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\n  \n 2019\n \n \n (3)\n \n \n
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\n \n\n \n \n \n \n \n \n In vitro and in vivo study of the toxicity of fullerenols С60, С70 and С120О obtained by an original two step method.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Materials Science and Engineering C, 104. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"InPaper\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 4 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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\n The toxicity of C60(OH)30, C70(OH)30, and C120O(OH)n fullerenols, prepared by a new original method, has been studied. This method allowed us to obtain high-purity fullerenols and eliminate the risks of synthesis of preparations containing insoluble fractions contaminated with impurities such as fullerenes not completely reacted by hydroxylation. All fullerenols were detected inside cultured cells. The MTT assay as well as the analysis of apoptosis and cell cycle showed that С60(ОН)30 and С70(OH)30 are non-toxic for cultured V79 и HeLa cells at concentrations exceeding physiological levels by an order of magnitude. С120O(OH)n caused low toxicity. Studies in Drosophila melanogaster showed that any preparations used did not result in a decreased lifespan or in behavior abnormalities in flies. © 2019 Elsevier B.V.\n
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\n \n\n \n \n \n \n \n \n State of aggregation and toxicity of aqueous fullerene solutions.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Applied Surface Science, 483: 69-75. 2019.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"StatePaper\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 2 downloads\n \n \n\n \n \n \n \n \n \n \n\n  \n \n \n\n\n\n
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\n An inevitable consequence of the growth of applications and corresponding production of fullerenes is the accumulation of these molecules in natural aquatic environments and biological systems. This raises the issue of evaluating toxicity of fullerenes and its relation to physical characteristics of fullerene solutions under various conditions. The given paper presents a detailed structural characterization of associations of fullerenes C 60 and C 70 in aqueous suspensions prepared by various methods. The found different temperature and coagulation stability of the systems under study is related to different characteristic aggregate sizes after preparation. The potential correlation between physical and toxic properties of fullerene water solutions is discussed basing on the extended viability tests conducted for living cell cultures (mammalian fibroblasts of Chinese hamster). © 2019 Elsevier B.V.\n
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\n \n\n \n \n \n \n \n \n Knockdown of the neuronal gene Lim3 at the early stages of development affects mitochondrial function and lifespan in Drosophila.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Mechanisms of Ageing and Development, 181: 29-41. 2019.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"KnockdownPaper\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 Understanding the molecular mechanisms underlying variation in lifespan is central to ensure long life. Lim3 encoding a homolog of the vertebrate Lhx3/4 transcription factors plays a key role in Drosophila neuron development. Here, we demonstrated that Lim3 knockdown early in life decreased survival of adult flies. To study the mechanisms underlying this effect, we identified embryonic Lim3 targets using combined RNA-seq and RT-qPCR analyses complemented by in silico analysis of Lim3 binding sites. Though genes with neuronal functions were revealed as Lim3 targets, the characteristics of neurons were not affected by Lim3 depletion. Many of the direct and indirect Lim3 target genes were associated with mitochondrial function, ATP-related activity, redox processes and antioxidant defense. Consistent with the observed changes in the embryonic transcription of these genes, ROS levels were increased in embryos, which could cause changes in the transcription of indirect Lim3 targets known to affect lifespan. We hypothesize that altered mitochondrial activity is crucial for the decrease of adult lifespan caused by Lim3 knockdown early in life. In adults that encountered Lim3 depletion early in life, the transcription of several genes remained altered, and mitochondrial membrane potential, ATP level and locomotion were increased, confirming the existence of carry-over effects. © 2019 Elsevier B.V.\n
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\n  \n 2018\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n Yeast red pigment modifies cloned human α-synuclein pathogenesis in Parkinson disease models in Saccharomyces cerevisiae and Drosophila melanogaster.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Neurochemistry International, 120: 172-181. 2018.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"YeastPaper\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 Recently, we identified the yeast red pigment (RP), a polymer of 1-(5′-Phosphoribosyl)-5-aminoimidazole, as a novel potential anti-amyloid agent for the therapy of neurodegenerative diseases. The purpose of this study was to further validate RP for treatment of Parkinson's disease (PD) and to clarify molecular mechanisms involved in the reduction of amyloid cytotoxicity. We investigated RP effects in vivo using Saccharomyces cerevisiae and Drosophila melanogaster PD models. Western blot analysis revealed reduction in the levels of insoluble α-synuclein in both models, while soluble α-synuclein decreased only in Drosophila. In both models RP significantly reduced α-synuclein cytotoxicity, as was revealed by immunohistochemistry in Drosophila (p < 0.001, n = 27 flies per genotype/assay) and by flow cytometry in yeast (p < 0.05). Data obtained from the yeast PD model suggests that RP antitoxic effects are associated with a drop in ROS accumulation, and slower cellular transition from the early to late apoptotic stage. Using Drosophila brain tissue sections, we have demonstrated that RP helps to compensate for an α-synuclein-mediated reduction in the number of dopaminergic neurons and leads to better performance in animal climbing tests (p < 0.001, n = 120–150 flies per genotype/assay). Taken together, these results demonstrate the potential of RP for the treatment of PD, at least in model systems. © 2018 Elsevier Ltd\n
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\n \n\n \n \n \n \n \n \n Ellipsoid Body and Medulla Defects and Locomotion Disturbances in sbr (small bristles) Mutants of Drosophila melanogaster.\n \n \n \n \n\n\n \n Yakimova, A.; Golubkova, E.; Sarantseva, S.; and Mamon, L.\n\n\n \n\n\n\n Russian Journal of Genetics, 54(6): 609-617. 2018.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"EllipsoidPaper\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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@ARTICLE{Yakimova2018609,\r\nauthor={Yakimova, A.O. and Golubkova, E.V. and Sarantseva, S.V. and Mamon, L.A.},\r\ntitle={Ellipsoid Body and Medulla Defects and Locomotion Disturbances in sbr (small bristles) Mutants of Drosophila melanogaster},\r\njournal={Russian Journal of Genetics},\r\nyear={2018},\r\nvolume={54},\r\nnumber={6},\r\npages={609-617},\r\ndoi={10.1134/S1022795418060145},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85049315581&doi=10.1134%2fS1022795418060145&partnerID=40&md5=512e3a77d1755cc256bf9f37a9dd38de},\r\naffiliation={Department of Genetics and Biotechnology, St. Petersburg State University, St. Petersburg, 199034, Russian Federation; National Research Center Kurchatov Institute–Petersburg Nuclear Physics Institute, Gatchina, Leningrad oblast, 188306, Russian Federation},\r\nabstract={The sbr gene is an ortholog of evolutionarily conservative nxf1 (nuclear export factor) genes that control nuclear-cytoplasmic transport of mRNA in various eukaryotic organisms. Mutations of sbr exhibit a broad range of pleiotropic effects, which are characteristic of “housekeeping” genes. Certain allele-specific manifestations of the sbr gene in neurogenesis and behavior facilitate a deeper understanding of not only universal but also highly specialized functions of this gene. Among such characteristic features of adult males with an sbr12 mutation are reduced locomotor activity as revealed in the negative geotaxis test and significant morphological disruptions of the ellipsoid body and the medulla, both of which are important for locomotion. The character of defects in the ellipsoid body and the medulla suggests that the SBR protein is essential for the normal formation and functioning of these nerve centers, and that the protein carries not only universal but also specialized functions. © 2018, Pleiades Publishing, Inc.},\r\nauthor_keywords={ellipsoid body;  locomotor behavior;  neurogenesis;  nxf1 (nuclear export factor);  optic lobe;  sbr (small bristles)},\r\n}
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\n The sbr gene is an ortholog of evolutionarily conservative nxf1 (nuclear export factor) genes that control nuclear-cytoplasmic transport of mRNA in various eukaryotic organisms. Mutations of sbr exhibit a broad range of pleiotropic effects, which are characteristic of “housekeeping” genes. Certain allele-specific manifestations of the sbr gene in neurogenesis and behavior facilitate a deeper understanding of not only universal but also highly specialized functions of this gene. Among such characteristic features of adult males with an sbr12 mutation are reduced locomotor activity as revealed in the negative geotaxis test and significant morphological disruptions of the ellipsoid body and the medulla, both of which are important for locomotion. The character of defects in the ellipsoid body and the medulla suggests that the SBR protein is essential for the normal formation and functioning of these nerve centers, and that the protein carries not only universal but also specialized functions. © 2018, Pleiades Publishing, Inc.\n
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\n  \n 2017\n \n \n (4)\n \n \n
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\n \n\n \n \n \n \n \n \n Tissue-specific transcription of the neuronal gene Lim3 affects Drosophila melanogaster lifespan and locomotion.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biogerontology, 18(5): 739-757. 2017.\n cited By 5\n\n\n\n
\n\n\n\n \n \n \"Tissue-specificPaper\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 The identity of neuronal cell types is established and maintained by the expression of neuronal genes coding for ion channels, neurotransmitters, and neuropeptides, among others. Some of these genes have been shown to affect lifespan; however, their role in lifespan control remains largely unclear. The Drosophila melanogaster gene Lim3 encodes a transcription factor involved in complicated motor neuron specification networks. We previously identified Lim3 as a candidate gene affecting lifespan. To obtain direct evidence of the involvement of Lim3 in lifespan control, Lim3 overexpression and RNAi knockdown were induced in the nervous system and muscles of Drosophila using the GAL4-UAS binary system. We demonstrated that Lim3 knockdown in the nervous system increased survival at an early age and that Lim3 knockdown in muscles both increased survival at an early age and extended median lifespan, directly establishing the involvement of Lim3 in lifespan control. Lim3 overexpression in nerves and muscles was deleterious and led to lethality and decreased lifespan, respectively. Lim3 misexpression in both nerves and muscles increased locomotion regardless of changes in lifespan, which indicated that the effects of Lim3 on lifespan and locomotion can be uncoupled. Decreased synaptic activity was observed in the neuromuscular junctions of individuals with Lim3 overexpression in muscles, in association with decreased lifespan. However, no changes in NMJ activity were associated with the positive shift in locomotion observed in all misexpression genotypes. Our data suggested that modifications in the microtubule network may be induced by Lim3 misexpression in muscles and cause an increase in locomotion. © 2017, Springer Science+Business Media Dordrecht.\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 \"TransmissionPaper\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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@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 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.\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 \"TransmissionPaper\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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@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 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.\n
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\n \n\n \n \n \n \n \n \n Human APP Gene Expression Alters Active Zone Distribution and Spontaneous Neurotransmitter Release at the Drosophila Larval Neuromuscular Junction.\n \n \n \n \n\n\n \n Saburova, E.; Vasiliev, A.; Kravtsova, V.; Ryabova, E.; Zefirov, A.; Bolshakova, O.; Sarantseva, S.; and Krivoi, I.\n\n\n \n\n\n\n Neural Plasticity, 2017. 2017.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"HumanPaper\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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@ARTICLE{Saburova2017,\r\nauthor={Saburova, E.A. and Vasiliev, A.N. and Kravtsova, V.V. and Ryabova, E.V. and Zefirov, A.L. and Bolshakova, O.I. and Sarantseva, S.V. and Krivoi, I.I.},\r\ntitle={Human APP Gene Expression Alters Active Zone Distribution and Spontaneous Neurotransmitter Release at the Drosophila Larval Neuromuscular Junction},\r\njournal={Neural Plasticity},\r\nyear={2017},\r\nvolume={2017},\r\ndoi={10.1155/2017/9202584},\r\nart_number={9202584},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-85026497907&doi=10.1155%2f2017%2f9202584&partnerID=40&md5=e664d727d85b573aedd63bc693a47882},\r\naffiliation={Department of General Physiology, St. Petersburg State University, St. Petersburg, 199034, Russian Federation; B.P. Konstantinov Petersburg Nuclear Physics Institute, National Research Centre Kurchatov Institute, Gatchina, 188300, Russian Federation; Department of Normal Physiology, Kazan State Medical University, Kazan, 420012, Russian Federation},\r\nabstract={This study provides further insight into the molecular mechanisms that control neurotransmitter release. Experiments were performed on larval neuromuscular junctions of transgenic Drosophila melanogaster lines with different levels of human amyloid precursor protein (APP) production. To express human genes in motor neurons of Drosophila, the UAS-GAL4 system was used. Human APP gene expression increased the number of synaptic boutons per neuromuscular junction. The total number of active zones, detected by Bruchpilot protein puncta distribution, remained unchanged; however, the average number of active zones per bouton decreased. These disturbances were accompanied by a decrease in frequency of miniature excitatory junction potentials without alteration in random nature of spontaneous quantal release. Similar structural and functional changes were observed with co-overexpression of human APP and β-secretase genes. In Drosophila line with expression of human amyloid-β42 peptide itself, parameters analyzed did not differ from controls, suggesting the specificity of APP effects. These results confirm the involvement of APP in synaptogenesis and provide evidence to suggest that human APP overexpression specifically disturbs the structural and functional organization of active zone and results in altered Bruchpilot distribution and lowered probability of spontaneous neurotransmitter release. © 2017 Ekaterina A. Saburova et al.},\r\ncorrespondence_address1={Krivoi, I.I.; Department of General Physiology, St. Petersburg State UniversityRussian Federation; email: iikrivoi@gmail.com},\r\npublisher={Hindawi Limited},\r\nissn={20905904},\r\ncoden={NEPLF},\r\npubmed_id={28770114},\r\nlanguage={English},\r\nabbrev_source_title={Neural Plast.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n This study provides further insight into the molecular mechanisms that control neurotransmitter release. Experiments were performed on larval neuromuscular junctions of transgenic Drosophila melanogaster lines with different levels of human amyloid precursor protein (APP) production. To express human genes in motor neurons of Drosophila, the UAS-GAL4 system was used. Human APP gene expression increased the number of synaptic boutons per neuromuscular junction. The total number of active zones, detected by Bruchpilot protein puncta distribution, remained unchanged; however, the average number of active zones per bouton decreased. These disturbances were accompanied by a decrease in frequency of miniature excitatory junction potentials without alteration in random nature of spontaneous quantal release. Similar structural and functional changes were observed with co-overexpression of human APP and β-secretase genes. In Drosophila line with expression of human amyloid-β42 peptide itself, parameters analyzed did not differ from controls, suggesting the specificity of APP effects. These results confirm the involvement of APP in synaptogenesis and provide evidence to suggest that human APP overexpression specifically disturbs the structural and functional organization of active zone and results in altered Bruchpilot distribution and lowered probability of spontaneous neurotransmitter release. © 2017 Ekaterina A. Saburova et al.\n
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\n \n\n \n \n \n \n \n \n The development of drosophila melanogaster under different duration space flight and subsequent adaptation to earth gravity.\n \n \n \n \n\n\n \n Ogneva, I.; Belyakin, S.; and Sarantseva, S.\n\n\n \n\n\n\n PLoS ONE, 11(11). 2016.\n cited By 2\n\n\n\n
