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Zhumadian, China

Zhou S.,Peking University | Yu D.,Beijing Hospital | Zhang H.,Zhumadian Central Hospital | Jiang L.,Beijing Hospital | And 3 more authors.
Cellular Physiology and Biochemistry | Year: 2015

Background: The aim of this study was to clarify the relationship among Rac1 expression and activation, oxidative stress and β cell dysfunction in obesity. Methods: In vivo, serum levels of glucose, insulin, oxidative stress markers and Rac1 expression were compared between ob/ob mice and C57BL/6J controls. Then, these variables were rechecked after the administration of the specific Rac1 inhibitor-NSC23766 in ob/ob mice. In vitro, NIT-1 β cells were cultured in a hyperglycemic and/or hyperlipidemic state with or without NSC23766, and the differences of Rac1 expression and translocation, NADPH oxidase(Nox) enzyme activity, reactive oxygen species (ROS) and insulin mRNA were observed. Results: ob/ob mice displayed abnormal glycometabolism, oxidative stress and excessive expression of Rac1 in the pancreas. NSC23766 injection inhibited the expression of Rac1 in the pancreas, along with amelioration of oxidative stress and glycometabolism in obese mice. Under hyperglycemic and/or hyperlipidemic conditions, Rac1 translocated to the cellular membrane, induced activation of the NADPH oxidase enzyme and oxidative stress, and simultaneously reduced the insulin mRNA expression in NIT-1 β cells. Inhibiting Rac1 activity could alleviate oxidative stress and meliorate the decline of insulin mRNA in β cells. Conclusions: Rac1 might contribute to oxidative stress systemically and locally in the pancreas in obesity. The excessive activation and expression of Rac1 in obesity were associated with β cell dysfunction through ROS production. © 2015 S. Karger AG, Basel.


Li X.-X.,Intensive Care Unit | Zhang Y.-G.,Intensive Care Unit | Wang D.,Intensive Care Unit | Chen Y.-F.,Zhumadian Central Hospital | Shan Y.-H.,Intensive Care Unit
Asian Pacific Journal of Cancer Prevention | Year: 2015

Objective: To explore the preventive effect of aspirin on the cardiovascular complications in prostate cancer after endocrinotherapy. Materials and Methods: A total of 92 patients with prostate cancer were divided into observation group (n=44) and control group (n=48). The control group was treated with medical castration plus anti-androgenic drugs. Based on the above treatment, the observation group was added aspirin. The follow-up duration was 2 years. The changes of partial prothrombin time (PT), activated partial thromboplastin time (APTT), platelet aggregation rate (PAG), prostate-specific antigen (PSA) and serum testosterone (T) before and after treatment as well as incidence of cardiovascular disease were observed. Results: The 2-year survival rates of patients without cardiovascular disease in observation group and control group were 95.45% (42/44) and 72.92% (35/48), respectively, and significant difference was presented between two groups by comparison to the survival rates (χ2=8.5453, p=0.0035). There was no statistical significance between two groups as well as before and after treatment regarding PT (p > 0.05). After treatment, APTT went down and PAG was gradually on the rise in control group, while PAG down and APTT on the rise increasingly in observation group. Significant differences were presented between two groups as well as before and after treatment (p < 0.01). Both PSA and T levels were decreased significantly in two groups after treatment (p < 0.01), but there was no statistical significant between two groups (p > 0.05). Conclusions: Application of endocrinotherapy in prostate cancer can easily lead to occurrence of cardiovascular disease, but cardiovascular complications can be prevented by aspirin, without affecting the effect of endocrinotherapy.


Gao Y.,Zhumadian Central Hospital | Li L.,Zhumadian Central Hospital | Song L.,Zhengzhou University
Oncology Letters | Year: 2015

