Fudan Taizhou Institute of Health science

Taizhou, China

Fudan Taizhou Institute of Health science

Taizhou, China
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Tang Y.,Fudan University | Tang Y.,Myopia Key Laboratory | Wang X.,Fudan University | Wang X.,Fudan Taizhou Institute of Health science | And 8 more authors.
Ophthalmology | Year: 2015

Purpose To study the current prevalence and causes of low vision and blindness in an adult Chinese population. Design Population-based, cross-sectional study. Participants We used a random cluster sampling method and evaluated 10 234 eligible subjects ≥45 years old (response rate, 78.1%) in the Taizhou Eye Study. Methods Examinations were performed from July 2012 through December 2013. Participants underwent a detailed examination, including uncorrected visual acuity, best-corrected visual acuity (BCVA), intraocular pressure, axial length, slit-lamp, and fundus examinations to evaluate the prevalence and primary causes of visual impairment (VI). Main Outcome Measures We defined low vision and blindness according to the World Health Organization (WHO) criteria (low vision: BCVA, <20/63-≥20/400; blindness: BCVA, <20/400 in the better eye) and United States criteria (low vision: BCVA, <20/40-≥20/200; blindness: BCVA, <20/200 in the better eye). Results Using the WHO BCVA criteria, the standardized prevalence of bilateral low vision and blindness were 5.1% and 1.0%, respectively. Using the United States BCVA criteria, the standardized prevalence were 12.8% and 1.5%, respectively. Using the WHO criteria, the primary causes of bilateral low vision and blindness were cataract (59.1% and 48.5%, respectively), myopic macular degeneration (17.6% and 17.2%, respectively), and age-related macular degeneration (11.6% and 10.1%, respectively). The primary causes of monocular low vision were cataract (55.6%), age-related macular degeneration (12.6%), and myopic macular degeneration (8.9%), whereas those of monocular blindness were cataract (46.8%), atrophy of eyeball or prosthetic eye (10.2%), and cornea opacity (7.3%). A further analysis revealed that in adults 45-59 years old, myopic macular degeneration (59.6% and 27.2%, respectively) and cataract (13.8% and 23.4%, respectively) were the leading causes of bilateral and monocular VI. In adults ≥60 years old, cataract (66.8% and 61.2%, respectively) and age-related macular degeneration (12.6% and 11.8%, respectively) were the primary causes of bilateral and monocular VI. Conclusions The prevalence of low vision and blindness in Chinese adults remains a severe public health problem. In the Taizhou Eye Study, cataract was the leading cause of low vision and blindness. Myopic macular degeneration and cataract were the primary causes of VI in adults 45-59 years and ≥60 years old, respectively. © 2015 American Academy of Ophthalmology.

Zhu J.,Fudan University | Zhu J.,Harbin Medical University | Wang M.,Fudan University | Zhu M.,Shanghai JiaoTong University | And 10 more authors.
Scientific Reports | Year: 2015

Single nucleotide polymorphisms (SNPs) in the PI3K/PTEN/AKT/mTOR signaling pathway may contribute to carcinogenesis. We genotyped five potentially functional PIK3R1 and mTOR SNPs in 1116 esophageal squamous cell cancer (ESCC) patients and 1117 cancer-free controls to assess their associations with ESCC risk. We observed no association with ESCC risk for any of the selected SNPs. However, the combined analysis of these SNPs revealed that subjects with one-to-three risk genotypes had an increased ESCC risk. Stratified analysis by body mass index (BMI) found that ESCC risk was significantly associated with each of three mTOR SNPs among subjects with BMI < 25.0. Specifically, we found that subjects carrying ≥ 1 risk genotypes had significantly increased ESCC risk, particularly for males, ever-smokers, ever-drinkers, and those with age > 60, or BMI < 25.0. Moreover, three mTOR haplotypes were associated with an increase in ESCC risk. Our meta-analysis of mTOR rs2295080 and cancer risk provided further evidence that mTOR SNPs might modulate cancer susceptibility. In this population, such risk effects might be modified by other risk factors, highlighting the importance of gene-environment interaction in esophageal carcinogenesis. Additional, larger studies are warranted to validate our findings.

