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| 1 | Targeting of the AKT/m-TOR Pathway: Biomarkers of Resistance to Cancer Therapy——AKT/m-TOR Pathway and Resistance to Cancer Therapy显示文摘Resistance to cancer therapy continues to be a major limitation for the successful treatment of cancer. There are many published studies on therapy resistance in breast and prostate cancers; however, there are currently no data on molecular markers associated with resistance. The conflicting data were reported regarding the AKT/m-TOR signaling pathway components as markers predicting resistance. The AKT/m-TOR signaling pathway is involved in the development of many human cancers; its activation is related to cell proliferation, angiogenesis, apoptosis, as well as to therapy resistance. Molecular alterations in the AKT/m-TOR signaling pathway provide a platform to identify universal markers associated with the development of resistance to cancer therapy. | Liudmila V SPIRINA Irina V KONDAKOVA Natalia V TARASENKO Elena M SLONIMSKAYA Evgeny A USYNIN Alexey K GORBUNOV Zahar A YURMAZOV Svetlana Yu CHIGEVSKAYA | 2018 | 中国肺癌杂志2018，21，1： | 18 |
| 2 | Effect of Helicobacter pylori on gastric epithelial cells显示文摘The gastrointestinal epithelium has cells with features that make them a powerful line of defense in innate mucosal immunity. Features that allow gastrointestinal epithelial cells to contribute in innate defense include cell barrier integrity, cell turnover, autophagy, and innate immune responses. Helicobacter pylori(H. pylori) is a spiral shape gram negative bacterium that selectively colonizes the gastric epithelium of more than half of the world's population. The infection invariably becomes persistent due to highly specialized mechanisms that facilitate H. pylori 's avoidance of this initial line of host defense as well as adaptive immune mechanisms. The host response is thus unsuccessful in clearing the infection and as a result becomes established as a persistent infection promoting chronic inflammation. In some individuals the associated inflammation contributes to ulcerogenesis or neoplasia. H. pylori has an array of different strategies to interact intimately with epithelial cells and manipulate their cellular processes and functions. Among the multiple aspects that H. pylori affects in gastric epithelial cells are their distribution of epithelial junctions, DNA damage, apoptosis, proliferation, stimulation of cytokine production, and cell transformation. Some of these processes are initiated as a result of the activation of signaling mechanisms activated on binding of H. pylori to cell surface receptors or via soluble virulence factors that gain access to the epithelium. The multiple responses by the epithelium to the infection contribute to pathogenesis associated with H. pylori. | Shatha Alzahrani Taslima T Lina Jazmin Gonzalez Irina V Pinchuk Ellen J Beswick Victor E Reyes | 2014 | World Journal of Gastroenterology2014，20，36： | 15 |
| 3 | Immune evasion strategies used by Helicobacter pylori显示文摘Helicobacter pylori(H. pylori) is perhaps the most ubiquitous and successful human pathogen, since it colonizes the stomach of more than half of humankind. Infection with this bacterium is commonly acquired during childhood. Once infected, people carry the bacteria for decades or even for life, if not treated. Persistent infection with this pathogen causes gastritis, peptic ulcer disease and is also strongly associated with the development of gastric cancer. Despite induction of innate and adaptive immune responses in the infected individual, the host is unable to clear the bacteria. One widely accepted hallmark of H. pylori is that it successfully and stealthily evades host defense mechanisms. Though the gastric mucosa is well protected against infection, H. pylori is able to reside under the mucus, attach to gastric epithelial cells and cause persistent infection by evading immune responses mediated by host. In this review, we discuss how H. pylori avoids innate and acquired immune response elements, uses gastric epithelial cells as mediators to manipulate host T cell responses and uses virulence factors to avoid adaptive immune responses by T cells to establish a persistent infection. We also discuss in this review how the genetic diversity of this pathogen helps for its survival. | Taslima T Lina Shatha Alzahrani Jazmin Gonzalez Irina V Pinchuk Ellen J Beswick Victor E Reyes | 2014 | World Journal of Gastroenterology2014，20，36： | 7 |
