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Institution

Fifth Affiliated Hospital of Xinjiang Medical University

HealthcareÜrümqi, China
About: Fifth Affiliated Hospital of Xinjiang Medical University is a healthcare organization based out in Ürümqi, China. It is known for research contribution in the topics: Apoptosis & Population. The organization has 241 authors who have published 139 publications receiving 1190 citations.


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Journal ArticleDOI
TL;DR: Evidence is provided that poly(I:C) potentiates liver injury in BALB/c mouse model of TCE-sensitization in a new mode of action that may explain increased risk of chemical-s Sensitization induced tissue damage by viral infection.

10 citations

Journal ArticleDOI
TL;DR: In this paper, the effects of polymethylmetnacrylate (PMMA) spacer loaded with different concentrations of vancomycin on the proliferative, osteogenic, and angiogenic capacity of the induced membrane were determined.
Abstract: Purpose The purpose of this study was to determine the effects of polymethylmetnacrylate (PMMA) spacer loaded with different concentrations of vancomycin on the proliferative, osteogenic, and angiogenic capacity of the induced membrane. Methods Varying concentrations of vancomycin (0, 1, 2, 4, 6, 8, and 10 g) were fully mixed with bone cement powder (40 g), resulting in seven experimental groups. Hollow cylindrical PMMA spacers (10-mm height, 3-mm external diameter, and 0.8-mm internal diameter) were formed by a mold and submerged in phosphate-buffered saline for antibiotic release by spectrophotometry. Eighty-four New Zealand white rabbits were evenly randomized into seven groups, and segmental radius shaft defects (10-mm) were created. Defects were filled with cylindrical PMMA spacers containing different vancomycin concentrations, and subsequently underwent intramedullary fixation with a retrograde Kirschner's wire. Tissue toxicity was assessed and the proliferative, osteogenic, and angiogenic capacity of induced membranes were qualitatively analyzed by immunohistochemistry and real-time PCR. Results No obvious toxicity was observed in the animal model. Alizarin red s staining and qualitative detection of type I collagen, CD31, Ki67, and STRO-1 by immunohistochemistry revealed an obvious decrease in the percentage of positively stained cells and in osteogenic capacity when the concentration of vancomycin was more than 6 g per cement dose. Quantitation of gene expression related to osteogenesis (Col1a, Alp, and Runx2), vascularization (Vegf, Tgfb1, and vWF), and proliferation (Oct4 and Stro-1) by real-time PCR revealed slight increases in the expression of selected genes at low vancomycin concentrations (1–4 g per cement dose), and relatively lower gene expression when the concentration of vancomycin was more than 6 g per cement dose. Conclusion PMMA spacers loaded with relatively low concentrations of vancomycin (1–4 g per cement dose) did not interfere with the proliferative, osteogenic, and angiogenic capacity of induced membranes, and even promoted their capacity. In contrast, spacers loaded with relatively high concentrations of vancomycin (6–10 g per cement dose) had negative effects on osteoblast viability, angiogenesis, and proliferation.

10 citations

Journal ArticleDOI
TL;DR: Levosimendan may protect against DOX-induced cardiotoxicity via modulation of the PTEN/Akt signaling pathway and reduce the cardiac dysfunction and attenuated the myocardial apoptosis induced by DOX in vivo and in vitro.
Abstract: Background and aims Myocyte apoptosis plays a critical role in the development of doxorubicin- (DOX-) induced cardiotoxicity. In addition to its cardiotonic effect, laboratory evidence indicates that levosimendan can inhibit apoptosis, but its role in DOX-induced cardiac injury remains unclear. Therefore, the present study is aimed at exploring whether levosimendan could attenuate DOX-induced cardiotoxicity. Methods Levosimendan (1 mg/kg) was administered to mice through oral gavage once daily for 4 weeks, and the mice were also subjected to an intraperitoneal injection of DOX (5 mg/kg) or saline, once a week for 4 weeks, to create a chronic model of DOX-induced cardiotoxicity. A morphological examination and biochemical analysis were used to evaluate the effects of levosimendan. H9C2 cells were used to verify the protective role of levosimendan in vitro. And an Akt inhibitor was utilized to verify the cardioprotection of levosimendan. Results Levosimendan reduced the cardiac dysfunction and attenuated the myocardial apoptosis induced by DOX in vivo and in vitro. Levosimendan also inhibited the activation of phosphatase and tensin homolog (PTEN) and upregulated P-Akt expression both in vivo and in vitro. And inhibition of Akt abolished the cardioprotection of levosimendan in vitro. Conclusion Levosimendan may protect against DOX-induced cardiotoxicity via modulation of the PTEN/Akt signaling pathway.

