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Dongguan, China

Zhang Y.,U.S. Center for Disease Control and Prevention | Zhang Y.,Huazhong University of Science and Technology | Tong Y.,U.S. Center for Disease Control and Prevention | Zhang Y.,BGI Shenzhen | And 12 more authors.
Molecular Neurobiology | Year: 2014

Genome-wide association studies (GWAS) of ischemic stroke (IS) have been performed on several cohorts of Caucasian or African population and Japanese, resulting in somewhat inconsistent conclusion. We aimed to identify susceptibility loci for IS by exome sequencing in a Chinese Han population. Exome sequencing was used to screen susceptibility loci among 100 cases and 100 matched controls. Significant SNPs from the first stage were verified in up to 3,554 participants from three hospital-based case-control studies. In the initial exome sequencing analysis, rs10489177 in c1orf156 gene located on chromosome 1q24 (p<1×10-8) and rs17118 in XYLB gene located on chromosome 3p21 (p<1×10-6) were found to be significantly associated with IS. In the following validation stage, significantly increased odds ratios were observed in individuals with rs10489177 GG (OR=2.02, 95 % CI=1.35-3.03) or rs17118 AA genotype (OR=1.50, 95 % CI=1.17-1.91). The rs10489177 GG genotype was associated with significantly increased risk for IS in individuals without hypertension (OR=2.78, 95 % CI=1.59-4.86) and in individuals without diabetes (OR=1.93, 95 % CI=1.27-2.94). In contrast, the rs17118 AA genotype may significantly increase the risk for IS, particularly for individuals with hypertension (OR=1.73, 95 % CI=1.08-2.78) and for individuals without diabetes (OR=1.52, 95 % CI=1.17-1.98) or non-smoker (OR=1.59, 95 % CI=1.16-2.19). Collectively, our study identified two novel loci (rs17118 and rs10489177) which were associated with an increased risk for IS in Chinese Han populations. Further studies are needed to confirm these associations in other populations and elucidate the biological mechanisms underlying the observed associations. © 2013 Springer Science+Business Media. Source

Wu L.,Southern Medical University | Wu L.,Songshan Lake Pearl Laboratory Animal Science &Tech. Co. | Wu L.,Guangzhou University | Liu W.,University of Tennessee Health Science Center | And 3 more authors.
Experimental Animals | Year: 2014

Obesity is a public health problem that increases the risk of metabolic disease, infertility, and other chronic health problems. The present study aimed to develop a new rat model for sex hormone disorder with overweight and Ca loss by intramuscular injection of exogenous leptin (LEP). Thirty female Sprague-Dawley (SD) rats (40 days old) were injected thrice intramuscularly with LEP or keyhole limpet hemocyanin immunogen. The following analyses were performed to determine the development of appetite, overweight, reproductive related-hormones, and calcium (Ca)/phosphorus (Pi) in SD rats: measurement of Lee’s index, body weight, food intake; serum Ca, Pi, and hormone tests by enzyme-linked immunosorbent analysis; histological analysis of abdominal fat; real-time polymerase chain reaction analysis of neuropeptide Y, pro-opiomelanocortin, gonadotropin-releasing hormone (Gnrh) mRNA, and gonadotropin-releasing hormone receptor (Gnrhr) mRNA expression; and western blotting analysis of enzyme phosphatidylinositol-3-kinase (PI3K). Rats injected with LEP immunogen displayed signifcantly increased body weight, food intake, Lee’s index, serum LEP, serum cortisol, fat deposition in the abdomen, and decreased hormones including follicle stimulating hormone, luteinizing hormone, estradiol, cholecystokinin, and Ca. Exogenous LEP administered intramuscularly also downregulate Gnrh and PI3K. In conclusion, exogenous LEP administered intramuscularly is a novel animal model for sex hormones disorder with overweight and Ca loss in SD rats. The downregulation of PI3K and Gnrh may be involved in the development of this animal model. ©2014 Japanese association for Laboratory animal Science. Source

Zeng C.,Sun Yat Sen University | Zeng C.,Guang Dong Medical College | Ke Z.-F.,Sun Yat Sen University | Yang Z.,Sun Yat Sen University | And 4 more authors.
Medical Oncology | Year: 2012

