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Gong Q.,Zhumadian City Center Hospital | Hou F.,Zhumadian City Center Hospital
Biochemical and Biophysical Research Communications | Year: 2016

The epithelial-mesenchymal transition (EMT) plays a significant role in renal tubulointerstitial fibrosis (TIF), which is one of hallmark pathological feature of diabetic nephropathy (DN). Angiotensin II via its type-1 receptor AT1R is involved in the development of TIF. The purpose of our study was aimed to investigate the effect of silencing of AT1R on EMT and elucidate the possible mechanism underling these effects. EMT was induced by high glucose (HG) in human proximal tubular epithelial cell line HK-2 cells. The mRNA levels of AT1R were determined. The expression of AT1R was silenced by small interfering RNA (siRNA) technology and confirmed by quantitative real time PCR (qRT-PCR). After transfection with siAT1R, cell viability and expression levels of epithelial cell marker (epithelial (E)-cadherin), mesenchymal cell marker (alpha-smooth muscle actin (α-SMA)), four transcriptional factors (snail, slug, twist, and ZEB-1) were determined, as well as the roles of mechanistic target of rapamycin (mTOR)/p70S6K signaling pathway. The levels of AT1R were significantly higher after exposure to HG (P < 0.05). Transfection with siAT1R had no effect on cell viability, but reversed HG-induced EMT by up-regulation of E-cadherin expression and decrease of α-SMA, snail, and twist levels. MTOR/p70S6K signaling pathway was highly activated in HK-2 cells cultured under HG, but was inhibited by transfection with siAT1R. Our results suggest that silencing of AT1R inhibits EMT induced by HG in HK-2 cells via inactivation of mTOR/p70S6K signaling pathway. Silencing of AT1R might be a new strategy to treat DN. © 2015 Elsevier Inc. All rights reserved. Source

Yang Y.,PLA Fourth Military Medical University | Yang Y.,Zhumadian City Center Hospital | Chen J.,Zhumadian City Center Hospital | Li L.,Zhumadian City Center Hospital | And 4 more authors.
Neurochemical Research | Year: 2013

The protective effect of the mild hypoxia to the epilepsy has been widely tested. Although it is found that the hypoxia protects the brain by up-regulation of hypoxia-inducible factor-1α, few focused on systematic comparisons between different mild hypoxia manipulations and their effects. The male Sprague-Dawley rats were observed following exposure to hypoxia before and after epilepsy for 3 days with 90 min per day. The effects of different mild hypoxia manipulations on kainic acid-induced epilepsy were compared from the perspective of morphology, molecular biology and behavioral test. Results showed that different mild hypoxia manipulations could inhibit the cell apoptosis of kainic acid-induced rat hippocampus and improve their physiological functions. The effect of preconditioning group was better than that of postconditioning group and that of preconditioning and postconditioning with mild hypoxia group was the best among all the groups. The result showed that the preconditioning and postconditioning of mild hypoxia was recommended pre- and post-epilepsy and exposure to mild hypoxia should be prolonged. These findings might provide new ideas and methods for the clinical treatment of epilepsy. © 2012 Springer Science+Business Media New York. Source

Yang Y.,Zhumadian City Center Hospital | Zhang Y.-G.,Zhumadian City Center Hospital | Lin G.-A.,159th Hospital of PLA | Xie H.-Q.,Zhumadian City Center Hospital | And 7 more authors.
PLoS ONE | Year: 2014

Chemotherapy-induced neuropathic pain (CNP) is the major dose-limiting factor in cancer chemotherapy. However, the neural mechanisms underlying CNP remain unclear. There is increasing evidence implicating the involvement of spinal endomorphin-2 (EM2) in neuropathic pain. In this study, we used a vincristine-evoked rat CNP model displaying mechanical allodynia and central sensitization, and observed a significant decrease in the expression of spinal EM2 in CNP. Also, while intrathecal administration of exogenous EM2 attenuated allodynia and central sensitization, the mu-opioid receptor antagonist β-funaltrexamine facilitated these events. We found that the reduction in spinal EM2 was mediated by increased activity of dipeptidylpeptidase IV, possibly as a consequence of chemotherapy-induced oxidative stress. Taken together, our findings suggest that a decrease in spinal EM2 expression causes the loss of endogenous analgesia and leads to enhanced pain sensation in CNP. © 2014 Yang et al. Source