10 citations

Journal ArticleDOI
TL;DR: Atorvastatin improves the cell proliferation, migration, and angiogenesis of EPCs via the miR-221/VEGFA axis and could be a potent agent against CSF, pending further in vivo and clinical investigations.
Abstract: The present study was aimed at investigating the detailed functions of atorvastatin, a lipid-lowering agent, in the pathogenesis of coronary slow flow (CSF), a clinical disease characterized by delayed angiographic coronary opacity without obstructive coronary disease. In the present study, we successfully identified isolated endothelial progenitor cells (EPCs) from the peripheral blood of patients with CSF. Their VEGFA protein levels were determined using immunoblotting analyses. We determined cell viability using MTT assays, cell migration capacity using Transwell assays, and the angiogenic capacity using a tube formation assay. The target association between miR-221 and VEGFA was validated with a luciferase reporter assay. Atorvastatin treatment increased EPC VEGFA protein levels, proliferation, migration, and angiogenesis. miR-221 expression was downregulated after atorvastatin treatment; miR-221 overexpression exerted an opposing effect to atorvastatin treatment on VEGFA protein, EPC proliferation, migration, and angiogenesis. The protective effects of atorvastatin treatment on VEGFA protein and EPCs could be significantly suppressed by miR-221 overexpression. miR-221 directly bound the VEGFA 3'UTR to inhibit its expression. In conclusion, atorvastatin improves the cell proliferation, migration, and angiogenesis of EPCs via the miR-221/VEGFA axis. Thus, atorvastatin could be a potent agent against CSF, pending further in vivo and clinical investigations.

10 citations

Journal ArticleDOI
TL;DR: It is demonstrated that CXCR7 suppression inhibits macrophages M1 polarization, chemotaxis and inflammation to ameliorate post- MI injury, providing novel insights and promising therapy approaches in post-MI treatment.
Abstract: Myocardial infarction (MI) is one of the primary causes leading to heart failure in coronary artery disease. However, the mechanisms of macrophage that dominate pathogenesis of MI remain unclear. Mice were induced with MI and pretreated with adenovirus containing indicated shRNA. Post-MI injuries were evaluated by echocardiography. BMDMs and post-MI LV macrophages were used to assess the significance of CXCR7. Macrophages’ migration was examined by chemotaxis assay, Cytokine production, phosphorylation of ERK1/2, p38 MAPK and JNK were measured by ELISA. CXCR7 in macrophages was up-regulated during M1 polarization and following MI in the murine model, with positive correlation with M1 markers but not M2 markers. Besides, CXCR7 down-regulation abolished macrophage M1 polarization. In addition, CXCR7 but not CXCR3 or CXCR4 controlled SDF-1 and I-TAC-mediated chemotaxis and inflammation in M1-like macrophages post-MI, signaling through activating ERK1/2, whereas p38 MAPK and JNK were not involved. Moreover, silencing CXCR7 ameliorated cardiac dysfunction by attenuating infarct area, LVEF and LVFS post-MI along with reduction of CXCR7 expression and ERK1/2 phosphorylation. Our data demonstrate that CXCR7 suppression inhibits macrophages M1 polarization, chemotaxis and inflammation to ameliorate post-MI injury, providing novel insights and promising therapy approaches in post-MI treatment.

10 citations


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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20222
202135
202019
201914
20189
201717