={5},\r\npages={421-429},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84864547092&partnerID=40&md5=2590d2dec40708fc6982709eb0c04e0c},\r\naffiliation={B. P. Konstantinov Petersburg Nuclear Physics Institute, Gatchina, Russian Federation; Institute for Experimental Medicine, St. Petersburg, Russian Federation; St. Petersburg State University, Russian Federation},\r\nabstract={Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the loss of neurocortical and hippocampal synapses that precedes amyloidosis and neurodegeneration and closely correlates with memory impairment. Mutations in the amyloid precursor protein (APP) cause familial AD and result in the increased production of amyloid-β-protein (Aβ). To gain insights into synaptic effects of APP, we expressed APP, mutant form APP-Swedish and BACE in the motor neurons of fly larvae. We have shown that targeted expression of APP (APP-Swedish) in Drosophila larval motor neurons causes significant morphological and functional changes in neuromuscular junctions (NMJs): a dramatic increase in the number of synaptic buttons and changes in exocytosis as revealed by incorporation of the styryl dye FM4-64. Analysis of the number and distribution of mitochondria showed that motor neurons overexpressing APP (APP-Swedish) had a significant reduction of functional mitochondria in the presynaptic terminal. Significant synaptic abnormalities were observed for APP (APP-Swedish) and human beta-secretase (BACE) resulting in secretion of amyloid beta protein (Aβ). We suggest that APP participates in regulation of synaptic functions and its elevated expression leads to synaptic pathology independently from neurotoxic effects of Aβ.},\r\nauthor_keywords={Alzheimer disease;  APP;  Drosophila melanogaster;  Neuromuscular junctions},\r\ncorrespondence_address1={Sarantseva, S.V.; B. P. Konstantinov Petersburg Nuclear Physics Institute, Gatchina, Russian Federation; email: svcsarl@yandcx.ru},\r\nissn={00413771},\r\ncoden={TSITA},\r\npubmed_id={22827040},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Morphological and functional abnormalities in neuromuscular junctions of Drosophila melanogaster induced by human APP gene expression.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 6(4): 326-334. 2012.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Morphological$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Apoptosis of peripheral blood lymphocytes in patients with LRRK2-associated Parkinson's disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 6(2): 171-175. 2012.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Apoptosis$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Human APP gene expression in nerve cells of Drosophila melanogaster causes alteration of synaptoptagmin 1 mRNA level.\n \n \n \n \n\n\n \n Sarantseva, S.; Rodin, D.; and Schwarzman, A.\n\n\n \n\n\n\n Doklady Biochemistry and Biophysics, 442(1): 19-21. 2012.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Human$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva201219,\r\nauthor={Sarantseva, S.V. and Rodin, D.I. and Schwarzman, A.L.},\r\ntitle={Human APP gene expression in nerve cells of Drosophila melanogaster causes alteration of synaptoptagmin 1 mRNA level},\r\njournal={Doklady Biochemistry and Biophysics},\r\nyear={2012},\r\nvolume={442},\r\nnumber={1},\r\npages={19-21},\r\ndoi={10.1134/S1607672912010061},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84858163762&doi=10.1134%2fS1607672912010061&partnerID=40&md5=4cfb55944bae9746805589a7bd68ca7f},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, St. Petersburg 188350, Russian Federation; Institute of Experimental Medicine, Russian Academy of Medical Sciences, ul. Popova 12, St. Petersburg 197376, Russian Federation},\r\n}

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\n \n\n \n \n \n \n \n \n The potential role of presenilin 1 in regulation of synaptic function.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Cell and Tissue Biology, 6(1): 60-68. 2012.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Glucocerebrosidase gene mutations are associated with Parkinson's disease in Russia.\n \n \n \n \n\n\n \n Emelyanov, A.; Boukina, T.; Yakimovskii, A.; Usenko, T.; Drosdova, A.; Zakharchuk, A.; Andoskin, P.; Dubina, M.; Schwarzman, A.; and Pchelina, S.\n\n\n \n\n\n\n Movement Disorders, 27(1): 158-159. 2012.\n cited By 26\n\n\n\n
\n\n\n\n \n \n $\"Glucocerebrosidase$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Emelyanov2012158,\r\nauthor={Emelyanov, A. and Boukina, T. and Yakimovskii, A. and Usenko, T. and Drosdova, A. and Zakharchuk, A. and Andoskin, P. and Dubina, M. and Schwarzman, A. and Pchelina, S.},\r\ntitle={Glucocerebrosidase gene mutations are associated with Parkinson's disease in Russia},\r\njournal={Movement Disorders},\r\nyear={2012},\r\nvolume={27},\r\nnumber={1},\r\npages={158-159},\r\ndoi={10.1002/mds.23950},\r\nnote={cited By 26},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84855914816&doi=10.1002%2fmds.23950&partnerID=40&md5=c889b2ca9424f2c476fcf9d0050845da},\r\naffiliation={Petersburg Nuclear Physics Institute, RAS, St. Petersburg, Russian Federation; Pavlov's State Medical University of Saint-Petersburg, St. Petersburg, Russian Federation; St. Petersburg Academic UniversityNanotechnology Research and Education Centre, RAS, St. Petersburg, Russian Federation; Research Centre for Medical Genetics, RAMS, Moscow, Russian Federation; St. Petersburg State University, St. Petersburg, Russian Federation},\r\ncorrespondence_address1={Pchelina, S.; Petersburg Nuclear Physics Institute. RAS, St. Petersburg, Russian Federation; email: sopchelina@hotmail.com},\r\nissn={08853185},\r\ncoden={MOVDE},\r\npubmed_id={21915911},\r\nlanguage={English},\r\nabbrev_source_title={Mov. Disord.},\r\ndocument_type={Letter},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2011\n \n \n (10)\n \n \n

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\n \n\n \n \n \n \n \n \n [Clinical features of LRRK2-associated Parkinson's disease].\n \n \n \n \n\n\n \n Pchelina, S.; Ivanova, O.; Emel'ianov, A.; and Iakimovskiǐ, A.\n\n\n \n\n\n\n Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova / Ministerstvo zdravookhraneniia i meditsinskoǐ promyshlennosti Rossiǐskoǐ Federatsii, Vserossiǐskoe obshchestvo nevrologov [i] Vserossiǐskoe obshchestvo psikhiatrov, 111(12): 56-62. 2011.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"[Clinical$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pchelina201156,\r\nauthor={Pchelina, S.N. and Ivanova, O.N. and Emel'ianov, A.K. and Iakimovskiǐ, A.F.},\r\ntitle={[Clinical features of LRRK2-associated Parkinson's disease].},\r\njournal={Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova / Ministerstvo zdravookhraneniia i meditsinskoǐ promyshlennosti Rossiǐskoǐ Federatsii, Vserossiǐskoe obshchestvo nevrologov [i] Vserossiǐskoe obshchestvo psikhiatrov},\r\nyear={2011},\r\nvolume={111},\r\nnumber={12},\r\npages={56-62},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84861438998&partnerID=40&md5=495d06b0eb1d177f07b8c2618ca683ca},\r\nabstract={Mutations in the Leucine Reach Repeat Kinase 2 (LRRK2) gene are the most frequent cause of familial Parkinson's disease (PD). Previously, we have sequenced the coding region of the LRRK2 gene in 85 PD patients and showed the prevalence of G2019S-associated PD (G2019S-PD) among all cases of LRRK2-associated PD in Russia. Screening of the most frequent LRRK2 mutations (G2019S, R1441C, R1441G) in the extended sample of PD patients (100 familial cases, 14 relatives and 230 sporadic cases) revealed two novel families with G2019S-PD in the addition to LRRK2-associated PD cases identified earlier. In summary, the frequency of LRRK2-associated PD among familial PD cases was estimated as 8%. The G2019S mutation was the most frequent (7% - in familial and 0.5% - in sporadic PD). Comparative analyses of the age-at-onset and main neurological symptoms in 13 patients with LRRK2-associated PD (8 with G2019S, 2 - V1613A and 1 - R1441C) and 80 PD patients without mutations in the LRRK2 gene did not reveal any differences. However, the G2019S LRRK2 mutation carriers had the increased rate of drug induced side-effects in comparison with genetically undefined patients (OR=6.4, p<0.02). The data obtained could improve our understanding of the pathogenesis of LRRK2-associated PD and be useful in clinical practice during disease therapy.},\r\ncorrespondence_address1={Pchelina, S.N.},\r\nissn={19977298},\r\npubmed_id={22433811},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh Nevrol Psikhiatr Im S S Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Association of apoprotein A-1 genetic variants with development of atherosclerosis in the population of St. Petersburg.\n \n \n \n \n\n\n \n Miroshnikova, V.; Rodygina, T.; Demina, E.; Kurjanov, P.; Urazgildeeva, S.; Gurevich, V.; and Schwarzman, A.\n\n\n \n\n\n\n Russian Journal of Genetics: Applied Research, 1(5): 411-415. 2011.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Association$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Miroshnikova2011411,\r\nauthor={Miroshnikova, V.V. and Rodygina, T.I. and Demina, E.P. and Kurjanov, P.S. and Urazgildeeva, S.A. and Gurevich, V.S. and Schwarzman, A.L.},\r\ntitle={Association of apoprotein A-1 genetic variants with development of atherosclerosis in the population of St. Petersburg},\r\njournal={Russian Journal of Genetics: Applied Research},\r\nyear={2011},\r\nvolume={1},\r\nnumber={5},\r\npages={411-415},\r\ndoi={10.1134/S207905971105011X},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84864750365&doi=10.1134%2fS207905971105011X&partnerID=40&md5=338a8e3af9b7f0e280005f8a11bcad7a},\r\naffiliation={Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Orlova Roshcha, Gatchina, Leningrad oblast 188300, Russian Federation; St. Petersburg Pavlov State Medical University, ul. Lva Tolstogo 6/8, St. Petersburg 197022, Russian Federation; Center of Atherosclerosis and Lipid Disorders, Federal State Medical Institution, Sokolov Clinical Hospital no. 122, Federal Medico-Biological Agency, pr. Kultury 4, St. Petersburg 194291, Russian Federation; Chair of Cardiology, St. Petersburg Sechenov State Medical Academy, Piskarevskii pr. 47, St. Petersburg 195067, Russian Federation},\r\nabstract={Apoprotein A-1 is the major protein of antiatherogenic high density lipoproteins and one of the key proteins regulating reverse cholesterol transport. The goal of this work was to study the association of the APOA1 gene polymorphism with development of atherosclerosis in the population of St. Petersburg. Allelic frequencies of polymorphic variants (-75)G/A and 83C/T of the APOA1 gene were determined in a group of patients with angiographically proven atherosclerosis and in the control group. Allele 83T of the APOA1 gene was associated with a lower risk of developing atherosclerosis in residents of St. Petersburg. © 2011 Pleiades Publishing, Ltd.},\r\nauthor_keywords={APOA1 gene;  apoprotein A1;  atherosclerosis;  reverse cholesterol transport},\r\ncorrespondence_address1={Miroshnikova, V. V.; Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Orlova Roshcha, Gatchina, Leningrad oblast 188300, Russian Federation},\r\nissn={20790597},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Genet. Appl. Res.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Compensatory function of transthyretin in Alzheimer's disease.\n \n \n \n \n\n\n \n Schwarzman, A.; and Sarantseva, S.\n\n\n \n\n\n\n Tsitologiya, 53(10): 772-777. 2011.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Compensatory$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman2011772,\r\nauthor={Schwarzman, A.L. and Sarantseva, S.V.},\r\ntitle={Compensatory function of transthyretin in Alzheimer's disease},\r\njournal={Tsitologiya},\r\nyear={2011},\r\nvolume={53},\r\nnumber={10},\r\npages={772-777},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84873043265&partnerID=40&md5=88bc2fbc53652793cc65e18728c9d6ec},\r\naffiliation={St. Petersburg Institute of Nuclear Physics, RAS, Gatchina, Russian Federation; Institute for Experimental Medicine, RAMS, St. Petersburg, Russian Federation},\r\nabstract={Alzheimer's disease (AD) is the most common form of age-related primary neurodegenerative diseases characterized by progressive memory loss, aphasia, and intellectual and mental breakdown. Pathogenesis of AD is based on the early synaptic dysfunction following neurodegeneration and neuronal death. According to modern concepts, the development of neuropathological processes is due to progressively deposited intermediates of amyloid fibrils that represent oligomers consisting of short peptide named amyloid beta protein (Aβ). In this context, it is reasonable to propose that one of the compensatory mechanisms of AD might be inhibition of Aβ oligomerization by sequestration or clearance of Aβ. Experiments with transgenic animals and epidemiological studies demonstrate that major protein of cerebrospinal fluid, transthyretin, is a natural neuroprotector that inhibits Aβ amyloid formation and restore cognitive functions. The study of Aβ-transthyretin complexes allowed to create peptides that are mimetics of transthyretin. These mimetics inhibit amyloid formation in vitro and, therefore, could be used in therapeutic treatment of AD.},\r\nauthor_keywords={Alzheimer's disease;  Amyloid beta protein;  Transthyretin},\r\ncorrespondence_address1={Schwarzman, A.L.; St. Petersburg Institute of Nuclear Physics, RAS, Gatchina, Russian Federation; email: aschwart1@yandex.ru},\r\nissn={00413771},\r\ncoden={TSITA},\r\npubmed_id={22232933},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n [Symptomatic epilepsy in inflammatory demyelinating diseases].\n \n \n \n \n\n\n \n Totolian, N.; Borisova, E.; Totolian, A.; Miliukhina, I.; Lapin, S.; Kodzaeva, A.; Prakhova, L.; Evdoshenko, E.; Kairbekova, E.; and Skoromets, A.\n\n\n \n\n\n\n Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova / Ministerstvo zdravookhraneniia i meditsinskoǐ promyshlennosti Rossiǐskoǐ Federatsii, Vserossiǐskoe obshchestvo nevrologov [i] Vserossiǐskoe obshchestvo psikhiatrov, 111(2 Suppl 2): 38-51. 2011.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"[Symptomatic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Totolian201138,\r\nauthor={Totolian, N.A. and Borisova, E.V. and Totolian, A.A. and Miliukhina, I.V. and Lapin, S.V. and Kodzaeva, A.I. and Prakhova, L.N. and Evdoshenko, E.P. and Kairbekova, E.I. and Skoromets, A.A.},\r\ntitle={[Symptomatic epilepsy in inflammatory demyelinating diseases].},\r\njournal={Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova / Ministerstvo zdravookhraneniia i meditsinskoǐ promyshlennosti Rossiǐskoǐ Federatsii, Vserossiǐskoe obshchestvo nevrologov [i] Vserossiǐskoe obshchestvo psikhiatrov},\r\nyear={2011},\r\nvolume={111},\r\nnumber={2 Suppl 2},\r\npages={38-51},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-80053329504&partnerID=40&md5=82ecdcf2f2e931f4928ae590356a52c8},\r\nabstract={Based on the own observations, we have summarized the features of symptomatic epilepsy in multiple sclerosis and conducted a clinical analysis of the most diagnostically difficult cases of inflammatory and demyelinating diseases in which epilepsy was the major clinical syndrome. The cases of post-infectious acute disseminated encephalomyelitis, idiopathic cerebral angiitis, Rasmussen's encephalitis are reviewed. Peculiarities of MRI structural brain lesions in these patients are discussed. The use of additional laboratory studies, including a study of cerebrospinal fluid, is considered.},\r\ncorrespondence_address1={Totolian, N.A.},\r\nissn={19977298},\r\npubmed_id={21916156},\r\nlanguage={Russian},\r\nabbrev_source_title={Zh Nevrol Psikhiatr Im S S Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Glycoprotein IIb-IIIa content and platelet aggregation in healthy volunteers and patients with acute coronary syndrome.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Platelets, 22(4): 243-251. 2011.\n cited By 18\n\n\n\n
\n\n\n\n \n \n $\"Glycoprotein$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n Glycoprotein (GP) IIb-IIIa (αIIbβ3-integrin) is the central receptor of platelet aggregation. Activated GP IIb-IIIa binds fibrinogen or von Willebrand factor, which forms molecular bridges between aggregating platelets. This review summarizes data on the relationship between GP IIb-IIIa expression on the platelet surface and platelet aggregating activity. GP IIb-IIIa number, measured as maximal binding of complex-specific monoclonal antibody, varied by approximately two fold in both healthy volunteers (n = 35) and patients with acute coronary syndrome (ACS) (n = 65). In healthy volunteers positive associations were observed between GP IIb-IIIa number and the level of ADP-induced aggregation when this relationship was analysed in untreated platelet-rich plasma (PRP) as well as upon in vitro addition of aspirin or non-saturating concentrations of GP IIb-IIIa blockers. In the same group of volunteers almost no differences in aggregating activity were detected between donors carrying the GP IIIa Pro33 allele (n = 15) and those with the GP IIIa Leu33Leu33 genotype (n = 20). No significant relationships were revealed between platelet aggregability and variations of plasma fibrinogen concentration. Positive correlation of the level of ADP-induced aggregation and GP IIb-IIIa content was detected in patients with ACS within the first hour upon admission to the hospital when they had already received aspirin, but not clopidogrel. However, there were no correlations between these parameters at days 3-5 and days 8-12 (before discharge). At these time points patients were treated not only with aspirin but were saturated with clopidogrel as well. In ACS patients we also evaluated the expression of another platelet adhesive receptor, GP Ib, and found a significant positive correlation between GP IIb-IIIa and GP Ib content. A strong association was also revealed between the number of both receptors and mean platelet volume. The latter observation indicated that individual variations of the number of glycoprotein molecules are mainly affected by platelet size but not the density of their expression on the platelet membrane. Possible usefulness of measuring GP IIb-IIIa content as a marker of increased platelet reactivity is discussed. © 2011 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.\n

