Fifth Affiliated Hospital of Xinjiang Medical University

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.

Echinococcus multilocularis induces surface high expression of inhibitory killer immunoglobulin-like receptor on natural killer cells.

Abstract: Alveolar echinococcosis (AE) is a malignant and fatal parasitic disease caused by the larvae of Echinococcus multilocularis (E. multilocularis), which inhibits the activity and proliferation of natural killer (NK) cells. In this study, the functional alteration of hepatic NK cells and their related molecules were studied. The AE-infected patient's tissue was fixed with formalin, embedded in paraffin, and stained with Masson's trichrome or hematoxylin and eosin (H&E). Single cells from AE-infected patient or E. multilocularis-infected mice were blocked with Fc-receptor (FcR), and stained with monoclonal antibodies, including CD16, CD56, CD3, KIR2DL1, granzyme B, perforin, Interferon gamma (IFN-γ), and tumor necrosis factor-α (TNFα) or isotype control, to measure molecules and cytokines of NK cells and analyzed by flow cytometry. The Sirius red staining was used to quantitate hepatic fibrosis by calculating quantitative collagen deposition. AE can adjust both the number of hepatic CD56+ NK cells and its KIR2DL1 expression processes. Moreover, the overexpression of KIR2DL1 in NK cells could downregulate the functioning of immune cells in the liver area close to parasitic lesions. The number and dysfunction of NK cells in E. multilocularis infection could be related to the molecule dynamics of cell surface inhibitory receptor Ly49A, leading to hepatic damage and progression of fibrosis. This study illustrated significant increase in hepatic fibrogenesis and apparent upregulation of hepatic CD56+ NK cell population and its KIR2DL1 expression in AE-infected patients. This opposite variation might be related to the impaired NK cells functioning, such as granzyme B, IFN-γ, and TNF-α secretion. In addition, the cell surface inhibitory receptor Ly49A was related to the intracellular cytokine secretion functions of NK cells.

Survivin Regulates Bad Gene Expression by Binding to Its Promoter and Modulates Cell Cycle and Apoptosis in Esophageal Carcinoma Cell.

Abstract: Esophageal cancer (EC) is the eighth most prevalent cancer and the sixth leading cause of cancer-related mortality worldwide. As an antiapoptotic and a proapoptotic protein, respectively, survivin and Bad play an important role in carcinogenesis of the most human cancers including EC. However, the regulatory relationships between them remain unclear. We sought to investigate the effects of survivin knockdown and overexpression on the expression of Bad gene, cell cycle progression, and apoptosis of esophageal carcinoma cell. The mRNA expression levels of survivin and Bad were determined in EC tissue samples. The knockdown and overexpression experiments were performed in ECA109 and KYSE450 cells via transfection with survivin overexpression and shRNA plasmids. A Bad overexpression experiment was conducted to confirm the biological effect on knockdown of survivin via modulating Bad expression. RT-qPCR and Western blot analysis were used to detect mRNA and protein expression, respectively. Cell cycle and apoptosis were analyzed by flow cytometry. The chromatin immunoprecipitation (ChIP) was conducted to determine the binding sites of survivin on the promoter of Bad gene. By analyzing the mRNA expression of survivin and Bad in 40 ESCC patient specimens, we found that the positive expression rate of survivin in tumor tissues (88%, 35/40) was remarkably high, compared with the distal nontumor tissues (48%, 19/40, p < 0.01). On the other hand, the positive expression rate of Bad in tumor tissues (70%, 28/40) was remarkably low, compared with the distal nontumor tissues (95%, 38/40, p < 0.01). Overexpression of survivin decreases Bad mRNA and protein expression and promotes transformation of cell cycle to S phase. Conversely, knockdown of survivin increases Bad mRNA and protein expression and induces cell cycle arrest and apoptosis. Bad overexpression inducing apoptosis of esophageal carcinoma cell shows the similar apoptotic effect with survivin knockdown. ChIP assays indicate that survivin directly binds to the Bad promoter region, diminishing the transcriptional activity of Bad. In conclusion, the result suggested that survivin regulates Bad gene expression by binding to its promoter and modulates cell cycle and apoptosis in esophageal carcinoma cell.

