Novosibirsk State Medical University
Novosibirsk, Russia
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Skidan I.N.,Bibkall RUS Ltd. | Gulyaev A.E.,Nazarbayev University | Kaznacheev K.S.,Novosibirsk State Medical University
Voprosy Pitaniia | Year: 2015

This review summarizes the most complete information on such fundamentally important quality parameters of goat milk as the cellular composition of somatic cells and the structure of cytoplasmic debris in milk. It also focuses on the characterization of an essential component of the energetic value and nutritional content of milk - milk fat globules and milk fat globule membranes. The survey also clarifies some of the terms and meanings of physiological processes associated with the formation of the milk of various ruminants and breast milk.

Barkhash A.V.,Georgia State University | Perelygin A.A.,Georgia State University | Babenko V.N.,RAS Institute of Cytology and Genetics | Myasnikova N.G.,Novosibirsk State Medical University | And 4 more authors.
Journal of Infectious Diseases | Year: 2010

The 2′-5′-oligoadenylate synthetase (2′-5′-OAS) family members are interferon-induced antiviral proteins. Twenty-three single nucleotide polymorphisms located within the OAS1, OAS2, OAS3, and OASL genes were analyzed in 142 patients with Russian tick-borne encephalitis. Statistically significant differences in genotype, allele, and haplotype frequencies for 3 OAS2 single nucleotide polymorphisms (rs1293762, rs15895, and rs1732778) and 2 OAS3 single nucleotide polymorphisms (rs2285932 and rs2072136) were detected between patients with central nervous system disease and both those with fever and/or meningitis and the control group. The data suggest a possible association between these 5 OAS single nucleotide polymorphisms and the outcome of tickborne encephalitis virus infection in a Russian population. © 2010 by the Infectious Diseases Society of America. All rights reserved.

Suhovskih A.V.,Novosibirsk State University | Aidagulova S.V.,Novosibirsk State Medical University | Kashuba V.I.,NASU Institute of Molecular Biology and Genetics | Kashuba V.I.,Karolinska Institutet | Grigorieva E.V.,Novosibirsk State University
Cell and Tissue Research | Year: 2015

Glycosylation changes occur widely in colon tumours, suggesting glycosylated molecules as potential biomarkers for colon cancer diagnostics. In this study, proteoglycans (PGs) expression levels and their transcriptional patterns are investigated in human colon tumours in vivo and carcinoma cells in vitro. According to RT-PCR analysis, normal and cancer colon tissues expressed a specific set of PGs (syndecan-1, perlecan, decorin, biglycan, versican, NG2/CSPG4, serglycin, lumican, CD44), while the expression of glypican-1, brevican and aggrecan was almost undetectable. Overall transcriptional activity of the PGs in normal and cancer tissues was similar, although expression patterns were different. Expression of decorin and perlecan was down-regulated 2-fold in colon tumours, while biglycan and versican expression was significantly up-regulated (6-fold and 3-fold, respectively). Expression of collagen1A1 was also increased 6-fold in colon tumours. However, conventional HCT-116 colon carcinoma and AG2 colon cancer-initiating cells did not express biglycan and decorin and were versican-positive and -negative, respectively, demonstrating an extracellular origin of the PGs in cancer tissue. Selective expression of heparan sulfate (HS) proteoglycans syndecan-1 and perlecan in the AG2 colon cancer-initiating cell line suggests these PGs as potential biomarkers for cancer stem cells. Overall transcriptional activity of the HS biosynthetic system was similar in normal and cancer tissues, although significant up-regulation of extracellular sulfatases SULF1/2 argues for a possible distortion of HS sulfation patterns in colon tumours. Taken together, the obtained results suggest versican, biglycan, collagen1A1 and SULF1/2 expression as potential microenvironmental biomarkers and/or targets for colon cancer diagnostics and treatment. © 2015, Springer-Verlag Berlin Heidelberg.

Krivoshapkin A.L.,Novosibirsk State Medical University | Zelman V.L.,University of Southern California
World Neurosurgery | Year: 2012

There is archaeological evidence that the first neurosurgical procedure in what is now known as Siberia was performed in 8005 ± 100 B.C. According to signs of bone growth, perhaps more than half of the individuals who received the ancient trepanations survived. In Siberia, the first operations on the human brain and spinal cord were performed in 1909 at Tomsk University Hospital by the outstanding Russian surgeon and professor Vladimir M. Mysh. Professor Mysh initially moved from Saint Petersburg to Tomsk and later to Novosibirsk. Nicolay N. Burdenko, the founder of Russian neurosurgery and the Moscow Neurosurgical Institution, began his medical education at the Tomsk Imperial University. In the 1950s, Professor Ksenia I. Kharitonova exerted her great influence upon the development of neurosurgery in Siberia. Since 1955, and for 30 years thereafter, Professor Kharitonova was recognized as a principal leader of Siberian neurosurgery. She applied every effort to spread neurosurgical knowledge, and she popularized best practices around Siberia and the Far East. Perestroika deconstructed and ultimately eliminated the orderly system of neurosurgical service in the Soviet Union. From another perspective, the process opened the window to the world. Fully equipped centers and clinics with state-of-the-art techniques for neuro-oncology, cerebrovascular diseases, neurotrauma, and spinal pathology management in Novosibirsk, Barnaul, Kemerovo, and Irkutsk were enabled. © 2012 Elsevier Inc.