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\n \n\n \n \n \n \n \n \n Reduced content of α-synuclein in peripheral blood leukocytes of patients with LRRK2-associated Parkinson's disease.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 150(6): 679-681. 2011.\n cited By 8\n\n\n\n
\n\n\n\n \n \n $\"Reduced$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n ABCA1 gene expression in peripheral blood lymphocytes and macrophages in patients with atherosclerosis.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Molecular Biology, 45(2): 258-262. 2011.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"ABCA1$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n [ABCA1 gene expression in peripheral blood lymphocytes and macrophages in patients with atherosclerosis].\n \n \n \n \n\n\n \n Demina, E.; Miroshnikova, V.; Rodygina, T.; Kur'ianov, P.; Vinogradov, A.; Denisenko, A.; and Shvartsman, A.\n\n\n \n\n\n\n Molekuliarnaia biologiia, 45(2): 289-293. 2011.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"[ABCA1$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Demina2011289,\r\nauthor={Demina, E.P. and Miroshnikova, V.V. and Rodygina, T.I. and Kur'ianov, P.S. and Vinogradov, A.G. and Denisenko, A.D. and Shvartsman, A.L.},\r\ntitle={[ABCA1 gene expression in peripheral blood lymphocytes and macrophages in patients with atherosclerosis].},\r\njournal={Molekuliarnaia biologiia},\r\nyear={2011},\r\nvolume={45},\r\nnumber={2},\r\npages={289-293},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-79960031498&partnerID=40&md5=881baf81e856f9c16cf0c48b4ba98049},\r\nabstract={ABCA1 transporter is known to play important role in the cholesterol transport from peripheral tissues. However its contribution in atherosclerosis development remains not completely understood. Using Real Time PCR, a significant reduction of ABCA1 mRNA level in leukocytes of patients with atherosclerosis was determined when compared with controls. Mean ABCA1 expression levels in leukocytes for the group of patients and for the control group are 0.57 +/- 0.28 and 0.93 +/- 0.14 (p = 0.02). At the same time we detected a significant increase of ABCA1 mRNA level in macrophages of patients when compared with controls. Mean ABCA1 expression levels in macrophages for the group of patients and for the control group are 1.32 +/- 0.10 and 0.90 +/- 0.14 (p = 0.014). In summary, we suggest that expression level of ABCA1 gene may contribute to the development of atherosclerosis.},\r\ncorrespondence_address1={Demina, E.P.},\r\nissn={00268984},\r\npubmed_id={21634116},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Biol. (Mosk.)},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Dendrimer D5 is a vector for peptide transport to brain cells.\n \n \n \n \n\n\n \n Sarantseva, S.; Bolshakova, O.; Timoshenko, S.; Kolobov, A.; and Schwarzman, A.\n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 150(4): 429-431. 2011.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"Dendrimer$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva2011429,\r\nauthor={Sarantseva, S.V. and Bolshakova, O.I. and Timoshenko, S.I. and Kolobov, A.A. and Schwarzman, A.L.},\r\ntitle={Dendrimer D5 is a vector for peptide transport to brain cells},\r\njournal={Bulletin of Experimental Biology and Medicine},\r\nyear={2011},\r\nvolume={150},\r\nnumber={4},\r\npages={429-431},\r\ndoi={10.1007/s10517-011-1160-z},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-79958268485&doi=10.1007%2fs10517-011-1160-z&partnerID=40&md5=03d1e714b41642bc890858ee832fc44c},\r\naffiliation={B. P. Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nabstract={Dendrimers are a new class of nonviral vectors for gene or drug transport. Dendrimer capacity to penetrate through the blood-brain barrier remaines little studied. Biotinylated polylysine dendrimer D5, similarly to human growth hormone biotinylated fragment covalently bound to D5 dendrimer, penetrates through the blood-brain barrier and accumulates in Drosophila brain after injection into the abdomen. Hence, D5 dendrimer can serve as a vector for peptide transport to brain cells. © 2011 Springer Science+Business Media, Inc.},\r\nauthor_keywords={Blood-brain barrier;  Dendrimers;  Drosophila;  Peptides;  Polylysine},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)07-04-00128, 09-04-00647},\r\n}

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\n \n\n \n \n \n \n \n \n Aspirin resistance in patients with acute coronary syndrome. Part 2.\n \n \n \n \n\n\n \n Frolova, N.; Shakhnovich, R.; Kaznacheeva, E.; Sirotkina, O.; and Dobrovolskyi, A.\n\n\n \n\n\n\n Cardiovascular Therapy and Prevention (Russian Federation), 10(2): 47-52. 2011.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Aspirin$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Frolova201147,\r\nauthor={Frolova, N.S. and Shakhnovich, R.M. and Kaznacheeva, E.M. and Sirotkina, O.V. and Dobrovolskyi, A.B.},\r\ntitle={Aspirin resistance in patients with acute coronary syndrome. Part 2},\r\njournal={Cardiovascular Therapy and Prevention (Russian Federation)},\r\nyear={2011},\r\nvolume={10},\r\nnumber={2},\r\npages={47-52},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84907931085&partnerID=40&md5=f5eabfe341d68cae381b06bda53668e3},\r\naffiliation={A.L. Myasnikov Research Institute of Clinical Cardiology, Russian Cardiology Scientific and Clinical Complex, Moscow, Russian Federation; B.P. Konstantinov St. Petersburg Institute of Nuclear Physics, Russian Academy of Science, St.-Petersburg, Russian Federation},\r\nabstract={Results: Aspirin resistance was diagnosed in 11% of ACS patients, receiving aspirin in a standard dose of 100 mg/d. The majority of aspirin-resistant patients had ACS with ST segment elevation (STE-ACS). In all aspirin-resistant individuals, the resistance was pharmacokinetic. The level of 11DHTxB2, increased at baseline in ACS patients and especially in those with STE-ACS, was reduced during aspirin therapy. The combination of high PLA and high 11DHTxB2 levels was typically associated with true aspirin resistance. In patients with metabolite levels >438 ng/mmol creatinine, prognosis was significantly worse than in those with lower levels of this parameter. In aspirinresistant patients, the levels of interleukin-6 (IL-6), IL-10, and C-reactive protein (CRP) at baseline and throughout the study were significantly higher than in aspirin-sensitive subjects. There was no significant association between aspirin resistance and Leu33Pro or A842G polymorphisms, while A842G polymorphism was more common in aspirin-resistant patients.\r\nConclusion: In aspirin-resistant patients, the level of TxA2 metabolite is increased (true resistance). In ACS individuals with high levels of 11DHTxB2, the prognosis was worse. Aspirin resistance could be linked to inflammation activation. There was no consistent association between aspirin resistance and studied genetic polymorphisms.\r\nAim: In patients with acute coronary syndrome (ACS), to investigate the prevalence of aspirin resistance, its clinical features, prognostic effects, and potential correction.\r\nMaterial and methods: The study included 100 ACS patients receiving aspirin. Aspirin resistance was diagnosed if at Day 7 of aspirin therapy, the level of platelet aggregation (PLA) with arachidonic acid was ≥20%. In addition, a thromboxane A2 (TxA2) metabolite - 11-dehydro-thromboxane B2 (11DHTxB2), as well as inflammation markers and genetic polymorphisms (sub-unit IIIa - Leu33Pro and cyclooxygenase-2 (COG) genes) were studied.},\r\nauthor_keywords={Acetylsalicylic acid;  Acute coronary syndrome;  Aspirin resistance;  Genetic polymorphisms;  Inflammation markers;  Platelet aggregation},\r\ncorrespondence_address1={Frolova, N.S.; A.L. Myasnikov Research Institute of Clinical Cardiology, Russian Cardiology Scientific and Clinical ComplexRussian Federation},\r\npublisher={Vserossiiskoe Obshchestvo Kardiologov},\r\nissn={17288800},\r\nlanguage={Russian},\r\nabbrev_source_title={Cardiovasc. Ther. Prev.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2010\n \n \n (2)\n \n \n

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\n \n\n \n \n \n \n \n \n Familial Alzheimer's disease mutations in the presenilin 1 gene reduce cell-cell adhesion in transfected fibroblasts.\n \n \n \n \n\n\n \n Schwarzman, A.; Sarantseva, S.; Runova, O.; Talalaeva, E.; and Vitek, M.\n\n\n \n\n\n\n Biophysics, 55(5): 760-764. 2010.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Familial$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman2010760,\r\nauthor={Schwarzman, A.L. and Sarantseva, S.V. and Runova, O.L. and Talalaeva, E.I. and Vitek, M.P.},\r\ntitle={Familial Alzheimer's disease mutations in the presenilin 1 gene reduce cell-cell adhesion in transfected fibroblasts},\r\njournal={Biophysics},\r\nyear={2010},\r\nvolume={55},\r\nnumber={5},\r\npages={760-764},\r\ndoi={10.1134/S0006350910050131},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-79951716708&doi=10.1134%2fS0006350910050131&partnerID=40&md5=d4a009952e1750e5a769bc2c9bb7855d},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningradskaya oblast 188300, Russian Federation; Institute of Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg 197376, Russian Federation; Division of Neurology, Duke University Medical Center, Durham, North Carolina 27710, United States},\r\nabstract={Experimental evidence has been obtained that mutations in the presenilin 1 (PS1) gene in familial Alzheimer's disease can lead to the disturbance of cell adhesion in model cell cultures. It was shown that, in L fibroblasts of mice with stable expression of GFP-PS1 cDNA containing G209V or E319G mutations, cell-cell interactions and the accumulation of GFP-PS1 cDNA in intercellular contacts are disturbed. Similar results were obtained in transfected human epithelial HEp2 cells. It is assumed that mutations in familial Alzheimer's disease lead to the disturbance of the functions of presenelin 1 in cell adhesion. © 2010 Pleiades Publishing, Ltd.},\r\nauthor_keywords={cell adhesion;  familial Alzheimer's disease;  HEp 2 cells;  L cells;  presenilin 1},\r\nfunding_details={10 04 00153, 09 04 00647},\r\n}

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\n \n\n \n \n \n \n \n \n Clopidogrel resistance in patients with acute coronary syndrome.\n \n \n \n \n\n\n \n Frolova, N.; Shakhnovich, R.; Sirotkina, O.; Dobrovolsky, A.; and Ruda, M.\n\n\n \n\n\n\n Terapevticheskii Arkhiv, 82(8): 14-20. 2010.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Clopidogrel$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Frolova201014,\r\nauthor={Frolova, N.S. and Shakhnovich, R.M. and Sirotkina, O.V. and Dobrovolsky, A.B. and Ruda, M.Ya.},\r\ntitle={Clopidogrel resistance in patients with acute coronary syndrome},\r\njournal={Terapevticheskii Arkhiv},\r\nyear={2010},\r\nvolume={82},\r\nnumber={8},\r\npages={14-20},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77957120381&partnerID=40&md5=6a810f465846498db7a4cc05727fafd8},\r\naffiliation={A. L. Myasnikov Institute of Clinical Cardiology, Russian Cardiology Research-and-Production Complex, Russian Agency for Medical Technologies, Russian Federation; B.P. Konstantinov Saint Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Russian Federation},\r\nabstract={Aim: to reveal the frequency of Clopidogrel resistance in patients with acute coronary syndrome (ACS) and its impact on prognosis in these patients. Subjects and methods. Seventy-five clopidogrel-treated patients with ACS were followed up. Optical aggregometry was conducted using ADP 20 μmol. The resistance criteria were baseline platelet aggregation, platelet aggregation on day 7, % &lt; 10%. Inflammatory markers (IL-6, IL-10, and C-reactive protein) were determined. Genetic polymorphisms (the IIIa subunit gene - Leu33Pro, the receptor P2Y12 C18T and G36T gene, and the CYP3 *A4(A-293G) gene) were studied. Results. According to the accepted resistance criteria, 54 (72%) patients were sensitive to Clopidogrel and 21 (28%) were resistant to the agent. The resistance was revealed in 7 (23%) of the patients with ECG ST-segment elevation and in 14 (31%) of those with ST-segment elevation. Before admission to the clinic, the unresponsive patients had significantly more frequently received the loading Clopidogrel dose of 300 mg while that latter was 600 mg in the responsive patients. As compared with the responsive patients, the unresponsive ones showed a significantly lower baseline antibody level that was increased on day 7. The Clopidogrel resistance determined by this criterion had no impact on prognosis. On dividing the patients by aggregation quartile values, poor manifestations insignificantly more frequently occurred in the third and fourth quartiles. No clear correlation was found between the occurrence of Clopidogrel resistance and the activation of an inflammatory process. The monozygous variant of the receptor P2Y 12 CT18T gene was insignificantly more frequently encountered in the unresponsive patients. Conclusion. The laboratory phenomenon of Clopidogrel resistance exists. Large multicenter studies of this issue are needed to identify simple and least expensive resistance methods and clear diagnostic criteria that enable the findings to be compared.},\r\nauthor_keywords={Acute coronary syndrome;  Clopidogrel;  Clopidogrel resistance;  Genetic polymorphisms;  Inflammatory markers;  Platelet aggregation},\r\ncorrespondence_address1={Frolova, N. S.; A. L. Myasnikov Institute of Clinical Cardiology, Russian Cardiology Research-and-Production Complex, Russian Agency for Medical TechnologiesRussian Federation; email: frolik78@mail.ru},\r\nissn={00403660},\r\ncoden={TEARA},\r\npubmed_id={20873239},\r\nlanguage={Russian},\r\nabbrev_source_title={Ter. Arkh.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2009\n \n \n (10)\n \n \n

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\n \n\n \n \n \n \n \n \n Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic drosophila model of Alzheimer's disease.\n \n \n \n \n\n\n \n Sarantseva, S.; Timoshenko, S.; Bolshakova, O.; Karaseva, E.; Rodin, D.; Schwarzman, A.; and Vitek, M.\n\n\n \n\n\n\n PLoS ONE, 4(12). 2009.\n cited By 43\n\n\n\n
\n\n\n\n \n \n $\"Apolipoprotein$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva2009,\r\nauthor={Sarantseva, S. and Timoshenko, S. and Bolshakova, O. and Karaseva, E. and Rodin, D. and Schwarzman, A.L. and Vitek, M.P.},\r\ntitle={Apolipoprotein E-mimetics inhibit neurodegeneration and restore cognitive functions in a transgenic drosophila model of Alzheimer's disease},\r\njournal={PLoS ONE},\r\nyear={2009},\r\nvolume={4},\r\nnumber={12},\r\ndoi={10.1371/journal.pone.0008191},\r\nart_number={e8191},\r\nnote={cited By 43},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77949510114&doi=10.1371%2fjournal.pone.0008191&partnerID=40&md5=8a9b648520a0c59765be60f68e28ad79},\r\naffiliation={Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Russian Federation; Institute for Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg, Russian Federation; Division of Neurology, Duke University Medical Center, Durham, NC, United States; Cognosci, Inc., Research Triangle Park, NC, United States},\r\nabstract={Background: Mutations of the amyloid precursor protein gene (APP) are found in familial forms of Alzheimer's disease (AD) and some lead to the elevated production of amyloid-b-protein (Ab). While Ab has been implicated in the causation of AD, the exact role played by Ab and its APP precursor are still unclear. Principal Findings: In our study, Drosophila melanogaster transgenics were established as a model to analyze AD-like pathology caused by APP overexpression. We demonstrated that age related changes in the levels and pattern of synaptic proteins accompanied progressive neurodegeneration and impairment of cognitive functions in APP transgenic flies, but that these changes may be independent from the generation of Ab. Using novel peptide mimetics of Apolipoprotein-E, COG112 or COG133 proved to be neuroprotective and significantly improved the learning and memory of APP transgenic flies. Conclusions: The development of neurodegeneration and cognitive deficits was corrected by injections of COG112 or COG133, novel mimetics of apolipoprotein-E (apoE) with neuroprotective activities. © 2009 Sarantseva et al.},\r\ncorrespondence_address1={Vitek, M. P.; Division of Neurology, Duke University Medical Center, Durham, NC, United States; email: Michael.Vitek@Duke.edu},\r\nissn={19326203},\r\npubmed_id={19997607},\r\nlanguage={English},\r\nabbrev_source_title={PLoS ONE},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Risk factors of thrombotic complications and prognosis of patients with chronic form of ischemic heart disease.\n \n \n \n \n\n\n \n Komarov, A.; Shakhmatova, O.; Stambolsky, D.; Rebrikov, D.; Kofiadi, I.; Sirotkina, O.; Deev, A.; and Panchenko, E.\n\n\n \n\n\n\n Kardiologiya, 49(11): 4-10. 2009.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Risk$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Komarov20094,\r\nauthor={Komarov, A.L. and Shakhmatova, O.O. and Stambolsky, D.V. and Rebrikov, D.V. and Kofiadi, I.A. and Sirotkina, O.V. and Deev, A.D. and Panchenko, E.P.},\r\ntitle={Risk factors of thrombotic complications and prognosis of patients with chronic form of ischemic heart disease},\r\njournal={Kardiologiya},\r\nyear={2009},\r\nvolume={49},\r\nnumber={11},\r\npages={4-10},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77949329226&partnerID=40&md5=6071dff3d62c96238d0322f6d42c28c1},\r\naffiliation={Russian Cardiology Scientific and Production Center, ul. Tretiya Cherepkovskaya 15a, 121552 Moscow, Russian Federation},\r\ncorrespondence_address1={Komarov, A.L.; Russian Cardiology Scientific and Production Center, ul. Tretiya Cherepkovskaya 15a, 121552 Moscow, Russian Federation},\r\nissn={00229040},\r\npubmed_id={20001975},\r\nlanguage={Russian},\r\nabbrev_source_title={Kardiologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Modern genetic approaches to searching for targets for medicinal preparations.\n \n \n \n \n\n\n \n Sarantseva, S.; and Schwarzman, A.\n\n\n \n\n\n\n Russian Journal of Genetics, 45(7): 761-770. 2009.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"Modern$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva2009761,\r\nauthor={Sarantseva, S.V. and Schwarzman, A.L.},\r\ntitle={Modern genetic approaches to searching for targets for medicinal preparations},\r\njournal={Russian Journal of Genetics},\r\nyear={2009},\r\nvolume={45},\r\nnumber={7},\r\npages={761-770},\r\ndoi={10.1134/S1022795409070011},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-70349957965&doi=10.1134%2fS1022795409070011&partnerID=40&md5=620601f03bd0b58864200ea1af43feea},\r\naffiliation={St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188300, Russian Federation; Institute of Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg, 197376, Russian Federation},\r\nabstract={In spite of a vast number of drug preparations used in medicine, advances in treating most socially important human diseases remain modest. Historically, many drugs were developed without clear understanding of the mechanisms of their action and were intended only for correcting symptoms of the disease. Identification of molecular targets in pharmacological screening new pharmaceuticals plays a key role not only in defining the strategy of the treatment, but also in understanding the general development of the disease. Sequencing of the genomes of various organisms, human in particular, and the development of new modern techniques of research have created the prerequisites for targeted screening for genes that are potentially interesting for development of new drugs. © Pleiades Publishing, Inc., 2009.},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)06-04-49571, 07-04-00128},\r\n}

