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.

Silencing of miR-23a attenuates hydrogen peroxide (H2O2) induced oxidative damages in ARPE-19 cells by upregulating GLS1: an in vitro study

Abstract: Oxidative damages contributes to age-related macular degeneration (AMD) caused vision blindness, but the molecular mechanisms are still largely unknown. This study managed to investigate this issue by conducting in vitro experiments. Oxidative stress were evaluated by L-012 dye, DHE staining and MDA assay. CCK-8 and colony formation assay were conducted to examine cell proliferation. Cell death was evaluated by trypan blue staining and Annexin V-FITC/PI double staining method through flow cytometry (FCM). The binding sites of miR-23a and GLS1 mRNA were predicted by online miRDB database and validated by dual-luciferase reporter gene system. Real-Time qPCR for miR-23a levels and Western Blot for protein expressions. The retinal pigment epithelial (RPE) cells (ARPE-19) were subjected to hydrogen peroxide (H2O2) stimulation to simulate AMD progression in vitro, and we identified a novel miR-23a/glutaminase-1 (GLS1) pathway that regulated H2O2 induced oxidative damages in ARPE-19 cells. Mechanistically, H2O2 induced oxidative stress, inhibited cell proliferation and induced cell death in ARPE-19 cells in a dose- and time-dependent manner. Also, H2O2 stimulation hindered cell invasion, migration and glutamine uptake in ARPE-19 cells. Interestingly, we proved that H2O2 increased miR-23a levels, while downregulated glutaminase-1 (GLS1) in ARPE-19 cells, and miR-23a targeted 3′ untranslated region (3′UTR) of GLS1 mRNA for GLS1 degradation. Finally, our data suggested that silencing miR-23a upregulated GLS1 to reverse the detrimental effects of H2O2 treatment on ARPE-19 cells. In general, analysis of the data suggested that miR-23a ablation upregulated GLS1 to attenuate H2O2 stimulation induced oxidative damages in ARPE-19 cells in vitro, and this study broadened our knowledge in this field, which might help to provide novel theranostic signatures for AMD.

Application of protein chip combined with SELDI‑TOF‑MS detection to investigate serum protein expression in patients with silicosis fibrosis

Abstract: The present study aimed to observe the identification of biomarkers of silicosis based on the differentially expressed serum proteins between normal healthy individuals and patients with silicosis fibrosis. A total number of 20 patients with clinically diagnosed silicosis were screened, which were designated as the foundation treatment group. In addition, 20 age-matched healthy patients attending a check-up at the physical examination department were selected. Serum samples were obtained and a combined protein chip with surface-enhanced laser desorption ionization flight mass spectrometry was applied to perform serum analysis. Data preprocessing, screening differences in peak, hierarchical cluster analysis, Principal Component Analysis, construction of a decision tree model, and prediction based on the differences between peaks corresponding to proteins were performed to analyze the data. The results revealed differences in the proteins in serum between the normal group and the group prior to foundation treatment prediction. The corresponding names of the protein peak, predicted protein, and gene name were as follows: M1948_00, complement c3 frag, C3; M2017_02, amyloid-βa4 protein, APP; and M2879_56, hepcidin, HAMP. Differentially expressed serum proteins in the normal group and the basis treatment group were predicted, including M2017_02, amyloid-βa4 protein, APP; M2879_56, hepcidin, HAMP; and M3224_97, fibrinogen-α chain frags, FGA. The differentially expressed serum proteins in the group prior to basis treatment and the group following basis treatment were predicted, including M2001_69, amyloid-βa4 protein, APP; M2017_02, amyloid-βa4 protein, APP, M4144_81, plasma protease c1 inhibitor frag, and SERPING1. In conclusion, there were differences in the proteins in serum between the patients with silicosis fibrosis and healthy individuals.

Relationship of UBA52 with MAU in Patients with Early Diabetic Nephropathy

Abstract: Objective To explore the expression of UBA52 and the relationship with MAU in patients with early diabetic nephropathy. Methods 20 diabetes( diabetic group) and 59 diabetic nephropathy patients( DN group) admitted by the Fifth Affiliated Hospital of Xinjiang Medical University from February 2012 to March 2013 were selected to be compared with 22 healthy people confirmed by physical check- up in this hospital( control group). The immunity transmission turbidity method was used to detect MAU of the three groups and ELISA was used to detect UBA52 in urine and blood. Results The differences of gender,age and BMI of the three groups were not significant( P 0. 05); the differences of blood sugar,glycosylated hemoglobin and total cholesterol of the three groups were significant( P 0. 05). Blood UBA52,urine UBA52,urinary protein and MAU of the three groups were significantly different( P 0. 05); blood,urine UBA52 levels,urinary protein and MAU of DN group were significantly higher than those of another two groups; urinary protein,MAU of diabetic group were significantly higher than those of control group( P 0. 05). Multiple linear regression analysis showed that MAU and glycosylated hemoglobin influenced urine UBA52 of DN patients( P 0. 05). Conclusion Blood and urine UBA52 levels increase in DN patients. MAU is the influencing factor for urine UBA52 level.

Investigation of the association between obesity and insulin-induced gene 1 polymorphism at 7q36.3 region in Uygur population in Xinjiang, China.

Abstract: BACKGROUND Obesity is a common heritable trait and a major risk factors of chronic and metabolic diseases. Insulin-induced gene 1 (INSIG1) is known to play important roles in cholesterol and triacylglycerol (TAG) metabolism. In the present study, our primary objective was to explore whether the single nucleotide polymorphisms (SNPs) in INSIG1 gene were associated with obesity in Uygur subjects, in Xinjiang, China. METHODS We designed a case-control study including 516 obese patients and 463 age- and sex-matched control subjects. Three SNPs (rs2721, rs9767875 and rs9719268) were genotyped using TaqMan SNP genotyping assays. RESULTS For rs2721, the distribution of genotypes, dominant model (GT + TT vs GG), recessive model (TT vs GT + GG) showed significant differences between obese patients and the controls (P = 0.008, P = 0.005 and P = 0.035, respectively). For rs9719268, the distribution of genotypes showed significant differences between obese patients and the controls (P = 0.004). The dominant model (GT + TT vs GG) of rs2721 and rs9719268 GT genotype remain significantly associated with obesity after adjustment for confounders (OR = 1.393, 95% CI = 1.047-1.853, P = 0.023; OR = 1.631, 95% CI = 1.059-2.512, P = 0.026). The TG levels were significantly higher in rs2721 GT/TT genotypes than that in GG genotypes (P<0.05). CONCLUSIONS Rs2721 and rs9719268 of INSIG1 gene are associated with obesity in Uygur subjects. Subjects with GT/TT genotype or T allele of rs2721 and GT genotype of rs9719268 were associated with an increased risk of obesity.