Pupyshev A.B.,Novosibirsk State Medical University
Tsitologiya | Year: 2011

Lysosomal membrane labilizing agents (incl. proapoptotic proteins of Bcl-2 family, LAPF, p53), estimation of lysosomal membrane permeabilization in living cells, the new data on differential permeabilization of lysosomal membranes, membrane stabilizing factors (incl. Hsp70), relations between lysosomal membrane damage, and initiation of apoptosis were considered. Signal effect of lysosomal membrane permeabilization is caused preferentially by release of cathepsin B and D in cytosol. Subsequent numerous pathways of apoptogenic signalization include proteolytic attack/activation on signal cytosolic proteins, mitochondria, procaspases, cell nuclei. The mainstream of the cell damage is connected with activation pf proapoptotic Bid and Bax, leading to permeabilization of the outer mitochondrial membrane, release of cytochrome c into cytosol and activation of caspase cascade. Translocation of the lysosoma enzymes in cytosol is capable to induce both the caspase-dependent and caspase-independent paths of apoptosis.

Olennikov D.N.,Russian Academy of Sciences | Kruglova M.Yu.,Novosibirsk State Medical University
Chemistry of Natural Compounds | Year: 2013

A total of 48 compounds and the new flavonoid glycoside ulmarioside, which was identified as quercetin-4′-O-α-rhamnopyranosyl-(1→6)- β-glucopyranoside (quercetin-4′-O-rutinoside), were isolated from Filipendula ulmaria (Rosaceae). Phenolic compounds from six species of Filipendula (F. camtschatica, F. denudata,F. palmata, F. stepposa, F. ulmaria, F. vulgaris) growing in Russia were compared. © 2013 Springer Science+Business Media New York.

Bondar I.A.,Novosibirsk State Medical University | Klimontov V.V.,Novosibirsk State Medical University | Simakova A.I.,Novosibirsk State Medical University
Terapevticheskii Arkhiv | Year: 2011

Obesity and overweight are now characterized as epidemics. It is shown that body overweight is associated with functional and structural changes in the kidneys. The results of epidemiological studies indicate that obesity can be the risk factor of chronic kidney disease (CKD) irrespective of the presence or absence of diabetes, arterial hypertension and other comorbidities. Manifestations of renal pathology in obese persons include microalbuminuria and proteinuria, hyperfiltration or impaired renal function. Glomerulomegaly and focal segmental glomerulosclerosis are the most typical structural signs of obesity-related nephropathy. More evidence is accumulated on the link between CKD in obesity and abnormalities in adypokine secretion (hyperleptinemia, lack of adiponectin), activation of rennin-angiotensin system, chronic inflammation, endothelial dysfunction, lipid accumulation, impaired renal hemodynamics and diminished nephron number related to body mass. A decrease of body weight following lifestyle modification or bariatric surgery leads to reduction in albuminuria and eliminates hyperfiltration in obese subjects. Thus, prevention and treatment of obesity may reduce CKD incidence in general population. © KQJUIEKTNB ABTOPOB, 2011.

Bondar' I.A.,Novosibirsk State Medical University | Shabel'nikova O.Y.,Novosibirsk State Regional Hospital
Diabetes Mellitus | Year: 2013

More than 100 genes associated with the risk of type 2 diabetes mellitus (T2DM) are now established. Most of them affect insulin secretion, adipogenesis and insulin resistance, but the exact molecular mechanisms determining their involvement in the pathogenesis of T2DM are not understood completely.

Kozlov V.A.,Novosibirsk State Medical University
Voprosy Onkologii | Year: 2016

There are numerous data in experimental and clinical medicine that convincing evidence on the leading role of the immune system in the pathogenesis of tumor diseases. Exactly immune cells such as cytotoxic T lymphocytes, NK cells, macrophages and dendritic cells have the ability to kill tumor cells. Under normal conditions the activity of these cells is a factor of inhibition proliferation and differentiation of tumor cells. An appearance of tumor itself, as uncontrolled cell growth and clinical manifestation, says that it was changed the cytotoxic activity of the cells causing tumor immunity. The main factor, if not the only reason for the decline of anti-tumor activity of the cells, is the formation of powerful extra- and inside-tumor suppressor mechanisms suppressing cytotoxic activity of anti-tumor immune-competent cells and allowing tumor cells to avoid surveillance by the immune system. It is showed that T and B cells, macrophages, and cells of myeloid origin suppressors possess these immunosuppressive properties. Therefore, in the future, methods to suppress functional activity of cells suppressors of various geneses can be the basis for immunotherapy of tumor growth.

Pupyshev A.B.,Novosibirsk State Medical University
Tsitologiya | Year: 2014

Molecular regulation of reparative/homeostatic autophagy induced by failure of vital resources and by cellular stress is considered. Extensive autophagy regulatory apparatus responds to starvation, insufficiency of growth factors and energy supply, accumulation of unfolded proteins (ER stress), reactive oxygen species, microbial invasion. Central sensor of the regulation is kinase mTOR. Part of the mTOR pool presented in lysosomes responds to the local level of amino acids and is able to induce autophagy under low rates of intralysosomal proteolysis. Autophagy is a self-regulated cell process, the peak of autophagy is followed by its regulatory weakening by amino acids formed in autophagolysosomes. Protective effect of autophagy is associated mainly with removal of permeabilized mitochondria generating ROS, and elimination of abnormally folded proteins. Autophagy has optimum of its activity: its deficiency leads to accelerated cellular aging, and the excessive autophagy brings to the deficiency of cellular survival resources and cell death. Autophagy cell death seems like a hyper- stimulated self-eating of the cell, but more probably that excessive autophagy disturbs cellular energy supply and switches on some specific cell death signalization (possibly associated with kinases c-Jun, DRP-1, PI3K class I etc.). Some approaches to use reparative autophagy for prevention of cell degeneration are considered.

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