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\n \n\n \n \n \n \n \n \n Ultrastructure of the hair in genetic prelingual deafness associated with the 35delg mutation in the connexin 26 gene (GJB2).\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 148(1): 79-81. 2009.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Ultrastructure$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Protein transduction domain peptide mediates delivery to the brain via the blood-brain barrier in Drosophila melanogaster.\n \n \n \n \n\n\n \n Sarantseva, S.; Bolshakova, O.; Timoshenko, S.; Kolobov, A.; Vitek, M.; and Schwarzman, A.\n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 3(2): 149-155. 2009.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Protein$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva2009149,\r\nauthor={Sarantseva, S.V. and Bolshakova, O.I. and Timoshenko, S.I. and Kolobov, A.A. and Vitek, M.P. and Schwarzman, A.L.},\r\ntitle={Protein transduction domain peptide mediates delivery to the brain via the blood-brain barrier in Drosophila melanogaster},\r\njournal={Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry},\r\nyear={2009},\r\nvolume={3},\r\nnumber={2},\r\npages={149-155},\r\ndoi={10.1134/S199075080902005X},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-65949086031&doi=10.1134%2fS199075080902005X&partnerID=40&md5=78b3d662faab8cbf2f177dc7c17e0507},\r\naffiliation={Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Leningrad oblast, Gatchina 188300, Russian Federation; State Research Institute of Highly Pure Biopreparations, ul. Pudozhskaya 7, St. Petersburg 197110, Russian Federation; Division of Neurology, Duke University Medical Center, Durham, NC 27710, United States; Institute for Experimental Medicine, Russian Academy of Medical Sciences, ul. Akademika Pavlova 12, St. Petersburg 197376, Russian Federation},\r\nabstract={The phenomenon of protein transduction represents internalization of short peptides known as protein transduction domains (PTD) by cells. It is widely used in the development of new preparations for treatment of various brain disorders. However, the drug discovery process is limited by lack of simple and reliable models of blood brain barrier (BBB). These models should meet two main criteria: they should be applicable for testing of large numbers of samples simultaneously reproduce the physiological and functional characteristics of mammalian (including) human BBB. The major goal of this study was to estimate the BBB-crossing ability of known PTD-peptides using Drosophila melanogaster BBB as the model. We demonstrate here that after abdominal administration the PTD-peptide penetratin, derived from a Drosophila Antennapedia homeodomain protein can cross Drosophila and deliver the apoE mimetic peptide exhibiting neuroprotective properties. © Pleiades Publishing, Ltd. 2009.},\r\nauthor_keywords={Antennapedia homeodomain;  Apolipoprotein E mimetic peptides;  Biotin;  Blood-brain barrier;  Drosophila melanogaster;  Penetratin;  Protein transduction domain;  Transport},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)07-04-00128, 06-04-49571},\r\n}

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\n \n\n \n \n \n \n \n \n Variations of glycoprotein IIb-IIIa (αIIb/β3-integrin) content in healthy donors. The influence on platelet aggregation activity and efficacy of aspirin action.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biochemistry (Moscow) Supplement Series B: Biomedical Chemistry, 3(1): 92-98. 2009.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Variations$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Genetic variants of platelet ADP receptor P2Y12 associated with changed platelet functional activity and development of cardiovascular diseases.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 45(2): 218-223. 2009.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Genetic variants of platelet ADP receptor P2Y12 associated with changed platelet functional activity and development of cardiovascular diseases.\n \n \n \n \n\n\n \n Sirotkina, O.; Zabotina, A.; Berkovich, O.; Bazhenova, E.; Vavilova, T.; and Shvartsman, A.\n\n\n \n\n\n\n Genetika, 45(2): 247-253. 2009.\n cited By 6\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina2009247,\r\nauthor={Sirotkina, O.V. and Zabotina, A.M. and Berkovich, O.A. and Bazhenova, E.A. and Vavilova, T.V. and Shvartsman, A.L.},\r\ntitle={Genetic variants of platelet ADP receptor P2Y12 associated with changed platelet functional activity and development of cardiovascular diseases},\r\njournal={Genetika},\r\nyear={2009},\r\nvolume={45},\r\nnumber={2},\r\npages={247-253},\r\nnote={cited By 6},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-64849087639&partnerID=40&md5=76d87775fbf32c5c8e9bc7fdfc2ae0b8},\r\nabstract={The key role in platelet aggregation is played by the platelet ADP receptor P2Y12, which is the target for antiaggregant drugs, clopidogrel and ticlopidine. At present, only sporadic data on genetic variants of platelet ADP receptor P2Y12 are available from literature, and their association with thromboembolic and cardiovascular diseases still remains obscure. Analysis of the group of subjects with high platelet reactivity resulted in identification of two nucleotide substitutions, C18T and G36T, in the coding region of the P2Y12 gene. The frequency of the P2Y12 T1 8 allele was higher in control group than in the group of patients survived from myocardial infarction at the age under 45 years (39% versus 28%, respectively, P = 0.04). Moreover, in the T18 carriers, platelet aggregation activity was lower than in the carriers of the wild-type genotype (0.84 +/- 0.05% versus 1.01 +/- 0.08%, respectively, P = 0.03). In the group of patients with early myocardial infarctions, a tendency towards the increased frequency of 16T allele in comparison with control group (20 and 12%, respectively, P = 0.07) was observed. The rate of ADP-induced platelet aggregation in the carriers of 16T allele from the control group was somewhat higher than in the subjects with the GG36 genotype (1.31 +/- 0.16% versus 1.12 +/- 0.06%, respectively, P = 0.07). The nucleotide substitutions identified were in absolute disequilibrium, i.e., allele T18 conformed to allele G36. On the contrary, allele C18 conformed to allele T36. Haplotype T18G36 was found to be responsible for the decreased risk of myocardial infarction and decreased platelet reactivity. It is suggested that polymorphisms of the P2Y12 gene identified can be used for determination of the risk group for myocardial infarction in the young males.},\r\ncorrespondence_address1={Sirotkina, O.V.},\r\nissn={00166758},\r\npubmed_id={19334620},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n\n

\n \n\n \n \n \n \n \n \n Protein transduction domain peptide mediates delivery to the brain via the blood-brain barrier in drosophila.\n \n \n \n \n\n\n \n Sarantseva, S.; Bolshakova, O.; Tunoshenko, S.; Kolobov, A.; Vitek, M.; and Schwarzman, A.\n\n\n \n\n\n\n Biomeditsinskaya Khimiya, 55(1): 41-49. 2009.\n cited By 6\n\n\n\n
\n\n\n\n \n \n $\"Protein$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva200941,\r\nauthor={Sarantseva, S.K. and Bolshakova, O.I. and Tunoshenko, S.I. and Kolobov, A.A. and Vitek, M.P. and Schwarzman, A.L.},\r\ntitle={Protein transduction domain peptide mediates delivery to the brain via the blood-brain barrier in drosophila},\r\njournal={Biomeditsinskaya Khimiya},\r\nyear={2009},\r\nvolume={55},\r\nnumber={1},\r\npages={41-49},\r\nnote={cited By 6},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-65349105042&partnerID=40&md5=54b580d1607cb31ad29acd3d22c6c8e4},\r\naffiliation={Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Leningrad district, Gatchina, 188300, Russian Federation; State Research Institute of Highly Pure Biopreparations, ul. Pudozhskaya 7, Saint-Petersburg, 197110, Russian Federation; Division of Neurology, Duke University Medical Center, Durham, NC 2771, United States; Institute for Experimental Medicine, Russian Academy of Medical Sciences, ul. Acad. Pavlova 12, Saint-Petersburg, 197376, Russian Federation},\r\nabstract={Protein transduction domain (PTD)-peptides greatly facilitate the delivery of high molecular weight macromolecules across the blood-brain barrier (BBB). This BBB-transport function is highly desirable and helps to enable the development of new therapeutics for treatment of brain disorders. However, the drug discovery process is limited by the generation of a simple and reliable BBB model that is amenable to testing of large number of samples and simultaneously, reproduces the physiological and functional characteristics of the human BBB. To address these challenges, we have studied whether the PTD-peptide penetratin, derived from a Drosophila Antennapedia homeodomain protein, is capable of crossing the BBB in Drosophila while carrying a cargo into the fly brain. An initial in vivo experiment in Drosophila showed that abdominal injection of biotin-tagged penetratin permeated the BBB. The same effect was observed for biotin-tagged penetratin fused with apoE mimetic peptide with demonstrated anti-inflammatory and neuroprotective activities.},\r\nauthor_keywords={Antennapedia Homeodomain;  Apolipoprotein E mimetic peptides;  Biotin;  Blood-brain barrier;  Drosophila melanogaster;  Penetratin;  Protein transduction domain;  Transport},\r\ncorrespondence_address1={Sarantseva, S. K.; Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Leningrad district, Gatchina, 188300, Russian Federation; email: svesar@omrb.pnpi.spb.ru},\r\npublisher={Russian Academy of Medical Sciences},\r\nissn={23106905},\r\npubmed_id={19351032},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomeditsinskaya Khim.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin.\n \n \n \n \n\n\n \n Sarantseva, S.; Bolshakova, O.; Timoshenko, S.; Rodin, D.; Vitek, M.; and Schwarzman, A.\n\n\n \n\n\n\n Russian Journal of Genetics, 45(1): 105-112. 2009.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Studying$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sarantseva2009105,\r\nauthor={Sarantseva, S.V. and Bolshakova, O.I. and Timoshenko, S.I. and Rodin, D.I. and Vitek, M. and Schwarzman, A.L.},\r\ntitle={Studying the pathogenesis of Alzheimer's disease in a Drosophila melanogaster model: Human APP overexpression in the brain of transgenic flies leads to deficit of the synaptic protein synaptotagmin},\r\njournal={Russian Journal of Genetics},\r\nyear={2009},\r\nvolume={45},\r\nnumber={1},\r\npages={105-112},\r\ndoi={10.1134/S1022795409010153},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-58149498442&doi=10.1134%2fS1022795409010153&partnerID=40&md5=3dd55141195f2e68c525679d2a58c93f},\r\naffiliation={St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad oblast 188306, Russian Federation; Division of Neurology, Duke University Medical Center, Durham, NC 27710, United States; Institute for Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg 197376, Russian Federation},\r\nabstract={Alzheimer's disease (AD) is a progressive neurodegenerative disease whose main pathomorphological sign is synapse degeneration in the cortex and hippocampus. Abnormal synaptogenesis precedes amyloidosis and neurodegeneration and correlates with memory impairment during the early clinical phase. Mutations in the amyloid precursor protein (APP) gene cause familial AD and enhance the secretion of amyloid-β protein (Aβ). However, it remains unclear in what way APP and Aβ- are involved in synaptic disorder in the absence of visible amyloid structures. In this study, the role of the human APP gene in synaptogenesis in transgenic lines of Drosophila melanogaster whose nerve cells express the human APP695 isoform, truncated APPs, and the presynaptic marker synaptotagmin containing the green fluorescent protein (GFP) sequence. The expression of APP and its truncated forms caused a decrease in the synaptotagmin content of antennal lobes (ALs) and mushroom bodies (MBs) of the D. melanogaster brain, as well as neurodegeneration that progressed with age. The results suggest that abnormal synaptogenesis and neurodegeneration occur in the Drosophila brain in the absence of β-. It is assumed that impaired cellular functions of APP and secretion of β- independently contribute to the pathogenesis of AD. © 2009 MAIK Nauka.},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)07–04–00 128, 06-04-49 571},\r\n}

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\n \n 2008\n \n \n (3)\n \n \n

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\n \n\n \n \n \n \n \n \n High Level of α-Synuclein mRNA in peripheral lymphocytes of patients with alcohol dependence syndrome.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 146(5): 609-611. 2008.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"High$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Screening for LRRK2 mutations in patients with Parkinson's disease in Russia: Identification of a novel LRRK2 variant.\n \n \n \n \n\n\n \n Pchelina, S.; Yakimovskii, A.; Emelyanov, A.; Ivanova, O.; Schwarzman, A.; and Singleton, A.\n\n\n \n\n\n\n European Journal of Neurology, 15(7): 692-696. 2008.\n cited By 22\n\n\n\n
\n\n\n\n \n \n $\"Screening$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pchelina2008692,\r\nauthor={Pchelina, S.N. and Yakimovskii, A.F. and Emelyanov, A.K. and Ivanova, O.N. and Schwarzman, A.L. and Singleton, A.B.},\r\ntitle={Screening for LRRK2 mutations in patients with Parkinson's disease in Russia: Identification of a novel LRRK2 variant},\r\njournal={European Journal of Neurology},\r\nyear={2008},\r\nvolume={15},\r\nnumber={7},\r\npages={692-696},\r\ndoi={10.1111/j.1468-1331.2008.02149.x},\r\nnote={cited By 22},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-44949116904&doi=10.1111%2fj.1468-1331.2008.02149.x&partnerID=40&md5=21c50cd46b1d43a96efbc402e717bd9b},\r\naffiliation={St. Petersburg State Pavlov Medical University, St. Petersburg, Russian Federation; Petersburg Nuclear Physics Institute, RAS, St. Petersburg, Russian Federation; Molecular Genetics Unit, NIA, NIH, Bethesda, MD, United States; Department of Molecular and Gene Technologies, St. Petersburg State Pavlov Medical University, L.Tolstogo str 6/8, St. Petersburg, 197089, Russian Federation},\r\nabstract={Background and purpose: Mutations in LRRK2, encoding leucine-rich repeat kinase 2 (or Dardarin), cause autosomal dominant Parkinson's disease (AdPD) and are also found in sporadic PD (sPD). To investigate the frequency of LRRK2 mutations in a sample of Russian PD patients. Methods: We sequenced the complete coding region of LRRK2 in 65 patients with AdPD and in 30 patients with sPD. Furthermore, in 20 patients with AdPD and in 159 patients with sPD we screened several common LRRK2 mutations (G2019S, R1441C/G/H, I2012T and I2020T). Results: Five AdPD patients had the LRRK2 G2019S mutation (5.9%, 5/85). In addition, we discovered a novel LRRK2 variant V1613A in a family with a tremor dominant form of AdPD; this variant was not present in controls. We identified two patients with LRRK2 mutations in sPD: one with the G2019S mutation (0.5; 1/189) and another with the previously described R1441C mutation (0,5; 1/189). Conclusions: LRRK2 mutations are common amongst patients with PD in Russia. The results also show that the G2019S mutation is the most frequent. We identified one novel mutation in a functional region of LRRK2. © 2008 The Author(s).},\r\nauthor_keywords={LRRK2;  Mutation;  Parkinson's disease},\r\ncorrespondence_address1={Pchelina, S. N.; Department of Molecular and Gene Technologies, St. Petersburg State Pavlov Medical University, L.Tolstogo str 6/8, St. Petersburg, 197089, Russian Federation; email: sopchelina@hotmail.com},\r\nissn={13515101},\r\ncoden={EJNEF},\r\npubmed_id={18435766},\r\nlanguage={English},\r\nabbrev_source_title={Eur. J. Neurol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Variations in glycoprotein IIb-IIIa (αIIb/β3-integrin) content in healthy donors. Influence on platelet aggregation activity and efficacy of aspirin action.\n \n \n \n \n\n\n \n Khaspekova, S.; Sirotkina, O.; Shimanova, Y.; and Mazurov, A.\n\n\n \n\n\n\n Biomeditsinskaya Khimiya, 54(3): 361-371. 2008.\n cited By 6\n\n\n\n
\n\n\n\n \n \n $\"Variations$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Khaspekova2008361,\r\nauthor={Khaspekova, S.G. and Sirotkina, O.V. and Shimanova, Y.V. and Mazurov, A.V.},\r\ntitle={Variations in glycoprotein IIb-IIIa (αIIb/β3-integrin) content in healthy donors. Influence on platelet aggregation activity and efficacy of aspirin action},\r\njournal={Biomeditsinskaya Khimiya},\r\nyear={2008},\r\nvolume={54},\r\nnumber={3},\r\npages={361-371},\r\nnote={cited By 6},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-51249091035&partnerID=40&md5=d57e91587aa065acf90d186e490856e7},\r\naffiliation={Cardiology Research and Production Complex, Russian Ministry O Health, 3rd Cherepkovskaya 15a, Moscow, 121552, Russian Federation; Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nabstract={Effects of fibrinogen receptor, glycoprotein (GP) IIb-IIIa (αII/β3-integrin) content, GP IIIa genetic polymorphism (substitution Leu33Pro) and fibrinogen concentration in blood plasma on platelet aggregation activity were studied in a group of healthy volunteers. The GP IIb-IIIa content on platelet surface in 3 5 tested donors varied (40-71)× 103 per platelet. Repeated measurements revealed that the GP Hb-IIIa content coefficient of variation was 9.5%, and deviations from mean levels did not exceed 20%. The level and rate of platelet aggregation induced by ADP (1.25-20 M) correlated with GP IIb-IIIa number (r from 0.315 to 0.591) and were higher in a group of donors with high in comparison with low GP IIb-IIIa content (&gt; 60 and (40-50)× 103 per platelet respectively). Aspirin, the inhibitor of thromboxane A2 synthesis, partially suppressed ADP-induced platelet aggregation. The level of residual aggregation in the presence of aspirin also correlated with GP IIb-IIIa content and increased in subjects with high receptor content. Parameters of ADP-induced aggregation did not differ in donors with GP IIIa Pro33(-) (Leu33Leu33, n = 20) and Pro33(+) (Leu33Pro33, n = 13, and Pro33Pro33, n = 2) genotype. GP IIb-IIIa content was also not affected by GP IIIa polymorphism. No significant correlations were found between the level and rate of platelet aggregation and fibrinogen concentration in blood plasma. The data obtained indicate that effects of GP IIb-IIIa variations in content on platelet aggregation are higher than GP IIIa Leu33Pro polymorphism and variations of fibrinogen concentration. High GP IIb-IIIa content is associated with increased platelet aggregation activity and decreased efficacy of aggregation inhibition by aspirin.},\r\nauthor_keywords={Fibrinogen;  Genetic polymorphism;  Glycoprotein IIb-IIIa;  Integrins;  Platelets},\r\ncorrespondence_address1={Khaspekova, S. G.; Cardiology Research and Production Complex, Russian Ministry O Health, 3rd Cherepkovskaya 15a, Moscow, 121552, Russian Federation; email: calab@cardio.ru},\r\npublisher={Russian Academy of Medical Sciences},\r\nissn={23106905},\r\npubmed_id={18712091},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomeditsinskaya Khim.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2007\n \n \n (4)\n \n \n

