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Xinxiang, China

Xinxiang Medical University is located at Xinxiang city in the northern part of Henan province of China.Xinxiang Medical University has a vast campus with about 7000 undergraduates.Foreign Students Programme of Xinxiang Medical University under the International Education Institute of XXMU, a foreign students programme, has been running successfully at the university since 2001.There are more than 120 foreign students pursuing Western Medicine studies at this college. Wikipedia.

Zhang L.F.,Xinxiang Medical University
Hepato-gastroenterology | Year: 2013

Diabetes mellitus (DM) has been considered to be relevant to an increased risk of several different types of cancers. However, its relationship with extrahepatic cholangiocarcinoma (ECC) remains unclear. To investigate a quantitative assessment of this relationship, we performed a meta-analysis to evaluate the association between diabetes and the risk of ECC. We identified studies by searching Embase (from 1 January 1974 to 30 June 2012), Medline (from 1 January 1966 to 30 June 2012), and the reference lists of related articles. Summary relative risks (RRs) with corresponding 95% CIs were calculated with a random-effects model. A total of 9 articles (4 case-control and 5 cohort studies) were included in this study. Compared with those without DM, individuals with DM had an increased risk of ECC (for case-control studies: summary OR=1.61, 95% CI: 1.05-2.49, p=0.063 for heterogeneity; for cohort studies: summary RR=1.61, 95% CI: 1.14-2.29, p=0.005 for heterogeneity). The funnel plot showed no evidence for publication bias concerning DM and the risk of ECC (Egger's test, p=0.699; Begg's test, p=0.175). These findings strongly reveal the positive link between DM and the increased risk of ECC.

Kou W.Z.,Xinxiang Medical University
African journal of traditional, complementary, and alternative medicines : AJTCAM / African Networks on Ethnomedicines | Year: 2013

We investigated the anti-tumor effects of Verbena officinalis extract on H22 tumor-bearing mice and its effect on immune function. Mice model of H22 solid tumor was established, the mice were divided into five groups and administered the extract, later, tumors were removed and inhibition rates were calculated; spleens were removed and spleen indices were calculated, and the sheep red blood cell-delayed-type hypersensitivity (SRBC-DTH) and the serum hemolysin level were determined. The Verbena officinalis extract had anti-tumor effect, with the inhibition rate reaching 38.78%, it also increased the spleen index to a certain extent, in addition, the changes in DTA and HA were not obvious compared with the model group. The Verbena officinalis extract had in vivo anti-tumor effect, while causing no damage on the immune function.

We performed a genome-wide association study of esophageal squamous cell carcinoma (ESCC) by genotyping 1,077 individuals with ESCC and 1,733 control subjects of Chinese Han descent. We selected 18 promising SNPs for replication in an additional 7,673 cases of ESCC and 11,013 control subjects of Chinese Han descent and 303 cases of ESCC and 537 control subjects of Chinese Uygur-Kazakh descent. We identified two previously unknown susceptibility loci for ESCC: PLCE1 at 10q23 (P(Han combined for ESCC) = 7.46 x 10(-56), odds ratio (OR) = 1.43; P(Uygur-Kazakh for ESCC) = 5.70 x 10(-4), OR = 1.53) and C20orf54 at 20p13 (P(Han combined for ESCC) = 1.21 x 10(-11), OR = 0.86; P(Uygur-Kazakh for ESCC) = 7.88 x 10(-3), OR = 0.66). We also confirmed association in 2,766 cases of gastric cardia adenocarcinoma cases and the same 11,013 control subjects (PLCE1, P(Han for GCA) = 1.74 x 10(-39), OR = 1.55 and C20orf54, P(Han for GCA) = 3.02 x 10(-3), OR = 0.91). PLCE1 and C20orf54 have important biological implications for both ESCC and GCA. PLCE1 might regulate cell growth, differentiation, apoptosis and angiogenesis. C20orf54 is responsible for transporting riboflavin, and deficiency of riboflavin has been documented as a risk factor for ESCC and GCA.

Wang H.,Xinxiang Medical University | Ye J.,Louisiana State University
Reviews in Endocrine and Metabolic Disorders | Year: 2015

Inflammation regulates energy metabolism in both physiological and pathological conditions. Pro-inflammatory cytokines involves in energy regulation in several conditions, such as obesity, aging (calorie restriction), sports (exercise), and cancer (cachexia). Here, we introduce a view of integrative physiology to understand pro-inflammatory cytokines in the control of energy expenditure. In obesity, chronic inflammation is derived from energy surplus that induces adipose tissue expansion and adipose tissue hypoxia. In addition to the detrimental effect on insulin sensitivity, pro-inflammatory cytokines also stimulate energy expenditure and facilitate adipose tissue remodeling. In caloric restriction (CR), inflammatory status is decreased by low energy intake that results in less energy supply to immnue cells to favor energy saving under caloric restriction. During physical exercise, inflammatory status is elevated due to muscle production of pro-inflammatory cytokines, which promote fatty acid mobilization from adipose tissue to meet the muscle energy demand. In cancer cachexia, chronic inflammation is elevated by the immune response in the fight against cancer. The energy expenditure from chronic inflammation contributes to weight loss. Immune tolerant cancer cells gains more nutrients during the inflammation. In these conditions, inflammation coordinates energy distribution and energy demand between tissues. If the body lacks response to the pro-inflammatory cytokines (Inflammation Resistance), the energy metabolism will be impaired leading to an increased risk for obesity. In contrast, super-induction of the inflammation activity leads to weight loss and malnutrition in cancer cachexia. In summary, inflammation is a critical component in the maintenance of energy balance in the body. Literature is reviewed in above fields to support this view. © 2014, Springer Science+Business Media New York.

Mahmoud A.M.,University of Illinois at Chicago | Yang W.,University of Illinois at Chicago | Yang W.,Xinxiang Medical University | Bosland M.C.,University of Illinois at Chicago
Journal of Steroid Biochemistry and Molecular Biology | Year: 2014

Soy isoflavones are dietary components for which an association has been demonstrated with reduced risk of prostate cancer (PCa) in Asian populations. However, the exact mechanism by which these isoflavones may prevent the development or progression of PCa is not completely understood. There are a growing number of animal and in vitro studies that have attempted to elucidate these mechanisms. The predominant and most biologically active isoflavones in soy products, genistein, daidzein, equol, and glycetin, inhibit prostate carcinogenesis in some animal models. Cell-based studies show that soy isoflavones regulate genes that control cell cycle and apoptosis. In this review, we discuss the literature relevant to the molecular events that may account for the benefit of soy isoflavones in PCa prevention or treatment. These reports show that although soy isoflavone-induced growth arrest and apoptosis of PCa cells are plausible mechanisms, other chemo protective mechanisms are also worthy of consideration. These possible mechanisms include antioxidant defense, DNA repair, inhibition of angiogenesis and metastasis, potentiation of radio- and chemotherapeutic agents, and antagonism of estrogen- and androgen-mediated signaling pathways. Moreover, other cells in the cancer milieu, such as the fibroblastic stromal cells, endothelial cells, and immune cells, may be targeted by soy isoflavones, which may contribute to soy-mediated prostate cancer prevention. In this review, these mechanisms are discussed along with considerations about the doses and the preclinical models that have been used. © Published by Elsevier Ltd.

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