\n\n\n\n \n \n \"ThePaper\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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@ARTICLE{Ogneva2016,\r\nauthor={Ogneva, I.V. and Belyakin, S.N. and Sarantseva, S.V.},\r\ntitle={The development of drosophila melanogaster under different duration space flight and subsequent adaptation to earth gravity},\r\njournal={PLoS ONE},\r\nyear={2016},\r\nvolume={11},\r\nnumber={11},\r\ndoi={10.1371/journal.pone.0166885},\r\nart_number={e0166885},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84998786449&doi=10.1371%2fjournal.pone.0166885&partnerID=40&md5=c7a206a3980e56ac016473a45ee4c5cd},\r\naffiliation={Cell Biophysics Group, State Scientific Center of Russian Federation, Institute of Biomedical Problems of the Russian Academy of Sciences, Moscow, Russian Federation; I. M. Sechenov First Moscow State Medical University, Moscow, Russian Federation; Institute of Molecular and Cellular Biology SB RAS, Novosibirsk, Russian Federation; B. P. Konstantinov Petersburg Nuclear Physics Institute National Research Centre, Kurchatov Institute, Gatchina, Russian Federation},\r\nabstract={In prospective human exploration of outer space, the need to preserve a species over several generations under changed gravity conditions may arise. This paper demonstrates our results in the creation of the third generation of fruit fly Drosophila melanogaster (third-stage larvae) during the 44.5-day space flight (Foton-M4 satellite (2014, Russia)), then the fourth generation on Earth and the fifth generation again in conditions of the 12-day space flight (2014, in the Russian Segment of the ISS). The species preserves fertility despite a number of changes in the level of expression and content of cytoskeletal proteins, which are the key components of the cleavage spindle and the contractile ring of cells. The results of transcriptome screening and space analysis of cytoskeletal proteins show that the exposure to weightless conditions leads to the increased transcription of metabolic genes, cuticle components and the decreased transcription of genes involved in morphogenesis, cell differentiation, cytoskeletal organization and genes associated with the plasma membrane. Subsequent exposure to the microgravity for 12 days resulted in an even more significant increase/decrease in the transcription of the same genes. On the contrary, the transition from the microgravity conditions to the gravity of Earth leads to the increased transcription of genes whose products are involved in the morphogenesis, cytoskeletal organization, motility of cells and transcription regulation, and to the decreased transcription of cuticle genes and proteolytic processes. © 2016 Ogneva et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.},\r\npublisher={Public Library of Science},\r\nissn={19326203},\r\ncoden={POLNC},\r\npubmed_id={27861601},\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 In prospective human exploration of outer space, the need to preserve a species over several generations under changed gravity conditions may arise. This paper demonstrates our results in the creation of the third generation of fruit fly Drosophila melanogaster (third-stage larvae) during the 44.5-day space flight (Foton-M4 satellite (2014, Russia)), then the fourth generation on Earth and the fifth generation again in conditions of the 12-day space flight (2014, in the Russian Segment of the ISS). The species preserves fertility despite a number of changes in the level of expression and content of cytoskeletal proteins, which are the key components of the cleavage spindle and the contractile ring of cells. The results of transcriptome screening and space analysis of cytoskeletal proteins show that the exposure to weightless conditions leads to the increased transcription of metabolic genes, cuticle components and the decreased transcription of genes involved in morphogenesis, cell differentiation, cytoskeletal organization and genes associated with the plasma membrane. Subsequent exposure to the microgravity for 12 days resulted in an even more significant increase/decrease in the transcription of the same genes. On the contrary, the transition from the microgravity conditions to the gravity of Earth leads to the increased transcription of genes whose products are involved in the morphogenesis, cytoskeletal organization, motility of cells and transcription regulation, and to the decreased transcription of cuticle genes and proteolytic processes. © 2016 Ogneva et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.\n
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\n  \n 2015\n \n \n (3)\n \n \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 \"ExpressionPaper\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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@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 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.\n
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\n \n\n \n \n \n \n \n \n Yeast red pigment modifies Amyloid beta growth in Alzheimer disease models in both Saccharomyces cerevisiae and Drosophila melanogaster.\n \n \n \n \n\n\n \n Nevzglyadova, O.; Mikhailova, E.; Amen, T.; Zenin, V.; Artemov, A.; Kostyleva, E.; Mezhenskaya, D.; Rodin, D.; Saifitdinova, A.; Khodorkovskii, M.; Sarantseva, S.; and Soidla, T.\n\n\n \n\n\n\n Amyloid, 22(2): 100-111. 2015.\n cited By 3\n\n\n\n
\n\n\n\n \n \n \"YeastPaper\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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@ARTICLE{Nevzglyadova2015100,\r\nauthor={Nevzglyadova, O.V. and Mikhailova, E.V. and Amen, T.R. and Zenin, V.V. and Artemov, A.V. and Kostyleva, E.I. and Mezhenskaya, D.A. and Rodin, D.I. and Saifitdinova, A.F. and Khodorkovskii, M.A. and Sarantseva, S.V. and Soidla, T.R.},\r\ntitle={Yeast red pigment modifies Amyloid beta growth in Alzheimer disease models in both Saccharomyces cerevisiae and Drosophila melanogaster},\r\njournal={Amyloid},\r\nyear={2015},\r\nvolume={22},\r\nnumber={2},\r\npages={100-111},\r\ndoi={10.3109/13506129.2015.1010038},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84934324177&doi=10.3109%2f13506129.2015.1010038&partnerID=40&md5=1c8e72f6ddee64a80ba62b27a680c9c8},\r\naffiliation={Institute of Cytology, RAS, St. Petersburg, Russian Federation; St. Petersburg State University, Dept. Genetics, St. Petersburg, Russian Federation; Petersburg Nuclear Physics Institute, National Research Centre kurchatov Institute, Gatchina, 188300, Russian Federation; St. Petersburg Polytechnic University, Analytical Center of Nano-and Biotechnologies, St. Petersburg, Russian Federation},\r\nabstract={The effect of yeast red pigment on amyloid-β (Aβ) aggregation and fibril growth was studied in yeasts, fruit flies and in vitro. Yeast strains accumulating red pigment (red strains) contained less amyloid and had better survival rates compared to isogenic strains without red pigment accumulation (white strains). Confocal and fluorescent microscopy was used to visualise fluorescent Aβ-GFP aggregates. Yeast cells containing less red pigment had more Aβ-GFP aggregates despite the lower level of overall GFP fluorescence. Western blot analysis with anti-GFP, anti-Aβ and A11 antibodies also revealed that red cells contained a considerably lower amount of Aβ GFP aggregates as compared to white cells. Similar results were obtained with exogenous red pigment that was able to penetrate yeast cells. In vitro experiments with thioflavine and TEM showed that red pigment effectively decreased Aβ fibril growth. Transgenic flies expressing Aβ were cultivated on medium containing red and white isogenic yeast strains. Flies cultivated on red strains had a significant decrease in Aβ accumulation levels and brain neurodegeneration. They also demonstrated better memory and learning indexes and higher locomotor ability. © 2015 Informa UK Ltd. All rights reserved.},\r\nauthor_keywords={Alzheimer disease;  Amyloid;  Aβ;  Neurodegeneration;  Yeast red pigment},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)14-04-01558a},\r\n}
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\n The effect of yeast red pigment on amyloid-β (Aβ) aggregation and fibril growth was studied in yeasts, fruit flies and in vitro. Yeast strains accumulating red pigment (red strains) contained less amyloid and had better survival rates compared to isogenic strains without red pigment accumulation (white strains). Confocal and fluorescent microscopy was used to visualise fluorescent Aβ-GFP aggregates. Yeast cells containing less red pigment had more Aβ-GFP aggregates despite the lower level of overall GFP fluorescence. Western blot analysis with anti-GFP, anti-Aβ and A11 antibodies also revealed that red cells contained a considerably lower amount of Aβ GFP aggregates as compared to white cells. Similar results were obtained with exogenous red pigment that was able to penetrate yeast cells. In vitro experiments with thioflavine and TEM showed that red pigment effectively decreased Aβ fibril growth. Transgenic flies expressing Aβ were cultivated on medium containing red and white isogenic yeast strains. Flies cultivated on red strains had a significant decrease in Aβ accumulation levels and brain neurodegeneration. They also demonstrated better memory and learning indexes and higher locomotor ability. © 2015 Informa UK Ltd. All rights reserved.\n
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\n \n\n \n \n \n \n \n \n GAPDH binders as potential drugs for the therapy of polyglutamine diseases: Design of a new screening assay.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n FEBS Letters, 589(5): 581-587. 2015.\n cited By 16\n\n\n\n
\n\n\n\n \n \n \"GAPDHPaper\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 Proteins with long polyglutamine repeats form a complex with glyceraldehyde-3-phosphate dehydrogenase (GAPDH), which enhances aggregation and cytotoxicity in models of Huntington disease. The aim of this study was to develop a novel assay for the screening of anti-aggregation compounds with a focus on the aggregation-promoting capacity of GAPDH. The assay includes a pure Q58 polyglutamine fragment, GAPDH, and a transglutaminase that links the two proteins. The feasibility of the new assay was verified using two GAPDH binders, hydroxynonenal and -(-)deprenyl, and the benzothiazole derivative PGL-135 which exhibits anti-aggregation effect. All three substances were shown to reduce aggregation and cytotoxicity in the cell and in the fly model of Spinocerebellar ataxia. © 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.\n
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\n  \n 2014\n \n \n (4)\n \n \n
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\n \n\n \n \n \n \n \n \n Effect of human APP gene overexpression on Drosophila melanogaster cholinergic and dopaminergic brain neurons.\n \n \n \n \n\n\n \n Bolshakova, O.; Zhuk, A.; Rodin, D.; Kislik, G.; and Sarantseva, S.\n\n\n \n\n\n\n Russian Journal of Genetics: Applied Research, 4(2): 113-121. 2014.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"EffectPaper\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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@ARTICLE{Bolshakova2014113,\r\nauthor={Bolshakova, O.I. and Zhuk, A.A. and Rodin, D.I. and Kislik, G.A. and Sarantseva, S.V.},\r\ntitle={Effect of human APP gene overexpression on Drosophila melanogaster cholinergic and dopaminergic brain neurons},\r\njournal={Russian Journal of Genetics: Applied Research},\r\nyear={2014},\r\nvolume={4},\r\nnumber={2},\r\npages={113-121},\r\ndoi={10.1134/S2079059714020026},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84899636645&doi=10.1134%2fS2079059714020026&partnerID=40&md5=a4407500eb0dc9c39b3265fba04593dc},\r\naffiliation={B.P. Konstantinov St. Petersburg Nuclear Physics Institute National Research Centre Kurchatov Inst., Gatchina, Russian Federation},\r\nabstract={We investigated the effects of overexpression of the human APP gene on the populations of cholinergic and dopaminergic brain neurons in the fruit fly, Drosophila melanogaster. The number of cholinergic neurons in the APP expressing young flies was the same as in the control and decreased significantly with age. The number of dopaminergic neurons in the APP expressing flies was significantly lower than in the control strain by the 15th day of life. Neurodegeneration was accompanied by deficiencies in memory and cognitive abilities in the flies overexpressing full-length APP (APP-Swedish), as well as in the strains with amyloid-β peptide production. © 2014 Pleiades Publishing, Ltd.},\r\nauthor_keywords={Alzeimer's disease;  amyloid-β peptide;  cholinergic neurons;  dopaminergic neurons;  Drosophila melanogaster;  neurodegeneration},\r\nfunding_details={Russian Foundation for Basic Research09-04-00647-a},\r\ncorrespondence_address1={Bolshakova, O. I.; B.P. Konstantinov St. Petersburg Nuclear Physics Institute National Research Centre Kurchatov Inst., Gatchina, Russian Federation; email: olya99991@yandex.ru},\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 We investigated the effects of overexpression of the human APP gene on the populations of cholinergic and dopaminergic brain neurons in the fruit fly, Drosophila melanogaster. The number of cholinergic neurons in the APP expressing young flies was the same as in the control and decreased significantly with age. The number of dopaminergic neurons in the APP expressing flies was significantly lower than in the control strain by the 15th day of life. Neurodegeneration was accompanied by deficiencies in memory and cognitive abilities in the flies overexpressing full-length APP (APP-Swedish), as well as in the strains with amyloid-β peptide production. © 2014 Pleiades Publishing, Ltd.\n
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\n \n\n \n \n \n \n \n \n Development of drosophila melanogaster in space flight.\n \n \n \n \n\n\n \n Ogneva, I.; Larina, I.; and Sarantseva, S.\n\n\n \n\n\n\n Aviakosmicheskaya i Ekologicheskaya Meditsina, 48(3): 5-11. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"DevelopmentPaper\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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@ARTICLE{Ogneva20145,\r\nauthor={Ogneva, I.V. and Larina, I.M. and Sarantseva, S.V.},\r\ntitle={Development of drosophila melanogaster in space flight},\r\njournal={Aviakosmicheskaya i Ekologicheskaya Meditsina},\r\nyear={2014},\r\nvolume={48},\r\nnumber={3},\r\npages={5-11},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84906925117&partnerID=40&md5=3bc15db7dda8482a5b2555151e10c100},\r\nabstract={The review deals with the available literary data on different aspects of Drosophila melanogaster vital functions in the conditions of real and modeled microgravity. The developmental stages, embryogenesis and aging, specifically, and behavioral reactions are discussed. The presented results of morphological as well as molecular genetic analyses are indicative of structural changes in early Drosophila embryos and their compensation during subsequent development, and formation of an adaptive gene-expression pattern in microgravity.},\r\nauthor_keywords={Drosophila;  Gene-expression pattern;  Microgravity;  Morphogenesis},\r\npublisher={Slovo Ltd},\r\nissn={0233528X},\r\npubmed_id={25163332},\r\nlanguage={Russian},\r\nabbrev_source_title={Aviakosmicheskaya Ekol. Med.},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n The review deals with the available literary data on different aspects of Drosophila melanogaster vital functions in the conditions of real and modeled microgravity. The developmental stages, embryogenesis and aging, specifically, and behavioral reactions are discussed. The presented results of morphological as well as molecular genetic analyses are indicative of structural changes in early Drosophila embryos and their compensation during subsequent development, and formation of an adaptive gene-expression pattern in microgravity.\n
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\n \n\n \n \n \n \n \n \n [Investigation of neuroprotective activity of apolipoprotein E peptide mimetic Cog1410 in transgenic lines of Drosophila melanogaster].\n \n \n \n \n\n\n \n Latypova, E.; Timoshenko, S.; Kislik, G.; Vitek, M.; Shvartsman, A.; and Sarantseva, S.\n\n\n \n\n\n\n Biomeditcombining double inverted brevesinskaicombining double inverted brevea khimiicombining double inverted brevea, 60(4): 515-521. 2014.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"[InvestigationPaper\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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@ARTICLE{Latypova2014515,\r\nauthor={Latypova, E.M. and Timoshenko, S.I. and Kislik, G.A. and Vitek, M. and Shvartsman, A.L. and Sarantseva, S.V.},\r\ntitle={[Investigation of neuroprotective activity of apolipoprotein E peptide mimetic Cog1410 in transgenic lines of Drosophila melanogaster].},\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={4},\r\npages={515-521},\r\ndoi={10.18097/pbmc20146004515},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84908283027&doi=10.18097%2fpbmc20146004515&partnerID=40&md5=8a773e3b0b4ac16929cda0a39e9ff9ef},\r\nabstract={The neuroprotective activity of apolipoprotein E (apoE) peptide mimetic Cog1410, containing amino acid sequence of the receptor-binding domain apoE, has been investigated in transgenic lines of Drosophila melanogaster expressing human APP and beta-secretase. Expression of two transgenes caused neuropathological processes attributed to Alzheimer's disease: neurodegeneration, cognitive abnormality and amyloid deposits formation in brain. It was shown that Cog 1410 reduces neurodegeneration in brain of transgenic flies and improves cognitive functions (odor recognition). These data suggest that Cog1410 is a potential neuroprotector that can be used in AD treatment.},\r\ncorrespondence_address1={Latypova, E.M.},\r\nissn={23106972},\r\npubmed_id={25249536},\r\nlanguage={Russian},\r\nabbrev_source_title={Biomed Khim},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n The neuroprotective activity of apolipoprotein E (apoE) peptide mimetic Cog1410, containing amino acid sequence of the receptor-binding domain apoE, has been investigated in transgenic lines of Drosophila melanogaster expressing human APP and beta-secretase. Expression of two transgenes caused neuropathological processes attributed to Alzheimer's disease: neurodegeneration, cognitive abnormality and amyloid deposits formation in brain. It was shown that Cog 1410 reduces neurodegeneration in brain of transgenic flies and improves cognitive functions (odor recognition). These data suggest that Cog1410 is a potential neuroprotector that can be used in AD treatment.\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 \"ThePaper\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 The neuroprotective activity of peptide mimetic of apolipoprotein E (apoE) Cog1410, containing the amino acid sequence of the apoE receptor-binding domain, has been investigated in transgenic Drosophila melanogaster strains expressing human APP and beta-secretase genes. Expression of double transgenes caused neuropathological processes typical for Alzheimer's disease (AD): neurodegeneration, cognitive impairments, and amyloid deposition in the brain. It was shown that Cog1410 reduces neurodegeneration in the brain of transgenic flies and improves cognitive functions (odor recognition). These data suggest that Cog1410 is a potential neuroprotector that can be used in AD treatment. © 2014 Pleiades Publishing, Ltd.\n
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\n  \n 2012\n \n \n (4)\n \n \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 \"MorphologicalPaper\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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@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
\n
\n\n\n
\n 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.\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 \"MorphologicalPaper\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 Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a 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 increased production of amyloid-β-protein (Aβ). To gain insight into the synaptic effects of APP protein in AD patients, wild-type APP, its mutant form APP-Swedish responsible for familial AD, and human beta-secretase gene were expressed in motor neurons of Drosophila melanogaster larvae. It was found that targeted expression of APP (APP-Swedish) in Drosophila larval motor neurons caused significant morphological and functional changes in neuromuscular junctions (NMJs)-a dramatic increase in the number of synaptic boutons and altered exocytosis 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 with APP (APP-Swedish) expression, as well as for double transgenes bearing APP (APP-Swedish) and human beta-secretase (BACE), which caused 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 Aβ neurotoxic effects. © 2012 Pleiades Publishing, Ltd.\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 \"HumanPaper\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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@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 \"ThePaper\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 One of the earliest neuropathological symptoms of Alzheimer's disease is the loss of synapses that precedes the formation of amyloid plaques and neurodegeneration. Although most cases of early-onset familial Alzheimer's disease are caused by mutations in the presenilin 1 (PS1) gene, the functions of PS1 and its role in synaptic dysfunction are not yet completely understood. In this paper, we analyzed PS1 intra- and extracellular distribution in cultures of mouse cortical embryonic neurons. We found that PS1 was concentrated on the surface of the growth cone and neurite contact sites. PS1 was also found in synapses where it was colocalized with synaptophysin. We obtained independent evidence of PS1 involvement in synaptic function by transfection of neurons with GFP-PS1cDNA. GFP was colocalized with synaptophysin in transfected cultures. GFP-immunoprecepitates from transfected neurons contained N-cadherin. This finding represents additional evidence of PS1 participation in the synapse formation. To evaluate the role of PS1 inactivation in the synaptic functions, we compare the synaptic density in neuronal cell cultures from knockout mice PS1 (-/-) and wild type mice PS1 (+/+). Our results obviously show that PS1 (-/-) cultures displayed lower number of morphological synapses compared to wild type culture PS1 (+/+). In summary, our findings show the role of PS1 in synaptic function. © 2012 Pleiades Publishing, Ltd.\n