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\n \n\n \n \n \n \n \n \n Genetic risk factors for development of myocardial infarction in young men living in North-West region of Russia.\n \n \n \n \n\n\n \n Pchelina, S.; Sirotkina, O.; Sheǐdina, A.; Taraskina, A.; Rodygina, T.; Demina, E.; Zabotina, A.; Mitupova, M.; Bazhenova, E.; Berkovich, O.; Shliakhto, E.; Shvartsman, A.; and Shvarts, E.\n\n\n \n\n\n\n Kardiologiia, 47(7): 29-34. 2007.\n cited By 8\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pchelina200729,\r\nauthor={Pchelina, S.N. and Sirotkina, O.V. and Sheǐdina, A.M. and Taraskina, A.E. and Rodygina, T.I. and Demina, E.P. and Zabotina, A.M. and Mitupova, M.I. and Bazhenova, E.A. and Berkovich, O.A. and Shliakhto, E.V. and Shvartsman, A.L. and Shvarts, E.I.},\r\ntitle={Genetic risk factors for development of myocardial infarction in young men living in North-West region of Russia},\r\njournal={Kardiologiia},\r\nyear={2007},\r\nvolume={47},\r\nnumber={7},\r\npages={29-34},\r\nnote={cited By 8},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-40949109019&partnerID=40&md5=78725c1ed5b851fd676ef6651bb06941},\r\nabstract={With the aim to detect genetic factors of risk of development of early myocardial infarction (MI) we studied 29 allele variants of 19 genes in 206 men who had survived MI in the age before 45 years and in 195 men of similar age without cardiovascular diseases. All subjects were inhabitants of North-West region of Russia. The following factors were associated with history of myocardial infarction: genotype RR191 of paraoxonase-1 (PON1) gene (RR 2.8 [95% CI: 1.24 - 6.30]), P1A2 allele of glycoprotein (GP) IIIa subunit of platelet fibrinogen receptor GPIIb/IIIa (RR 1.8 [95% CI: 1.11 - 2.93]), and Met145 allele of GPIbalpha platelet von Willebrand factor receptor gene. Genotype CC ( - 108) PON1 was associated with lowered risk of MI development (RR 0.6 [95% CI: 0.40 - 0.91]). During 7 years of follow-up 30 men from MI group died of recurrent acute coronary syndromes. In the group of those who died we noted increased prevalence of P1A2 GPIIIa allele compared with those who survived (p < 0.03). The results allow to suggest that contribute to development of MI in young men factors associated with elevation of functional state of platelets and levels of oxidized lipids in blood plasma.},\r\ncorrespondence_address1={Pchelina, S.N.},\r\nissn={00229040},\r\npubmed_id={18260892},\r\nlanguage={Russian},\r\nabbrev_source_title={Kardiologiia},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Effects of platelet glycoprotein IIb-IIIa number and glycoprotein IIIa Leu33Pro polymorphism on platelet aggregation and sensitivity to glycoprotein IIb-IIIa antagonists.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Platelets, 18(7): 506-514. 2007.\n cited By 21\n\n\n\n
\n\n\n\n \n \n $\"Effects$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n\n\n

\n We investigated the influence of glycoprotein (GP) IIIa Leu33Pro polymorphism, platelet GP IIb-IIIa number, and plasma fibrinogen concentration on platelet aggregation and antiaggregatory action of GP IIb-IIIa antagonists. Healthy volunteers with GP IIIa Pro33(-) (Leu33Leu33, n = 20) and Pro33(+) (Leu33Pro33, n = 13, and Pro33Pro33, n = 2) genotypes were included into the study. GP IIIa Leu33Pro substitution was associated with the increase of the level and rate of platelet microaggregate formation induced by GP IIb-IIIa activating antibody CRC54 (100, 200, 400 μg/ml) against the epitope within 1-100 residues of GP IIIa N-terminal part (p from 0.001 to 0.047). No significant differences were detected between parameters of platelet aggregation induced by ADP (1.25, 2.5, 5.0, 20 μM) in GP IIIa Pro33(+) and Pro33(-) donors. GP IIb-IIIa antagonist Monafram (F(ab')2 fragment of GP-IIb-IIIa blocking antibody CRC64) (1, 2, 3 μg/ml), but not eptifibatide (50, 100, 150 ng/ml) inhibited ADP-induced aggregation slightly less efficiently in GP IIIa Pro33(+) group (p < 0.05 at 1 and 2 μg/ml Monafram). GP IIb-IIIa number (evaluated as maximal binding of 125I-labelled antibody CRC64) varied from 40.5 to 80.8 × 103 per platelet with no significant influence of GP IIIa genotype. Consistent correlations were revealed between GP IIb-IIIa quantity and the level and rate of ADP-induced aggregation (r from 0.353 to 0.583, p from <0.001 to 0.037) as well as resistance (level of residual aggregation) to both GP IIb-IIIa antagonists (r from 0.345 to 0.602, p from <0.001 to 0.042). ADP-induced aggregation was considerably increased and efficiency of GP IIb-IIIa antagonists decreased in donors with high in comparison with low GP IIb-IIIa quantity (>60 and 40-50 × 103 per platelet respectively, p < 0.01 for most tests). No correlations were observed between all tested parameters and plasma fibrinogen concentration. Our results indicate that inter-individual variability of platelet GP IIb-IIIa number significantly affects platelet aggregation and antiaggregatory effects of GP IIb-IIIa antagonists. Contribution of this factor is higher than that of GP IIIa Leu33Pro polymorphism and variations of fibrinogen concentration. © 2007 Informa UK Ltd.\n

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\n \n\n \n \n \n \n \n \n Participation of IIb-IIIa glycoprotein in spontaneous platelet aggregation.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 143(4): 422-425. 2007.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"Participation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Mutation screen of the GAD2 gene and association study of alcoholism in three populations.\n \n \n \n \n\n\n \n Lappalainen, J.; Krupitsky, E.; Kranzler, H.; Lue, X.; Remizov, M.; Pchelina, S.; Taraskina, A.; Zvartau, E.; Räsanen, P.; Makikyro, T.; Somberg, L.; Krystal, J.; Stein, M.; and Gelernter, J.\n\n\n \n\n\n\n American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics, 144(2): 183-192. 2007.\n cited By 21\n\n\n\n
\n\n\n\n \n \n $\"Mutation$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Lappalainen2007183,\r\nauthor={Lappalainen, J. and Krupitsky, E. and Kranzler, H.R. and Lue, X. and Remizov, M. and Pchelina, S. and Taraskina, A. and Zvartau, E. and Räsanen, P. and Makikyro, T. and Somberg, L.K. and Krystal, J.H. and Stein, M.B. and Gelernter, J.},\r\ntitle={Mutation screen of the GAD2 gene and association study of alcoholism in three populations},\r\njournal={American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics},\r\nyear={2007},\r\nvolume={144},\r\nnumber={2},\r\npages={183-192},\r\ndoi={10.1002/ajmg.b.30377},\r\nnote={cited By 21},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-34047272984&doi=10.1002%2fajmg.b.30377&partnerID=40&md5=d10dc896688b44bf3b958c83e7c37a5d},\r\naffiliation={Department of Psychiatry, Yale University School of Medicine, New Haven, CT, United States; VA Connecticut Healthcare System, West Haven, CT, United States; St. Petersburg State Pavlov Medical University, St. Petersburg, Russian Federation; Department of Psychiatry, University of Connecticut School of Medicine, Farmington, CT, United States; Department of Psychiatry, University of Oulu, Oulu, Finland; Department of Psychiatry, University of California, San Diego, CA, United States; Yale University, VA Connecticut Healthcare System, Psychiatry 116A2, 950 Campbell Ave, West Haven, CT 06516, United States},\r\nabstract={Synaptic actions of γ-amino butyric acid (GABA) have been implicated in many facets of ethanol's effects and risk for alcoholism. We examined whether variation in glutamate decarboxylase-2 (GAD2), a gene encoding for a major enzyme in the synthesis of GABA, contributes to risk of alcohol dependence (AD). We screened GAD2 for sequence variants using dHPLC in a population of 96 individuals. Several single nucleotide polymorphisms (SNPs), including four rare non-synonymous polymorphisms, were identified. Thirteen SNPs located in the GAD2 gene were genotyped in a sample of 113 Russian males with AD and 100 Russian male controls. These analyses revealed a modest association between the functional GAD2 -243 A > G SNP (rs2236418) and AD (allele P = 0.038, genotype P = 0.008). An additional sample of 138 Russian males with AD were genotyped for the GAD2 -243 A > G. These analyses supported an association of this polymorphism with AD (combined sample allele P = 0.038, genotype P = 0.0009). We extended these findings to additional populations: a sample of 538 college students assessed using the AUDIT and a sample of European-American (EA) AD subjects (n = 235) and controls (n = 310). Analyses in these populations did not support a role for GAD2 in alcoholism. In summary, the results of an extensive search for an association of GAD2 with AD suggest that variation in GAD2 is not a major risk factor for AD in EAs. The functional promoter GAD2 -243 A > G variant may influence risk for AD in some populations, or its role may be limited to susceptibility to severe AD. © 2006 Wiley-Liss, Inc.},\r\nauthor_keywords={Alcoholism;  GABA;  Genetics;  Glutamate decarboxylase;  Polymorphism},\r\ncorrespondence_address1={Lappalainen, J.; Yale University, VA Connecticut Healthcare System, Psychiatry 116A2, 950 Campbell Ave, West Haven, CT 06516, United States; email: jaakko.lappalainen@yale.edu},\r\nissn={15524841},\r\ncoden={AJMGE},\r\npubmed_id={17034009},\r\nlanguage={English},\r\nabbrev_source_title={Am. J. Med. Genet. Part B Neuropsychiatr. Genet.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n

\n \n 2006\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n G2019S LRRK2 mutation in familial and sporadic Parkinson's disease in Russia.\n \n \n \n \n\n\n \n Pchelina, S.; Yakimovskii, A.; Ivanova, O.; Emelianov, A.; Zakharchuk, A.; and Schwarzman, A.\n\n\n \n\n\n\n Movement Disorders, 21(12): 2234-2236. 2006.\n cited By 17\n\n\n\n
\n\n\n\n \n \n $\"G2019S$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pchelina20062234,\r\nauthor={Pchelina, S.N. and Yakimovskii, A.F. and Ivanova, O.N. and Emelianov, A.K. and Zakharchuk, A.H. and Schwarzman, A.L.},\r\ntitle={G2019S LRRK2 mutation in familial and sporadic Parkinson's disease in Russia},\r\njournal={Movement Disorders},\r\nyear={2006},\r\nvolume={21},\r\nnumber={12},\r\npages={2234-2236},\r\ndoi={10.1002/mds.21134},\r\nnote={cited By 17},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-33846408281&doi=10.1002%2fmds.21134&partnerID=40&md5=c3f05dde5052fb088bb5c49cf1e176cb},\r\naffiliation={Petersburg Nuclear Physics Institute, RAS, St. Petersburg, Russian Federation; St. Petersburg State Pavlov Medical University, L. Tolstogo str. 6/8, St. Petersburg, Russian Federation; St. Petersburg Cuty Geriatric Center, St. Peterburg, Russian Federation},\r\nabstract={Among mutations associated with autosomal dominant an sporadic Parkinson's disease (PD) the G2019S substitution in the leucine-rich repeat kinase 2 (LRRK2) gene is the most frequently identified. To estimate its frequency in Russia, we analyzed 208 patients with PD from the Northwestern region of Russia. Of these, 51 patients were probands from families with PD compatible with autosomal dominant inheritance. The control group represented 161 subjects without neurological disorders settled in the same region. The frequency of the G2019S mutation was greater in familial PD (2 [3.9%] of 51) than in sporadic PD) (1 [0.6%] of 157). In addition, this mutation was found in the proband's father, who also had PD, in 1 PD family, and in 1 carrier without signs of PD at age 40 in another PD family. All carriers were heterozygous for the G2019S mutation and reported the Ashkenazi Jewish origin. The mutation was not found in the control group. © 2006 Movement Disorder Society.},\r\nauthor_keywords={LRRK2;  Mutation;  Parkinson's disease;  Russia},\r\ncorrespondence_address1={Pchelina, S.N.; Department of Molecular and Gene Technologies, St. Petersburg State Pavlov Medical University, L. Tolstogo str. 6/8, St. Petersburg, Russian Federation; email: sopchelina@hotmail.com},\r\nissn={08853185},\r\ncoden={MOVDE},\r\npubmed_id={17044089},\r\nlanguage={English},\r\nabbrev_source_title={Mov. Disord.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2005\n \n \n (6)\n \n \n