| 4 | Linagliptin alleviates fatty liver disease in diabetic db/db mice显示文摘AIM To study the effects of linagliptin on the structural signs of non-alcoholic fatty liver disease(NAFLD) in db/db mice. METHODS Male diabetic db /db mice(BKS.Cg-Dock7m+/+Leprdb/J) aged 10 wk received the dipeptidyl peptidase 4(DPP4) inhibitor linagliptin(10 mg/kg) or saline as a placebo once per day by gavage for 8 wk. Intact db/db mice served as controls. Structural changes in the liver were analyzed from light and electron microscopic images of sections from intact, placebo-treated and linagliptin-treated animals. We estimated the changes in hepatocytes, sinusoidal cells, liver microvasculature and lymphatic roots. Hepatic staining for lymphatic vessel endothelial hyaluronan receptor-1(LYVE-1) was assessed by immunohistochemistry. RESULTS In 18-wk-old diabetic mice, liver steatosis(predominantly microvesicular and mediovesicular steatosis) was accompanied by dilation of the roots of the lymphatic system, interlobular blood vessels and bile canaliculi. Compared to saline-treated mice, linagliptin-treated mice exhibited a reduction in the mean numeral densities of hepatocytes with lipid droplets(92.4% ± 1.7% vs 64.9% ± 5.8% per field of view, P = 0.0002) and a lower proportion of hepatocytes with a high density of lipid droplets(20.7% ± 3.6% vs 50.4% ± 3.1%, P = 0.0007). We observed heterogeneous hepatocytes and relatively preserved cell structures in the linagliptin group. Dilation of blood and lymphatic vessels, as well as ultrastructural changes in the hepatocyte endoplasmic reticulum and mitochondria, were alleviated by linagliptin treatment. In intact and placebo-treated mice, immunohistochemical staining for LYVE-1 was observed in the endothelial cells of interlobular lymphatic vessels and on the membranes of some endothelial sinusoidal cells. We observed an enlarged LYVE-1 reaction area in linagliptin-treated mice compared to intact and placebo-treated mice. The improvement in the structural parameters of the liver in linagliptin-treated mice was independent to changes in the plasma glucose levels. CONCLUSION The DPP4 inhibitor linagliptin alleviates liver steatosis and structural changes in the hepatic microvasculature and lymphatic roots in a model of NAFLD in diabetic db/db mice. | Svetlana V Michurina Irina Ju Ishenko Vadim V Klimontov Sergey A Archipov Natalia E Myakina Marina A Cherepanova Eugenii L Zavjalov Galina V Koncevaya Vladimir I Konenkov | 2016 | World Journal of Diabetes2016，7，19： | 2 |
| 5 | Regenerative medicine of pancreatic islets显示文摘The pancreas became one of the first objects of regenerative medicine,since other possibilities of dealing with the pancreatic endocrine insufficiency were clearly exhausted.The number of people living with diabetes mellitus is currently approaching half a billion,hence the crucial relevance of new methods to stimulate regeneration of the insulin-secretingβ-cells of the islets of Langerhans.Natural restrictions on the islet regeneration are very tight;nevertheless,the islets are capable of physiological regeneration viaβ-cell self-replication,direct differentiation of multipotent progenitor cells and spontaneousα-toβ-orδ-toβ-cell conversion(trans-differentiation).The existing preclinical models ofβ-cell dysfunction or ablation(induced surgically,chemically or genetically)have significantly expanded our understanding of reparative regeneration of the islets and possible ways of its stimulation.The ultimate goal,sufficient level of functional