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\n  \n 2011\n \n \n (3)\n \n \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 \"CompensatoryPaper\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
\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
\n
\n\n\n
\n 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.\n
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\n \n\n \n \n \n \n \n \n Potential role of presenilin 1 in regulation of synaptic function.\n \n \n \n \n\n\n \n Schwarzmaii, A.; Sarantseva, S.; and Vitek, M.\n\n\n \n\n\n\n Tsitologiya, 53(12): 959-967. 2011.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"PotentialPaper\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
\n
@ARTICLE{Schwarzmaii2011959,\r\nauthor={Schwarzmaii, A.L. and Sarantseva, S.V. and Vitek, M.P.},\r\ntitle={Potential role of presenilin 1 in regulation of synaptic function},\r\njournal={Tsitologiya},\r\nyear={2011},\r\nvolume={53},\r\nnumber={12},\r\npages={959-967},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-84858143189&partnerID=40&md5=d923fbc359648180b08cfc37059027fb},\r\naffiliation={Petersburg Institute of Nuclear Physics RAS, Gatchina, Russian Federation; Institute for Experimental Medicine RAMS, St. Petersburg, Russian Federation; Division of Neurology, Duke University Medical Center, Durham, NC, United States},\r\nabstract={One of the earliest neuropathological symptoms of Alzheimer's disease is the loss of synapses, which preceed the formation of amyloidosis and neurodegeneration. Although most cases of early-onset familial Alzheimer's disease are caused by mutations in the presenilin 1 (PSl) gene, the functions of PSl and its role in synaptic disfunction are not yet completely understood. In this paper we analysed of the intracellular and extracellular distribution of PSl in the cultures of mouse cortical embryonic neurons. We found that PSl is concentrated on the surface of the growth cone and at neurite contact sites. PSl was also found in synapses where it is co-localized with synaptophysin. Independent evidense of involvment of PSl in synaptic function we obtained by transfection of neurons with GFP-PS1 cDNA. GFP was colocalized with synaptophysin in transfected cultures. GFP-immunoprecepitatcs from transfected neurons contained processed N-cadherin. This result presents an additional proof of involvment PSl in synapse formation. To evaluate the role of PSl inactivation in the synaptic functions, we compare synaptic density in neuronal cell cultures from PSl knockout mice PSl (-/-) and wild type mice PSl (+/+). Our results clearly show that PS 1(-/-) displayed a low number of morphological synapses in comparing with wild type culture PSl(+/+). In summary, our results indicate a role of PSl in synaptic function.},\r\nauthor_keywords={Alzheimer's disease;  APP;  Presenilin;  Synapses},\r\ncorrespondence_address1={Schwarzmaii, A.L.; Petersburg Institute of Nuclear Physics RAS, Gatchina, Russian Federation; email: svesarl@yandex.ru},\r\nissn={00413771},\r\ncoden={TSITA},\r\npubmed_id={22359955},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n One of the earliest neuropathological symptoms of Alzheimer's disease is the loss of synapses, which preceed the formation of amyloidosis and neurodegeneration. Although most cases of early-onset familial Alzheimer's disease are caused by mutations in the presenilin 1 (PSl) gene, the functions of PSl and its role in synaptic disfunction are not yet completely understood. In this paper we analysed of the intracellular and extracellular distribution of PSl in the cultures of mouse cortical embryonic neurons. We found that PSl is concentrated on the surface of the growth cone and at neurite contact sites. PSl was also found in synapses where it is co-localized with synaptophysin. Independent evidense of involvment of PSl in synaptic function we obtained by transfection of neurons with GFP-PS1 cDNA. GFP was colocalized with synaptophysin in transfected cultures. GFP-immunoprecepitatcs from transfected neurons contained processed N-cadherin. This result presents an additional proof of involvment PSl in synapse formation. To evaluate the role of PSl inactivation in the synaptic functions, we compare synaptic density in neuronal cell cultures from PSl knockout mice PSl (-/-) and wild type mice PSl (+/+). Our results clearly show that PS 1(-/-) displayed a low number of morphological synapses in comparing with wild type culture PSl(+/+). In summary, our results indicate a role of PSl in synaptic function.\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 \"DendrimerPaper\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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@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}
\n
\n\n\n
\n 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.\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 \"FamilialPaper\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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@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 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.\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 Shvartsman, A.; Sarantseva, S.; Runova, O.; Talalaeva, E.; and Vitek, M.\n\n\n \n\n\n\n Biofizika, 55(5): 862-867. 2010.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"[FamilialPaper\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
\n
@ARTICLE{Shvartsman2010862,\r\nauthor={Shvartsman, 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={Biofizika},\r\nyear={2010},\r\nvolume={55},\r\nnumber={5},\r\npages={862-867},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-78149237903&partnerID=40&md5=2335c9dbde6f598a9da3b817fd12e74d},\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.},\r\ncorrespondence_address1={Shvartsman, A.L.},\r\nissn={00063029},\r\npubmed_id={21033353},\r\nlanguage={Russian},\r\nabbrev_source_title={Biofizika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n 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.\n
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\n  \n 2009\n \n \n (7)\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 \"ApolipoproteinPaper\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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@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
\n
\n\n\n
\n 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.\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 \"ModernPaper\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
@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}
\n
\n\n\n
\n 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.\n
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\n \n\n \n \n \n \n \n \n Modern genetic approaches to the search for targets for medicinal preparations.\n \n \n \n \n\n\n \n Sarantseva, S.; and Shvartsman, A.\n\n\n \n\n\n\n Genetika, 45(7): 869-880. 2009.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"ModernPaper\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
\n
@ARTICLE{Sarantseva2009869,\r\nauthor={Sarantseva, S.V. and Shvartsman, A.L.},\r\ntitle={Modern genetic approaches to the search for targets for medicinal preparations},\r\njournal={Genetika},\r\nyear={2009},\r\nvolume={45},\r\nnumber={7},\r\npages={869-880},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-70349567551&partnerID=40&md5=f273508e28a3e534677a6859ae0b8516},\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 aimed only at correcting symptoms of the disease. Identification of molecular targets in pharmacological screening of 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 designing new drugs.},\r\ncorrespondence_address1={Sarantseva, S.V.},\r\nissn={00166758},\r\npubmed_id={19705737},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Review},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n 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 aimed only at correcting symptoms of the disease. Identification of molecular targets in pharmacological screening of 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 designing new drugs.\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 \"ProteinPaper\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
@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}
\n
\n\n\n
\n 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.\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.\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 \"ProteinPaper\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
\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 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.\n
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\n \n\n \n \n \n \n \n \n Studying 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.; Bol'shakova, O.; Timoshenko, S.; Rodin, D.; Vitek, M.; and Shvartsman, A.\n\n\n \n\n\n\n Genetika, 45(1): 119-126. 2009.\n cited By 5\n\n\n\n
\n\n\n\n \n \n \"StudyingPaper\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
\n
@ARTICLE{Sarantseva2009119,\r\nauthor={Sarantseva, S.V. and Bol'shakova, O.I. and Timoshenko, S.I. and Rodin, D.I. and Vitek, M.P. and Shvartsman, A.L.},\r\ntitle={Studying 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={Genetika},\r\nyear={2009},\r\nvolume={45},\r\nnumber={1},\r\npages={119-126},\r\nnote={cited By 5},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-63049133912&partnerID=40&md5=b9247ce4cb04d9578611d8a0e28af84e},\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-beta-protein (Abeta). However, it remains unclear in what way APP and Abeta 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 driving the sequence of the green fluorescent protein. The expression of APP and its truncated forms caused a decrease in the synaptotagmin content of antennal lobes and mushroom lobes of the D. melanogaster brain, as well as neurodegeneration that progressed with age. The results suggest that that abnormal synaptogenesis and neurodegeneration occur in the Drosophila brain in the absence of Abeta. It is assumed that impaired cellular functions of APP and secretion of Abeta independently contribute to the pathogenesis of AD.},\r\ncorrespondence_address1={Sarantseva, S.V.},\r\nissn={00166758},\r\npubmed_id={19239106},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n 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-beta-protein (Abeta). However, it remains unclear in what way APP and Abeta 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 driving the sequence of the green fluorescent protein. The expression of APP and its truncated forms caused a decrease in the synaptotagmin content of antennal lobes and mushroom lobes of the D. melanogaster brain, as well as neurodegeneration that progressed with age. The results suggest that that abnormal synaptogenesis and neurodegeneration occur in the Drosophila brain in the absence of Abeta. It is assumed that impaired cellular functions of APP and secretion of Abeta independently contribute to the pathogenesis of AD.\n
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\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 \"StudyingPaper\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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@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}
\n
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\n 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.\n
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\n \n\n \n \n \n \n \n \n Degeneration of growth cones in a culture of embryonic neurons of mouse with presenilin 1 knockout.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biophysics, 53(6): 550-554. 2008.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"DegenerationPaper\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 A comparative study of growth cone morphology in cultured embryonic neurons derived from wild type PS1(+/+) and knockout PS1(-/-) mice has been performed. Growth cones from wild type PS1(+/+) mice were well spread and usually formed radially continuous and regular lamellar extensions, short filopodia. In contrast, most growth cones from knockout PS1(-/-) mice collapsed after 3-4 days in culture. Summarizing these data, we suggest that PS1 plays an important role in growth cone structure by stabilizing the integrity of the cytoskeleton. The growth cone collapse may be the main reason of abnormal neuronal migration and impaired synaptic function in PS1(-/-) mice. © 2008 Pleiades Publishing, Ltd.\n
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\n \n\n \n \n \n \n \n \n Degeneration of growth cones in a culture of embryonic neurons of mouse with presenilin 1 gene knockout.\n \n \n \n \n\n\n \n Shvartsman, A.; Sarantseva, S.; Solov'ev, K.; Runova, O.; Talalaeva, E.; and Vitek, M.\n\n\n \n\n\n\n Biofizika, 53(6): 1008-1013. 2008.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"DegenerationPaper\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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@ARTICLE{Shvartsman20081008,\r\nauthor={Shvartsman, A.L. and Sarantseva, S.V. and Solov'ev, K.V. and Runova, O.L. and Talalaeva, E.I. and Vitek, M.P.},\r\ntitle={Degeneration of growth cones in a culture of embryonic neurons of mouse with presenilin 1 gene knockout},\r\njournal={Biofizika},\r\nyear={2008},\r\nvolume={53},\r\nnumber={6},\r\npages={1008-1013},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-61549108285&partnerID=40&md5=680d601d07db699c04d978e2ce906ba1},\r\nabstract={A comparative study of growth cone morphology in cultured embryonic neurons derived from wild type PS 1(+/+) and knockout PS 1(-/-) mice has been performed. Growth cones from wild type PS 1(+/+) mice were well spread and usually formed radially continuous and regular lamellar extensions with numerous filopodia. In contrast, most growth cones from knockout PS 1(-/-) mice exhibited small lamellar extensions, short filopodia, and pure adhesion. A significant amount of growth cones from knockout PS 1(-/-) mice collapsed after 3-4 days in culture. It was suggested that PS 1 plays an important role in growth cone structure by stabilizing the integrity of the cytoskeleton. The growth cone collapse may be the main reason for abnormal neuronal migration and impaired synaptic function in PS 1(-/-) mice.},\r\ncorrespondence_address1={Shvartsman, A.L.},\r\nissn={00063029},\r\npubmed_id={19137685},\r\nlanguage={Russian},\r\nabbrev_source_title={Biofizika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n A comparative study of growth cone morphology in cultured embryonic neurons derived from wild type PS 1(+/+) and knockout PS 1(-/-) mice has been performed. Growth cones from wild type PS 1(+/+) mice were well spread and usually formed radially continuous and regular lamellar extensions with numerous filopodia. In contrast, most growth cones from knockout PS 1(-/-) mice exhibited small lamellar extensions, short filopodia, and pure adhesion. A significant amount of growth cones from knockout PS 1(-/-) mice collapsed after 3-4 days in culture. It was suggested that PS 1 plays an important role in growth cone structure by stabilizing the integrity of the cytoskeleton. The growth cone collapse may be the main reason for abnormal neuronal migration and impaired synaptic function in PS 1(-/-) mice.\n
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\n \n\n \n \n \n \n \n \n Epigenetic effect of the rad201(G1) mutation in a system with mobilization of nonautonomous P elements in Drosophila.\n \n \n \n \n\n\n \n Khromykh, I.; Varentsova, E.; Sarantseva, S.; and Kotlovanova, L.\n\n\n \n\n\n\n Genetika, 44(3): 346-352. 2008.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"EpigeneticPaper\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
\n
@ARTICLE{Khromykh2008346,\r\nauthor={Khromykh, I.M. and Varentsova, E.P. and Sarantseva, S.V. and Kotlovanova, L.V.},\r\ntitle={Epigenetic effect of the rad201(G1) mutation in a system with mobilization of nonautonomous P elements in Drosophila},\r\njournal={Genetika},\r\nyear={2008},\r\nvolume={44},\r\nnumber={3},\r\npages={346-352},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-51549119174&partnerID=40&md5=e01aee0f4b1b7d225954c0cad7b88060},\r\nabstract={The effect on P-element activity in somatic cells was studied for a repair mutation localized in the Drosophila genome in the region of the rad201 and Rad51C overlapping genes. When one of the parents carried nonautonomous P elements and the rad201 mutation and the other carried a P-transposase source, a high dominant pupal lethality was observed in the progeny heterozygous for the mutant allele and their sibs homozygous for the rad201+ wild-type allele. The sib response was due to the epigenetic effect of the rad201 mutation and was maintained through at least two generations. The specifics of the epigenetic effect are discussed in terms of its possible association with P transpositions and mitotic crossing over events determined by P transposase. Based on the results of genetic and genomic DNA analyses of the rad201 mutant, it was assumed that the phenomenon in question was determined by several genetic factors.},\r\ncorrespondence_address1={Khromykh, I.M.},\r\nissn={00166758},\r\npubmed_id={18664138},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n The effect on P-element activity in somatic cells was studied for a repair mutation localized in the Drosophila genome in the region of the rad201 and Rad51C overlapping genes. When one of the parents carried nonautonomous P elements and the rad201 mutation and the other carried a P-transposase source, a high dominant pupal lethality was observed in the progeny heterozygous for the mutant allele and their sibs homozygous for the rad201+ wild-type allele. The sib response was due to the epigenetic effect of the rad201 mutation and was maintained through at least two generations. The specifics of the epigenetic effect are discussed in terms of its possible association with P transpositions and mitotic crossing over events determined by P transposase. Based on the results of genetic and genomic DNA analyses of the rad201 mutant, it was assumed that the phenomenon in question was determined by several genetic factors.\n
\n\n\n
\n\n\n
\n \n\n \n \n \n \n \n \n DNA reparation parameters during epigenetic effect of the rad201(G1) mutation in Drosophila.\n \n \n \n \n\n\n \n Kotlovanova, L.; Varentsova, E.; Sarantseva, S.; and Khromykh, I.\n\n\n \n\n\n\n Genetika, 44(3): 353-358. 2008.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"DNAPaper\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
\n