Desmoglein 3 contributes to tumorigenicity of pancreatic ductal adenocarcinoma through activating Src–FAK signaling

Abstract: Desmogleins (DSGs), with the ability to link adjacent cells, have been shown to participate in the development of malignancy. DSG3 was up-regulated in various cancers, including lung, head and neck...

Chemopreventive effect of galangin against benzo(a)pyrene-induced stomach tumorigenesis through modulating aryl hydrocarbon receptor in Swiss albino mice:

Abstract: The present study was aimed to evaluate the chemopreventive potential of galangin against benzo(a)pyrene (BaP)-induced stomach carcinogenesis in Swiss albino mice. Stomach cancer was induced in experimental mice using BaP oral administration. The mice were treated with galangin (10 mg/kg b.wt.) before and during BaP administration. Oral administration of galangin at a dose of 10 mg/kg b.wt. significantly (p < 0.05) prevented the tumor incidence, tumor volume in the experimental animals. Further, galangin pretreatment prevents BaP-induced lipid peroxidation and restores BaP-mediated loss of cellular antioxidants status. It has also been found that galangin prevents BaP-induced activation of phase I detoxification enzymes. Furthermore, galangin pretreatment prevented the BaP-induced overexpression of cytochrome P450s isoform genes (CYP1A1, CYP1B1), aryl hydrocarbon receptor system (AhR, ARNT), transcriptional activators (CBP/p300, NF-kB), tumor growth factors, proto-oncogenes, invasion markers (TGFB, SRC-1, MYC, iNOS, MMP2, MMP9) and Phase II metabolic isoenzyme genes (GST) in the stomach tissue homogenate when compared to the control groups. The western blot results confirm that galangin (10 mg/kg. b.wt.) treatment significantly prevented the BaP-mediated expression of ArR, ARNT, and CYP1A1 proteins in the mouse stomach tissue. Therefore, the present results confirm that galangin prevents BaP-induced stomach carcinogenesis probably through modulating ArR and ARNT expression in the experimental mice.

Correction: Epidemiological investigation into the prevalence of abnormal inter-arm blood pressure differences among different ethnicities in Xinjiang, China.

Abstract: Objectives The prevalence of and risk factors for IAD among different ethnicity groups was unknown. Our aim was to investigate the prevalence of and risk factors for IAD among Han, Uygur and Kazakh ethnicities in Xinjiang. China. Methods In total, 14,618 adult participants (7,799 males and 6,819 females) were recruited from the Cardiovascular Risk Survey. A 4-stage stratified cluster random sampling method was used. The participants’ personal information and medical history were assessed by questionnaire. IAD was diagnosed by a noninvasive arteriosclerosis analyzer. Results The prevalence of abnormal IAD among the general population was 14.3%, with 12.5% in the Han, 14.9% in the Uygur, and 16.4% in the Kazakh populations. The prevalence of abnormal IAD among the hypertensive population was 19.4%, with 17.0% in the Han, 18.1% in the Uygur, and 22.7% in the Kazakh populations. The prevalence of abnormal IAD increased with age (all P 0.05). Multivariate logistic regression analysis showed that age more than 45 years, obesity and hypertriglyceridemia were significantly associated with a higher prevalence of IAD. There were different risk factors for abnormal IAD in different ethnicities. Middle or old age, obesity, ABI and diabetes mellitus were risk factors for the Han population, smoking was a risk factor in the Uygur population, and obesity and PAD were risk factors in the Kazakh population. Conclusion The prevalence of abnormal IAD in the Kazakh participants was higher than that in the Han and Uygur populations among both the general population and the hypertensive population in Xinjiang, China. The main risk factors of IAD were age, obesity, and triglyceride levels. Different ethnicities had different kinds of risk factors for IAD.