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Eldarov Ch. M. Nikitina I. V. Kirtbaya A. R. Chagovets V. V. Ionov O. V. Bobrov M. Yu. 《Russian Journal of Bioorganic Chemistry》2019,45(2):165-172
Russian Journal of Bioorganic Chemistry - The early period of postnatal development of premature infants is often complicated by bacterial infections, in particular respiratory infections, which in... 相似文献
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E. A. Nikitina A. V. Medvedeva Yu. F. Dolgaya L. I. Korochkin G. V. Pavlova E. V. Savvateeva-Popova 《Journal of Evolutionary Biochemistry and Physiology》2012,48(5-6):529-539
Molecular mechanisms of the synapse and dendrite integrity maintenance and their disruption in psychiatric and neurodegenerative diseases (NDD) are being studied intensively to identify target genes for therapeutic activities. It is suggested that synapse is a tripartite system in which glia, alongside with well-studied pre- and postsynaptic neurons, represents a third, poorly studied partner in synaptic transmission involved in a positive feedback loop between the other two partners. It is the glia cell-derived neurotrophic factor (GDNF) and the transmembrane proteins, neuregulins, that mediate bidirectional coupling between presynaptic neurons and their postsynaptic targets. Neuregulins are structurally related to the epidermal growth factor and have a cytoplasmic domain that interacts with intracellular LIM kinase 1 (LIMK1), the key enzyme of actin remodeling. Since neurons and axons that do not receive a sufficient GDNF supply are at risk of degeneration and synapse elimination, GDNF became a central target factor in human NDD therapy. The delivery of GDNF-producing stem cells to the nidus of neurodegeneration by transplantation surgery is an efficient tool for NDD treatment. A new approach is proposed based on the use of the Drosophila heat shock (hs) promoter that responds to the mammalian body temperature and ensures constant expression of the human GDNF gene. The Drosophila models facilitate studying the role of each component of the bidirectional signaling between pre- and postsynaptic neurons in the development of the key diagnostic NDD symptom—a defective memory formation resulted from synaptic atrophy. To assess the efficiency of memory formation depending on the level of GDNF and LIMK1 brain expression, we used the Drosophila strains simulating different nervous system disorders: GDNF, the transgenic flies that carry the human GDNF gene under hs-promoter, l(1)ts403, the mutants with disruption of heat shock proteins (HSPs) mRNA nuclear trafficking, and agn ts3 carrying a mutation in LIMK1 gene. We investigated at the behavioral (learning/memory) level the functional connections between GDNF, LIMK1 and HSP signaling transductions that might offer promising targets for complex approaches to NDD treatment. 相似文献
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E. S. Naumova G. I. Naumov T. N. Nikitina A. Zh. Sadykova V. I. Kondratieva 《Microbiology》2012,81(2):216-223
Molecular genetic identification of 52 Kluyveromyces strains from VKM, mainly of dairy origin, was carried out. Restriction analysis of 5.8S-ITS rDNA fragments was used to differentiate
between Kl. lactis var. lactis, Kl. lactis var. drosophilarum (European population of “krassilnikovii”), and Kl. marxianus. Kl. lactis was shown to differ from Kl. marxianus in its ability to assimilate α-glucosides: maltose, melezitose, and α-methyl-glucoside. 相似文献
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This study assesses the efficacy of a fixed dose of Ropren(?) (a plant preparation isolated from the neutral fraction of an extract of spruce needles) on cognitive impairment in rats with β-amyloid peptide-(25-35)-induced amnesia. Ropren(?) was administered at a dose of 8.6mg/kg for 28 days, per os, to rats with β-amyloid peptide-(25-35)-induced amnesia. Cognitive performance was assessed using the passive avoidance paradigm and the Morris water maze and behavior was assessed using the open field test. After four weeks, Ropren(?) treatment significantly improved non-spatial and spatial learning in rats with β-amyloid peptide-(25-35)-induced amnesia. The results of the present study suggest that Ropren(?), a novel plant preparation, ameliorates cognitive deficiencies in an animal model relevant to Alzheimer's disease. 相似文献