PubMed | Fudan University, Karolinska Institutet, Taixing Peoples Hospital and Fudan Taizhou Institute of Health science
Type: Journal Article | Journal: PloS one | Year: 2015

Poor oral health has been linked with an increased risk of esophageal squamous cell carcinoma (ESCC). We investigated whether alteration of oral microbiota is associated with ESCC risk. Fasting saliva samples were collected from 87 incident and histopathologicallly diagnosed ESCC cases, 63 subjects with dysplasia and 85 healthy controls. All subjects were also interviewed with a questionnaire. V3-V4 region of 16S rRNA was amplified and sequenced by 454-pyrosequencing platform. Carriage of each genus was compared by means of multivariate-adjusted odds ratios derived from logistic regression model. Relative abundance was compared using Metastats method. Beta diversity was estimated using Unifrac and weighted Unifrac distances. Principal coordinate analysis (PCoA) was applied to ordinate dissimilarity matrices. Multinomial logistic regression was used to compare the coordinates between different groups. ESCC subjects had an overall decreased microbial diversity compared to control and dysplasia subjects (P<0.001). Decreased carriage of genera Lautropia, Bulleidia, Catonella, Corynebacterium, Moryella, Peptococcus and Cardiobacterium were found in ESCC subjects compared to non-ESCC subjects. Multinomial logistic regression analyses on PCoA coordinates also revealed that ESCC subjects had significantly different levels for several coordinates compared to non-ESCC subjects. In conclusion, we observed a correlation between altered salivary bacterial microbiota and ESCC risk. The results of our study on the saliva microbiome are of particular interest as it reflects the shift in microbial communities. Further studies are warranted to verify this finding, and if being verified, to explore the underlying mechanisms.

Lin R.,Hainan Medical College | Lin R.,Tongji University | Lei Y.,University of Texas at Austin | Yuan Z.,Fudan Taizhou Institute of Health science | And 2 more authors.
Annals of Human Genetics | Year: 2012

There are controversies in reports on the association of the angiotensinogen (AGT) gene polymorphisms with the risk of developing pre-eclampsia (PE). We performed a meta-analysis to examine the association between the AGT polymorphisms and PE risk: M235T (31 studies involving 2555 patients and 6114 controls) and T174M (six studies involving 681 patients and 2076 controls). For the M235T polymorphism, the TT genotype increased the PE risk as compared to the MM genotype (odds ratio 1.61, 95% confidence intervals 1.22-2.14, P= 0.001). When stratified by ethnicity, the TT genotype remained significantly associated with higher PE risk in Caucasians and Mongolians but not in Africans. Similar results were also obtained under all three genetic models of the M235T polymorphism. For the T174M polymorphism, no significant association was found in the comparisons (MT vs. TT and MM vs. TT) and under any genetic models. The analysis excluding the highly significant Hardy-Weinberg equilibrium-violating studies and sensitivity analysis further strengthened the validity of these associations. No publication bias was observed in this study. This meta-analysis demonstrates that the AGT M235T polymorphism is significantly associated with PE whereas the T174M polymorphism is not. © 2012 The Authors Annals of Human Genetics © 2012 Blackwell Publishing Ltd/University College London.

He J.,Fudan University | Wang M.-Y.,Fudan University | Qiu L.-X.,Fudan University | Zhu M.-L.,Fudan University | And 14 more authors.
Molecular Carcinogenesis | Year: 2013

Mammalian target of rapamycin complex 1 (mTORC1) plays an important role in maintaining proper cellular functions, and genetic variations in this complex may affect cancer risk. In this study, we examined the associations between eight potential functional single nucleotide polymorphisms in the mTORC1 genes (rs2536T>C and rs1883965G>A for mTOR, rs3160T>C, and rs26865A>G for mLST8, rs3751934C>A, rs1062935T>C, rs3751932T>C, and rs12602885G>A for Raptor, not included in published gastric cancer genome-wide association studies) and gastric cancer risk in 1125 gastric cancer cases and 1196 cancer-free controls. We performed conditional logistic regression and multifactor dimensionality reduction (MDR) analyses to assess their associations with gastric cancer risk. We also used false-positive report probabilities (FPRP) for assessing significant findings. We found that only the rs1883965A variant genotypes were associated with an increased risk of gastric cancer (AG vs. GG: adjusted odds ratio (OR)=1.26, 95% confidence interval (CI)=1.00-1.59; AA vs. GG: adjusted OR=1.85, 95% CI=0.67-5.16 and dominant model: adjusted OR=1.28, 95% CI=1.03-1.61). Patients with ≥1 risk genotypes of mTOR had significant increased risk (adjusted OR=1.25, 95% CI=1.04-1.49), compared with those having zero risk genotypes. In the stratified analysis, the risk effect of the rs1883965 AG/AA genotypes was evident in subgroups of ever-smokers, non-gastric cardia adenocarcinoma and clinical stage I+II, which were noteworthy findings as evaluated by FPRP. The MDR analysis identified smoking status and rs1883965 as the strongest two-factors for gastric cancer risk. These data support the hypothesis that functional polymorphisms of mTOR may contribute to gastric cancer risk. Clearly, our results require validation in larger studies with different ethnic populations. © 2013 Wiley Periodicals, Inc.