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\n \n\n \n \n \n \n \n \n Clinical value of allele variants of cytochrome CYP2C9 gene for anticoagulation therapy with warfarin.\n \n \n \n \n\n\n \n Sirotkina, O.; Ulitina, A.; Taraskina, A.; Kadinskaya, M.; Vavilova, T.; Pchelina, S.; and Schwarts, E.\n\n\n \n\n\n\n Kardiologiya, 45(4): 61-63. 2005.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Clinical$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina200561,\r\nauthor={Sirotkina, O.V. and Ulitina, A.S. and Taraskina, A.E. and Kadinskaya, M.I. and Vavilova, T.V. and Pchelina, S.N. and Schwarts, E.I.},\r\ntitle={Clinical value of allele variants of cytochrome CYP2C9 gene for anticoagulation therapy with warfarin},\r\njournal={Kardiologiya},\r\nyear={2005},\r\nvolume={45},\r\nnumber={4},\r\npages={61-63},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-33644955020&partnerID=40&md5=79148a97228d86733dc3a4258fe38ba5},\r\naffiliation={I.P. Pavlov St.-Peterburg State Medical University},\r\nabstract={Warfarin is metabolized by cytochrome CYP2C9 and its pharmacokinetic properties depend on structural polymorphisms of CYP2C9 gene. We studied frequencies of allele variants of CYP2C9 gene and associations of individual reaction to warfarin intake with genotype of CYP2C9 gene. Population frequencies of CYP2C9×1, CYP2C9×2, CYP2C9×3 alleles of CYP2C9 gene in St-Petersburg were 82.66, 11.11, and 6.32%, respectively. Carriers of CYP2C9×2 and CYP2C9×3 alleles more rapidly achieved therapeutic levels of hypocoagulation and required significantly lower weekly doses of warfarin.},\r\nauthor_keywords={CYP2C9 gene;  Pharmacogenetics;  Warfarin},\r\ncorrespondence_address1={Sirotkina, O.V.; I.P. Pavlov St.-Peterburg State Medical University},\r\nissn={00229040},\r\npubmed_id={15940194},\r\nlanguage={Russian},\r\nabbrev_source_title={Kardiologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Selection of peptides binding to the amyloid b-protein reveals potential inhibitors of amyloid formation.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Amyloid, 12(4): 199-209. 2005.\n cited By 23\n\n\n\n
\n\n\n\n \n \n $\"Selection$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n\n \n \n \n \n \n \n Novel mutation of the GPIIIa gene in the Russian population, Leu40Arg, linked to the Leu33Pro.\n \n \n \n \n\n\n \n Sirotkina, O.; Shaydina, A.; Vavilova, T.; and Schwartz, E.\n\n\n \n\n\n\n Genetika, 41(6): 838-843. 2005.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Novel$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina2005838,\r\nauthor={Sirotkina, O.V. and Shaydina, A.M. and Vavilova, T.V. and Schwartz, E.I.},\r\ntitle={Novel mutation of the GPIIIa gene in the Russian population, Leu40Arg, linked to the Leu33Pro},\r\njournal={Genetika},\r\nyear={2005},\r\nvolume={41},\r\nnumber={6},\r\npages={838-843},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-26944462373&partnerID=40&md5=562b7b4ad90f9c49cf5ee58faba677d8},\r\naffiliation={St. Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Leningrad oblast, Gatchina, 188350, Russian Federation; St. Petersburg Pavlov State Medical University, St. Petersburg, 197022, Russian Federation},\r\nabstract={Glycoprotein IIb/IIIa complex, a platelet surface fibrinogen receptor, plays a key role in producing primary hemostasis. At present, only a single mutation in the GPIIIa gene, Leu33Pro, and a single mutation in the GPIIb gene, Ile843Ser, has been described. The mutations are known to enhance signaling functions of the receptor and are associated with the development of arterial thromboses. In the present study, we describe a novel GPIIIa mutation, which is T to G nucleotide substitution in position 1585, resulting in the replacement of Leu for Arg in position 40 of the amino acid sequence of the protein.},\r\ncorrespondence_address1={Sirotkina, O.V.; St. Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Leningrad oblast, Gatchina, 188350, Russian Federation; email: olga_sirotkina@mail.ru},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={16080610},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Novel mutation of the GPIIIa gene in the Russian population, Leu40Arg, linked to the Leu33Pro.\n \n \n \n \n\n\n \n Sirotkina, O.; Shaydina, A.; Vavilova, T.; and Schwartz, E.\n\n\n \n\n\n\n Russian Journal of Genetics, 41(6): 683-687. 2005.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Novel$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Sirotkina2005683,\r\nauthor={Sirotkina, O.V. and Shaydina, A.M. and Vavilova, T.V. and Schwartz, E.I.},\r\ntitle={Novel mutation of the GPIIIa gene in the Russian population, Leu40Arg, linked to the Leu33Pro},\r\njournal={Russian Journal of Genetics},\r\nyear={2005},\r\nvolume={41},\r\nnumber={6},\r\npages={683-687},\r\ndoi={10.1007/s11177-005-0145-2},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-23744441034&doi=10.1007%2fs11177-005-0145-2&partnerID=40&md5=a5d61768b645085189fd610085570da5},\r\naffiliation={St. Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Leningrad Oblast, Gatchina, 188350, Russian Federation; St. Petersburg Pavlov State Medical University, St. Petersburg, 197022, Russian Federation},\r\nabstract={Glycoprotein IIb/IIIa complex, a platelet surface fibrinogen receptor, plays a key role in producing primary hemostasis. At present, only a single mutation in the GPIIIa gene, Leu33Pro, and a single mutation in the GPIIb gene, Ile843Ser, has been described. The mutations are known to enhance signaling functions of the receptor and are associated with the development of arterial thromboses. In the present study, we describe a novel GPIIIa mutation, which is T to G nucleotide substitution in position 1585, resulting in the replacement of Leu for Arg in position 40 of the amino acid sequence of the protein. © 2005 Pleiades Publishing, Inc.},\r\ncorrespondence_address1={Sirotkina, O.V.; St. Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Leningrad Oblast, Gatchina, 188350, Russian Federation; email: olga-sirotkina@mail.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Association between alcoholism and γ-amino butyric acid α2 receptor subtype in a Russian population.\n \n \n \n \n\n\n \n Lappalainen, J.; Krupitsky, E.; Remizov, M.; Pchelina, S.; Taraskina, A.; Zvartau, E.; Somberg, L.; Covault, J.; Kranzler, H.; Krystal, J.; and Gelernter, J.\n\n\n \n\n\n\n Alcoholism: Clinical and Experimental Research, 29(4): 493-498. 2005.\n cited By 157\n\n\n\n
\n\n\n\n \n \n $\"Association$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Lappalainen2005493,\r\nauthor={Lappalainen, J. and Krupitsky, E. and Remizov, M. and Pchelina, S. and Taraskina, A. and Zvartau, E. and Somberg, L.K. and Covault, J. and Kranzler, H.R. and Krystal, J.H. and Gelernter, J.},\r\ntitle={Association between alcoholism and γ-amino butyric acid α2 receptor subtype in a Russian population},\r\njournal={Alcoholism: Clinical and Experimental Research},\r\nyear={2005},\r\nvolume={29},\r\nnumber={4},\r\npages={493-498},\r\ndoi={10.1097/01.ALC.0000158938.97464.90},\r\nnote={cited By 157},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-20244368365&doi=10.1097%2f01.ALC.0000158938.97464.90&partnerID=40&md5=bb09638cda9e8200741e971fb961fe72},\r\naffiliation={Department of Psychiatry, Yale University, School of Medicine, New Haven, CT, United States; VA Connecticut Healthcare System, West Haven, CT, United States; St. Petersburg State Pavlov Med. U., St. Petersburg, Russian Federation; Department of Psychiatry, University of Connecticut, School of Medicine, Farmington, CT, United States; Yale University, VA Connecticut Healthcare System, Psychiatry 116A2, 950 Campbell Avenue, West Haven, CT 06516, United States},\r\nabstract={Background: Two recent large genetic studies in the US population have reported association between genetic variation in γ-amino butyric acid α2 receptor subtype (GABRA2) and risk for alcohol dependence. The goal of this study was to test whether GABRA2 is associated with alcohol dependence in a sample of Russian alcohol-dependent men. Methods: A total of 113 Russian alcohol-dependent men and 100 male population control subjects were recruited in St. Petersburg and genotyped for seven GABRA2 single-nucleotide polymorphisms (SNPs) using real-time PCR (TaqMan). Six SNPs were located in a GABRA2 haplotype block previously associated with alcohol dependence (AD) in the US population. SNPs and haplotypes were tested for an association to AD using χ2 analysis and a likelihood ratio-based statistic implemented in the software COCAPHASE. Results: Significant associations between two SNPs and AD were observed (p &lt; 0.05). In addition, a trend-level association was observed between AD and three adjacent SNPs (p &lt; 0.1). Associated alleles were carried in a haplotype that was present at frequencies of 0.37 and 0.48 in the control and alcohol-dependent populations, respectively (p &lt; 0.06). Tight linkage disequilibrium spanning from the central portion of the gene to the 3′ end was observed in this population. Comparison of the findings to the previously published studies in the US population revealed a highly similar linkage disequilibrium pattern in this population. Conclusions: These findings suggest that genetic variants of GABRA2 increase risk for AD in the Russian population and provide additional support to the hypothesis that polymorphic variation at the GABRA2 locus plays an important role in predisposing to AD at least in European-ancestry populations. Copyright © 2005 by the Research Society on Alcoholism.},\r\nauthor_keywords={Alcoholism;  Association;  GABA;  Genetics;  Russian Population},\r\ncorrespondence_address1={Lappalainen, J.; Yale University, VA Connecticut Healthcare System, Psychiatry 116A2, 950 Campbell Avenue, West Haven, CT 06516, United States; email: jaakko.lappalainen@yale.edu},\r\nissn={01456008},\r\ncoden={ACRSD},\r\npubmed_id={15834213},\r\nlanguage={English},\r\nabbrev_source_title={Alcohol. Clin. Exp. Res.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The frequency of cytochrome P450 2C9 genetic variants in the Russian population and their associations with individual sensitivity to warfarin therapy.\n \n \n \n \n\n\n \n Pchelina, S.; Sirotkina, O.; Taraskina, A.; Vavilova, T.; Shwarzman, A.; and Schwartz, E.\n\n\n \n\n\n\n Thrombosis Research, 115(3): 199-203. 2005.\n cited By 12\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pchelina2005199,\r\nauthor={Pchelina, S.N. and Sirotkina, O.V. and Taraskina, A.E. and Vavilova, T.V. and Shwarzman, A.L. and Schwartz, E.I.},\r\ntitle={The frequency of cytochrome P450 2C9 genetic variants in the Russian population and their associations with individual sensitivity to warfarin therapy},\r\njournal={Thrombosis Research},\r\nyear={2005},\r\nvolume={115},\r\nnumber={3},\r\npages={199-203},\r\ndoi={10.1016/j.thromres.2004.08.020},\r\nnote={cited By 12},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-11144343361&doi=10.1016%2fj.thromres.2004.08.020&partnerID=40&md5=6c913f02c1c95a86f34ade40fd008200},\r\naffiliation={S.-Petersburg Pavlov State Med. U., St. Petersburg, Russia, Russian Federation; Petersburg Nuclear Physics Institute, St. Petersburg, Russia, Russian Federation; S.-Petersburg Pavlov State Med. U., L. Tolstogo Street, 6/8, St. Petersburg, 197022 F., Russian Federation},\r\nauthor_keywords={CYP2C9 polymorphism;  Oral anticoagulants;  Pharmacogenetics;  Warfarin therapy},\r\ncorrespondence_address1={S.-Petersburg Pavlov State Med. U., St. Petersburg, RussiaRussian Federation; email: sopchelina@hotmail.com},\r\nissn={00493848},\r\ncoden={THBRA},\r\npubmed_id={15617742},\r\nlanguage={English},\r\nabbrev_source_title={Thromb. Res.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2004\n \n \n (4)\n \n \n

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\n \n\n \n \n \n \n \n \n Models of inter-group difference of the homeostasis system in patients with artificial heart valves and the set of laboratory parameters.\n \n \n \n \n\n\n \n Vavilova, T.; Razorenov, G.; Kadinskaya, M.; Sirotkina, O.; Pchelina, S.; Emanuel, V.; Orlovsky, P.; and Gritsenko, V.\n\n\n \n\n\n\n Klinichescheskaya Laboratornaya Diagnostika, (10): 41-44. 2004.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Models$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Vavilova200441,\r\nauthor={Vavilova, T.V. and Razorenov, G.I. and Kadinskaya, M.I. and Sirotkina, O.V. and Pchelina, S.N. and Emanuel, V.L. and Orlovsky, P.I. and Gritsenko, V.V.},\r\ntitle={Models of inter-group difference of the homeostasis system in patients with artificial heart valves and the set of laboratory parameters},\r\njournal={Klinichescheskaya Laboratornaya Diagnostika},\r\nyear={2004},\r\nnumber={10},\r\npages={41-44},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-9344251633&partnerID=40&md5=a33ea3ab98968dfc4894cdf9f45f10f7},\r\nabstract={Patients with artificial heart valves (AHV) belong to a unique multi-component model of the homeostasis system presenting an interaction of activated coagulation processes and pharmacological effects, on the one hand, and genetic peculiarities functioning homeostatic mechanisms, on the other hand. The described method was evaluated on the basis of multi-factor mathematic analysis by information-metry. The data obtained provided for isolating the most information-dense laboratory indices and some genetic polymorphisms describing the shaping of continuous intravascular coagulation of stage III in AHV patients. The clinicians and laboratory experts are offered a practical instrument for the diagnosis (prognostication) of the above condition. It was proven as necessary to examine (by the morphofunctional method) the intravascular activation of platelets and to determine the D-dimer in the remote period after prosthesis of heart valves.},\r\nissn={08692084},\r\npubmed_id={15584400},\r\nlanguage={Russian},\r\nabbrev_source_title={Klin. Lab. Diagn.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n The influence of hereditary thrombophilic mechanisms on the degree of permanent intravascular coagulation in patients with artificial heart valves [Vliianie nasledstvennykh trombofilicheskikh mekhanizmov na stepen' postoiannogo vnutrisosudistogo svertyvaniia u bol'nykh s iskusstvennymi klapanami serdtsa.].\n \n \n \n \n\n\n \n Vavilova, T.; Sirotkina, O.; Razorenov, G.; Razorenova, T.; Emanuél', V.; Gritsenko, V.; Orlovskiǐ, P.; Doǐnikov, D.; Sharafutdinov, V.; Karpov, S.; Kuznetsov, A.; and Kadinskaia, M.\n\n\n \n\n\n\n Vestnik khirurgii imeni I. I. Grekova, 163(5): 89-94. 2004.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Vavilova200489,\r\nauthor={Vavilova, T.V. and Sirotkina, O.V. and Razorenov, G.I. and Razorenova, T.S. and Emanuél', V.L. and Gritsenko, V.V. and Orlovskiǐ, P.I. and Doǐnikov, D.N. and Sharafutdinov, V.E. and Karpov, S.A. and Kuznetsov, A.A. and Kadinskaia, M.I.},\r\ntitle={The influence of hereditary thrombophilic mechanisms on the degree of permanent intravascular coagulation in patients with artificial heart valves [Vliianie nasledstvennykh trombofilicheskikh mekhanizmov na stepen' postoiannogo vnutrisosudistogo svertyvaniia u bol'nykh s iskusstvennymi klapanami serdtsa.]},\r\njournal={Vestnik khirurgii imeni I. I. Grekova},\r\nyear={2004},\r\nvolume={163},\r\nnumber={5},\r\npages={89-94},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-15944378909&partnerID=40&md5=e6fb827968bdc23b61715d50e832e72a},\r\nabstract={The genotyping of 40 patients with artificial heart valves (AHV) was performed after prosthesis of the mitral and aotic valves with bicuspid AHV (Medinzh-2 and CarboMedics). The patients took phenylin and varfarin. The patients' genotype was estimated by the thrombophylic genes: factor V Leiden (FVL), prothrombin G20210A, methylene tetrahydrofolate reductase C677T, G/A--455FGB, 4G/5G PAI-1, PI A1/A2 GPIIIa. The genes determining the thrombocytic activity or the vascular wall state substantially influence the third degree of the intensity of the permanent intravascular coagulation (PIC-3) independent of the degree of correction of hemostasis of oral anticoagulants. The addition of anti-aggregants to therapy is the only that can normalize functional activity of thrombocytes in patients with AHV having such defects. The laboratory detection of the genetic defects is of great practical importance for the determination of risk groups of formation of PIC-3 and the strategy of antithrombotic protection of patients with AHV.},\r\ncorrespondence_address1={Vavilova, T.V.},\r\nissn={00424625},\r\npubmed_id={15651704},\r\nlanguage={Russian},\r\nabbrev_source_title={Vestn Khir Im I I Grek},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: Effects of FAD mutations.\n \n \n \n \n\n\n \n Baki, L.; Shioi, J.; Wen, P.; Shao, Z.; Schwarzman, A.; Gama-Sosa, M.; Neve, R.; and Robakis, N.\n\n\n \n\n\n\n EMBO Journal, 23(13): 2586-2596. 2004.\n cited By 227\n\n\n\n
\n\n\n\n \n \n $\"PS1$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Baki20042586,\r\nauthor={Baki, L. and Shioi, J. and Wen, P. and Shao, Z. and Schwarzman, A. and Gama-Sosa, M. and Neve, R. and Robakis, N.K.},\r\ntitle={PS1 activates PI3K thus inhibiting GSK-3 activity and tau overphosphorylation: Effects of FAD mutations},\r\njournal={EMBO Journal},\r\nyear={2004},\r\nvolume={23},\r\nnumber={13},\r\npages={2586-2596},\r\ndoi={10.1038/sj.emboj.7600251},\r\nnote={cited By 227},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-3343005434&doi=10.1038%2fsj.emboj.7600251&partnerID=40&md5=2ddcc14539d32c1990a04bf3a6b5e9ad},\r\naffiliation={Department of Psychiatry, Fishberg Res. Ctr. for Neurobiology, Mount Sinai School of Medicine, New York, NY, United States; Dept. of Psychiat. and Behav. Sci., State Univ. New York at Stony Brook, Stony Brook, NY, United States; Department of Psychiatry, McLean Hospital, Harvard University, Belmont, MA, United States; Mount Sinai School of Medicine, NYU, Annenberg Bldg., One Gustave Levy Pl., New York, NY 10029, United States},\r\nabstract={Phosphatidylinositol 3-kinase (PI3K) promotes cell survival and communication by activating its downstream effector Akt kinase. Here we show that PS1, a protein involved in familial Alzheimer's disease (FAD), promotes cell survival by activating the PI3K/Akt cell survival signaling. This function of PS1 is unaffected by γ-secretase inhibitors. Pharmacological and genetic evidence indicates that PS1 acts upstream of Akt, at or before PI3K kinase. PS1 forms complexes with the p85 subunit of PI3K and promotes cadherin/PBK association. Furthermore, conditions that inhibit this association prevent the PS1-induced PI3K/Akt activation, indicating that PS1 stimulates PI3K/Akt signaling by promoting cadherin/PI3K association. By activating PI3K/Akt signaling, PS1 promotes phosphorylation/inactivation of glycogen synthase kinase-3 (GSK-3), suppresses GSK-3-dependent phosphorylation of tau at residues overphosphorylated in AD and prevents apoptosis of confluent cells. PS1 FAD mutations inhibit the PS1-dependent PI3K/Akt activation, thus promoting GSK-3 activity and tau overphosphorylation at AD-related residues. Our data raise the possibility that PS1 may prevent development of AD pathology by activating the PI3K/Akt signaling pathway. In contrast, FAD mutations may promote AD pathology by inhibiting this pathway.},\r\nauthor_keywords={Alzheimer's disease;  Cadherin;  PBK;  Presenilin;  Tau},\r\ncorrespondence_address1={Robakis, N.K.; Mount Sinai School of Medicine, NYU, Annenberg Bldg., One Gustave Levy Pl., New York, NY 10029, United States; email: nikos.robakis@mssm.edu},\r\nissn={02614189},\r\ncoden={EMJOD},\r\npubmed_id={15192701},\r\nlanguage={English},\r\nabbrev_source_title={EMBO J.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Amyloidogenic and anti-amyloidogenic properties of recombinant transthyretin variants.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Amyloid, 11(1): 1-9. 2004.\n cited By 37\n\n\n\n
\n\n\n\n \n \n $\"Amyloidogenic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n 2003\n \n \n (1)\n \n \n

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\n \n\n \n \n \n \n \n \n The combination of glycoprotein IIIa PlA polymorphism with polymorphism of serotonin transporter as an independent strong risk factor for the occurrence of coronary thrombosis.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Molecular Genetics and Metabolism, 79(3): 229-230. 2003.\n cited By 8\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

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\n \n 2002\n \n \n (5)\n \n \n

