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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: Environmental and urinary cadmium levels were raised in this group of welders and were associated with raised markers of renal tubular dysfunction, and the values were close to the level for chronic Cadmium poisoning in China.
Abstract: Background Occupational exposure to welding fumes has been associated with several diseases including metal fume fever, lung cancer, welder's pneumoconiosis and manganism. However, there are few reports on cadmium-induced renal tubular dysfunction in welders. Aims To evaluate the body burden of cadmium and cadmium-induced proteinuria in a group of Chinese welders. Methods Cadmium concentrations in the breathing zone and in urine were measured by atomic absorption spectrometry. β(2)-microglobulin (β(2)-MG) in urine as a marker of renal tubular function was measured using an ELISA kit. All urinary parameters were adjusted by urinary creatinine (Cr). Results A total of 103 welders participated. The concentration of airborne cadmium in the welders' breathing zones ranged from 5 to 86 μg/m(3), and 17% of samples exceeded the threshold limit value. Six welders' urinary cadmium levels exceeded the Chinese recommended reference value. Urinary β(2)-MG levels increased significantly with increasing urinary cadmium levels and in two welders, the values were close to the level for chronic cadmium poisoning in China. Conclusions Environmental and urinary cadmium levels were raised in this group of welders and were associated with raised markers of renal tubular dysfunction. The exact source of the cadmium warrants further assessment.

26 citations

Journal ArticleDOI
TL;DR: The study provides a new clue for mitochondrial DNA in the etiology of T2DM in Chinese Uyghur population and predicts two markers of haplogroup D4 and H, predicted to affect the structure of MT-ATP8 and 16S RNA, respectively, and may be involved in the pathogenesis of T1DM.
Abstract: A hospital-based case-control study was conducted to investigate potential association between mitochondrial DNA and Type 2 diabetes mellitus (T2DM) in Chinese Uyghur population. We sequenced mitochondrial DNA from 210 Uyghur individuals including 88 T2DM patients and 122 controls. Using haplogroup classification and association test, we found that haplogroup H (odds ratio [OR] = 1.40; 95% confidence interval [CI]: 1.20–1.64; P = 0.0005138) and D4 (odds ratio = 1.47; 95% CI: 1.22–1.77; P = 0.001064) were associated with an increased risk of T2DM in Chinese Uyghur population. Two markers of haplogroup D4 and H, MT-ATP8 m.8414 T > G (p.Leu17Phe) and m.2706 G > A encoding 16S rRNA in mitochondria, were predicted to affect the structure of MT-ATP8 and 16S RNA, respectively, and may be involved in the pathogenesis of T2DM. Our study provides a new clue for mitochondrial DNA in the etiology of T2DM in Chinese Uyghur population.

25 citations

Journal ArticleDOI
TL;DR: It is indicated that miR-142-3p may participate in the regulation of the body’s inflammatory response through the LPS-TLR-TNF-α signaling pathway in chronic rhinosinusitis with nasal polyposis.
Abstract: Objective:Previous studies suggested that microRNAs played an important role in the progression of inflammation and remodeling of chronic rhinosinusitis with nasal polyposis. However, the abnormal ...

22 citations

Journal ArticleDOI
TL;DR: The result suggested that metabolic disorders and gut microbiota dysbiosis occurred in Uyghur T2DM and IGR, and the results provide a theoretical basis for studying the pathological mechanism for further research.
Abstract: Objective. Gut microbiota and their metabolites play an important role in the development of type 2 diabetes mellitus (T2DM). This research was designed to study the relationship between gut microbiota and faecal metabolites of Uyghur newly onset T2DM and impaired glucose regulation (IGR) patients. Materials and Methods. A total of 60 different glycemic Uyghur subjects were enrolled and divided into T2DM, IGR, and normal glucose tolerance (NGT) groups. Metagenomics and LC-MS-based untargeted faecal metabolomics were employed. Correlations between bacterial composition and faecal metabolomics were evaluated. Results. We discovered that the composition and diversity of gut microbiota in newly onset T2DM and IGR were different from those in NGT. The α-diversity was higher in NGT than in T2DM and IGR; β-diversity analysis revealed apparent differences in the bacterial community structures between patients with T2DM, IGR, and NGT. LC-MS faecal metabolomics analysis discovered different metabolomics features in the three groups. Alchornoic acid, PE (14 : 0/20 : 3), PI, L-tyrosine, LysoPC (15 : 0), protorifamycin I, pimelic acid, epothilone A, 7-dehydro-desmosterol, L-lysine, LysoPC (14 : 1), and teasterone are the most significant differential enriched metabolites. Most of the differential enriched metabolites were involved in metabolic processes, including carbohydrate metabolism, starch and sucrose metabolism, phenylpropanoid biosynthesis, and biosynthesis of amino acids. Procrustes analysis and correlation analysis identified correlations between gut microbiota and faecal metabolites. Matricin was positively correlated with Bacteroides and negatively correlated with Actinobacteria; protorifamycin I was negatively correlated with Actinobacteria; epothilone A was negatively correlated with Actinobacteria and positively correlated with Firmicutes; PA was positively correlated with Bacteroides and negatively correlated with Firmicutes; and cristacarpin was positively correlated with Actinobacteria; however, this correlation relationship does not imply causality. Conclusions. This study used joint metagenomics and metabolomics analyses to elucidate the relationship between gut microbiota and faecal metabolites in different glycemic groups, and the result suggested that metabolic disorders and gut microbiota dysbiosis occurred in Uyghur T2DM and IGR. The results provide a theoretical basis for studying the pathological mechanism for further research.

22 citations

Journal ArticleDOI
TL;DR: It is proposed that PKM2 regulates cell proliferation, migration, and invasion via phosphorylation of STAT3 through TGF‐β1‐induced EMT.
Abstract: Recent studies have demonstrated pleiotropic roles of pyruvate kinase isoenzyme type M2 (PKM2) in tumor progression. However, the precise mechanisms underlying the effects of PKM2 on esophageal squamous cell carcinoma (ESCC) metastasis and transforming growth factor β1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) remain to be established. In this study, we observed upregulation of PKM2 in ESCC tissues that was markedly associated with lymph node metastasis and poor prognosis. High PKM2 expression in tumor tissues frequently coincided with the high pSTAT3Tyr705 expression and low E-cadherin expression. Furthermore, altered PKM2 expression was significantly associated with proliferation, migration, and invasion of ESCC cells, in addition to expression patterns of EMT markers (Snail, E-cadherin, and vimentin) and pSTAT3Tyr705 /STAT3 ratio. Overexpression of STAT3 significantly attenuated the effects of PKM2 knockdown on cell proliferation and motility as well as expression of pSTAT3 Tyr705 and EMT markers. Consistently, stable short hairpin RNA (shRNA)-mediated silencing of PKM2 reversed the effects of TGF-β1 treatment, specifically, upregulation of PKM2, phosphorylation of STAT3 at Tyr705, and increased EMT, migration, and invasion. We propose that PKM2 regulates cell proliferation, migration, and invasion via phosphorylation of STAT3 through TGF-β1-induced EMT. Our findings collectively provide mechanistic insights into the tumor-promoting role of PKM2, supporting its prognostic value and the therapeutic utility of PKM2 inhibitors as potential antitumor agents in ESCC.

21 citations


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