@ARTICLE{Kotlovanova2008353,\r\nauthor={Kotlovanova, L.V. and Varentsova, E.R. and Sarantseva, S.V. and Khromykh, I.M.},\r\ntitle={DNA reparation parameters during epigenetic effect of the rad201(G1) mutation in Drosophila},\r\njournal={Genetika},\r\nyear={2008},\r\nvolume={44},\r\nnumber={3},\r\npages={353-358},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-51549101489&partnerID=40&md5=1e4e1872216bb689306c8bb68794a650},\r\nabstract={Cell estimates of genetic damage repair were obtained to characterize the epigenetic effect of the rad201(G1) mutation. The estimates included morphological defects (malformations); the frequency of chromosome aberrations in somatic cells; and somatic mosaicism, reflecting double-strand break repair via conversion. The range and frequency of malformations significantly differed between the rad201(G1) epigenetic effect and irradiation. A high pupal lethality, detected upon P-element mobilization, was not associated with an increase in the frequency of cells with chromosome aberrations, while somatic mosaicism was far greater. The results are discussed in the context of differences between radiation and P-element mutagenesis.},\r\ncorrespondence_address1={Kotlovanova, L.V.},\r\nissn={00166758},\r\npubmed_id={18664139},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n Cell estimates of genetic damage repair were obtained to characterize the epigenetic effect of the rad201(G1) mutation. The estimates included morphological defects (malformations); the frequency of chromosome aberrations in somatic cells; and somatic mosaicism, reflecting double-strand break repair via conversion. The range and frequency of malformations significantly differed between the rad201(G1) epigenetic effect and irradiation. A high pupal lethality, detected upon P-element mobilization, was not associated with an increase in the frequency of cells with chromosome aberrations, while somatic mosaicism was far greater. The results are discussed in the context of differences between radiation and P-element mutagenesis.\n
\n\n\n
\n\n\n
\n \n\n \n \n \n \n \n \n Cell estimates of genetic damage repair under the epigenetic effect of the rad201(G1) mutation in Drosophila.\n \n \n \n \n\n\n \n Kotlovanova, L.; Varentsova, E.; Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Russian Journal of Genetics, 44(3): 301-305. 2008.\n cited By 2\n\n\n\n
\n\n\n\n \n \n \"CellPaper\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
@ARTICLE{Kotlovanova2008301,\r\nauthor={Kotlovanova, L.V. and Varentsova, E.R. and Sarantseva, S.V. and Khromykh, Yu.M.},\r\ntitle={Cell estimates of genetic damage repair under the epigenetic effect of the rad201(G1) mutation in Drosophila},\r\njournal={Russian Journal of Genetics},\r\nyear={2008},\r\nvolume={44},\r\nnumber={3},\r\npages={301-305},\r\ndoi={10.1007/s11177-008-3009-8},\r\nnote={cited By 2},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-43249113472&doi=10.1007%2fs11177-008-3009-8&partnerID=40&md5=405d8ae3a6dd7b268cd8038e95aeb36a},\r\naffiliation={Konstantinov St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad oblast, 188350, Russian Federation},\r\nabstract={Cell estimates of genetic damage repair were obtained to characterize the epigenetic effect of the rad201(G1) mutation. The estimates included morphological defects (malformations); the frequency of chromosome aberrations in somatic cells; and somatic mosaicism, reflecting double-strand break repair via conversion. The range and frequency of malformations significantly differed between the rad201(G1) epigenetic effect and irradiation. A high pupal lethality, detected upon P-element mobilization, was not associated with an increase in the frequency of cells with chromosome aberrations, while somatic mosaicism was far greater. The results are discussed in the context of differences between radiation and P-element mutagenesis. © 2008 MAIK Nauka.},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)07-04-01168},\r\n}
\n
\n\n\n
\n Cell estimates of genetic damage repair were obtained to characterize the epigenetic effect of the rad201(G1) mutation. The estimates included morphological defects (malformations); the frequency of chromosome aberrations in somatic cells; and somatic mosaicism, reflecting double-strand break repair via conversion. The range and frequency of malformations significantly differed between the rad201(G1) epigenetic effect and irradiation. A high pupal lethality, detected upon P-element mobilization, was not associated with an increase in the frequency of cells with chromosome aberrations, while somatic mosaicism was far greater. The results are discussed in the context of differences between radiation and P-element mutagenesis. © 2008 MAIK Nauka.\n
\n\n\n
\n\n\n
\n \n\n \n \n \n \n \n \n Epigenetic effect of the rad201(G1) mutation in a system with mobilization of nonautonomous P elements in Drosophila.\n \n \n \n \n\n\n \n Khromykh, Y.; Varentsova, E.; Sarantseva, S.; and Kotlovanova, L.\n\n\n \n\n\n\n Russian Journal of Genetics, 44(3): 295-300. 2008.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"EpigeneticPaper\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
@ARTICLE{Khromykh2008295,\r\nauthor={Khromykh, Yu.M. and Varentsova, E.R. and Sarantseva, S.V. and Kotlovanova, L.V.},\r\ntitle={Epigenetic effect of the rad201(G1) mutation in a system with mobilization of nonautonomous P elements in Drosophila},\r\njournal={Russian Journal of Genetics},\r\nyear={2008},\r\nvolume={44},\r\nnumber={3},\r\npages={295-300},\r\ndoi={10.1007/s11177-008-3008-9},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-43249085329&doi=10.1007%2fs11177-008-3008-9&partnerID=40&md5=290eb960830bc8a90ae0ca97b32532b6},\r\naffiliation={Konstantinov St. Petersburg Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, Leningrad oblast, 188350, Russian Federation},\r\nabstract={The effect on P-element activity in somatic cells was studied for a repair mutation localized in the Drosophila genome in the region of the rad201 and Rad51C overlapping genes. When one of the parents carried nonautonomous P elements and the rad201 mutation and the other carried a P-transposase source, a high dominant pupal lethality was observed in the progeny heterozygous for the mutant allele and their sibs homozygous for the rad201 + wild-type allele. The sib response was due to the epigenetic effect of the rad201 mutation and was maintained through at least two generations. The specifics of the epigenetic effect are discussed in terms of its possible association with P transpositions and mitotic crossing over events determined by P transposase. Based on the results of genetic and genomic DNA analyses of the rad201 mutant, it was assumed that the phenomenon in question was determined by several genetic factors. © 2008 MAIK Nauka.},\r\nfunding_details={Российский Фонд Фундаментальных Исследований (РФФИ)07-04-01168},\r\n}
\n
\n\n\n
\n The effect on P-element activity in somatic cells was studied for a repair mutation localized in the Drosophila genome in the region of the rad201 and Rad51C overlapping genes. When one of the parents carried nonautonomous P elements and the rad201 mutation and the other carried a P-transposase source, a high dominant pupal lethality was observed in the progeny heterozygous for the mutant allele and their sibs homozygous for the rad201 + wild-type allele. The sib response was due to the epigenetic effect of the rad201 mutation and was maintained through at least two generations. The specifics of the epigenetic effect are discussed in terms of its possible association with P transpositions and mitotic crossing over events determined by P transposase. Based on the results of genetic and genomic DNA analyses of the rad201 mutant, it was assumed that the phenomenon in question was determined by several genetic factors. © 2008 MAIK Nauka.\n
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\n  \n 2007\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n The influence of sodium nitrite on the osmoresistance of Chinese hamster cells.\n \n \n \n \n\n\n \n Bolshakova, O.; Sverdlov, A.; Timoshenko, S.; Nikanorova, N.; and Grachev, S.\n\n\n \n\n\n\n Tsitologiya, 49(7): 576-580. 2007.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"ThePaper\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
\n
@ARTICLE{Bolshakova2007576,\r\nauthor={Bolshakova, O.I. and Sverdlov, A.G. and Timoshenko, S.I. and Nikanorova, N.G. and Grachev, S.A.},\r\ntitle={The influence of sodium nitrite on the osmoresistance of Chinese hamster cells},\r\njournal={Tsitologiya},\r\nyear={2007},\r\nvolume={49},\r\nnumber={7},\r\npages={576-580},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-34948844992&partnerID=40&md5=93b31ff652de5e229146afc64ef825ac},\r\naffiliation={St. Petersburg Nuclear Physics Institute RAS, Gatchina, Leningrad District, Russian Federation},\r\nabstract={We have previously demonstrated that incubation of V-79 cells in the medium containing the nitric oxide donor, NaNO2, increases cell resistance to damaging effect of γ;-rays, UV radiation and hyperthermia. In the present study, we investigated the effects of the nitric oxide donor on the sensitivity of V-79 cells to changes in osmomolarity of the medium by adding different amounts of sodium chloride or water. We found that pretreatment of the cells with NaNO2 resulted in a significant increase in the number of growing cells in 48 h after the treatment. The osmomolarity-dependent morphological changes in cultured cells were also substantially diminished following NaNO2 treatment. This effect could be observed under both hyper- and hypoosmosis, and was dependent on concentration of sodium chloride in hypertonic medium (being maximal under 0.17 M NaCl) and on the amount of water in hypotonic medium (being maximal under 1.1 times the dilution with water). In the experiments with increased osmomolarity, we found that the observed increase in the number of growing cells following NaNO2 treatment was accompanied with a significant increase of the mitotic index. These findings indicate that nitric oxide increases cell resistance to the damaging effects of osmotic shock in the way which is simi-lar to the protective effect of these molecules against radiation and hyperthermia. Similarities in the effects of NaNO2 under different conditions leading to cell damage suggest that nitric oxide might serve as the universal factor participating in recovery of damaged cells and mediating increased cellular resistance to the damaging conditions.},\r\ncorrespondence_address1={Bolshakova, O.I.; St. Petersburg Nuclear Physics Institute RAS, Gatchina, Leningrad District, Russian Federation},\r\nissn={00413771},\r\ncoden={TSITA},\r\npubmed_id={17918342},\r\nlanguage={Russian},\r\nabbrev_source_title={Tsitologiya},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n We have previously demonstrated that incubation of V-79 cells in the medium containing the nitric oxide donor, NaNO2, increases cell resistance to damaging effect of γ;-rays, UV radiation and hyperthermia. In the present study, we investigated the effects of the nitric oxide donor on the sensitivity of V-79 cells to changes in osmomolarity of the medium by adding different amounts of sodium chloride or water. We found that pretreatment of the cells with NaNO2 resulted in a significant increase in the number of growing cells in 48 h after the treatment. The osmomolarity-dependent morphological changes in cultured cells were also substantially diminished following NaNO2 treatment. This effect could be observed under both hyper- and hypoosmosis, and was dependent on concentration of sodium chloride in hypertonic medium (being maximal under 0.17 M NaCl) and on the amount of water in hypotonic medium (being maximal under 1.1 times the dilution with water). In the experiments with increased osmomolarity, we found that the observed increase in the number of growing cells following NaNO2 treatment was accompanied with a significant increase of the mitotic index. These findings indicate that nitric oxide increases cell resistance to the damaging effects of osmotic shock in the way which is simi-lar to the protective effect of these molecules against radiation and hyperthermia. Similarities in the effects of NaNO2 under different conditions leading to cell damage suggest that nitric oxide might serve as the universal factor participating in recovery of damaged cells and mediating increased cellular resistance to the damaging conditions.\n
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\n  \n 2006\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n Presenilin 1 expression on the cell surface in motile polarized cells.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Biophysics, 51(5): 740-743. 2006.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"PresenilinPaper\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 Most cases of early-onset familial Alzheimer's disease are caused by mutations in the presenilin 1 gene. Nonetheless, the function of presenilin 1 are not yet completely understood. It was shown that endogenous presenilin 1, as well as the adhesion protein CD44, is concentrated on the surface of lamellipodia of polarized T cells (Jurkat cells) after adhesion to a collagen matrix. This phenomenon was not observed for another surface protein of T cells, T cell receptor, which is not involved in cell adhesion processes. In cultures of primary mouse cortical neurons, presenilin 1 was concentrated on the surface of the growth cone and at neurite contact sites. The concentration of presenilin 1 on the surface of structures that determine cell motility and intercellular contacts suggests that presenilin 1 plays an important role in cell adhesion in motile polarized cells. © Nauka/Interperiodica 2006.\n
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\n \n\n \n \n \n \n \n \n Expression of presenilin 1 on the cell surface in motile polarized cells.\n \n \n \n \n\n\n \n Shvartsman, A.; Sarantseva, S.; Tatishcheva, I.; Runova, O.; Talalaeva, E.; and Vitek, M.\n\n\n \n\n\n\n Biofizika, 51(5): 839-843. 2006.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"ExpressionPaper\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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@ARTICLE{Shvartsman2006839,\r\nauthor={Shvartsman, A.L. and Sarantseva, S.V. and Tatishcheva, I.A. and Runova, O.L. and Talalaeva, E.I. and Vitek, M.P.},\r\ntitle={Expression of presenilin 1 on the cell surface in motile polarized cells},\r\njournal={Biofizika},\r\nyear={2006},\r\nvolume={51},\r\nnumber={5},\r\npages={839-843},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-39049190925&partnerID=40&md5=041a3d5ee2821e0eb4b7da898dd51373},\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 not yet completely understood. We showed that endogenous PS1 and the adhesion protein CD44 are redistributed on the surface of cell projections (lamellipodia) in polarized T- lymphocytes (Jurkat cells) after the adhesion to a collagen matrix. This effect was not observed for another surface protein of T lymphocytes, which is not involved in cell adhesion processes, the T cell receptor. In primary cultures of mouse cortical neurons, PS1 was concentrated at the surface of extended growth cones and at the sites of neurite contacts. The concentration of PS1 at the surface of cellular structures that promote cell motility and cell contacts suggests an important role of PSI in cell adhesion in motile polarized cells.},\r\ncorrespondence_address1={Shvartsman, A.L.},\r\nissn={00063029},\r\npubmed_id={17131822},\r\nlanguage={Russian},\r\nabbrev_source_title={Biofizika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n 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 not yet completely understood. We showed that endogenous PS1 and the adhesion protein CD44 are redistributed on the surface of cell projections (lamellipodia) in polarized T- lymphocytes (Jurkat cells) after the adhesion to a collagen matrix. This effect was not observed for another surface protein of T lymphocytes, which is not involved in cell adhesion processes, the T cell receptor. In primary cultures of mouse cortical neurons, PS1 was concentrated at the surface of extended growth cones and at the sites of neurite contacts. The concentration of PS1 at the surface of cellular structures that promote cell motility and cell contacts suggests an important role of PSI in cell adhesion in motile polarized cells.\n
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\n  \n 2004\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n New characteristic of Drosophila rad(2)201G1 mutation: Epigenetic inheritance of repair defect through meiosis and connection with Rad51C gene.\n \n \n \n \n\n\n \n Khromykh, Y.; Varentsova, E.; Sarantseva, S.; and Kotlovanova, L.\n\n\n \n\n\n\n Doklady Akademii Nauk, 395(6): 847-849. 2004.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"NewPaper\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
\n
@ARTICLE{Khromykh2004847,\r\nauthor={Khromykh, Yu.M. and Varentsova, E.R. and Sarantseva, S.V. and Kotlovanova, L.V.},\r\ntitle={New characteristic of Drosophila rad(2)201G1 mutation: Epigenetic inheritance of repair defect through meiosis and connection with Rad51C gene},\r\njournal={Doklady Akademii Nauk},\r\nyear={2004},\r\nvolume={395},\r\nnumber={6},\r\npages={847-849},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-8644274865&partnerID=40&md5=9e209ae072a359c28bfc256ddb461750},\r\naffiliation={Peterb. Inst. Yad. Fiz., Sankt-Peterburg, Russian Federation},\r\nabstract={The effect of rad(2)201G1 mutation on DNA reparation in Drosophila has been studied. Experimental system of mobilization of P-elements with P-transposase has been used as a model. The existence of inheritable mechanism of gene regulation in DNA reparation control has been demonstrated. Reparation deficiency has been probably meiosis-mediated. The rad201 appeared to be a mutant allele of Rad51C gene.},\r\ncorrespondence_address1={Khromykh, Yu.M.; Peterb. Inst. Yad. Fiz., Sankt-Peterburg, Russian Federation},\r\nissn={08695652},\r\ncoden={DAKNE},\r\nlanguage={Russian},\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 The effect of rad(2)201G1 mutation on DNA reparation in Drosophila has been studied. Experimental system of mobilization of P-elements with P-transposase has been used as a model. The existence of inheritable mechanism of gene regulation in DNA reparation control has been demonstrated. Reparation deficiency has been probably meiosis-mediated. The rad201 appeared to be a mutant allele of Rad51C gene.\n
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\n \n\n \n \n \n \n \n \n New characteristics of Drosophila mutation Rad(2)201G1: epigenetic transmission of a repair defect via meiosis and association with the Rad51C gene.\n \n \n \n \n\n\n \n Khromykh, Y.; Varentsova, E.; Sarantseva, S.; and Kotlovanova, L.\n\n\n \n\n\n\n Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections / translated from Russian, 395: 163-165. 2004.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"NewPaper\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
\n
@ARTICLE{Khromykh2004163,\r\nauthor={Khromykh, Y.M. and Varentsova, E.R. and Sarantseva, S.V. and Kotlovanova, L.V.},\r\ntitle={New characteristics of Drosophila mutation Rad(2)201G1: epigenetic transmission of a repair defect via meiosis and association with the Rad51C gene.},\r\njournal={Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections / translated from Russian},\r\nyear={2004},\r\nvolume={395},\r\npages={163-165},\r\ndoi={10.1023/B:DOBS.0000025248.45915.3e},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-4344703363&doi=10.1023%2fB%3aDOBS.0000025248.45915.3e&partnerID=40&md5=c20c9ce7b92495105b7d4d8676d1665a},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, St. Petersburg, Russian Federation},\r\ncorrespondence_address1={Khromykh, Y.M.},\r\nissn={00124966},\r\npubmed_id={15255153},\r\nlanguage={English},\r\nabbrev_source_title={Dokl. Biol. Sci.},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n  \n 2002\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n Increase of the radiation resistance of eucaryotic cells by means of sodium nitrite serving as an NO donor.\n \n \n \n \n\n\n \n Grachev, S.; Sverdlov, A.; Bol'shakova, O.; Timoshenko, S.; and Nikanorova, N.\n\n\n \n\n\n\n Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections / translated from Russian, 383: 103-105. 2002.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"IncreasePaper\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
