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Hu Y.-R.,Central South University | Zhao Y.,Central South University | Sun Y.-W.,Central South University | Lu W.-D.,Tumor Hospital of Shaanxi Province | And 6 more authors.
Cardiovascular Pathology | Year: 2010

Background: Nanobacterium contributes to pathological calcification in human renal stones and psammoma bodies in ovarian cancer. Pathological calcification is also present in cardiac valves with rheumatic heart disease. The aim of this study was to detect, isolate, culture, and characterize nanobacteria-like material from human calcified cardiac valves with rheumatic heart disease. Methods: Normal and calcified cardiac valve groups, as well as positive (nanobacteria strain Se90) and negative (serum radiated with 30 kGy of γ-ray) control groups, were included in this study. Part of each valve was immunostained with nanobacterial antibody 8D10, and the remaining parts were homogenized, filtered, and maintained in culture. The cultures were checked with a microscope weekly. Culture medium at different time points was analyzed with a spectrophotometer. The cultures maintained for 3 weeks were further examined with immunofluorescence double staining and transmission electron microscopy. Results: While 26 of 29 calcified valves stained positive for 8D10 antibody, all normal valves stained negative. Mobile tiny particles were observed under a microscope in the calcified valve group and the Se90 group. Optical densities were significantly different among groups (P<.001). Immunofluorescence double staining displayed tiny green fluorescence particles in the calcified valve group, in the Se90 group, and in two samples of the normal valve group. Transmission electron microscopy analysis indicated that cultured particles from calcified valves ranging in size from 88 to 341 nm had an obvious cell membrane structure similar to that of Se90. Conclusions: The nanobacteria-like material has been isolated and cultured from calcified cardiac valves with rheumatic heart disease, and its characteristics are similar to those of Se90. © 2010 Elsevier Inc. All rights reserved. Source


Deng Z.,Xian Jiaotong University | Shi X.,Minzu University of China | Shi X.,National Engineering Research Center for Miniaturized Detection Systems | Liu Q.,Tumor Hospital of Shaanxi Province | And 6 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016

Background: As one important cancer in world, breast cancer is a hot topic for researchers. A large number of genome-wide association studies of persons with breast cancer have widely studied the association between rs3803662 and breast cancer risk. However, the results remain inconclusive. So, we want to clarify the association between them through a classical statistics method: a meta-analysis. Methods and results: We mined the literature for publications on the TNRC9 rs3803662 polymorphism and breast cancer risk. We then performed a meta-analysis on the genotype data. To assess the association, we estimated odds ratios (ORs) with 95% confidence intervals (CIs). We performed sensitivity analysis, heterogeneity tests, cumulative meta-analysis, and bias assessment. Our meta-analysis confirmed that TNRC9 rs3803662 polymorphisms increased breast cancer risk using thirteen casecontrol studies. These data are consistent for all genetic models: the allele model, the dominant model, the recessive model, and the additive model. The results of subgroup analysis suggest that the association in Caucasians appeared more significant than in Asians. Conclusions: Our study suggests that TNRC9 rs3803662 polymorphisms may be a risk-conferring factor for breast cancer. Further functional studies on the role of rs3803662 in breast cancer pathogenesis are warranted. © 2016, E-Century Publishing Corporation. All rights reserved. Source


Guo X.,PLA Fourth Military Medical University | Li D.,PLA Fourth Military Medical University | Wu Y.,PLA Fourth Military Medical University | Chen Y.,PLA Fourth Military Medical University | And 6 more authors.
Lung Cancer | Year: 2015