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\n \n\n \n \n \n \n \n \n Allelic polymorphism of the tetM determinant in Mycoplasma hominis and Ureaplasma urealyticum clinical isolates resistant to tetracyclines.\n \n \n \n \n\n\n \n Soroka, A.; Akopian, T.; Taraskina, A.; Baitsur, M.; Savicheva, A.; and Govorun, V.\n\n\n \n\n\n\n Genetika, 38(11): 1463-1469. 2002.\n cited By 9\n\n\n\n
\n\n\n\n \n \n $\"Allelic$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Soroka20021463,\r\nauthor={Soroka, A.E. and Akopian, T.A. and Taraskina, A.E. and Baitsur, M.V. and Savicheva, A.M. and Govorun, V.M.},\r\ntitle={Allelic polymorphism of the tetM determinant in Mycoplasma hominis and Ureaplasma urealyticum clinical isolates resistant to tetracyclines},\r\njournal={Genetika},\r\nyear={2002},\r\nvolume={38},\r\nnumber={11},\r\npages={1463-1469},\r\nnote={cited By 9},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036834609&partnerID=40&md5=1a329e7a0d7aa9f6fb4486ea9eb028c7},\r\naffiliation={Research Institute of Physicochemical Medicine, Moscow, 119992, Russian Federation; Ott Institute of Obstetrics and Gynecology, Russian Academy of Medical Sciences, St. Petersburg, 199034, Russian Federation; Outpatient Hospital No. 1, Medical Center Attached to the Administrative Department of the President of Russian Federation, Moscow, Russian Federation},\r\nabstract={Of the 130 clinical isolates of Mycoplasma hominis from patients with nonspecific inflammatory diseases of the urogenital tract (UGT), approximately 10% contained the tet(M) gene after the course of treatment with tetracyclines. This gene was found in nine (25%) of the 36 Ureaplasma urealyticum clinical isolates. The nucleotide sequence of 13 tet(M) genes in TcR clinical isolates of M. hominis and five genes in U. urealyticum TcR clinical isolates was determined. A comparison of nucleotide sequences of eight tetM genes of different origin and tet(M) genes of Gardnerella vaginalis and M. hominis and U. urealyticum clinical isolates showed that the mosaic structure of the tet(M) gene is completely identical in 11 of 13 M. hominis TcR isolates but belongs to an unidentified allele different from those described earlier, Another new allelic variant of tet(M) was found in two isolates. In three of five TcR clinical isolates of U. urealyticum, a tet(M) gene, whose mosaic structure was identical to that of tet(M) reported previously for ureaplasmas, and also two new allelic variants, which have not been described so far, were found.},\r\ncorrespondence_address1={Soroka, A.E.; Research Institute of Physicochemical Medicine, Moscow, 119992, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={12500671},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Allelic Polymorphism of the tet(M) Determinant in Mycoplasma hominis and Ureaplasma urealyticum Clinical Isolates Resistant to Tetracyclines.\n \n \n \n \n\n\n \n Soroka, A.; Akopyan, T.; Taraskina, A.; Baitsur, M.; Savicheva, A.; and Govorun, V.\n\n\n \n\n\n\n Russian Journal of Genetics, 38(11): 1236-1241. 2002.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Allelic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Soroka20021236,\r\nauthor={Soroka, A.E. and Akopyan, T.A. and Taraskina, A.E. and Baitsur, M.V. and Savicheva, A.M. and Govorun, V.M.},\r\ntitle={Allelic Polymorphism of the tet(M) Determinant in Mycoplasma hominis and Ureaplasma urealyticum Clinical Isolates Resistant to Tetracyclines},\r\njournal={Russian Journal of Genetics},\r\nyear={2002},\r\nvolume={38},\r\nnumber={11},\r\npages={1236-1241},\r\ndoi={10.1023/A:1021138809273},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0347616594&doi=10.1023%2fA%3a1021138809273&partnerID=40&md5=ab7e8b9920cf87983f883e00e34261cc},\r\naffiliation={Res. Inst. of Physicochemical Med., Moscow, 119992, Russian Federation; Ott Inst. of Obstet. and Gynecology, Russian Academy of Medical Sciences, St. Petersburg, 199034, Russian Federation; Outpatient Hospital No. 1, Medical Center Attached, Admin. Dept. the Pres. of Russ. Fed., Moscow, Russian Federation},\r\nabstract={Of the 130 clinical isolates of Mycoplasma hominis from patients with nonspecific inflammatory diseases of the urogenital tract (UGT), approximately 10% contained the tet(M) gene after the course of treatment with tetracyclines. This gene was found in nine (25%) of the 36 Ureaplasma urealyticum clinical isolates. The nucleotide sequence of 13 tet(M) genes in TcR clinical isolates of M. hominis and five genes in U. urealyticum TcR clinical isolates was determined. A comparison of nucleotide sequences of eight tetM genes of different origin and tet(M) genes of Gardnerella vaginalis and M. hominis and U. urealyticum clinical isolates showed that the mosaic structure of the tet(M) gene is completely identical in 11 of 13 M. hominis TcR isolates but belongs to an unidentified allele different from those described earlier. Another new allelic variant of tet(M) was found in two isolates. In three of five TcR clinical isolates of U. urealyticum, a tet(M) gene, whose mosaic structure was identical to that of tet(M) reported previously for ureaplasmas, and also two new allelic variants, which have not been described so far, were found.},\r\ncorrespondence_address1={Soroka, A.E.; Res. Inst. of Physicochemical Med., Moscow, 119992, Russian Federation; email: n_e_w@newmail.ru},\r\nissn={10227954},\r\nlanguage={English},\r\nabbrev_source_title={Russ. J. Gen.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Drift of tetM determinant in urogenital microbiocenosis containing mycoplasmas during treatment with a tetracycline antibiotic.\n \n \n \n \n\n\n \n Taraskina, A.; Savicheva, A.; Akopian, T.; Soroka, A.; Momynaliev, K.; and Govorun, V.\n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 134(1): 60-63. 2002.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"Drift$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Taraskina200260,\r\nauthor={Taraskina, A.E. and Savicheva, A.M. and Akopian, T.A. and Soroka, A.E. and Momynaliev, K.T. and Govorun, V.M.},\r\ntitle={Drift of tetM determinant in urogenital microbiocenosis containing mycoplasmas during treatment with a tetracycline antibiotic},\r\njournal={Bulletin of Experimental Biology and Medicine},\r\nyear={2002},\r\nvolume={134},\r\nnumber={1},\r\npages={60-63},\r\ndoi={10.1023/A:1020664807029},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036665010&doi=10.1023%2fA%3a1020664807029&partnerID=40&md5=d43744d4353aed2be0f8505ce216e5bc},\r\naffiliation={Laboratory of Microbiology, D.O. Ott Inst. of Obstet./Gynecol., Russian Academy of Medical Sciences, St. Petersburg, Russian Federation; Lab. of Gene Eng. and Immunogenet., Institute of Physicochem. Medicine, Ministry of Health of Russian Fed., Moscow, Russian Federation},\r\nabstract={We studied the correlation between genetic transfer of tetM determinant in Tn916 conjugative transposon by urogenital mycoplasmas (Mycoplasma hominis and Ureaplasma urealyticum) and changes in the bacterial repertoire during treatment with a tetracycline antibiotic. Basic conditions favoring the nonspecific transfer of tetM determinant into mollicute cells are determined and the allele polymorphism of tetM determinant in clinical strains of M. hominis and U. urealyticum is evaluated. The structure of tetM gene in clinical mycoplasma and ureaplasma strains s characterized by a peculiar mosaic pattern and differs from all previously described alleles of this gene. The results suggest that tetracycline resistance in mollicutes is determined by mechanisms alternative to genetic transfer of tetM determinant.},\r\nauthor_keywords={Allele polymorphism;  Antibiotic resistance;  Mycoplasma hominis;  tetM determinant;  Ureaplasma urealyticum},\r\ncorrespondence_address1={Taraskina, A.E.; Laboratory of Microbiology, D.O. Ott Inst. of Obstet./Gynecol., Russian Academy of Medical Sciences, St. Petersburg, Russian Federation},\r\nissn={00074888},\r\ncoden={BEXBA},\r\npubmed_id={12459871},\r\nlanguage={English},\r\nabbrev_source_title={Bull. Exp. Biol. Med.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Interaction between the platelet IIb/IIIa receptor gene and serotonin transporter gene is involved in the formation of the predisposition to myocardial infarction in young men.\n \n \n \n \n\n\n \n Demidova, D.; Sirotkina, O.; Kudinov, S.; and Schwartz, E.\n\n\n \n\n\n\n Doklady. Biochemistry and biophysics, 387: 335-337. 2002.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Interaction$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Demidova2002335,\r\nauthor={Demidova, D.V. and Sirotkina, O.V. and Kudinov, S.V. and Schwartz, E.I.},\r\ntitle={Interaction between the platelet IIb/IIIa receptor gene and serotonin transporter gene is involved in the formation of the predisposition to myocardial infarction in young men.},\r\njournal={Doklady. Biochemistry and biophysics},\r\nyear={2002},\r\nvolume={387},\r\npages={335-337},\r\ndoi={10.1023/A:1021752416254},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0038499723&doi=10.1023%2fA%3a1021752416254&partnerID=40&md5=9a8ceb51212eda1e25da711df59110b0},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, St. Petersburg 188350, Russian Federation; St. Petersburg State Medical University, St. Petersburg, Russian Federation},\r\ncorrespondence_address1={Demidova, D.V.},\r\nissn={16076729},\r\npubmed_id={12577616},\r\nlanguage={English},\r\nabbrev_source_title={Dokl. Biochem. Biophys.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Gene-gene interaction between platelet glycoprotein IIIa and serotonin transporter genes in predisposition to miocardial infarction in young men.\n \n \n \n \n\n\n \n Demidova, D.; Sirotkina, O.; Kudinov, S.; and Shvarts, E.\n\n\n \n\n\n\n Doklady Akademii Nauk, 387(6): 827-830. 2002.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Gene-gene$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Demidova2002827,\r\nauthor={Demidova, D.V. and Sirotkina, O.V. and Kudinov, S.V. and Shvarts, E.I.},\r\ntitle={Gene-gene interaction between platelet glycoprotein IIIa and serotonin transporter genes in predisposition to miocardial infarction in young men},\r\njournal={Doklady Akademii Nauk},\r\nyear={2002},\r\nvolume={387},\r\nnumber={6},\r\npages={827-830},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036958225&partnerID=40&md5=04617ada053c7454c885ad364b5b2787},\r\npublisher={National Academy of Sciences},\r\nissn={08695652},\r\ncoden={DAKNE},\r\nabbrev_source_title={Dokl Akad Nauk},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 2001\n \n \n (5)\n \n \n

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\n \n\n \n \n \n \n \n \n Genetic heterogeneity of Mycoplasma hominis clinical isolates detected during observation of patients with recurrent urogenital inflammation.\n \n \n \n \n\n\n \n Soroka, A.; Momynaliev, K.; Taraskina, A.; Savicheva, A.; and Govorun, V.\n\n\n \n\n\n\n Bulletin of Experimental Biology and Medicine, 132(1): 663-665. 2001.\n cited By 7\n\n\n\n
\n\n\n\n \n \n $\"Genetic$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Soroka2001663,\r\nauthor={Soroka, A.E. and Momynaliev, K.T. and Taraskina, A.M. and Savicheva, A.M. and Govorun, V.M.},\r\ntitle={Genetic heterogeneity of Mycoplasma hominis clinical isolates detected during observation of patients with recurrent urogenital inflammation},\r\njournal={Bulletin of Experimental Biology and Medicine},\r\nyear={2001},\r\nvolume={132},\r\nnumber={1},\r\npages={663-665},\r\ndoi={10.1023/A:1012528311987},\r\nnote={cited By 7},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035682997&doi=10.1023%2fA%3a1012528311987&partnerID=40&md5=c72291b6c3b4218fde78425bd4cb1e4b},\r\naffiliation={Laboratory of Gene Engineering and Immunogenetics, Institute of Physico-Chemical Medicine, Ministry of Health of Russian Federation, Moscow, Russian Federation; Laboratory of Clinical Microbiology, D. O. Ott Institute of Obstetrics and Gynecology, Russian Academy of Medical Sciences, St. Petersburg, Russian Federation},\r\nabstract={A rapid reproducible effective method for molecular typing of Mycoplasma hominis strains based on random amplified polymorphic DNA (RAPD) technique was developed. RAPD detected genetic heterogeneity of genomes of Mycoplasma hominis clinical isolates and showed changes in the genomes of Mycoplasma hominis clinical isolates from patients with chronic infection.},\r\nauthor_keywords={Genetic heterogeneity;  Mycoplasma hominis;  RAPD},\r\ncorrespondence_address1={Soroka, A.E.; Lab. of Gene Eng. and Immunogenetics, Inst. of Physico-Chemical Medicine, Min. of Health of Russian Federation, Moscow, Russian Federation},\r\nissn={00074888},\r\ncoden={BEXBA},\r\npubmed_id={11687848},\r\nlanguage={English},\r\nabbrev_source_title={Bull. Exp. Biol. Med.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Changes in the hemostatic system in patients with inherited thrombophilia caused by mutation of coagulation factor V (Leyden's factor V).\n \n \n \n \n\n\n \n Papayan, L.; Kobilyanskaya, V.; Sheidina, A.; Baranovskaya, S.; Sirotkina, O.; Kargin, V.; Saltykova, N.; Belyazo, O.; Golovina, O.; Papayan, K.; and Tarkovskaya, L.\n\n\n \n\n\n\n Terapevticheskii Arkhiv, 73(7): 47-51. 2001.\n cited By 2\n\n\n\n
\n\n\n\n \n \n $\"Changes$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Papayan200147,\r\nauthor={Papayan, L.P. and Kobilyanskaya, V.A. and Sheidina, A.M. and Baranovskaya, S.S. and Sirotkina, O.V. and Kargin, V.D. and Saltykova, N.B. and Belyazo, O.Ye. and Golovina, O.G. and Papayan, K.A. and Tarkovskaya, L.R.},\r\ntitle={Changes in the hemostatic system in patients with inherited thrombophilia caused by mutation of coagulation factor V (Leyden's factor V)},\r\njournal={Terapevticheskii Arkhiv},\r\nyear={2001},\r\nvolume={73},\r\nnumber={7},\r\npages={47-51},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035236395&partnerID=40&md5=de93214a1fe59503fb2bab5d6aa5b756},\r\nabstract={Aim. To study the incidence of mutation of Leyden's factor V in patients with venous thrombosis and the hemostatic system in carrier of this genetic defect. Materials and methods. A hundred and one patients aged 15-69 years who had venous thrombosis and 10 individuals with mutation of Leyden's factor V without manifestations in the history of thrombosis were examined. Factor V gene mutations and the thrombocyle and plasma links of hemostasis were determined by routine methods. Results. The Leyden's factor V genotype Arg506 → Gln was detected in 17 of the 101 patients with venous thrombosis. Patients and asymptomatic individuals with this factor were found to have significant hypercoagulation, as evidenced by lower activated protein C-resistance index, higher factor VIII (von Willebrand's factor) activity, elevated von Willebrand's factor antigen levels, and enhanced intravascular platelet activation. In the presence of lupoid anticoagulant, hypercoagulation increased and protein C activity decreased. Conclusion. Detection of signs of hypercoagulation in patients with inherited thrombophilia at recovery in carriers of Leyden's factor V without clinical manifestations of thrombosis shows it necessary to make a particularly careful monitoring of the hemostatic system in these subjects. This is especially important for hypercoagulation-predisposing situations, such as pregnancy, surgical interventions, long-term immobilization, use of contraceptives, etc. when preventive measures may be used to prevent thrombotic events.},\r\nauthor_keywords={Hemostatic system;  Inherited thrombophilia;  Leyden's factor V;  Venous thrombosis},\r\nissn={00403660},\r\ncoden={TEARA},\r\npubmed_id={11523408},\r\nlanguage={Russian},\r\nabbrev_source_title={Ter. Arkh.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Cdc2 phosphorylation of nucleolin demarcates mitotic stages and Alzheimer's disease pathology.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Neurobiology of Aging, 22(4): 517-528. 2001.\n cited By 71\n\n\n\n
\n\n\n\n \n \n $\"Cdc2$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Paraoxonase 1 Met-Leu 54 polymorphism is associated with Parkinson's disease.\n \n \n \n \n\n\n \n Akhmedova, S.; Yakimovsky, A.; and Schwartz, E.\n\n\n \n\n\n\n Journal of the Neurological Sciences, 184(2): 179-182. 2001.\n cited By 67\n\n\n\n
\n\n\n\n \n \n $\"Paraoxonase$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Akhmedova2001179,\r\nauthor={Akhmedova, S.N. and Yakimovsky, A.K. and Schwartz, E.I.},\r\ntitle={Paraoxonase 1 Met-Leu 54 polymorphism is associated with Parkinson's disease},\r\njournal={Journal of the Neurological Sciences},\r\nyear={2001},\r\nvolume={184},\r\nnumber={2},\r\npages={179-182},\r\ndoi={10.1016/S0022-510X(01)00439-7},\r\nnote={cited By 67},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035283113&doi=10.1016%2fS0022-510X%2801%2900439-7&partnerID=40&md5=f654bb95c6383e3bd5ed66a72b1a39d4},\r\naffiliation={Laboratory of Human Molecular Genetics, St. Petersburg Nuclear Physics Institute, Russian Academy of Science, St. Petersburg Area, Gatchina 188350, Russian Federation; Department of Normal Physiology, St. Petersburg State Medical University, L. Tolstoy St. 6/8, St. Petersburg 197189, Russian Federation},\r\nabstract={Two up-to-date known paraoxonase 1 (PON1) polymorphisms (Gln-Arg 191 and Leu-Met 54) affect the hydrolysis of toxic oxons and might intensify effects of pollutants, organophosphates and other environmental chemicals in development of Parkinson's disease (PD). We reported previously that PON1 G1n-Arg 191 polymorphism did not influence on the susceptibility to PD. In the present study we have investigated the PON1 Leu-Met 54 polymorphism in 117 patients with sporadic idiopathic PD. A new approach for Leu-Met 54 polymorphism genotyping has been developed. We have showed the frequency of the Met 54 allele of PON1 to be significantly increased in patients with PD compared with the controls (χ2=8.63, df=1, P&lt;0.003). The relative risk of PD in the Met 54 allele carriers has been estimated to be 2.3 fold higher than in homozygotes for the L allele. Moreover it appeared to be even 5.15 higher in the subgroup of patients with early-onset PD. We suggest that the Met 54 allele may be considered to be an independent risk factor for PD. This mutation could probably cause PON1 impaired metabolism of environmental neurotoxins and might be responsible for neurodegeneration. Copyright © 2001 .},\r\nauthor_keywords={Organophosphates;  Paraoxonase;  Parkinson's disease},\r\ncorrespondence_address1={Schwartz, E.I.; Lab. Human Molecular Genetics, St. Petersburg Nuclear Physics Inst., Russian Academy of Science, St. Petersburg Area, Gatchina 188350, Russian Federation; email: schwartz@mail.line.ru},\r\nissn={0022510X},\r\ncoden={JNSCA},\r\npubmed_id={11239953},\r\nlanguage={English},\r\nabbrev_source_title={J. Neurol. Sci.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n The role of Alzheimer’s disease-related presenilin 1 in intercellular adhesion.\n \n \n \n \n\n\n \n Singh, N.; Talalayeva, Y.; Tsiper, M.; Romanov, V.; Dranovsky, A.; Colflesh, D.; Rudamen, G.; Vitek, M.; Shen, J.; Yang, X.; Goldgaber, D.; and Schwarzman, A.\n\n\n \n\n\n\n Experimental Cell Research, 263(1): 1-13. 2001.\n cited By 28\n\n\n\n
\n\n\n\n \n \n $\"The$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Singh20011,\r\nauthor={Singh, N. and Talalayeva, Y. and Tsiper, M. and Romanov, V. and Dranovsky, A. and Colflesh, D. and Rudamen, G. and Vitek, M.P. and Shen, J. and Yang, X. and Goldgaber, D. and Schwarzman, A.L.},\r\ntitle={The role of Alzheimer’s disease-related presenilin 1 in intercellular adhesion},\r\njournal={Experimental Cell Research},\r\nyear={2001},\r\nvolume={263},\r\nnumber={1},\r\npages={1-13},\r\ndoi={10.1006/excr.2000.5098},\r\nnote={cited By 28},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035242437&doi=10.1006%2fexcr.2000.5098&partnerID=40&md5=34fe4506af7b22c824a4812c95f27a0f},\r\naffiliation={Department of Psychiatry, SUNY at Stony Brook, Stony Brook, NY 11794, United States; Department of Medicine, SUNY at Stony Brook, Stony Brook, NY 11794, United States; UMIC, SUNY at Stony Brook, Stony Brook, NY 11794, United States; Department of Neurology, Duke University Medical Center, Durham, NY 27710, United States; Center for Neurologic Diseases, Brigham and Women’s Hospital, Boston, MA 02115, United States},\r\nabstract={Most cases of familial early-onset Alzheimer’s disease are caused by mutations in the presenilin 1 (PS1) gene. However, the cellular functions of PS1 are unknown. We showed predominant localization of PS1 to cell-cell contacts of the plasma membrane in human prostate epithelial tissue and in a human epithelial cell line HEp2 stably transfected with an inducible PS1 construct. PS1 co-immunoprecipitated with β-catenin from cell lysates of stable transfectants. Conversely, PS1 lacking the PS1-β-catenin interaction site did not co-immunoprecipitate with β-catenin and was not recruited to the cell-cell contacts. L cells, which do not form tight intercellular contacts, formed clusters of adhered cells after stable transfection with GFP-PSl cDNA and demonstrated a clear preference for independent aggregation in the mixed cultures. However, L cells transfected with mutant GFP-PSl constructs, which had a truncated N-terminus of PS1 or deleted PSl-β-catenin interaction site, failed to form intercellular contacts. In addition, in primary cultures of mouse cortical neurons PS1 was highly concentrated on the surface of extended growth cones. Taken together, our results suggest an important role of PS1 in intercellular adhesion in epithelial cells and neurons. © 2001 Academic Press.},\r\nauthor_keywords={Alzheimer’s disease;  Cell-cell adhesion;  Epithelial cells;  Presenilin 1;  Primary neuronal cultures},\r\nissn={00144827},\r\npubmed_id={11161700},\r\nlanguage={English},\r\nabbrev_source_title={Exp. Cell Res.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n