\n
@ARTICLE{Grachev2002103,\r\nauthor={Grachev, S.A. and Sverdlov, A.G. and Bol'shakova, O.I. and Timoshenko, S.I. and Nikanorova, N.G.},\r\ntitle={Increase of the radiation resistance of eucaryotic cells by means of sodium nitrite serving as an NO donor.},\r\njournal={Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections / translated from Russian},\r\nyear={2002},\r\nvolume={383},\r\npages={103-105},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036510823&partnerID=40&md5=dae2cb945222df3796cd3c5bc9377606},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Leningrad Oblast, Russia, 188350, Russian Federation},\r\ncorrespondence_address1={Grachev, S.A.},\r\nissn={00124966},\r\npubmed_id={12053556},\r\nlanguage={English},\r\nabbrev_source_title={Dokl. Biol. Sci.},\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 of the eucariotic cells radioresistance using a donor of NO-sodium salt of nitrous acid.\n \n \n \n \n\n\n \n Grachev, S.; Sverdlov, A.; Bol'shakova, O.; Timoshenko, S.; and Nikanorova, N.\n\n\n \n\n\n\n Doklady Akademii Nauk, 383(4): 559-562. 2002.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"IncreasePaper\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
\n
@ARTICLE{Grachev2002559,\r\nauthor={Grachev, S.A. and Sverdlov, A.G. and Bol'shakova, O.I. and Timoshenko, S.I. and Nikanorova, N.G.},\r\ntitle={Increase of the eucariotic cells radioresistance using a donor of NO-sodium salt of nitrous acid},\r\njournal={Doklady Akademii Nauk},\r\nyear={2002},\r\nvolume={383},\r\nnumber={4},\r\npages={559-562},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0036418526&partnerID=40&md5=b193cc6240d09377455702f6dbe64f0b},\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 (4)\n \n \n
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\n \n\n \n \n \n \n \n \n The interaction of the rad201 gene with genes mei-9 and mei-41 in germline cells of drosophila females.\n \n \n \n \n\n\n \n Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Genetika, 37(7): 926-929. 2001.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"ThePaper\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
\n
@ARTICLE{Sarantseva2001926,\r\nauthor={Sarantseva, S.V. and Khromykh, Y.M.},\r\ntitle={The interaction of the rad201 gene with genes mei-9 and mei-41 in germline cells of drosophila females},\r\njournal={Genetika},\r\nyear={2001},\r\nvolume={37},\r\nnumber={7},\r\npages={926-929},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035405314&partnerID=40&md5=b242fa1523df560f57f2f1e8d6c2368e},\r\naffiliation={St. Petersburg Konstantinov Institute of Nuclear Physics, Gatchina, Leningrad ablast, 188350, Russian Federation},\r\nabstract={The effect of Drosophila mutation rad201GI together with mutations mei-41DS and mei-9° on the sensitivity of oocytes to induction of dominant lethals (DLs) was studied. To this end, the frequencies of spontaneous and gamma-radiation-induced DLs in consecutive egg batches of females carrying double or single mutations were estimated. Since the effects of the mutations examined are expressed only at the previtellogenetic stages of oogenesis, only newly hatched (0-5-hour-old) females, whose oocytes did not develop farther than stage 7, were irradiated. The results obtained indicated that in intact and irradiated oocytes of double mutants mei-9 rad201GI and mei-41D5 rad201G1, mutation rad201Gl epistatically suppresses the mutations of the both mei genes.},\r\ncorrespondence_address1={Sarantseva, S.V.; St. Petersburg Konstantinov Institute of Nuclear Physics, Gatchina, Leningrad ablast, 188350, Russian Federation; email: khromykh@omrb.pnpi.spb.ru},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={11558232},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n The effect of Drosophila mutation rad201GI together with mutations mei-41DS and mei-9° on the sensitivity of oocytes to induction of dominant lethals (DLs) was studied. To this end, the frequencies of spontaneous and gamma-radiation-induced DLs in consecutive egg batches of females carrying double or single mutations were estimated. Since the effects of the mutations examined are expressed only at the previtellogenetic stages of oogenesis, only newly hatched (0-5-hour-old) females, whose oocytes did not develop farther than stage 7, were irradiated. The results obtained indicated that in intact and irradiated oocytes of double mutants mei-9 rad201GI and mei-41D5 rad201G1, mutation rad201Gl epistatically suppresses the mutations of the both mei genes.\n
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\n \n\n \n \n \n \n \n \n Effects of gamma-radiation in oogenesis of drosophila mutants defective for repair and meiotic recombination.\n \n \n \n \n\n\n \n Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Genetika, 37(6): 770-778. 2001.\n cited By 3\n\n\n\n
\n\n\n\n \n \n \"EffectsPaper\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
\n
@ARTICLE{Sarantseva2001770,\r\nauthor={Sarantseva, S.V. and Khromykh, Y.M.},\r\ntitle={Effects of gamma-radiation in oogenesis of drosophila mutants defective for repair and meiotic recombination},\r\njournal={Genetika},\r\nyear={2001},\r\nvolume={37},\r\nnumber={6},\r\npages={770-778},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0035377169&partnerID=40&md5=a4427154efe97c878c3876f407e897ba},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Gatchina, Leningrad ablast, 188350, Russian Federation},\r\nabstract={Effects of mutations rad201, mei-9, and mei-41 on cell sensitivity to gamma-radiation in Drosophila oogenesis were studied. Females of the control (Oregon R) and mutant strains were irradiated at a dose of 15 Gy. For 9 days after the irradiation, the number of eggs in consecutive day batches, the frequency of dominant lethals (DLs) among the eggs, and the cytologically recorded distribution of oocytes for stages of their development, and the frequency of egg chamber degeneration in female ovaries were estimated. As a result of joint analysis of the data, different oogenesis stages were characterized with regard to the frequency of two radiation-induced events: appearance of DLs in oocytes and degeneration of egg chambers due to apoptosis of nurse cells. It was shown that the mutations affect these parameters only at particular stages of early oogenesis, at which previtellogenetic growth of egg follicles and meiotic recombination in oocytes occur. Mutation rad201G1 increased the frequency of DLs and egg chamber degeneration, mei-41DS affected only the DL frequency, and mei-9°, in addition to enhancing the chamber degeneration frequency, promoted radiation "rescue" of some oocytes from the DL induction.},\r\ncorrespondence_address1={Sarantseva, S.V.; Konstantinov Institute of Nuclear Physics, Gatchina, Leningrad ablast, 188350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={11517763},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n Effects of mutations rad201, mei-9, and mei-41 on cell sensitivity to gamma-radiation in Drosophila oogenesis were studied. Females of the control (Oregon R) and mutant strains were irradiated at a dose of 15 Gy. For 9 days after the irradiation, the number of eggs in consecutive day batches, the frequency of dominant lethals (DLs) among the eggs, and the cytologically recorded distribution of oocytes for stages of their development, and the frequency of egg chamber degeneration in female ovaries were estimated. As a result of joint analysis of the data, different oogenesis stages were characterized with regard to the frequency of two radiation-induced events: appearance of DLs in oocytes and degeneration of egg chambers due to apoptosis of nurse cells. It was shown that the mutations affect these parameters only at particular stages of early oogenesis, at which previtellogenetic growth of egg follicles and meiotic recombination in oocytes occur. Mutation rad201G1 increased the frequency of DLs and egg chamber degeneration, mei-41DS affected only the DL frequency, and mei-9°, in addition to enhancing the chamber degeneration frequency, promoted radiation \"rescue\" of some oocytes from the DL induction.\n
\n\n\n
\n\n\n
\n \n\n \n \n \n \n \n \n The Interaction of the rad201 Gene with Genes mei-9 and mei-41 in Germline Cells of Drosophila Females.\n \n \n \n \n\n\n \n \n\n\n \n\n\n\n Russian Journal of Genetics, 37(7): 764-767. 2001.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"ThePaper\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
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\n The effect of Drosophila mutation rad201G1 together with mutations mei-41D5 and mei-9a on the sensitivity of oocytes to induction of dominant lethals (DLs) was studied. To this end, the frequencies of spontaneous and gamma-radiation-induced DLs in consecutive egg batches of females carrying double or single mutations were estimated. Since the effects of the mutations examined are expressed only at the previtellogenetic stages of oogenesis, only newly hatched (0-5-hour-old) females, whose oocytes did not develop farther than stage 7, were irradiated. The results obtained indicated that in intact and irradiated oocytes of double mutants mei-9a rad201G1 and mei-41D5 rad201G1, mutation rad201G1 epistatically suppresses the mutations of the both mei genes.\n
\n\n\n
\n\n\n
\n \n\n \n \n \n \n \n \n Effects of Gamma-Radiation in Oogenesis of Drosophila Mutants Defective for Repair and Meiotic Recombination.\n \n \n \n \n\n\n \n Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Russian Journal of Genetics, 37(6): 631-638. 2001.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"EffectsPaper\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
@ARTICLE{Sarantseva2001631,\r\nauthor={Sarantseva, S.V. and Khromykh, Yu.M.},\r\ntitle={Effects of Gamma-Radiation in Oogenesis of Drosophila Mutants Defective for Repair and Meiotic Recombination},\r\njournal={Russian Journal of Genetics},\r\nyear={2001},\r\nvolume={37},\r\nnumber={6},\r\npages={631-638},\r\ndoi={10.1023/A:1016669123397},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0347708981&doi=10.1023%2fA%3a1016669123397&partnerID=40&md5=469fc7683b1d1c12c9c7c063b21ece34},\r\naffiliation={Konstantinov Inst. of Nucl. Physics, Gatchina, Leningrad oblast, 188350, Russian Federation},\r\nabstract={Effects of mutations rad201, mei-9, and mei-41 on cell sensitivity to gamma-radiation in Drosophila oogenesis were studied. Females of the control (Oregon R) and mutant strains were irradiated at a dose of 15 Gy. For 9 day s after the irradiation, the number of eggs in consecutive day batches, the frequency of dominant lethals (DLs) among the eggs, and the cytologically recorded distribution of oocytes for stages of their development, and the frequency of egg chamber degeneration in female ovaries were estimated. As a result of joint analysis of the data, different oogenesis stages were characterized with regard to the frequency of two radiation-induced events: appearance of DLs in oocytes and degeneration of egg chambers due to apoptosis of nurse cells. It was shown that the mutations affect these parameters only at particular stages of early oogenesis, at which previtellogenetic growth of egg follicles and meiotic recombination in oocytes occur. Mutation rad201G1 increased the frequency of DLs and egg chamber degeneration, mei-41D5 affected only the DL frequency, and mei-9a, in addition to enhancing the chamber degeneration frequency, promoted radiation "rescue" of some oocytes from the DL induction.},\r\ncorrespondence_address1={Sarantseva, S.V.; Konstantinov Inst. of Nucl. Physics, Gatchina, Leningrad oblast, 188350, Russian Federation; email: khromykh@omrb.pnpi.spb.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
\n
\n\n\n
\n Effects of mutations rad201, mei-9, and mei-41 on cell sensitivity to gamma-radiation in Drosophila oogenesis were studied. Females of the control (Oregon R) and mutant strains were irradiated at a dose of 15 Gy. For 9 day s after the irradiation, the number of eggs in consecutive day batches, the frequency of dominant lethals (DLs) among the eggs, and the cytologically recorded distribution of oocytes for stages of their development, and the frequency of egg chamber degeneration in female ovaries were estimated. As a result of joint analysis of the data, different oogenesis stages were characterized with regard to the frequency of two radiation-induced events: appearance of DLs in oocytes and degeneration of egg chambers due to apoptosis of nurse cells. It was shown that the mutations affect these parameters only at particular stages of early oogenesis, at which previtellogenetic growth of egg follicles and meiotic recombination in oocytes occur. Mutation rad201G1 increased the frequency of DLs and egg chamber degeneration, mei-41D5 affected only the DL frequency, and mei-9a, in addition to enhancing the chamber degeneration frequency, promoted radiation \"rescue\" of some oocytes from the DL induction.\n
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\n  \n 1999\n \n \n (4)\n \n \n
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\n \n\n \n \n \n \n \n \n A Study on the UV Sensitivity of Embryogenesis in Drosophila Lines with Different Repair Abilities.\n \n \n \n \n\n\n \n Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Russian Journal of Genetics, 35(2): 151-156. 1999.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"APaper\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
\n
@ARTICLE{Sarantseva1999151,\r\nauthor={Sarantseva, S.V. and Khromykh, Yu.M.},\r\ntitle={A Study on the UV Sensitivity of Embryogenesis in Drosophila Lines with Different Repair Abilities},\r\njournal={Russian Journal of Genetics},\r\nyear={1999},\r\nvolume={35},\r\nnumber={2},\r\npages={151-156},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0346394597&partnerID=40&md5=24b87635f9483b7ea1c89eaefa1f9440},\r\naffiliation={Konstantinov Nucl. Phys. Inst. St.P., Gatchina, St. Petersburg 188350, Russian Federation},\r\nabstract={Sensitivity of Drosophila embryos to the lethal effect of UV rays was studied in mutants rad202G1 and mei-9a (a homologue of the gene for xeroderma pigmentosum) that are deficient in excision repair, the mutant mei-41D5 (a homologue of the gene for AT) with distorted check-point function in the cell cycle, and wild-type line Oregon R. The mortality of embryos, which were exposed to radiation within the 0.5 - 16-h interval of embryonic life, served as a criterion of sensitivity. During this interval of embryogenesis, the multicellular system of Drosophila embryo consecutively passes through a set of well studied cell cycle modifications. It was of interest to compare UV sensitivity at these stages recorded at the organism level. The induced embryonic lethality was tested by means of determining the dose - effect relationship followed by an estimation of corresponding values of the LD50 dose characterizing the pattern of age-associated changes of the character. The obtained data were analyzed in relation to the specificity of the mutagenic effect of UV irradiation, the features of Drosophila development, and repair deficiency of each studied mutant. The interval of the pronounced effect of UV irradiation on embryo viability was shown to be limited to 13 h from the beginning of embryonic life. During this interval, the UV sensitivity of embryogenesis in mutant lines is much higher than in the line of normal genotype. Moreover, at the level of LD50 doses that individually characterize each line, this sensitivity did not exhibit a relation to the mitotic status of cells, in contrast with the effects of rarely ionizing radiation. UV-inducible embryo lethalities that are caused by the mortality of dividing and nondividing cells are either equal (line Oregon R and mutants rad202G1 and mei-41D5) or even extreme in the case of damage of amitotically growing cells (the mei-9a mutant). Possible mechanisms of these manifestations are discussed.},\r\ncorrespondence_address1={Sarantseva, S.V.; Konstantinov Nucl. Phys. Inst. St.P., Gatchina, St. Petersburg 188350, Russian Federation; email: khromykh@omrb.pnpi.spb.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
\n
\n\n\n
\n Sensitivity of Drosophila embryos to the lethal effect of UV rays was studied in mutants rad202G1 and mei-9a (a homologue of the gene for xeroderma pigmentosum) that are deficient in excision repair, the mutant mei-41D5 (a homologue of the gene for AT) with distorted check-point function in the cell cycle, and wild-type line Oregon R. The mortality of embryos, which were exposed to radiation within the 0.5 - 16-h interval of embryonic life, served as a criterion of sensitivity. During this interval of embryogenesis, the multicellular system of Drosophila embryo consecutively passes through a set of well studied cell cycle modifications. It was of interest to compare UV sensitivity at these stages recorded at the organism level. The induced embryonic lethality was tested by means of determining the dose - effect relationship followed by an estimation of corresponding values of the LD50 dose characterizing the pattern of age-associated changes of the character. The obtained data were analyzed in relation to the specificity of the mutagenic effect of UV irradiation, the features of Drosophila development, and repair deficiency of each studied mutant. The interval of the pronounced effect of UV irradiation on embryo viability was shown to be limited to 13 h from the beginning of embryonic life. During this interval, the UV sensitivity of embryogenesis in mutant lines is much higher than in the line of normal genotype. Moreover, at the level of LD50 doses that individually characterize each line, this sensitivity did not exhibit a relation to the mitotic status of cells, in contrast with the effects of rarely ionizing radiation. UV-inducible embryo lethalities that are caused by the mortality of dividing and nondividing cells are either equal (line Oregon R and mutants rad202G1 and mei-41D5) or even extreme in the case of damage of amitotically growing cells (the mei-9a mutant). Possible mechanisms of these manifestations are discussed.\n
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\n \n\n \n \n \n \n \n \n A study on the UV sensitivity of embryogenesis in drosophila lines with different repair abilities.\n \n \n \n \n\n\n \n Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Genetika, 35(2): 203-208. 1999.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"APaper\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
\n