activity ofβ-cells or their substitutes can be achieved by two prospective broad strategies:β-cell replacement andβ-cell regeneration.The“regeneration”strategy aims to maintain a preserved population ofβ-cells through in situ exposure to biologically active substances that improveβ-cell survival,replication and insulin secretion,or to evoke the intrinsic adaptive mechanisms triggering the spontaneous non-β-toβ-cell conversion.The“replacement”strategy implies transplantation ofβ-cells(as non-disintegrated pancreatic material or isolated donor islets)orβ-like cells obtained ex vivo from progenitors or mature somatic cells(for example,hepatocytes orα-cells)under the action of small-molecule inducers or by genetic modification.We believe that the huge volume of experimental and clinical studies will finally allow a safe and effective solution to a seemingly simple goal-restoration of the functionally activeβ-cells,the innermost hope of millions of people globally. | Irina V Arutyunyan Timur Kh Fatkhudinov Andrey V Makarov Andrey V Elchaninov Gennady T Sukhikh | 2020 | World Journal of Gastroenterology2020，26，22： | 2 |
| 6 | Late miocene to pliocene paleogeography of the Paratethys and its relation to the Mediterranean显示文摘 | PoPov S V IRINA G S LUBOV B I | 2006 | Pataeogeography Palaeoclimatology Palaeoecology2006，238，： | 1 |
| 7 | Structure of antigenic sites on the haemagglutinin molecule of H5 avian influenza virus and phenotypic variation of escape mutants显示文摘 | Nikolai V K Irina A R Natalia A I | 2002 | J Gen Virol2002，83，： | 1 |
| 8 | Epitope mapping of the hemagglutinin molecule of a highly pathogenic HSN1 influenza virus by using monoclonal antibodies显示文摘 | Nikolai V K Irina A R Elena A G | 2007 | J Virol2007，81，12： | 1 |
| 9 | 3 ' -Minor groove binder-DNA probe increase sequence specificity at PCR extension temperatures显示文摘 | IGOR V K IRINA A A ALAN M | 2000 | Nucleic Acids Res2000，28，2： | 1 |
| 10 | Structure of anti- gen-ic sites on the haemagglutinin molecule of H5 avian influen- za v-irus and phenotypic variation of escape mutants 显示文摘 | Nikolai V K Irina A R Natalia A I | 2002 | J Gen Virol2002，83，： | 1 |
| 11 | Astigmatism outcomes of horizontal temporal versus nasal clear corneal incision cataract surgery显示文摘 | Irina SB Edward Y Susan V | | 0，，02： | 1 |
| 12 | Structure of antigenic sites on the haemagglutinin molecule of H5 avian influenza virus and phenotypie variation of escape mutants 显示文摘 | Nikolai V Kaverin Irina A | 2002 | Journal of General Virology2002，83，： | 1 |
| 13 | Control of Exciton Migration Efficiency in Disordered J-Aggregates 显示文摘 | ALEXANDER V S IRINA I F ROMAN S G | 2010 | J Phys Chem C2010，114，2： | 1 |
| 14 | Frequency and clinical determinants of post stroke depression 显示文摘 | TARJA A L IRINA S RISTO V | 1998 | Stroke1998，29，26： | 1 |
| 15 | Phenanthrene metabolism by Pseudomonas and Burkholderia strains显示文摘 | Natalia V Balashova Irina A Koshelava Nicolai P | 1999 | Process Biochemistry1999，35，： | 1 |
| 16 | Microwave assisted acid diges- tion of siliceous and organically based matrices 显示文摘 | Irina V Kubrakova Andrei A | 1998 | Mendeleev Communications1998，，8： | 1 |
| 17 | Two opposite effects of cofilin on the thermal unfolding of F- actin : a differential scanning calorimetric study 显示文摘 | Irina V Dedova Olga P Nikolaeva Valeria V Mikhailova | 2004 | Biophysical Chemistry2004，110，： | 1 |
| 18 | Mitochondrial ATP synthase levels in brown adipose tissue are governed by the c-Fo subunit P1 isoform显示文摘 | Tatiana V K Irina G S Ulf A | 2008 | FASEB J2008，22，： | 1 |
| 19 | Osteoblast ontogeny and implications for bone pathology: an oyerview 显示文摘 | Irina Titorencu Vasile Pruna Victor V Jinga | 2013 | Cell and Tissue Research2013，11，： | 1 |
| 20 | Mycoplasmahominis and Ureaplasma urealyticum in midtrimester arnniotic fluid: Association with amniotie fluid cytokine levels amd pregnalley outcome 显示文摘 | SriramCP Santosh V Irina K | 2001 | Am J Ohstet Gynecol2001，191，4： | 1 |
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