The survival rate of glioma patients is very low, and a lack of effective diagnostic techniques are available at present. The current study aimed to investigate the expression of p16 and Survivin and their association with proliferation and apoptosis in gliomas, as well as patient characteristics and prognosis. In total, 62 glioma specimens were surgically resected and pathologically confirmed at the Zhumadian Central Hospital (Zhumadian, China) between June 2008 and February 2014. Clinical data, including the gender and age of the patients, as well as the location, infiltration degree, size and pathological stage of the glioma, was collected. In order to evaluate the expression of p16 and Survivin in the gliomas, the Ki-67 labeling index was used to evaluate cell proliferation activity. The number of argyrophilic nucleolar organizer regions and the rate of cellular apoptosis was examined using the terminal deoxynucleotidyl transferase dUTP nick end labeling method. The results were analyzed using SPSS 14.0 statistical software. The positive rate of p16 gene expression in the gliomas was 46.77% (29 cases), and p16 gene expression was positively correlated with the differentiation status, tumor size and pre-operative symptoms. The positive rate of Survivin expression in the gliomas was 69.88% (58 cases), and Survivin expression was positively correlated with tumor size, differentiation status and clinical stage. The proliferation activity of the gliomas was enhanced with increasing p16 and Survivin expression, while apoptosis was inhibited. In conclusion, the overexpression of p16 and Survivin was closely associated with uncontrolled cell proliferation and the inhibition of apoptosis in gliomas. The combined analysis of the expression of p16 and Survivin in gliomas may provide guidance with respect to the clinical diagnosis, evaluation, treatment and prognosis of patients with glioma. © 2015, Spandidos Publications. All rights reserved.


Hu J.-L.,Zhumadian Central Hospital | Yang Z.,Zhengzhou University | Tang J.-R.,Zhumadian Central Hospital | Fu X.-Q.,Zhumadian Central Hospital | Yao L.-J.,Zhumadian Central Hospital
Asian Pacific Journal of Cancer Prevention | Year: 2013

The aim of this study was evaluated the prevalence of Treg cells in peripheral blood in patients with gastric cancer, and investigate the effect of gastric cancer cells on their differentiation. ELISA was employed to assess the concentrations of TGF-β and IL-10 in gastric cancer patients' serum. Then, mouse gastric cancer cells were co-cultured with T lymphocytes or T lymphocytes + anti-TGF-β. Flow cytometric analysis and RT-PCR were then performed to detect Treg cells and TGF-β and IL-10 expression in gastric cancer cells. Our data showed that the expression of TGF-β and IL-10 in the patients with gastric cancer was increased compared to the case with healthy donors. The population of Treg cells and the expression levels of TGF-β and IL-10 in the co-culture group were much higher than in the control group (18.6% vs 9.5%) (P < 0.05). Moreover, the population of Treg cells and the expression levels of TGF-β and IL-10 in the co-culture systerm were clearly decreased after addition of anti-TGF-β (7.7% vs 19.6%) (P < 0.01). In conclusion, gastric cancer cells may induce Treg cell differentiation through TGF-β, and further promote immunosuppression.


Liu T.Y.,Zhumadian Central Hospital | Zhang H.,Huanghuai University | Du S.M.,Zhumadian Central Hospital | Li J.,Zhumadian Central Hospital | Wen X.H.,Zhumadian Central Hospital
Genetics and Molecular Research | Year: 2016

This study investigated the expression of microRNA-210 (miR-210) in tissue and serum of renal carcinoma patients and its effect on renal carcinoma cell proliferation, apoptosis, and invasion. Thirty-two renal carcinoma patients in our hospital were selected as the study group and 32 people receiving a physical examination were selected as the control group. miR-210 expression in the serum of renal carcinoma patients and in healthy subjects was quantified by real-time polymerase chain reaction. After miR-210 overexpression and inhibition in ACHN cells in human renal carcinoma, ACHN cell proliferation, apoptosis, and invasion were detected by CCK-8, flow cytometry, and a transwell invasion assay. The expression of miR-210 was significantly higher in renal carcinoma than in corresponding paracarcinoma tissues (P < 0.001). The expression of miR-210 was significantly higher in the serum of renal carcinoma than in the control group (P < 0.001). ACHN cell proliferation and invasion were significantly increased and apoptosis was significantly decreased (P < 0.05) when miR-210 was overexpressed. ACHN cell proliferation and invasion were significantly decreased and apoptosis was significantly increased (P < 0.05) when miR-210 was inhibited. In conclusion, miR-210 was highly expressed in tissues and serum of renal carcinoma patients. miR-210 could promote the proliferation and invasion of renal carcinoma cells and inhibit the apoptosis of renal cell carcinoma cells. © FUNPEC-RP.

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