Previous studies have demonstrated that the expression of prostate-specific membrane antigen (PSMA) is restricted to endothelium from tumor-associated neovasculature. But the expression of PSMA in osteosarcoma and its clinical significance are unknown. Using immunohistochemical analysis and quantum dot probes, we found that 46.7% (21/45) of the osteosarcoma showed positive staining for PSMA while no PSMA staining in osteofibrous dysplasia. The expression and localization of PSMA was confirmed by CD34 staining. More importantly, the expression of PSMA is correlated with tumor size, pulmonary metastasis and worse survival (survival rate 63.2% in the PSMA-negative group versus 36.6% in the PSMApositive group). Thus, PSMA could be used as an independent prognostic marker for the osteosarcoma patients, and PSMA staining in tumor-associated neovasculature may be a potential target for antineovasculature-based therapy in osteosarcoma. Copyright © Springer Science+Business Media, LLC 2011. Source

Song Y.,China Pharmaceutical University | Yang Z.,Sun Yat Sen University | Ke Z.,Sun Yat Sen University | Yao Y.,Guang Dong Medical College | And 5 more authors.
Cancer Epidemiology | Year: 2012

Aim: Protein 14-3-3γ is an important member of the 14-3-3 family that play important roles in the regulation of various cellular processes. The aim of the study is to investigate the association between 14-3-3γ expression and the clinicopathological features of patients with breast cancer. Methods: The expression of 14-3-3γ was detected by Western blot in both foci of breast cancer and adjacent non-cancerous tissues. In addition, 14-3-3γ expression was analyzed by immunohistochemistry in 60 clinicopathologically characterized breast cancer cases. The association of 14-3-3γ expression with survival of the patients were analyzed. Results: The expression level of 14-3-3γ protein in breast cancer were significantly higher than that in non-cancerous mammary gland tissues. Moreover, high expression of 14-3-3γ correlated with tumor size and tumor grade (all P< 0.05). Patients with high 14-3-3γ expression had worse overall survival rate than that with low expression (P<0.05). Furthermore, multivariate analysis showed that 14-3-3γ expression was an independent predictor of overall survival (HR, 0.196; 95%CI, 0.043-0.892; P=0.035). Conclusions: Our data suggest for the first time that the increased expression of 14-3-3γ in breast cancer is associated significantly with tumor progression and poor prognosis. 14-3-3γ may be a novel and potential prognostic marker for breast cancer. © 2012 Elsevier Ltd. Source

Ke Z.-F.,Sun Yat Sen University | Mao X.,Sun Yat Sen University | Zeng C.,Guang Dong Medical College | He S.,Sun Yat Sen University | And 2 more authors.
Medical Oncology | Year: 2013

Expression of astrocyte-elevated gene-1 (AEG-1), a novel oncoprotein, has been shown to promote cell growth and inhibit apoptosis, but the underlying molecular mechanisms and its functional significance in non-small cell lung cancer (NSCLC) remain to be elucidated. In the present study, statistical analysis displayed a significant correlation of AEG-1 expression with clinical staging (P = 0.048), differentiation (P = 0.019) and lymph node metastasis (P = 0.032). Simultaneously, the overall survival time in patients with higher AEG-1 expression was obviously shorter than that in patients with lower expression of AEG-1 (P < 0.001). Furthermore, we found that AEG-1 could inhibit apoptotic cell death in L-78 cells, as assessed by MTT, TUNEL and flow cytometry assay. After treating L-78 cells with AEG-1 siRNA, caspase-3 protein was significantly up-regulated and Bcl-2 protein was markedly decreased in L-78 cells, which was verified by the immunohistochemistry results about AEG-1, caspase-3 and Bcl-2. Furthermore, PI3K p110 protein and phosphorylated Akt were also largely attenuated by the treatment of AEG-1 siRNA. In conclusion, our results indicated that AEG-1 played a crucial role in the carcinogenesis of NSCLC and could inhibit apoptosis via activating cell survival signaling (enhancing the level of anti-apoptotic protein Bcl-2 and the activation of PI3K/Akt pathway). © 2013 Springer Science+Business Media New York. Source

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