\n \n 2000\n \n \n (1)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n Analysis of regions determining resistence to fluoroquinolones in genes gyrA and parC in clinical isolates of Mycoplasma hominis [Analiz raionov, opredeliaiushchikh rezistentnost' k ftorkhinolonam, genov gyrA i parC v klinicheskikh izoliatakh Mycoplasma hominis.].\n \n \n \n \n\n\n \n Gushchin, A.; Ladygina, V.; Govorun, V.; Taraskina, A.; and Savicheva, A.\n\n\n \n\n\n\n Molekuliarnaia genetika, mikrobiologiia i virusologiia, (4): 33-35. 2000.\n cited By 4\n\n\n\n
\n\n\n\n \n \n $\"Analysis$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Gushchin200033,\r\nauthor={Gushchin, A.E. and Ladygina, V.G. and Govorun, V.M. and Taraskina, A.M. and Savicheva, A.M.},\r\ntitle={Analysis of regions determining resistence to fluoroquinolones in genes gyrA and parC in clinical isolates of Mycoplasma hominis [Analiz raionov, opredeliaiushchikh rezistentnost' k ftorkhinolonam, genov gyrA i parC v klinicheskikh izoliatakh Mycoplasma hominis.]},\r\njournal={Molekuliarnaia genetika, mikrobiologiia i virusologiia},\r\nyear={2000},\r\nnumber={4},\r\npages={33-35},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0033641962&partnerID=40&md5=42e6fcb0ee98a12acebe7f4ea1689d39},\r\naffiliation={Laboratory of Gene Engineering and Immunogenetics, Institute of Physico-Chemical Medicine, Ministry of Health of Russian Federation, St. Petersburg, Russian Federation},\r\nabstract={Fifteen strains of M. hominis isolated from patients with urogenital inflammations were analyzed. Variations in the quinolone resistance-determining regions (QRDR) have been found in fluoroquinolone-resistant M. hominis clinical isolates in comparison with the reference PG21 strain. In one isolate, parC had Asn substitute at position 91.},\r\ncorrespondence_address1={Gushchin, A.E.},\r\nissn={02080613},\r\npubmed_id={11186458},\r\nlanguage={Russian},\r\nabbrev_source_title={Mol. Gen. Mikrobiol. Virusol.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n

\n \n 1999\n \n \n (2)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n Endogenous presenilin 1 redistributes to the surface of lamellipodia upon adhesion of Jurkat cells to a collagen matrix.\n \n \n \n \n\n\n \n Schwarzman, A.; Singh, N.; Tsiper, M.; Gregori, L.; Dranovsky, A.; Vitek, M.; Glabe, C.; St. George-Hyslop, P.; and Goldgaber, D.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences of the United States of America, 96(14): 7932-7937. 1999.\n cited By 63\n\n\n\n
\n\n\n\n \n \n $\"Endogenous$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman19997932,\r\nauthor={Schwarzman, A.L. and Singh, N. and Tsiper, M. and Gregori, L. and Dranovsky, A. and Vitek, M.P. and Glabe, C.G. and St. George-Hyslop, P.H. and Goldgaber, D.},\r\ntitle={Endogenous presenilin 1 redistributes to the surface of lamellipodia upon adhesion of Jurkat cells to a collagen matrix},\r\njournal={Proceedings of the National Academy of Sciences of the United States of America},\r\nyear={1999},\r\nvolume={96},\r\nnumber={14},\r\npages={7932-7937},\r\ndoi={10.1073/pnas.96.14.7932},\r\nnote={cited By 63},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0033529331&doi=10.1073%2fpnas.96.14.7932&partnerID=40&md5=7eeb8e758b2af8874593611cec7fd714},\r\naffiliation={Dept. of Psychiatry/Behavioral Sci., Health Sciences Center, State University of New York, Stony Brook, NY 11794-8101, United States},\r\nabstract={Most familial early-onset Alzheimer's disease cases are caused by mutations in the presenilin 1 (PS1) gene. Subcellular localization of the endogenous PS1 is essential for understanding its function, interactions with proteins, and role in Alzheimer's disease. Although numerous studies revealed predominant localization of PS1 to endoplasmic reticulum and Golgi, there are conflicting reports on the localization of PSI to the cell surface. We found that endogenous PS1 is highly expressed in T lymphocytes (Jurkat cells). Using a variety of methods, we present evidence that endogenous PSI is localized to the cell surface in addition to intracellular membrane compartments. Moreover, PS1 appeared in high levels on the surface of lamellipodia upon adhesion of the cells to a collagen matrix. The redistribution of PS1 in adhered cells was strikingly similar to that of the well characterized adhesion protein CD44. Cell surface PS1 formed complexes in vivo with actin-binding protein filamin (ABP-280), which is known to form bridges between cell surface receptors and cytoskeleton and mediate cell adhesion and cell motility. Taken together, our results suggest a role of PS1 in cell adhesion and/or cell-matrix interaction.},\r\ncorrespondence_address1={Goldgaber, D.; Dept. of Psychiatry/Behavioral Sci., Health Sciences Center, State University of New York, Stony Brook, NY 11794-8101, United States; email: dgoldgaber@mail.psychiatry.sunysb.edu},\r\npublisher={National Academy of Sciences},\r\nissn={00278424},\r\ncoden={PNASA},\r\npubmed_id={10393925},\r\nlanguage={English},\r\nabbrev_source_title={Proc. Natl. Acad. Sci. U. S. A.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n\n \n \n \n \n \n \n Gln→Arg 191 polymorphism of paraoxonase and Parkinson's disease.\n \n \n \n \n\n\n \n Akhmedova, S.; Anisimov, S.; Yakimovsky, A.; and Schwartz, E.\n\n\n \n\n\n\n Human Heredity, 49(3): 178-180. 1999.\n cited By 27\n\n\n\n
\n\n\n\n \n \n $\"Gln→Arg$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Akhmedova1999178,\r\nauthor={Akhmedova, S. and Anisimov, S. and Yakimovsky, A. and Schwartz, E.},\r\ntitle={Gln→Arg 191 polymorphism of paraoxonase and Parkinson's disease},\r\njournal={Human Heredity},\r\nyear={1999},\r\nvolume={49},\r\nnumber={3},\r\npages={178-180},\r\ndoi={10.1159/000022868},\r\nnote={cited By 27},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0032587920&doi=10.1159%2f000022868&partnerID=40&md5=ffff4cd8e9c8abfe26909d68ed37a6b3},\r\naffiliation={Lab. of Human Molecular Genetics, St. Petersburg Nucl. Phys. Institute, Russian Academy of Science, St. Petersburg, Russian Federation; Department of Normal Physiology, St. Petersburg Stt. Med. University, St. Petersburg, Russian Federation; St. Petersburg Inst. of Nucl. Phys., St. Petersburg area, Gatchina 188350, Russian Federation},\r\nabstract={We investigated the Gln→Arg 191 polymorphism in paraoxonase (PON1) in St. Petersburg population, in three clinically differentiated groups of patients with Parkinson's disease (PD) and in the symptomatic tremor group. A new approach for Gln→Arg 191 PON1 polymorphism genotyping is suggested. No significant differences in the groups studies as compared to the controls was observed.},\r\nauthor_keywords={Organophosphates;  Paraxonase;  Parkinson's disease},\r\ncorrespondence_address1={Schwartz, E.; St. Petersburg Inst. Nuclear Physics, St. Petersburg area, Gatchina 188350, Russian Federation; email: schwartz@lnpi.spb.su},\r\nissn={00015652},\r\ncoden={HUHEA},\r\npubmed_id={10364684},\r\nlanguage={English},\r\nabbrev_source_title={Hum. Hered.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n\n

\n \n 1997\n \n \n (1)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n Molecular Genetic and Toxico-Ecological Basis of Etiology and Pathogenesis of Parkinson's Disease.\n \n \n \n \n\n\n \n Yakimovsky, A.; Pushnova, E.; Akhmedova, S.; and Avtonomov, V.\n\n\n \n\n\n\n Zhurnal Nevropatolgii i Psikhiatrii im. S S Korsakova, 97(4): 69-73. 1997.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"Molecular$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Yakimovsky199769,\r\nauthor={Yakimovsky, A.F. and Pushnova, E.A. and Akhmedova, S.N. and Avtonomov, V.V.},\r\ntitle={Molecular Genetic and Toxico-Ecological Basis of Etiology and Pathogenesis of Parkinson's Disease},\r\njournal={Zhurnal Nevropatolgii i Psikhiatrii im. S S Korsakova},\r\nyear={1997},\r\nvolume={97},\r\nnumber={4},\r\npages={69-73},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-77950341322&partnerID=40&md5=21b8e7d6baeede52c95e1919a4f1045c},\r\npublisher={Media Sfera},\r\nissn={00444588},\r\npubmed_id={9214197},\r\nlanguage={Russian},\r\nabbrev_source_title={Zhurnal Nevropatolgii Psikhiatrii im. S S Korsakova},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

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\n \n 1996\n \n \n (2)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n Interaction of transthyretin with amyloid β-protein: Binding and inhibition of amyloid formation.\n \n \n \n \n\n\n \n Schwarzman, A.; and Goldgaber, D.\n\n\n \n\n\n\n CIBA Foundation Symposia, (199): 146-164. 1996.\n cited By 62\n\n\n\n
\n\n\n\n \n \n $\"Interaction$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman1996146,\r\nauthor={Schwarzman, A.L. and Goldgaber, D.},\r\ntitle={Interaction of transthyretin with amyloid β-protein: Binding and inhibition of amyloid formation},\r\njournal={CIBA Foundation Symposia},\r\nyear={1996},\r\nnumber={199},\r\npages={146-164},\r\nnote={cited By 62},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0030329641&partnerID=40&md5=3a83db4522a27d2e79b706fb6b212cca},\r\naffiliation={Department of Psychiatry, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-8101, United States},\r\nabstract={Aggregated amyloid β-protein (Aβ) is a key component of the amyloid depositions found in the brains of patients with Alzheimer's disease. In contrast, in cerebrospinal fluid (CSF), Aβ is found in a soluble form. The analysis of complexes of Aβ with CSF proteins in a KBr gradient revealed an association of Aβ only with free proteins and not with lipoprotein particles. Transthyretin (TTR), a second major CSF protein, formed SDS-stable complexes with Aβ and significantly decreased the rate of Aβ fibril formation. In physiological buffers and CSF, TTR exclusively decreased the level of Aβ pentamers. Endogenous TTR-Aβ complexes were detected in human CSF by immunoprecipitation. Using site-directed mutagenesis and computer-assisted modelling, we identified amino acid residues on the surface of the TTR monomer that interact with Aβ. Specific TTR immunoreactivity was detected in multiple cortical neurons and astrocytes in the human brain. We propose that Aβ binding proteins play a key role in the modulation of Aβ aggregation and normally prevent amyloid formation in biological fluids and in the brain.},\r\ncorrespondence_address1={Schwarzman, A.L.; Department of Psychiatry, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-8101, United States},\r\nissn={03005208},\r\npubmed_id={8915609},\r\nlanguage={English},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n CYP2D6 genotyping in a Russian population using a novel approach for identification of the CYP2D6A mutation.\n \n \n \n \n\n\n \n Akhmedova, S.; Pushnova, E.; Anisimov, S.; Bogdanova, L.; Bova, L.; and Schwartz, E.\n\n\n \n\n\n\n Biochemical and Molecular Medicine, 58(2): 234-236. 1996.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"CYP2D6$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Akhmedova1996234,\r\nauthor={Akhmedova, S.N. and Pushnova, E.A. and Anisimov, S. and Bogdanova, L.A. and Bova, L.K. and Schwartz, E.I.},\r\ntitle={CYP2D6 genotyping in a Russian population using a novel approach for identification of the CYP2D6A mutation},\r\njournal={Biochemical and Molecular Medicine},\r\nyear={1996},\r\nvolume={58},\r\nnumber={2},\r\npages={234-236},\r\ndoi={10.1006/bmme.1996.0054},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0030217818&doi=10.1006%2fbmme.1996.0054&partnerID=40&md5=4dd8306f3047c553a2003c7d48701c48},\r\naffiliation={Petersburg Inst. of Nuclear Physics, St. Petersburg region 188350, Russian Federation; Biol./Biotechnology Research Program, Lawrence Livermore Natl. Laboratory, University of California, P.O. Box 808, L-452, Livermore, CA 94550, United States; Department of Medical Genetics, St. Petersburg Pediat. Med. Academy, Litovskaya str. 2, St. Petersburg 194100, Russian Federation; St. Petersburg Munic. Geriatric Ctr., Leninski pr. 116, St. Petersburg 196066, Russian Federation},\r\nabstract={The frequency of 29A and 29B mutations in the CYP2D6 gene, the most common mutations among Caucasoid PM (debrisoquine 4-hydroxylase defficient) individuals, has been analyzed in the Russian population. For the detection of the 29A mutation, a new one-step ARMS PCR approach has been developed. The frequency of the 29B mutant allele in Russians appeared to be significantly lower than in other Caucasoid populations, and this observation can be explained by the mixed origin of the population inhabiting Russia. Comparative analysis of the mutation frequencies among individuals of various ages showed no age-related differences.},\r\n}