@ARTICLE{Sarantseva1999203,\r\nauthor={Sarantseva, S.V. and Khromykh, Yu.M.},\r\ntitle={A study on the UV sensitivity of embryogenesis in drosophila lines with different repair abilities},\r\njournal={Genetika},\r\nyear={1999},\r\nvolume={35},\r\nnumber={2},\r\npages={203-208},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0033070297&partnerID=40&md5=305dd5341c71d8bbe9f1cd155f8606ca},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nabstract={Sensitivity of Drosophila embryos to lethal effect of UV rays was studied in mutants rad202Gl and mei-9a (a homologue of the gene for xeroderma pigmentosum) that are deficient in excision repair, the mutant mei-41D5 (a homologue of the gene for AT) with distorted check-point function in the cell cycle, and wild-type line Oregon R. The mortality of embryos, which were exposed to radiation'within the 0.5-16-h interval of embryonic life, served as a criterion of sensitivity. During this interval of embryogenesis, the multicellular system of Drosophila embryo sequentially consecutively passes through a set of well studied cell cycle modifications. It was of interest to compare UV sensitivity at these stages recorded at the organism level. The induced embryonic lethality was tested by means of determining the dose-effect relationship followed by an estimation of corresponding values of the LD50 dose characterizing the pattern of age-associated changes of the character. The obtained data were analyzed in relation to the specificity of the mutagenic effect of UV irradiation, the features of Drosophila development, and repair deficiency of each studied mutant. The interval of the pronounced effect of UV irradiation on embryo viability was shown to be limited to 13 h from the beginning of embryonic life. During this interval, the UV sensitivity of embryogenesis in mutant lines is much higher than in the line of normal genotype. Moreover, at the level of LD50 doses that individually characterize each line, this sensitivity did not exhibit a relation to the mitotic status of cells, in contrast with the effects of rarely ionizing radiation. UV-inducible embryo lethalities that are caused by the mortality of dividing and nondividing cells are whether equal (line Oregon R and mutants rad202Gl and mei-41D5) or even extremum in the case of damage of amitotically growing cells (the mei-9a mutant). Possible mechanisms of these manifestations are discussed.},\r\ncorrespondence_address1={Sarantseva, S.V.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={10495937},\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 Sensitivity of Drosophila embryos to lethal effect of UV rays was studied in mutants rad202Gl and mei-9a (a homologue of the gene for xeroderma pigmentosum) that are deficient in excision repair, the mutant mei-41D5 (a homologue of the gene for AT) with distorted check-point function in the cell cycle, and wild-type line Oregon R. The mortality of embryos, which were exposed to radiation'within the 0.5-16-h interval of embryonic life, served as a criterion of sensitivity. During this interval of embryogenesis, the multicellular system of Drosophila embryo sequentially consecutively passes through a set of well studied cell cycle modifications. It was of interest to compare UV sensitivity at these stages recorded at the organism level. The induced embryonic lethality was tested by means of determining the dose-effect relationship followed by an estimation of corresponding values of the LD50 dose characterizing the pattern of age-associated changes of the character. The obtained data were analyzed in relation to the specificity of the mutagenic effect of UV irradiation, the features of Drosophila development, and repair deficiency of each studied mutant. The interval of the pronounced effect of UV irradiation on embryo viability was shown to be limited to 13 h from the beginning of embryonic life. During this interval, the UV sensitivity of embryogenesis in mutant lines is much higher than in the line of normal genotype. Moreover, at the level of LD50 doses that individually characterize each line, this sensitivity did not exhibit a relation to the mitotic status of cells, in contrast with the effects of rarely ionizing radiation. UV-inducible embryo lethalities that are caused by the mortality of dividing and nondividing cells are whether equal (line Oregon R and mutants rad202Gl and mei-41D5) or even extremum in the case of damage of amitotically growing cells (the mei-9a mutant). Possible mechanisms of these manifestations are discussed.\n
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\n \n\n \n \n \n \n \n \n Effect of unithiol on cystamine toxicity in dogs [Vliianie unitiola na toksicheskie éffekty tsistamina u sobak.].\n \n \n \n \n\n\n \n Grachev, S.; Sverdlov, A.; Nikanorova, N.; and Timoshenko, S.\n\n\n \n\n\n\n Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk, 39(2-3): 261-263. 1999.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"EffectPaper\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
\n
@ARTICLE{Grachev1999261,\r\nauthor={Grachev, S.A. and Sverdlov, A.G. and Nikanorova, N.G. and Timoshenko, S.I.},\r\ntitle={Effect of unithiol on cystamine toxicity in dogs [Vliianie unitiola na toksicheskie éffekty tsistamina u sobak.]},\r\njournal={Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk},\r\nyear={1999},\r\nvolume={39},\r\nnumber={2-3},\r\npages={261-263},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0033093812&partnerID=40&md5=bb2efbc59081c0815669db072f386c24},\r\naffiliation={B.P. Konstantinov Petersburg Nuclear Physics Institute, Russian Academy of Sciences, Gatchina, Russian Federation},\r\nabstract={In experiments with dogs it was shown that administration of unithiol before administration of cystamine decreases toxic effect of the last: period of excitation induced by cystamine is shortened, the time of emetic reaction decreases and expression of the emetic reaction to this preparation is diminished, the recorded EKG changes of conditions of heart decrease.},\r\ncorrespondence_address1={Grachev, S.A.email: Grachev@lnpi.spb.su},\r\nissn={08698031},\r\npubmed_id={10366950},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiats Biol Radioecol},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n In experiments with dogs it was shown that administration of unithiol before administration of cystamine decreases toxic effect of the last: period of excitation induced by cystamine is shortened, the time of emetic reaction decreases and expression of the emetic reaction to this preparation is diminished, the recorded EKG changes of conditions of heart decrease.\n
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\n \n\n \n \n \n \n \n \n Increased efficacy of radiation protection against fission neutrons using unithiol [Povyshenie éffektivnosti khimicheskoi zashchity ot neitronov deleniia s pomoshch'iu unitiola.].\n \n \n \n \n\n\n \n Grachev, S.; Sverdlov, A.; Nikanorova, N.; and Timoshenko, S.\n\n\n \n\n\n\n Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk, 39(2-3): 258-260. 1999.\n cited By 3\n\n\n\n
\n\n\n\n \n \n \"IncreasedPaper\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
\n
@ARTICLE{Grachev1999258,\r\nauthor={Grachev, S.A. and Sverdlov, A.G. and Nikanorova, N.G. and Timoshenko, S.I.},\r\ntitle={Increased efficacy of radiation protection against fission neutrons using unithiol [Povyshenie éffektivnosti khimicheskoi zashchity ot neitronov deleniia s pomoshch'iu unitiola.]},\r\njournal={Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk},\r\nyear={1999},\r\nvolume={39},\r\nnumber={2-3},\r\npages={258-260},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0033093699&partnerID=40&md5=6e4f62812267b52c5b3de590b261ce51},\r\naffiliation={B.P. Konstantinov Petersburg Nuclear Physics Institute, Russuan Academy of Sciences, Gatchina, Russian Federation},\r\nabstract={It was found that the combination of unithiol (Sodium salt of 2,3-dimercapto-1-propansulfonic acid) with cystamine and AET diminished their toxicity. The optimum ratio for the antitoxic effect is 0.5 molar equivalent of unithiol per radioprotective 1.0 equivalent of thiol. Animals withstand big doses of protectors well, that gives an opportunity to use increased amounts of cystamine and AET. In the experiments with circular irradiation of male (CBA x C57B1)F1 mice weighing 18-22 g with fission neutrons (the neutron mean energy was 0.85 MeV, the contribution of gamma-quanta to the total was 25%, dose rate was 14 cGy/min) it was shown that the combination of unithiol with cystamine and AET enhances their radioprotective effect: the DRF of cystamine (150 mg/kg)--1.1, and the DRF of the combination of cystamine (300 mg/kg) with unithiol (152 mg/kg)--1.2; the DRF of AET (150 mg/kg)--1.2, the DRF of the combination of AET (300 mg/kg) with unithiol--1.4. Thus, the enhancement of dose of the radioprotectors, which was made possible as a result of their combination with unithiol, leads to enhancement of efficacy of chemical protection against fission neutron irradiation as much as 10-20%. Efficacy of AET is found to be comparable to efficacy of this protector in conditions of X-rays irradiation.},\r\ncorrespondence_address1={Grachev, S.A.email: Grachev@lnpi.spb.su},\r\nissn={08698031},\r\npubmed_id={10366949},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiats Biol Radioecol},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n It was found that the combination of unithiol (Sodium salt of 2,3-dimercapto-1-propansulfonic acid) with cystamine and AET diminished their toxicity. The optimum ratio for the antitoxic effect is 0.5 molar equivalent of unithiol per radioprotective 1.0 equivalent of thiol. Animals withstand big doses of protectors well, that gives an opportunity to use increased amounts of cystamine and AET. In the experiments with circular irradiation of male (CBA x C57B1)F1 mice weighing 18-22 g with fission neutrons (the neutron mean energy was 0.85 MeV, the contribution of gamma-quanta to the total was 25%, dose rate was 14 cGy/min) it was shown that the combination of unithiol with cystamine and AET enhances their radioprotective effect: the DRF of cystamine (150 mg/kg)–1.1, and the DRF of the combination of cystamine (300 mg/kg) with unithiol (152 mg/kg)–1.2; the DRF of AET (150 mg/kg)–1.2, the DRF of the combination of AET (300 mg/kg) with unithiol–1.4. Thus, the enhancement of dose of the radioprotectors, which was made possible as a result of their combination with unithiol, leads to enhancement of efficacy of chemical protection against fission neutron irradiation as much as 10-20%. Efficacy of AET is found to be comparable to efficacy of this protector in conditions of X-rays irradiation.\n
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\n  \n 1998\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Characterization of the adaptive response to the action of gamma-rays, induced by low doses of 14C in Chinese hamster fibroblasts [Kharakteristika adaptivnogo otveta k deistviiu gamma-luchei, indutsirovannogo malymi dozami 14C v fibroblastakh kitaiskogo khomiachka.].\n \n \n \n \n\n\n \n Gilliano, N.; Bol'shakova, O.; Lavrova, G.; Konevega, L.; Bikineeva, E.; and Noskin, L.\n\n\n \n\n\n\n Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk, 38(5): 663-671. 1998.\n cited By 3\n\n\n\n
\n\n\n\n \n \n \"CharacterizationPaper\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
\n
@ARTICLE{Gilliano1998663,\r\nauthor={Gilliano, N.I. and Bol'shakova, O.I. and Lavrova, G.A. and Konevega, L.V. and Bikineeva, E.G. and Noskin, L.A.},\r\ntitle={Characterization of the adaptive response to the action of gamma-rays, induced by low doses of 14C in Chinese hamster fibroblasts [Kharakteristika adaptivnogo otveta k deistviiu gamma-luchei, indutsirovannogo malymi dozami 14C v fibroblastakh kitaiskogo khomiachka.]},\r\njournal={Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk},\r\nyear={1998},\r\nvolume={38},\r\nnumber={5},\r\npages={663-671},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0032151422&partnerID=40&md5=75c2ac79005b569a5446c94977298da1},\r\naffiliation={Petersburg Nuclear Physics Institute, Russian Academy of Science, Gatchina, Russian Federation},\r\nabstract={It has been studied the correlation of the mitotic activity of the chromosome aberrations and apoptosis, in the V-79 cells pre-exposure to an adapting dose of ionizing radiation from 14C-thymidine prior to an acute challenge dose of gamma-rays. In spite of that the incubation of the cells with isotope increased of the yield of the chromosome aberrations, but the cells became more resistant to following gamma-irradiation. Increasing the adaptive dose of the 14C on degree didn't influence on the present of the adaptive response. However, using concentrations of the 14C damaged metaphase/anaphase transition and cells blocked in this check-point by apoptotic death. The results suggest, that the cellular selection has been involved in 14C-induced adaptive response, estimated by level of asymmetric chromosome aberrations in V-79 cells.},\r\ncorrespondence_address1={Gilliano, N.I.},\r\nissn={08698031},\r\npubmed_id={9876490},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiats Biol Radioecol},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n It has been studied the correlation of the mitotic activity of the chromosome aberrations and apoptosis, in the V-79 cells pre-exposure to an adapting dose of ionizing radiation from 14C-thymidine prior to an acute challenge dose of gamma-rays. In spite of that the incubation of the cells with isotope increased of the yield of the chromosome aberrations, but the cells became more resistant to following gamma-irradiation. Increasing the adaptive dose of the 14C on degree didn't influence on the present of the adaptive response. However, using concentrations of the 14C damaged metaphase/anaphase transition and cells blocked in this check-point by apoptotic death. The results suggest, that the cellular selection has been involved in 14C-induced adaptive response, estimated by level of asymmetric chromosome aberrations in V-79 cells.\n
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\n  \n 1997\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n Selective expression of the rad201 radiosensitivity gene mutation in Drosophila embryogenesis.\n \n \n \n \n\n\n \n Varentsova, E.; Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Genetika, 33(2): 205-210. 1997.\n cited By 3\n\n\n\n
\n\n\n\n \n \n \"SelectivePaper\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
\n
@ARTICLE{Varentsova1997205,\r\nauthor={Varentsova, E.R. and Sarantseva, S.V. and Khromykh, Yu.M.},\r\ntitle={Selective expression of the rad201 radiosensitivity gene mutation in Drosophila embryogenesis},\r\njournal={Genetika},\r\nyear={1997},\r\nvolume={33},\r\nnumber={2},\r\npages={205-210},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0031062457&partnerID=40&md5=a74b9de729d582c823dd5ea8b83cabfc},\r\naffiliation={Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nabstract={Embryonic sensitivity to the lethal effect of y-irradiation was compared in a radiosensitive mutant strain rad201Gl and a control radioresistant strain of Drosophila during the first 9 h of embryonic development. Embryonic radiosensitivity was analyzed with regard to the physiological age of embryos at the time of exposure to radiation. In the wild-type embryos, age-dependent variations of radiosensitivity were shown to be closely associated with genetically determined alterations in mitotic cycle structure, synchronism, and duration of separate phases. The rad201 gene mutation, which disrupts repair of chromosome damage in female germ cells and somatic cells of Drosophila, is expressed selectively during the period studied. The mutation had no effect on lethality at the stages of cleavage division, which represent alternation of S and M phases of the cell cycle. However, it caused an increase in lethality at the stage of postblastodermal mitotic divisions, whose onset is associated with a transformation of the organization and functions of genetic material and the appearance of G2 in the cell cycle. This transformation seems to be required for the functioning of the repair system affected by radZOl.},\r\ncorrespondence_address1={Varentsova, E.R.; Konstantinov Institute of Nuclear Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={9162698},\r\nlanguage={Russian},\r\nabbrev_source_title={Genetika},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n Embryonic sensitivity to the lethal effect of y-irradiation was compared in a radiosensitive mutant strain rad201Gl and a control radioresistant strain of Drosophila during the first 9 h of embryonic development. Embryonic radiosensitivity was analyzed with regard to the physiological age of embryos at the time of exposure to radiation. In the wild-type embryos, age-dependent variations of radiosensitivity were shown to be closely associated with genetically determined alterations in mitotic cycle structure, synchronism, and duration of separate phases. The rad201 gene mutation, which disrupts repair of chromosome damage in female germ cells and somatic cells of Drosophila, is expressed selectively during the period studied. The mutation had no effect on lethality at the stages of cleavage division, which represent alternation of S and M phases of the cell cycle. However, it caused an increase in lethality at the stage of postblastodermal mitotic divisions, whose onset is associated with a transformation of the organization and functions of genetic material and the appearance of G2 in the cell cycle. This transformation seems to be required for the functioning of the repair system affected by radZOl.\n
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\n \n\n \n \n \n \n \n \n Selective Expression of the rad201 Radiosensitivity Gene Mutation in Drosophila Embryogenesis.\n \n \n \n \n\n\n \n Varentsova, E.; Sarantseva, S.; and Khromykh, Y.\n\n\n \n\n\n\n Russian Journal of Genetics, 33(2): 153-157. 1997.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"SelectivePaper\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
\n
@ARTICLE{Varentsova1997153,\r\nauthor={Varentsova, E.P. and Sarantseva, S.V. and Khromykh, Yu.M.},\r\ntitle={Selective Expression of the rad201 Radiosensitivity Gene Mutation in Drosophila Embryogenesis},\r\njournal={Russian Journal of Genetics},\r\nyear={1997},\r\nvolume={33},\r\nnumber={2},\r\npages={153-157},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-1542607484&partnerID=40&md5=66b89ac578cfe56dfb89a40bdcd61738},\r\naffiliation={Konstantinov Inst. of Nucl. Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\r\nabstract={Embryonic sensitivity to the lethal effect of γ-irradiation was compared in a radiosensitive mutant strain rad201G1 and a control radioresistant strain of Drosophila during the first 9 h of embryonic development. Embryonic radiosensitivity was analyzed with regard to the physiological age of embryos at the time of exposure to radiation. In wild-type embryos, age-dependent variations of radiosensitivity were shown to be closely associated with genetically determined alterations in mitotic cycle structure, synchronism, and duration of separate phases. The rad201 gene mutation, which disrupts repair of chromosome damage in female germ cells and somatic cells of Drosophila, is expressed selectively during the period studied. The mutation had no effect on lethality at the stages of cleavage division, which represent alternation of S and M phases of the cell cycle. However, it caused an increase in lethality at the stage of postblastodermal mitotic divisions, whose onset is associated with a transformation of the organization and functions of genetic material and the appearance of G2 in the cell cycle. This transformation seems to be required for the functioning of the repair system affected by rad201.},\r\ncorrespondence_address1={Varentsova, E.P.; Konstantinov Inst. of Nucl. Physics, Russian Academy of Sciences, Gatchina, 188350, Russian Federation},\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
\n
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\n Embryonic sensitivity to the lethal effect of γ-irradiation was compared in a radiosensitive mutant strain rad201G1 and a control radioresistant strain of Drosophila during the first 9 h of embryonic development. Embryonic radiosensitivity was analyzed with regard to the physiological age of embryos at the time of exposure to radiation. In wild-type embryos, age-dependent variations of radiosensitivity were shown to be closely associated with genetically determined alterations in mitotic cycle structure, synchronism, and duration of separate phases. The rad201 gene mutation, which disrupts repair of chromosome damage in female germ cells and somatic cells of Drosophila, is expressed selectively during the period studied. The mutation had no effect on lethality at the stages of cleavage division, which represent alternation of S and M phases of the cell cycle. However, it caused an increase in lethality at the stage of postblastodermal mitotic divisions, whose onset is associated with a transformation of the organization and functions of genetic material and the appearance of G2 in the cell cycle. This transformation seems to be required for the functioning of the repair system affected by rad201.\n