Qiu L.-X.,Fudan University | He J.,Guangzhou University | Cheng L.,Fudan University | Zhou F.,Fudan University | And 15 more authors.
Oncotarget | Year: 2015

Published data on the association between PRKAA1 rs13361707 T > C polymorphism and gastric cancer (GCa) susceptibility were inconclusive. To derive a more precise estimation of the association, we conducted a large-scale GCa study of 1,124 cases and 1,194 controls to confirm this association in an Eastern Chinese population. Our results showed that the C allele of PRKAA1 rs13361707 increased the GC risk in the study population [CT vs. TT, odds ratio (OR) = 1.72, 95% confidence interval (CI) = 1.40-2.12; CC vs. TT, OR = 2.15, 95%CI = 1.70-2.71; CT/CC vs. TT, OR = 1.86, 95%CI = 1.53-2.26; CC vs.TT/CT, OR = 1.49, 95%CI = 1.24-1.79]. In addition, the association of C allele with an increased GCa risk was still significant in subgroups, when stratified by age, sex, tumor site, drinking and smoking status. Moreover, the findings in the present study were validated by our further meta-analysis. In summary, these results indicated that the C allele of PRKAA1 rs13361707 was a low-penetrate risk factor for GCa.

Wei W.-J.,Fudan University | Wang Y.-L.,Fudan University | Li D.-S.,Fudan University | Wang Y.,Fudan University | And 14 more authors.
PLoS ONE | Year: 2013

Background: Rs2910164, a Single nucleotide polymorphism (SNP) located in the precursor microRNA sequence of miR-146a, is the only MicroRNA sequence SNP studied in papillary thyroid cancer (PTC). Association studies had been performed in US and UK-Northern European populations, but results were inconsistence. This study evaluated the association between rs2910164 and the risk of PTC as well as benign thyroid tumor (BN), and examined the clinicopathological characteristics of PTC and BN for different genotypes. Methods: This case-control study genotyped rs2910164 in 753 PTCs, 484 BNs and 760 controls in a Chinese Han population. Clinicopathological and genetic data were collected and compared. Multivariate logistic regression was performed to calculate adjusted odds ratios (ORs). Results: There were no differences in rs2910164 genotype distributions between the three groups. PTC cases with three genotypes (CC, CG, GG) had similar clinicopathological characteristics except the existence of "para-cancer" BN (PTC/BN, P = 0.006). PTC/BN patients were older (P = 0.009), and had smaller cancer lesions (P<0.001), lower serum thyrotropin levels (1.82±1.42 vs. 2.21±1.74, P = 0.04), and lower rates of level VI lymph node metastasis (20.8% vs. 52.7%, P<0.001) and lateral neck lymph node metastasis (11.5% vs. 23.0%, P = 0.011) compared with PTC only. Then we supposed a possible progression from BN to PTC which may involve rs2910164 in and performed a multivariate logistic regression analysis of PTC/BN and BN cases to determine risk factors of this progression. Results showed that the rs2910164 GG homozygote (OR = 2.25, 95% CI 1.22-4.14, P = 0.01) was the only risk factor in this study. Conclusion: Rs2910164 was not associated with increased risk of PTC and BN in Chinese patients, but may play a latent role in the transformation from BN to PTC. © 2013 Wei et al.

He J.,Fudan University | Xu Y.,Fudan University | Qiu L.-X.,Fudan University | Li J.,Fudan University | And 11 more authors.
PLoS ONE | Year: 2012

Background: Inherited functional single nucleotide polymorphisms (SNPs) in DNA repair genes may alter DNA repair capacity and thus contribute to cancer risk. Methods: Three ERCC1 functional SNPs (rs2298881C>A, rs3212986C>A and rs11615G>A) and two XPF/ERCC4 functional SNPs (rs2276466C>G and rs6498486A>C) were genotyped for 1125 gastric adenocarcinoma cases and 1196 cancer-free controls by Taqman assays. Odds ratios (OR) and 95% confidence intervals (CI) were used to estimate risk associations, and false-positive report probabilities (FPRP) were calculated for assessing significant findings. Results: ERCC1 rs2298881C and rs11615A variant genotypes were associated with increased gastric cancer risk (adjusted OR = 1.33, 95% CI = 1.05-1.67 for rs2298881 AC/CC and adjusted OR = 1.23, 95% CI = 1.05-1.46 for rs11615 AG/AA, compared with their common genotype AA and GG, respectively). Patients with 2-3 ERCC1 risk genotypes had significant increased risk (adjusted OR = 1.56, 95% CI = 1.27-1.93), compared with those with 0-1 ERCC1 risk genotypes, and this risk was more significantly in subgroups of never drinkers, non-gastric cardia adenocarcinoma (NGCA) and clinical stage I+II. All these risks were not observed for XPF SNPs. Conclusions: These findings suggest that functional ERCC1 SNPs may contribute to risk of gastric cancer. Larger and well-designed studies with different ethnic populations are needed to validate our findings. © 2012 He et al.

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