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\n \n 1995\n \n \n (2)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n USF binds to the APBα sequence in the promoter of the amyloid β-protein precursor gene.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Nucleic Acids Research, 23(14): 2734-2741. 1995.\n cited By 31\n\n\n\n
\n\n\n\n \n \n $\"USF$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Frequency of a specific cytochrome P4502D6B (CYP2D6B) mutant allele in clinically differentiated groups of patients with Parkinson disease.\n \n \n \n \n\n\n \n Akhmedova, S.; Pushnova, E.; Yakimovsky, A.; Avtonomov, V.; and Schwartz, E.\n\n\n \n\n\n\n Biochemical and Molecular Medicine, 54(2): 88-90. 1995.\n cited By 18\n\n\n\n
\n\n\n\n \n \n $\"Frequency$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Akhmedova199588,\r\nauthor={Akhmedova, S.N. and Pushnova, E.A. and Yakimovsky, A.F. and Avtonomov, V.V. and Schwartz, E.I.},\r\ntitle={Frequency of a specific cytochrome P4502D6B (CYP2D6B) mutant allele in clinically differentiated groups of patients with Parkinson disease},\r\njournal={Biochemical and Molecular Medicine},\r\nyear={1995},\r\nvolume={54},\r\nnumber={2},\r\npages={88-90},\r\ndoi={10.1006/bmme.1995.1012},\r\nnote={cited By 18},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0029050430&doi=10.1006%2fbmme.1995.1012&partnerID=40&md5=85943f129343457362ec22addf348c59},\r\naffiliation={Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, St. Petersburg, Russian Federation; St. Petersburg Pediatric Medical Institute, Litovskaya Str. 2, St. Petersburg 194100, Russian Federation; Pavlov Institute of Nuclear Physics, Russian Academy of Sciences, St. Petersburg, Russian Federation; Municipal Gastello Hospital (N 20), St. Petersburg, Russian Federation},\r\nabstract={The frequency of the cytochrome P4502D6B CYP2D6B (29B) mutant allele has been determined in three clinically distinct groups of patients with Parkinson disease. No differences in mutation frequency among the patients with the rigidity-akinetic and monosymptomatic tremor forms has been observed compared to the healthy control group, while in the group with akinetic-rigidity tremor symptoms the frequency of heterozygous wt/29B individuals was significantly increased. Therefore, individuals bearing the CYP2D6B mutation appear to be predisposed to the development of this particular form of Parkinson disease, and the presence of the 29B mutation in the genotype may serve as an additional diagnostic criterium for the clinical differentiation of patients with Parkinson disease. © 1995 by Academic Press, Inc.},\r\ncorrespondence_address1={Schwartz, E.I.; Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, St. Petersburg, Russian Federation},\r\nissn={10773150},\r\nlanguage={English},\r\nabbrev_source_title={BIOCHEM. MOL. MED.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n

\n \n 1994\n \n \n (3)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n Transthyretin sequesters amyloid β protein and prevents amyloid formation.\n \n \n \n \n\n\n \n Schwarzman, A.; Gregori, L.; Vitek, M.; Lyubski, S.; Strittmatter, W.; Enghilde, J.; Bhasin, R.; Silverman, J.; Weisgraber, K.; Coyle, P.; Zagorski, M.; Talafous, J.; Eisenberg, M.; Saunders, A.; Roses, A.; and Goldgaber, D.\n\n\n \n\n\n\n Proceedings of the National Academy of Sciences of the United States of America, 91(18): 8368-8372. 1994.\n cited By 290\n\n\n\n
\n\n\n\n \n \n $\"Transthyretin$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman19948368,\r\nauthor={Schwarzman, A.L. and Gregori, L. and Vitek, M.P. and Lyubski, S. and Strittmatter, W.J. and Enghilde, J.J. and Bhasin, R. and Silverman, J. and Weisgraber, K.H. and Coyle, P.K. and Zagorski, M.G. and Talafous, J. and Eisenberg, M. and Saunders, A.M. and Roses, A.D. and Goldgaber, D.},\r\ntitle={Transthyretin sequesters amyloid β protein and prevents amyloid formation},\r\njournal={Proceedings of the National Academy of Sciences of the United States of America},\r\nyear={1994},\r\nvolume={91},\r\nnumber={18},\r\npages={8368-8372},\r\ndoi={10.1073/pnas.91.18.8368},\r\nnote={cited By 290},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027999030&doi=10.1073%2fpnas.91.18.8368&partnerID=40&md5=d600d8db8de320883e0a4aea9f18ab74},\r\naffiliation={Department of Psychiatry, School of Medicine, State Univ. New York at Stony Brook, Stony Brook, NY 11794, United States; Department of Pathology, School of Medicine, State Univ. New York at Stony Brook, Stony Brook, NY 11794, United States; Department of Neurology, School of Medicine, State Univ. New York at Stony Brook, Stony Brook, NY 11794, United States; Department of Pharmacology, School of Medicine, State Univ. New York at Stony Brook, Stony Brook, NY 11794, United States; Picower Inst. for Medical Research, Manhasset, NY 11030, United States; Department of Medicine (Neurology), Joseph Kathleen Bryan Alzheimer's R., Durham, NC 27710, United States; Department of Pathology, Duke University Medical Center, Durham, NC 27710, United States; Department of Pathology, J. David Gladstone Inst. C., University of California, San Francisco, CA 94110, United States; Department of Chemistry, Case Western Reserve University, Cleveland, OH 44106, United States},\r\nabstract={The cardinal pathological features of Alzheimer disease are depositions of aggregated amyloid β protein (Aβ) in the brain and cerebrovasculature. However, the Aβ is found in a soluble form in cerebrospinal fluid in healthy individuals and patients with Alzheimer disease. We postulate that sequestration of Aβ precludes amyloid formation. Failure to sequester Aβ in Alzheimer disease may result in amyloidosis. When we added Aβ to cerebrospinal fluid of patients and controls it was rapidly sequestered into stable complexes with transthyretin. Complexes with apolipoprotein E, which has been shown to bind Aβ in vitro, were not observed in cerebrospinal fluid. Additional in vitro studies showed that both purified transthyretin and apolipoprotein E prevent amyloid formation.},\r\nauthor_keywords={sequestration},\r\ncorrespondence_address1={Goldgaber, D.; Department of Psychiatry, School of Medicine, State University of New York, Stony Brook, NY 11794, United States},\r\npublisher={National Academy of Sciences},\r\nissn={00278424},\r\ncoden={PNASA},\r\npubmed_id={8078889},\r\nlanguage={English},\r\nabbrev_source_title={PROC. NATL. ACAD. SCI. U. S. A.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n A rapid and simple DNA fingerprinting method using RLFP and SSCP analysis of the hypervariable noncoding region of human mitochondrial DNA.\n \n \n \n \n\n\n \n Pushnova, E.; Akhmedova, S.; Shevtsov, S.; and Schwartz, E.\n\n\n \n\n\n\n Human Mutation, 3(3): 292-296. 1994.\n cited By 5\n\n\n\n
\n\n\n\n \n \n $\"A$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Pushnova1994292,\r\nauthor={Pushnova, E.A. and Akhmedova, S.N. and Shevtsov, S.P. and Schwartz, E.I.},\r\ntitle={A rapid and simple DNA fingerprinting method using RLFP and SSCP analysis of the hypervariable noncoding region of human mitochondrial DNA},\r\njournal={Human Mutation},\r\nyear={1994},\r\nvolume={3},\r\nnumber={3},\r\npages={292-296},\r\ndoi={10.1002/humu.1380030318},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0028267752&doi=10.1002%2fhumu.1380030318&partnerID=40&md5=71340bd83e23b5640db9a78ac7df38dd},\r\naffiliation={Center of Molecular Diagnostics, St. Petersburg Pediatric Medical Institute, St. Petersburg, 194100, Russian Federation; St. Petersburg Nuclear Physics Institute, The Russian Academy of Sciences, St. Petersburg, 194100, Russian Federation},\r\nabstract={A simple method for identification of individuals and maternity testing has been developed. This technique includes PCR amplification of the 199‐bp hypervariable portion of the noncoding region of human mtDNA, digestion with RsaI and subsequent SSCP analysis of restriction fragments with DNA silver staining. Using this approach we have analysed the DNA fingerprint patterns of the family members. The fingerprints of maternally related individuals appeared to be identical in three generations, while maternally unrelated members of the family showed differences in their fingerprints, either in SSCP or both RFLP and SSCP patterns. Sequencing data have confirmed the results obtained. Further DNA fingerprinting analysis of 19 unrelated mother–child pairs by means of the method described revealed complete identity of the fingerprint patterns within the pairs. The probability of a random fingerprint match for two maternally unrelated individuals was estimated as 8%. © 1994 Wiley‐Liss, Inc. Copyright © 1994 Wiley‐Liss, Inc., A Wiley Company},\r\nauthor_keywords={DNA fingerprinting, Mitochondrial DNA;  Mother–child pairs},\r\ncorrespondence_address1={Schwartz, E.I.; Center of Molecular Diagnostics, St. Petersburg Pediatric Medical Institute, St. Petersburg, 194100, Russian Federation},\r\nissn={10597794},\r\npubmed_id={7912606},\r\nlanguage={English},\r\nabbrev_source_title={Hum. Mutat.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n\n

\n \n\n \n \n \n \n \n \n Ceruloplasmin gene defect associated with epilepsy in EL mice.\n \n \n \n \n\n\n \n Garey, C.; Schwarzman, A.; Rise, M.; and Seyfried, T.\n\n\n \n\n\n\n Nature Genetics, 6(4): 426-431. 1994.\n cited By 18\n\n\n\n
\n\n\n\n \n \n $\"Ceruloplasmin$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Garey1994426,\r\nauthor={Garey, C.E. and Schwarzman, A.L. and Rise, M.L. and Seyfried, T.N.},\r\ntitle={Ceruloplasmin gene defect associated with epilepsy in EL mice},\r\njournal={Nature Genetics},\r\nyear={1994},\r\nvolume={6},\r\nnumber={4},\r\npages={426-431},\r\ndoi={10.1038/ng0494-426},\r\nnote={cited By 18},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0028362686&doi=10.1038%2fng0494-426&partnerID=40&md5=ec044ebdd0c77a967f8ed7220edc0fb4},\r\naffiliation={Department of Biology, Boston College, Chestnut Hill, MA, 02167, United States},\r\nabstract={Epilepsy is a dominant trait in EL mice, a model for human complex partial seizures. We recently mapped the major gene, EI−1, to chromosome 9 near the predicted location for the ceruloplasmin (Cp) gene. We now present evidence for a partial duplication in the Cp gene in EL mice. This Cp duplication is coinherited with seizures in backcross generations and is associated with enhanced expression of Cp mRNA and increased Cp oxidase activity. Moreover, the duplication is associated with an enhanced frequency of double recombinants, simulating negative interference. The findings are relevant to the basic mechanisms of epilepsy and to theories of genetic recombination and gene mapping. © 1994 Nature Publishing Group.},\r\ncorrespondence_address1={Seyfried, T.N.; Department of Biology, Boston College, Chestnut Hill, MA, 02167, United States},\r\nissn={10614036},\r\npubmed_id={7914452},\r\nlanguage={English},\r\nabbrev_source_title={Nat. Genet.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n

\n \n 1993\n \n \n (1)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n Sequestration of Amyloid β‐Peptide.\n \n \n \n \n\n\n \n GOLDGABER, D.; SCHWARZMAN, A.; BHASIN, R.; GREGORI, L.; SCHMECHEL, D.; SAUNDERS, A.; ROSES, A.; and STRITTMATTER, W.\n\n\n \n\n\n\n Annals of the New York Academy of Sciences, 695(1): 139-143. 1993.\n cited By 29\n\n\n\n
\n\n\n\n \n \n $\"Sequestration$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{GOLDGABER1993139,\r\nauthor={GOLDGABER, D. and SCHWARZMAN, A.I. and BHASIN, R. and GREGORI, L. and SCHMECHEL, D. and SAUNDERS, A.M. and ROSES, A.D. and STRITTMATTER, W.J.},\r\ntitle={Sequestration of Amyloid β‐Peptide},\r\njournal={Annals of the New York Academy of Sciences},\r\nyear={1993},\r\nvolume={695},\r\nnumber={1},\r\npages={139-143},\r\ndoi={10.1111/j.1749-6632.1993.tb23042.x},\r\nnote={cited By 29},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0027425059&doi=10.1111%2fj.1749-6632.1993.tb23042.x&partnerID=40&md5=9023dad426614905748b4de5348e9353},\r\naffiliation={Department of Psychiatry and Behavioral Science, State University of New York, Stony Brook, New York, 11794-8101, United States; Department of Medicine (Neurology), Joseph and Kathleen Bryan Alzheimer's Disease Research Center, Duke University Medical Center, Durham, North Carolina, 27710, United States},\r\nabstract={Amyloid β‐protein, or β/A4, is a 4‐kilodalton peptide that forms poorly soluble extracellular depositions of amyloid in brains and leptomeninges of patients with Alzheimer's disease (AD), Down's syndrome (DS), and hereditary cerebral hemorrhage with amyloidosis‐Dutch type (HCHWA‐D). β/A4 peptide is a derivative of a large transmembrane glycoprotein (APP) and is found in the extracellular space, i.e., in the cerebrospinal fluid and serum of individuals with and without AD and in the conditioned media of many different cells grown in culture.1 The mechanism by which normally produced amyloid β peptide forms extracellular aggregates in patients is unknown. One possible explanation is a failure of a mechanism for removal of the β/A4 peptide that prevents this highly aggregating peptide from forming extracellular amyloid depositions. Copyright © 1993, Wiley Blackwell. All rights reserved},\r\ncorrespondence_address1={GOLDGABER, D.; Department of Psychiatry and Behavioral Science, State University of New York, Stony Brook, New York, 11794-8101, United States},\r\nissn={00778923},\r\npubmed_id={8239272},\r\nlanguage={English},\r\nabbrev_source_title={Ann. New York Acad. Sci.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n

\n \n 1992\n \n \n (1)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n De novo mutation within the intron-exon junction in the PiZ allele of the alpha-1-antitrypsin gene.\n \n \n \n \n\n\n \n Schwarzman, A.; Kowalska, A.; Rujner, J.; Vlasov, M.; and Gaitskhoki, V.\n\n\n \n\n\n\n Human Genetics, 90(1-2): 169-170. 1992.\n cited By 0\n\n\n\n
\n\n\n\n \n \n $\"De$ Paper\n \n \n\n \n \n doi\n \n \n\n \n link\n \n \n\n bibtex\n \n\n \n \n \n abstract \n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Schwarzman1992169,\r\nauthor={Schwarzman, A.L. and Kowalska, A. and Rujner, J. and Vlasov, M.S. and Gaitskhoki, V.S.},\r\ntitle={De novo mutation within the intron-exon junction in the PiZ allele of the alpha-1-antitrypsin gene},\r\njournal={Human Genetics},\r\nyear={1992},\r\nvolume={90},\r\nnumber={1-2},\r\npages={169-170},\r\ndoi={10.1007/BF00210767},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026785645&doi=10.1007%2fBF00210767&partnerID=40&md5=473a6ccbaa625c4d2469c5578670ca7e},\r\naffiliation={Research Institute for Experimental Medicine, St. Petersburgh, Russian Federation; Institute of Human Genetics, Polish Academy of Sciences, Poznan, Poland; Institute of Child Health, Warsaw, Poland; Institute of Molecular Genetics, Moscow, Russian Federation},\r\nabstract={A proband homozygous for the PiZ allele of the alpha-1-antitrypsin gene was found to be a heterozygous carrier of the additional nucleotide substitution (C-T) within the intron IV-exon V junction (position 9955 in intron IV, 3bp upstream of its 3′-splice site). This mutation was not found in DNA from either the PiZ heterozygous parents or the PiZ homozygous brother of proband. © 1992 Springer-Verlag.},\r\ncorrespondence_address1={Schwarzman, A.L.; Department of Biology, Boston College, Chestnut Hill, 02167, MA, United States},\r\npublisher={Springer-Verlag},\r\nissn={03406717},\r\ncoden={HUGED},\r\npubmed_id={1427771},\r\nlanguage={English},\r\nabbrev_source_title={Hum Genet},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n

\n\n\n\n\n\n

\n\n

\n \n 1985\n \n \n (1)\n \n \n

\n \n \n

\n \n\n \n \n \n \n \n \n Assignment of ceruplasmin gene to metaphase chromosomes of laboratory rats by direct in situ hybridization with the specific DNA-probes.\n \n \n \n \n\n\n \n Baranov, V.; Schwarzman, A.; and Gorbunova, V.\n\n\n \n\n\n\n Genetika, 21(1): 23-30. 1985.\n cited By 1\n\n\n\n
\n\n\n\n \n \n $\"Assignment$ Paper\n \n \n\n \n\n \n link\n \n \n\n bibtex\n \n\n \n\n \n\n \n \n \n \n \n \n \n\n \n \n \n\n\n\n

@ARTICLE{Baranov198523,\r\nauthor={Baranov, V.S. and Schwarzman, A.L. and Gorbunova, V.N.},\r\ntitle={Assignment of ceruplasmin gene to metaphase chromosomes of laboratory rats by direct in situ hybridization with the specific DNA-probes},\r\njournal={Genetika},\r\nyear={1985},\r\nvolume={21},\r\nnumber={1},\r\npages={23-30},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021956487&partnerID=40&md5=cece1a22c278d7f286a581bba6444207},\r\naffiliation={Research Institute for Experimental Medicine, Academy of Medical Sciences of the USSR, Leningrad},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={4038670},\r\nlanguage={Russian},\r\nabbrev_source_title={GENETIKA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n

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