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\n  \n 1994\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n Decrease of toxic effects of aminothiol radiation-protective agents and increase of chemical protection action against ionizing radiation by the use of unithiol [Snizhenie toksicheskogo deǐstviia aminotiolovykh radioprotektorov i povyshenie éffekta khimicheskoǐ zashchity ot ioniziruiushcheǐ radiatsii s pomoshchiu unitiola.].\n \n \n \n \n\n\n \n Grachev, S.; Sverdlov, A.; Nikanorova, N.; Bol'shakova, O.; and Korolva, I.\n\n\n \n\n\n\n Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk, 34(3): 424-429. 1994.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"DecreasePaper\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
\n
@ARTICLE{Grachev1994424,\r\nauthor={Grachev, S.A. and Sverdlov, A.G. and Nikanorova, N.G. and Bol'shakova, O.I. and Korolva, I.K.},\r\ntitle={Decrease of toxic effects of aminothiol radiation-protective agents and increase of chemical protection action against ionizing radiation by the use of unithiol [Snizhenie toksicheskogo deǐstviia aminotiolovykh radioprotektorov i povyshenie éffekta khimicheskoǐ zashchity ot ioniziruiushcheǐ radiatsii s pomoshchiu unitiola.]},\r\njournal={Radiatsionnaia biologiia, radioecologiia / Rossiiskaia akademiia nauk},\r\nyear={1994},\r\nvolume={34},\r\nnumber={3},\r\npages={424-429},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0028435828&partnerID=40&md5=7fbfc0eeb997dcd9dfb31f4dea9a28c0},\r\nabstract={It has been shown that unithiol diminishes toxic action of cysteamine, AET, and disulfide of WR-1065 on mice. This permits to enhance protection of animals against X-rays by increasing of protector doses. The effect of unithiol on cysteamine action in rats was the same. Antitoxic effect of unithiol on cysteamine was shown both at i.p. and p.o. protector administration. The effect was also revealed in Chinese hamster V-79 cell culture. Combined disulfide of cysteamine and unithiol was synthetized, which ensures effective prolonged protection against ionizing radiation.},\r\ncorrespondence_address1={Grachev, S.A.},\r\nissn={08698031},\r\npubmed_id={8069380},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiats Biol Radioecol},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n It has been shown that unithiol diminishes toxic action of cysteamine, AET, and disulfide of WR-1065 on mice. This permits to enhance protection of animals against X-rays by increasing of protector doses. The effect of unithiol on cysteamine action in rats was the same. Antitoxic effect of unithiol on cysteamine was shown both at i.p. and p.o. protector administration. The effect was also revealed in Chinese hamster V-79 cell culture. Combined disulfide of cysteamine and unithiol was synthetized, which ensures effective prolonged protection against ionizing radiation.\n
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\n \n\n \n \n \n \n \n \n Cytogenetic analysis of the chromosome region containing the Drosophila radiosensitivity gene. I. Cytogenetic mapping of the radiosensitivity gene [Tsitogeneticheskiǐ analiz uchastka khromosomy, soderzhashchego gen radiochuvstvitel'nosti drozofily.I. Tsitogeneticheskoe kartirovanie gena radiochuvstvitel'nosti.].\n \n \n \n \n\n\n \n Konev, A.; Varentsova, E.; Levina, V.; Sarantseva, S.; and Khromykh, I.\n\n\n \n\n\n\n Genetika, 30(2): 192-200. 1994.\n cited By 4\n\n\n\n
\n\n\n\n \n \n \"CytogeneticPaper\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
\n
@ARTICLE{Konev1994192,\r\nauthor={Konev, A.I. and Varentsova, E.R. and Levina, V.V. and Sarantseva, S.V. and Khromykh, I.M.},\r\ntitle={Cytogenetic analysis of the chromosome region containing the Drosophila radiosensitivity gene. I. Cytogenetic mapping of the radiosensitivity gene [Tsitogeneticheskiǐ analiz uchastka khromosomy, soderzhashchego gen radiochuvstvitel'nosti drozofily.I. Tsitogeneticheskoe kartirovanie gena radiochuvstvitel'nosti.]},\r\njournal={Genetika},\r\nyear={1994},\r\nvolume={30},\r\nnumber={2},\r\npages={192-200},\r\nnote={cited By 4},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0028374035&partnerID=40&md5=d89e88e89f3c35f4fa2604d626ce6d68},\r\nabstract={Eleven deletions were obtained in the rad(2)201 radiosensitivity gene region and the 41-45B4 fragment duplication in the Y chromosome were made by using chromosome rearrangements that transfer the material of the 44F - 45D site of chromosome 2 in Drosophila melanogaster to heterochromatin. The locus rad(2)201 was mapped in thin band region 45B3 by using these rearrangements and 13 deletions isolated before. Analysis of the complementation of the rad(2)201G1 radiosensitivity mutation by lethals and chromosome rearrangements in the 44F2-3; 45C5-6 region did not reveal any lethal alleles of this gene. The translocation T(Y;2)G6 was isolated; in this translocation, the change of the rad(2)201 gene expression causes high sensitivity of rad(2)201G1/T(Y;2)G6 heterozygotes of the initiation of the radiation-induced morphoses, while the survival rate of individuals remains at the level of wild-type flies.},\r\ncorrespondence_address1={Konev, A.I.},\r\nissn={00166758},\r\npubmed_id={8045381},\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 Eleven deletions were obtained in the rad(2)201 radiosensitivity gene region and the 41-45B4 fragment duplication in the Y chromosome were made by using chromosome rearrangements that transfer the material of the 44F - 45D site of chromosome 2 in Drosophila melanogaster to heterochromatin. The locus rad(2)201 was mapped in thin band region 45B3 by using these rearrangements and 13 deletions isolated before. Analysis of the complementation of the rad(2)201G1 radiosensitivity mutation by lethals and chromosome rearrangements in the 44F2-3; 45C5-6 region did not reveal any lethal alleles of this gene. The translocation T(Y;2)G6 was isolated; in this translocation, the change of the rad(2)201 gene expression causes high sensitivity of rad(2)201G1/T(Y;2)G6 heterozygotes of the initiation of the radiation-induced morphoses, while the survival rate of individuals remains at the level of wild-type flies.\n
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\n  \n 1992\n \n \n (1)\n \n \n
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\n \n \n
\n \n\n \n \n \n \n \n \n Molecular-genetic analysis of radiation-induced mutation of the white gene, inserted in the 45D region of the second Drosophila melanogaster chromosome [Molekuliarno-geneticheskiǐ analiz radiatsionno indutsirovannykh mutatsiǐ gena white, insertirovannogo v raǐon 45D vtoroǐ khromosomy Drosophila melanogaster.].\n \n \n \n \n\n\n \n Anashchenko, V.; Sarantseva, S.; and Konev, A.\n\n\n \n\n\n\n Doklady Akademii nauk SSSR, 322(1): 161-165. 1992.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"Molecular-geneticPaper\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
\n
@ARTICLE{Anashchenko1992161,\r\nauthor={Anashchenko, V.A. and Sarantseva, S.V. and Konev, A.I.},\r\ntitle={Molecular-genetic analysis of radiation-induced mutation of the white gene, inserted in the 45D region of the second Drosophila melanogaster chromosome [Molekuliarno-geneticheskiǐ analiz radiatsionno indutsirovannykh mutatsiǐ gena white, insertirovannogo v raǐon 45D vtoroǐ khromosomy Drosophila melanogaster.]},\r\njournal={Doklady Akademii nauk SSSR},\r\nyear={1992},\r\nvolume={322},\r\nnumber={1},\r\npages={161-165},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0026464274&partnerID=40&md5=82b5fbb5b041a1263b5db977469ce34a},\r\ncorrespondence_address1={Anashchenko, V.A.},\r\nissn={00023264},\r\npubmed_id={1511665},\r\nlanguage={Russian},\r\nabbrev_source_title={Dokl Akad Nauk SSSR},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n  \n 1991\n \n \n (1)\n \n \n
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\n \n \n
\n \n\n \n \n \n \n \n \n Study of radiation mutagenesis in the 44-45 region of Drosophila melanogaster chromosome 2.\n \n \n \n \n\n\n \n Konev Yu., A.; Varentsova, E.; Sarantseva, S.; and Khromykh Yu., M.\n\n\n \n\n\n\n Genetika, 27(1): 77-87. 1991.\n cited By 3\n\n\n\n
\n\n\n\n \n \n \"StudyPaper\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
\n
@ARTICLE{KonevYu.199177,\r\nauthor={Konev Yu., A. and Varentsova, E.R. and Sarantseva, S.V. and Khromykh Yu., M.},\r\ntitle={Study of radiation mutagenesis in the 44-45 region of Drosophila melanogaster chromosome 2},\r\njournal={Genetika},\r\nyear={1991},\r\nvolume={27},\r\nnumber={1},\r\npages={77-87},\r\nnote={cited By 3},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0025846106&partnerID=40&md5=4b5503df12a885d9a4e6d73f92bd94fb},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, Academy of Sciences of the USSR, Gatchina, Russia},\r\nissn={00166758},\r\ncoden={GNKAA},\r\npubmed_id={1903758},\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 1987\n \n \n (2)\n \n \n
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\n \n \n
\n \n\n \n \n \n \n \n \n Efficacy of hyperthermia during fast neutron irradiation of Ehrlich carcinoma [Effektivnost' gipertermii pri obluchenii bystrymi neǐtronami kartsinomy Erlikha.].\n \n \n \n \n\n\n \n Letov, V.; Averin, S.; and Bol'shakova, O.\n\n\n \n\n\n\n Medicinskaa radiologia, 32(5): 49-51. 1987.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"EfficacyPaper\n  \n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\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
\n
@ARTICLE{Letov198749,\r\nauthor={Letov, V.N. and Averin, S.A. and Bol'shakova, O.I.},\r\ntitle={Efficacy of hyperthermia during fast neutron irradiation of Ehrlich carcinoma [Effektivnost' gipertermii pri obluchenii bystrymi neǐtronami kartsinomy Erlikha.]},\r\njournal={Medicinskaa radiologia},\r\nyear={1987},\r\nvolume={32},\r\nnumber={5},\r\npages={49-51},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023339514&partnerID=40&md5=8277d7638627c3e72b565c6e9cd3920d},\r\ncorrespondence_address1={Letov, V.N.},\r\nissn={00258334},\r\npubmed_id={3586924},\r\nlanguage={Russian},\r\nabbrev_source_title={Med Radiol (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 Repair of damages to human lymphocytes induced by fractionated irradiation with fast neutrons.\n \n \n \n \n\n\n \n Bolshakova, O.; and Letov, V.\n\n\n \n\n\n\n Radiobiologiya, 27(4): 481-484. 1987.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"RepairPaper\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
\n
@ARTICLE{Bolshakova1987481,\r\nauthor={Bolshakova, O.I. and Letov, V.N.},\r\ntitle={Repair of damages to human lymphocytes induced by fractionated irradiation with fast neutrons},\r\njournal={Radiobiologiya},\r\nyear={1987},\r\nvolume={27},\r\nnumber={4},\r\npages={481-484},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0023615726&partnerID=40&md5=b9eb690eadc32992b10086aa5eb40348},\r\naffiliation={Siberian Department of the National Cancer Research Centre, USSR Academy of Medical Sciences, Tomsk},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={3628728},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n  \n 1986\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n A radiomodifying effect of acute hypoxia on neutron-irradiated mice and dogs.\n \n \n \n \n\n\n \n Sverdlov, A.; Kalmykova, G.; Timoshenko, S.; and Nikanorova, N.\n\n\n \n\n\n\n Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft . [et al], 162(8): 525-530. 1986.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"APaper\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
\n
@ARTICLE{Sverdlov1986525,\r\nauthor={Sverdlov, A.G. and Kalmykova, G.I. and Timoshenko, S.I. and Nikanorova, N.G.},\r\ntitle={A radiomodifying effect of acute hypoxia on neutron-irradiated mice and dogs.},\r\njournal={Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft . [et al]},\r\nyear={1986},\r\nvolume={162},\r\nnumber={8},\r\npages={525-530},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0022760209&partnerID=40&md5=a881b7240aa540050795f392e11b16fe},\r\nabstract={Anoxia increased the survival of neutron irradiated mice with DMF = 1.66. As to haemopoietic stem cells neutron irradiated in vivo, DMF was 1.8. With X-irradiation DMF was 2.49 and 2.94, respectively. Anoxia decreased the damage of the intestinal mucous membrane after a whole-body neutron irradiation with a dose 3.0 Gy. A protective effect of acute hypoxia was demonstrated on dogs exposed to fast neutrons (4.0 Gy). Breathing of 10% gas hypoxic mixture protected more than half of the exposed animals from death and provided the development of a light form of radiation sickness instead of a serious one.},\r\ncorrespondence_address1={Sverdlov, A.G.},\r\nissn={01797158},\r\npubmed_id={3764676},\r\nlanguage={English},\r\nabbrev_source_title={Strahlenther Onkol},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n Anoxia increased the survival of neutron irradiated mice with DMF = 1.66. As to haemopoietic stem cells neutron irradiated in vivo, DMF was 1.8. With X-irradiation DMF was 2.49 and 2.94, respectively. Anoxia decreased the damage of the intestinal mucous membrane after a whole-body neutron irradiation with a dose 3.0 Gy. A protective effect of acute hypoxia was demonstrated on dogs exposed to fast neutrons (4.0 Gy). Breathing of 10% gas hypoxic mixture protected more than half of the exposed animals from death and provided the development of a light form of radiation sickness instead of a serious one.\n
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\n  \n 1984\n \n \n (2)\n \n \n
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\n \n\n \n \n \n \n \n \n Radiation-induced changes in the critical organs of rats irradiated during parabiosis.\n \n \n \n \n\n\n \n Timoshenko, S.; Bogatyrev, A.; and Nikanorova, N.\n\n\n \n\n\n\n Radiobiologiya, 24(3): 400-403. 1984.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"Radiation-inducedPaper\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
\n
@ARTICLE{Timoshenko1984400,\r\nauthor={Timoshenko, S.I. and Bogatyrev, A.V. and Nikanorova, N.G.},\r\ntitle={Radiation-induced changes in the critical organs of rats irradiated during parabiosis},\r\njournal={Radiobiologiya},\r\nyear={1984},\r\nvolume={24},\r\nnumber={3},\r\npages={400-403},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021434189&partnerID=40&md5=1fb640c9da18c73058e5d1f95637ba91},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, USSR Academy of Sciences, Gatchina},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={6739748},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\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 A radiomodifying effect of hypoxia on neutron-irradiated mice.\n \n \n \n \n\n\n \n Kalmykova, G.; Timoshenko, S.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 24(2): 190-194. 1984.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"APaper\n  \n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\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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@ARTICLE{Kalmykova1984190,\r\nauthor={Kalmykova, G.I. and Timoshenko, S.I. and Sverdlov, A.G.},\r\ntitle={A radiomodifying effect of hypoxia on neutron-irradiated mice},\r\njournal={Radiobiologiya},\r\nyear={1984},\r\nvolume={24},\r\nnumber={2},\r\npages={190-194},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0021358379&partnerID=40&md5=70478e3b10644142c1318185d9846b73},\r\naffiliation={B.P. Konstantinov Leningrad Institute of Nuclear Physics, USSR Academy of Sciences, Gatchina},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={6374745},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n  \n 1982\n \n \n (1)\n \n \n
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\n \n \n
\n \n\n \n \n \n \n \n \n Comparative characteristics of radiation damage to the small intestine of mice exposed to X-rays and fission neutrons at different stages of the postnatal development.\n \n \n \n \n\n\n \n Bogatyrev, A.; Timoshenko, S.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 22(1): 76-81. 1982.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"ComparativePaper\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
\n
@ARTICLE{Bogatyrev198276,\r\nauthor={Bogatyrev, A.V. and Timoshenko, S.I. and Sverdlov, A.G.},\r\ntitle={Comparative characteristics of radiation damage to the small intestine of mice exposed to X-rays and fission neutrons at different stages of the postnatal development},\r\njournal={Radiobiologiya},\r\nyear={1982},\r\nvolume={22},\r\nnumber={1},\r\npages={76-81},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0020051416&partnerID=40&md5=82494131dbba0910ddf4ecdbcd34a82e},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., USSR Acad. Sci., Gatchina},\r\nabstract={Age-related changes were detected in the manifestation of radiation injury to the small intestine of mice exposed to X-rays and fission neutrons. All signs of the intestinal lesion were more pronounced in the newborn and 2-wk-old mice than in 4-wk and pubertal animals. This, perhaps, is due to different rate of renewal of cells on the villi at different stages of the postnatal development of mice.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={7063656},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n Age-related changes were detected in the manifestation of radiation injury to the small intestine of mice exposed to X-rays and fission neutrons. All signs of the intestinal lesion were more pronounced in the newborn and 2-wk-old mice than in 4-wk and pubertal animals. This, perhaps, is due to different rate of renewal of cells on the villi at different stages of the postnatal development of mice.\n
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\n  \n 1981\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Morphological characteristic of radiation-induced affection of the small intestine mucosa of mice treated with homologous bone marrow cells.\n \n \n \n \n\n\n \n Bogatyrev, A.; Timoshenko, S.; Nikanorova, N.; and Kalmykova, G.\n\n\n \n\n\n\n Radiobiologiya, 21(6): 929-932. 1981.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"MorphologicalPaper\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
\n
@ARTICLE{Bogatyrev1981929,\r\nauthor={Bogatyrev, A.V. and Timoshenko, S.I. and Nikanorova, N.G. and Kalmykova, G.I.},\r\ntitle={Morphological characteristic of radiation-induced affection of the small intestine mucosa of mice treated with homologous bone marrow cells},\r\njournal={Radiobiologiya},\r\nyear={1981},\r\nvolume={21},\r\nnumber={6},\r\npages={929-932},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0019812079&partnerID=40&md5=f2e8065e0299c48118ef3603e4d60a95},\r\naffiliation={Leningrad Inst. Nucl. Phys., USSR Acad. Sci., Gatchina},\r\nabstract={A study was made of the radiation injury to small intestine mucosa of mice after postirradiation treatment with homologous bone marrow. The obtained results show that transplantation of the bone marrow cells increases the survival rate of mice and produces a beneficial effect on the small intestine mucosa. It is suggested that the administered bone marrow cells favor the recovery of a total pool of both hemopoietic and stem cells of the intestine, perform a trephocytic function and increase the resistance of the organism to infection.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={7034041},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n A study was made of the radiation injury to small intestine mucosa of mice after postirradiation treatment with homologous bone marrow. The obtained results show that transplantation of the bone marrow cells increases the survival rate of mice and produces a beneficial effect on the small intestine mucosa. It is suggested that the administered bone marrow cells favor the recovery of a total pool of both hemopoietic and stem cells of the intestine, perform a trephocytic function and increase the resistance of the organism to infection.\n