Introduction: Non-small cell lung cancer (NSCLC) is characterized by poor prognosis and only a few molecular markers may be potentially used to predict the outcome. Metabolic reprogramming is a hallmark of cancer, including the alterations of tricarboxylic acid (TCA) cycle key enzymes. However, the significance of single nucleotide polymorphisms (SNPs) in genes encoding these key enzymes has not been investigated in NSCLC. Patients and methods: In this study, we genotyped 18 potentially functional SNPs in 7 genes belonging to 3 TCA cycle enzyme families (SDH, FH and IDH) using Sequenom iPLEX genotyping system in a cohort of 500 NSCLC patients. Multivariate Cox proportional hazards model and Kaplan-Meier curve were used for the survival analysis. Results: Our results showed that SDHC gene: SNP rs12064957, IDH2 gene: SNP rs11540478 and FH gene: SNP rs1414493 were associated with overall survival (OS) and SDHA gene: SNP rs13173911, IDH2 gene: SNP rs4932158 were associated with recurrence-free survival (RFS) of NSCLC patients. Unfavorable genotypes of these SNPs showed a significant cumulative effect on OS and RFS of NSCLC patients (both P<. 0.001). Furthermore, survival tree analysis indicated that FH: rs1414493 was the primary risk factor contributing to OS of NSCLC patients and the IDH2: rs4932158 was the primary risk factor contributing to RFS of NSCLC patients. Conclusion: Our data suggest that SNPs in TCA cycle key enzyme genes may serve as potential biomarkers to predict the outcomes of NSCLC. Further studies with different ethnicities are needed to validate our findings and generalize their clinical utility. © 2014 Elsevier Ireland Ltd. Source


Wu C.,Peking Union Medical College | Wang Z.,U.S. National Institutes of Health | Wang Z.,SAIC | Song X.,Xinxiang Medical University | And 165 more authors.
Nature Genetics | Year: 2014

We conducted a joint (pooled) analysis of three genome-wide association studies (GWAS) of esophageal squamous cell carcinoma (ESCC) in individuals of Chinese ancestry (5,337 ESCC cases and 5,787 controls) with 9,654 ESCC cases and 10,058 controls for follow-up. In a logistic regression model adjusted for age, sex, study and two eigenvectors, two new loci achieved genome-wide significance, marked by rs7447927 at 5q31.2 (per-allele odds ratio (OR) = 0.85, 95% confidence interval (CI) = 0.82-0.88; P = 7.72 × 10-20) and rs1642764 at 17p13.1 (per-allele OR = 0.88, 95% CI = 0.85-0.91; P = 3.10 × 10-13). rs7447927 is a synonymous SNP in TMEM173, and rs1642764 is an intronic SNP in ATP1B2, near TP53. Furthermore, a locus in the HLA class II region at 6p21.32 (rs35597309) achieved genome-wide significance in the two populations at highest risk for ESSC (OR = 1.33, 95% CI = 1.22-1.46; P = 1.99 × 10-10). Our joint analysis identifies new ESCC susceptibility loci overall as well as a new locus unique to the population in the Taihang Mountain region at high risk of ESCC. © 2014 Nature America, Inc. All rights reserved. Source


Abnet C.C.,U.S. National Institutes of Health | Wang Z.,U.S. National Institutes of Health | Wang Z.,SAIC | Song X.,Xinxiang Medical University | And 173 more authors.
Human Molecular Genetics | Year: 2012

Genome-wide association studies have identified susceptibility loci for esophageal squamous cell carcinoma (ESCC). We conducted a meta-analysis of all single-nucleotide polymorphisms (SNPs) that showed nominally significant P-values in two previously published genome-wide scans that included a total of 2961 ESCC cases and 3400 controls. The meta-analysis revealed five SNPs at 2q33 with P< 5 × 10 -8, and the strongest signal was rs13016963, with a combined odds ratio (95% confidence interval) of 1.29 (1.19-1.40) and P= 7.63 × 10 -10. An imputation analysis of 4304 SNPs at 2q33 suggested a single association signal, and the strongest imputed SNP associations were similar to those from the genotyped SNPs. We conducted an ancestral recombination graph analysis with 53 SNPs to identify one or more haplotypes that harbor the variants directly responsible for the detected association signal. This showed that the five SNPs exist in a single haplotype along with 45 imputed SNPs in strong linkage disequilibrium, and the strongest candidate was rs10201587, one of the genotyped SNPs. Our meta-analysis found genome-wide significant SNPs at 2q33 that map to the CASP8/ALS2CR12/TRAK2 gene region. Variants in CASP8 have been extensively studied across a spectrum of cancers with mixed results. The locus we identified appears to be distinct from the widely studied rs3834129 and rs1045485 SNPs in CASP8. Future studies of esophageal and other cancers should focus on comprehensive sequencing of this 2q33 locus and functional analysis of rs13016963 and rs10201587 and other strongly correlated variants. Published by Oxford University Press 2012. Source

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