Li W.-G.,Zhumadian City Center Hospital | Zhao L.,Zhumadian City Center Hospital | Zhao H.,Zhumadian City Center Hospital
Transplantation Proceedings | Year: 2015

The aim of this work was to understand the epidemiologic characteristics of TB and human immunodeficiency virus (HIV) dual infection cases, thus providing the basis for effective prevention and control measures. On the basis of HIV/TB screening of new and old TB and HIV/acquired immunodeficiency syndrome (AIDS) patients registered in 4 regions of Urumqi, Xinjiang, People's Republic of China, from 2012 to 2014, an analysis was made of the epidemiologic characteristics and risk factors of people suffering from HIV/TB dual infection. A total of 2,645 TB patients were tested for HIV antibodies, of whom 128 tested positive, showing a detection rate of 4.8%; TB patients ≥35 years old had 0.26 times (95% confidence interval [CI], 0.18-0.40) the risk of HIV infection than those 18-35 years old, and pulmonary and extrapulmonary TB patients with positive smear had, respectively, 0.43 times (95% CI, 0.28-0.66) and 1.79 times (95% CI, 1.09-2.94) the risk of HIV infection than those with negative smear. And 1,195 HIV/AIDS patients were screened for TB, of whom 91 were positive, showing an infection rate of 7.6%; male HIV/AIDS patients had 12.2 times (95% CI, 6.4-23.1) the risk of TB infection than female patients, and HIV/AIDS patients with CD4 cells ≤200/μL had 20.4 times (95% CI, 11.8-35.3) the risk of TB infection than those with CD4 cells >200/μL. TB and HIV/AIDS patients in Urumqi from 2012 to 2014 suffered from high HIV and TB infection rates, so relevant measures should be taken to intervene, especially for TB patients ≥35 years old, those with positive smear, extrapulmonary TB patients, male HIV/AIDS patients, and those with CD4 cells ≤200/μL. © 2015 by Elsevier Inc. All rights reserved. Source

Xu H.,Zhumadian City Center Hospital | Feng Y.,Zhumadian City Center Hospital | Jia Z.,Zhumadian City Center Hospital | Yang J.,Zhumadian City Center Hospital | And 6 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2016

We conducted a case-control study to investigate the association of ERCC1 (rs3212986) and ERCC2 (rs13181) gene polymorphisms with the susceptibility to bladder cancer. A total of 194 bladder cancer patients and 240 control subjects were recruited from the Zhumadian City Center Hospital between March 2012 and March 2014. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was taken to genotype ERCC1 rs3212986 and ERCC2 rs13181. A significant difference was found between the genotype distributions of ERCC1 rs3212986 between the two groups by chi-square test (Χ2 = 6.01, P = 0.04). Unconditional logistic regression analyses showed that subjects carrying the CC genotype of ERCC1 rs3212986 were associated with a higher risk of developing bladder cancer than those carrying the AA genotype, and the adjusted OR (95% CI) was 2.05 (1.10-3.83) (P = 0.01). Moreover, we found that the CC genotype of ERCC1 rs3212986 had 1.8 fold risk of bladder cancer compared to the AA+AC genotype (OR = 1.80, 95% CI = 1.01-3.21; P = 0.03). However, we did not find any significant association between the ERCC2 rs13181 polymorphism and susceptibility to bladder cancer. In conclusion, we suggest that the ERCC1 rs3212986 gene polymorphism influences the development of bladder cancer in co-dominant and recessive models. Source

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