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\n  \n 1979\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Analysis of radiosensitivity of mice with respect to age.\n \n \n \n \n\n\n \n Bogatirev, A.; Timoshenko, S.; Nikanorova, N.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 19(2): 225-228. 1979.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"AnalysisPaper\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
\n
@ARTICLE{Bogatirev1979225,\r\nauthor={Bogatirev, A.V. and Timoshenko, S.I. and Nikanorova, N.G. and Sverdlov, A.G.},\r\ntitle={Analysis of radiosensitivity of mice with respect to age},\r\njournal={Radiobiologiya},\r\nyear={1979},\r\nvolume={19},\r\nnumber={2},\r\npages={225-228},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0018447945&partnerID=40&md5=0570e6abfd7ad3b30646105b496f38f3},\r\naffiliation={B.P. Konstantinov Leningrad Inst. Nucl. Phys., USSR Acad. Sci., Gatchina},\r\nabstract={In order to elucidate mechanisms of age variations radiosensitivity of mice, a study was made of the sensitivity of in vitro irradiated bone marrow stem cells, taken from animals of different age, and postradiation recovery of leukocyte content of peripheral blood and cellularity of bone marrow and spleen. Using the method of spleen colonies, similar affections were revealed in bone marrow cells of animals of different age. The degree of recovery of the hemopoietic cell pool was significantly lower in newborn mice than in adults after exposure to a dose (LD(50/30)) equally effective with respect to mortality.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={472153},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
\n\n\n
\n In order to elucidate mechanisms of age variations radiosensitivity of mice, a study was made of the sensitivity of in vitro irradiated bone marrow stem cells, taken from animals of different age, and postradiation recovery of leukocyte content of peripheral blood and cellularity of bone marrow and spleen. Using the method of spleen colonies, similar affections were revealed in bone marrow cells of animals of different age. The degree of recovery of the hemopoietic cell pool was significantly lower in newborn mice than in adults after exposure to a dose (LD(50/30)) equally effective with respect to mortality.\n
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\n  \n 1976\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Morphological characteristics of a radiation induced damage to the small intestine of mice irradiated at different stages of their postnatal development (Russian).\n \n \n \n \n\n\n \n Timoshenko, S.; Bogatyrev, A.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 16(6): 847-851. 1976.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"MorphologicalPaper\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
\n
@ARTICLE{Timoshenko1976847,\r\nauthor={Timoshenko, S.I. and Bogatyrev, A.V. and Sverdlov, A.G.},\r\ntitle={Morphological characteristics of a radiation induced damage to the small intestine of mice irradiated at different stages of their postnatal development (Russian)},\r\njournal={Radiobiologiya},\r\nyear={1976},\r\nvolume={16},\r\nnumber={6},\r\npages={847-851},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0017022983&partnerID=40&md5=15a854842290551c4c22ae980161bcd4},\r\naffiliation={B. P. Konstantinov Inst. Nucl. Phys., USSR Acad. Sci., Leningrad},\r\nabstract={Radiation induced damages to the small intestine mucosa of mice of different ages have been comparatively studied. The data obtained show distinct morphological variations in the development of a gastric syndrome in mice of different ages. Inspite of the fact that the character of a radiation injury to crypts was similar irrespective of the age of animals, the state of villi was different. This is probably due to the kinetic peculiarities of the cell population of the small intestine of mice being at different stages of the postnatal development.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={1027025},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n Radiation induced damages to the small intestine mucosa of mice of different ages have been comparatively studied. The data obtained show distinct morphological variations in the development of a gastric syndrome in mice of different ages. Inspite of the fact that the character of a radiation injury to crypts was similar irrespective of the age of animals, the state of villi was different. This is probably due to the kinetic peculiarities of the cell population of the small intestine of mice being at different stages of the postnatal development.\n
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\n  \n 1975\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Protective effect of cystafos against radiation delivered to mice at different stages of postnatal development (Russian).\n \n \n \n \n\n\n \n Timoshenko, S.; and Bogatyriov, A.\n\n\n \n\n\n\n Radiobiologiya, 15(1): 154-158. 1975.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"ProtectivePaper\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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@ARTICLE{Timoshenko1975154,\r\nauthor={Timoshenko, S.I. and Bogatyriov, A.V.},\r\ntitle={Protective effect of cystafos against radiation delivered to mice at different stages of postnatal development (Russian)},\r\njournal={Radiobiologiya},\r\nyear={1975},\r\nvolume={15},\r\nnumber={1},\r\npages={154-158},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016612110&partnerID=40&md5=d328f031db9afa03ec71198468b4315b},\r\naffiliation={B.P. Konstantinov Inst. Nucl. Phys., USSR Acad. Sci., Leningrad},\r\nabstract={The radioprotective action of cystafos against ionizing radiation delivered to animals at different stages of their postnatal development was investigated. The preparation exerted a pronounced protective effect at all the stages studied at radiation dose levels which cause damage to the hemopoietic system and the digestive tract.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={1144718},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n The radioprotective action of cystafos against ionizing radiation delivered to animals at different stages of their postnatal development was investigated. The preparation exerted a pronounced protective effect at all the stages studied at radiation dose levels which cause damage to the hemopoietic system and the digestive tract.\n
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\n  \n 1974\n \n \n (5)\n \n \n
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\n \n\n \n \n \n \n \n \n Chemical protection in neutron irradiation of animals [K voprosu o khimicheskoǐ zashchite pri obluchenii zhivotnykh neǐtronami].\n \n \n \n \n\n\n \n Sverdlov, A.; Bogatyrev, A.; Nikanorova, N.; Timoshenko, S.; and Krasotskaia, G.\n\n\n \n\n\n\n Radiobiologiya, 14(3): 359-362. 1974.\n cited By 1\n\n\n\n
\n\n\n\n \n \n \"ChemicalPaper\n  \n \n\n \n\n \n link\n  \n \n\n bibtex\n \n\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
\n
@ARTICLE{Sverdlov1974359,\r\nauthor={Sverdlov, A.G. and Bogatyrev, A.V. and Nikanorova, N.G. and Timoshenko, S.I. and Krasotskaia, G.I.},\r\ntitle={Chemical protection in neutron irradiation of animals [K voprosu o khimicheskoǐ zashchite pri obluchenii zhivotnykh neǐtronami]},\r\njournal={Radiobiologiya},\r\nyear={1974},\r\nvolume={14},\r\nnumber={3},\r\npages={359-362},\r\nnote={cited By 1},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016063602&partnerID=40&md5=6af6fb0b49d304103fb278b16a079743},\r\ncorrespondence_address1={Sverdlov, A.G.},\r\nissn={00338192},\r\npubmed_id={4846001},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiobiologiia},\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 dose fractionation on the survival of animals irradiated at different stages of their postnatal development (Russian).\n \n \n \n \n\n\n \n Bogatirev, A.; Timoshenko, S.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 14(6): 928-931. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"InfluencePaper\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
\n
@ARTICLE{Bogatirev1974928,\r\nauthor={Bogatirev, A.V. and Timoshenko, S.I. and Sverdlov, A.G.},\r\ntitle={Influence of dose fractionation on the survival of animals irradiated at different stages of their postnatal development (Russian)},\r\njournal={Radiobiologiya},\r\nyear={1974},\r\nvolume={14},\r\nnumber={6},\r\npages={928-931},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016122562&partnerID=40&md5=522be7eb60c51f7de491ce6f39222d80},\r\naffiliation={B.P. Konstantinov Inst. Nucl. Phys., USSR Acad. Sci., Leningrad},\r\nabstract={Influence of dose fractionation of the survival of animals irradiated at different stages of their postnatal development was studied. An age dependence was observed in the reduction of the lethal effect of fractionated exposure. Fractionation of the dose into three fractions does not change the yield of radiation damage in newborn and 1 wk old animals. It appears that the rate of the repair processes in mice and rats of the given age is much lower than that in animals of other ages.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={4450005},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n Influence of dose fractionation of the survival of animals irradiated at different stages of their postnatal development was studied. An age dependence was observed in the reduction of the lethal effect of fractionated exposure. Fractionation of the dose into three fractions does not change the yield of radiation damage in newborn and 1 wk old animals. It appears that the rate of the repair processes in mice and rats of the given age is much lower than that in animals of other ages.\n
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\n \n\n \n \n \n \n \n \n Radioprotective effects of 5 methoxytryptamine (mexamine) and cystamine in mice irradiated at different stages of postnatal development (Russian).\n \n \n \n \n\n\n \n Timoshenko, S.; Bogatyrov, A.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 14(4): 564-567. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"RadioprotectivePaper\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
\n
@ARTICLE{Timoshenko1974564,\r\nauthor={Timoshenko, S.I. and Bogatyrov, A.V. and Sverdlov, A.G.},\r\ntitle={Radioprotective effects of 5 methoxytryptamine (mexamine) and cystamine in mice irradiated at different stages of postnatal development (Russian)},\r\njournal={Radiobiologiya},\r\nyear={1974},\r\nvolume={14},\r\nnumber={4},\r\npages={564-567},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016086572&partnerID=40&md5=8a7a46bbfe1ea1f049b4fcc5b16b894d},\r\naffiliation={Inst. Jadern. Fiz., AN SSSR, Leningrad, Russian Federation},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={4438609},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\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 Study in cellular mechanism of the radioprotective action of 5 methoxytryptamine ('mexamine') on colony forming cells of bone marrow (Russian).\n \n \n \n \n\n\n \n Bogatyrov, A.; Nikanorova, N.; Timoshenko, S.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 14(2): 290-292. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"StudyPaper\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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@ARTICLE{Bogatyrov1974290,\r\nauthor={Bogatyrov, A.V. and Nikanorova, N.G. and Timoshenko, S.I. and Sverdlov, A.G.},\r\ntitle={Study in cellular mechanism of the radioprotective action of 5 methoxytryptamine ('mexamine') on colony forming cells of bone marrow (Russian)},\r\njournal={Radiobiologiya},\r\nyear={1974},\r\nvolume={14},\r\nnumber={2},\r\npages={290-292},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016366534&partnerID=40&md5=6517fc6e7276608470db9237009d6a6b},\r\naffiliation={B.P. Konstantinov Inst. Nucl. Phys., USSR Acad. Sci., Leningrad},\r\nabstract={Mexamine (5 methoxytryptamine) and some of the sulfur bearing protectors were administered to mice in radioprotective doses, then their bone marrow cells were isolated and irradiated in vitro. All protectors applied increased the survival of colony forming cells. This effect was not produced by preiiradiation hypoxia. The data obtained indicate a cellular, but not hypoxic, mechanism of the protective action of mexamine.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={4832889},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n Mexamine (5 methoxytryptamine) and some of the sulfur bearing protectors were administered to mice in radioprotective doses, then their bone marrow cells were isolated and irradiated in vitro. All protectors applied increased the survival of colony forming cells. This effect was not produced by preiiradiation hypoxia. The data obtained indicate a cellular, but not hypoxic, mechanism of the protective action of mexamine.\n
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\n \n\n \n \n \n \n \n \n Radioprotective efficiency of shielding of bone marrow of mice exposed to ionizing radiation at different stages of their postnatal development (Russian).\n \n \n \n \n\n\n \n Bogatyriov, A.; Timoshenko, S.; Nikanorova, N.; and Shabarova, A.\n\n\n \n\n\n\n Radiobiologiya, 14(4): 600-603. 1974.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"RadioprotectivePaper\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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@ARTICLE{Bogatyriov1974600,\r\nauthor={Bogatyriov, A.V. and Timoshenko, S.I. and Nikanorova, N.G. and Shabarova, A.I.},\r\ntitle={Radioprotective efficiency of shielding of bone marrow of mice exposed to ionizing radiation at different stages of their postnatal development (Russian)},\r\njournal={Radiobiologiya},\r\nyear={1974},\r\nvolume={14},\r\nnumber={4},\r\npages={600-603},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0016277576&partnerID=40&md5=5952b73990229b9b0ea226df3723e454},\r\naffiliation={B.P. Konstantinov Inst. Nucl. Phys., USSR Acad. Sci., Leningrad},\r\nabstract={Shielding of a definite volume of bone marrow during an irradiation of mice at different stages of postnatal development produced a varying effect on the survival of animals. The least pronounced protective action of shielding was observed in the newborn mice. The efficacy of shielding increases with age. The protective effect, however, is observed unequivocally only at dose levels directly damaging the hemopoietic system. The less marked protective effect of bone marrow shielding observed in newborn mice is probably due to the inability of stem cells to form new hemopoietic colonies.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={4438621},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n Shielding of a definite volume of bone marrow during an irradiation of mice at different stages of postnatal development produced a varying effect on the survival of animals. The least pronounced protective action of shielding was observed in the newborn mice. The efficacy of shielding increases with age. The protective effect, however, is observed unequivocally only at dose levels directly damaging the hemopoietic system. The less marked protective effect of bone marrow shielding observed in newborn mice is probably due to the inability of stem cells to form new hemopoietic colonies.\n
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\n  \n 1973\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Dynamics of post irradiation death of mice and rats irradiated at different stages of the postnatal development (Russian).\n \n \n \n \n\n\n \n Bogatyrov, A.; Timoshenko, S.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 13(5): 786-788. 1973.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"DynamicsPaper\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
\n
@ARTICLE{Bogatyrov1973786,\r\nauthor={Bogatyrov, A.V. and Timoshenko, S.I. and Sverdlov, A.G.},\r\ntitle={Dynamics of post irradiation death of mice and rats irradiated at different stages of the postnatal development (Russian)},\r\njournal={Radiobiologiya},\r\nyear={1973},\r\nvolume={13},\r\nnumber={5},\r\npages={786-788},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015668442&partnerID=40&md5=c83bc24e4a7714af83973af3ed28b0fe},\r\naffiliation={B.P. Konstantinov Inst. Nucl. Phys., Acad. Sci. USSR, Leningrad},\r\nabstract={Age related features of radiosensitivity and radiation induced death of X irradiated mice were detected. Newborn and one or two wk old animals died mainly of hemopoietic system lesions, while in 4 wk old mice lesions of the digestive tract were predominant.},\r\nissn={00338192},\r\ncoden={RADOA},\r\npubmed_id={4763071},\r\nlanguage={Russian},\r\nabbrev_source_title={RADIOBIOLOGIYA},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
\n
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\n Age related features of radiosensitivity and radiation induced death of X irradiated mice were detected. Newborn and one or two wk old animals died mainly of hemopoietic system lesions, while in 4 wk old mice lesions of the digestive tract were predominant.\n
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\n  \n 1972\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n Chemical protection of newborn mice from the effects of ionizing radiation [Khimicheskaia zashchita novorozhdennykh mysheǐ ot vozdeǐstviia ioniziruiushchego izlucheniia.].\n \n \n \n \n\n\n \n Bogatyrev, A.; Timoshenko, S.; and Sverdlov, A.\n\n\n \n\n\n\n Radiobiologiya, 12(3): 454-458. 1972.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"ChemicalPaper\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
\n
@ARTICLE{Bogatyrev1972454,\r\nauthor={Bogatyrev, A.V. and Timoshenko, S.I. and Sverdlov, A.G.},\r\ntitle={Chemical protection of newborn mice from the effects of ionizing radiation [Khimicheskaia zashchita novorozhdennykh mysheǐ ot vozdeǐstviia ioniziruiushchego izlucheniia.]},\r\njournal={Radiobiologiya},\r\nyear={1972},\r\nvolume={12},\r\nnumber={3},\r\npages={454-458},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0015345781&partnerID=40&md5=3b12612cdcd18a0ecaf7b2f6e7d15da8},\r\ncorrespondence_address1={Bogatyrev, A.V.},\r\nissn={00338192},\r\npubmed_id={5052708},\r\nlanguage={Russian},\r\nabbrev_source_title={Radiobiologiia},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n\r\n
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\n  \n 1968\n \n \n (1)\n \n \n
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\n \n\n \n \n \n \n \n \n A group disease of trichinelliasis in the Pechora district of the Komi ASSR [Gruppovoe zabolevanie trikhinellezom v Pechorskom raǐone Komi ASSR.].\n \n \n \n \n\n\n \n Sorochenko, E.; and Bol'shakova, O.\n\n\n \n\n\n\n Meditsinskaya Parazitologiya i Parazitarnye Bolezni, 37(4): 483. 1968.\n cited By 0\n\n\n\n
\n\n\n\n \n \n \"APaper\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
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@ARTICLE{Sorochenko1968483,\r\nauthor={Sorochenko, E.V. and Bol'shakova, O.I.},\r\ntitle={A group disease of trichinelliasis in the Pechora district of the Komi ASSR [Gruppovoe zabolevanie trikhinellezom v Pechorskom raǐone Komi ASSR.]},\r\njournal={Meditsinskaya Parazitologiya i Parazitarnye Bolezni},\r\nyear={1968},\r\nvolume={37},\r\nnumber={4},\r\npages={483},\r\nnote={cited By 0},\r\nurl={https://www.scopus.com/inward/record.uri?eid=2-s2.0-0014312815&partnerID=40&md5=79fafa0bfdfea1b9759e53f5785edd60},\r\ncorrespondence_address1={Sorochenko, E.V.},\r\nissn={00258326},\r\npubmed_id={5732634},\r\nlanguage={Russian},\r\nabbrev_source_title={Med Parazitol (Mosk)},\r\ndocument_type={Article},\r\nsource={Scopus},\r\n}\r\n
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