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Articles by Y Zheng
Total Records ( 9 ) for Y Zheng
  S Huang , Y Zheng , P. J Foster , W Huang and M. He

Objective  To assess the prevalence and causes of visual impairment and blindness in adults living in an urban area of southern China.

Methods  Random cluster sampling was used to identify the adults 50 years and older living in the Liwan district of Guangzhou, China. Presenting visual acuity (PVA) with habitual correction and best-corrected visual acuity (BCVA) based on autorefraction and subjective refraction were measured using the Early Treatment Diabetic Retinopathy Study visual chart. Blindness and low vision were defined according to World Health Organization criteria. Eyes with visual impairment were assigned 1 principal cause for the impairment.

Results  Visual acuity measurements were available for 1399 adults 50 years and older (75.3% participation rate). The prevalence of blindness and low vision based on the PVA was 0.6% (95% confidence interval, 0.2%-1.0%) and 10.1% (95% confidence interval, 8.5%-11.7%), respectively. These rates were reduced to 0.5% and 3.1% when the BCVA was considered. Based on the PVA, the principal causes for blindness were cataract (39.6%), glaucoma (11.0%), and myopic maculopathy (6.6%). The majority of low vision cases were attributable to cataract (45.3%) and uncorrected refractive error (43.9%).

Conclusion  The majority of eye diseases leading to visual impairment are potentially treatable in this population.

  Y Zheng , J Zhu and A. Roy

A powerful technique for inference concerning spatial dependence in a random field is to use spectral methods based on frequency domain analysis. Here we develop a nonparametric Bayesian approach to statistical inference for the spectral density of a random field. We construct a multi-dimensional Bernstein polynomial prior for the spectral density and devise a Markov chain Monte Carlo algorithm to simulate from the posterior of the spectral density. The posterior sampling enables us to obtain a smoothed estimate of the spectral density as well as credible bands at desired levels. Simulation shows that our proposed method is more robust than a parametric approach. For illustration, we analyse a soil data example.

  A Beeghly Fadiel , W Lu , J. R Long , X. o Shu , Y Zheng , Q Cai , Y. T Gao and W. Zheng

Matrix metalloproteinase-2 (MMP-2) is a well-known mediator of cancer metastasis but is also thought to be involved in several aspects of cancer development, including cell growth and inflammation. We comprehensively characterized genetic variation across the MMP-2 gene and evaluated associations with breast cancer risk using a two-phase (phase 1 and phase 2) study design. A total of 39 polymorphisms were genotyped among 6,066 Chinese women participating in the Shanghai Breast Cancer Study, a population-based case-control study. Two MMP-2 promoter polymorphisms were found to have consistent results between phase 1 and phase 2 participants, and to be significantly associated with breast cancer risk among all genotyped participants. Minor allele homozygotes for rs11644561 (G/A) were found to have a decreased risk of breast cancer [odds ratio (OR), 0.6; 95% confidence interval (CI), 0.3-1.0] compared with major allele homozygotes, as were minor allele homozygotes for rs11643630 (T/G) compared with major allele homozygotes (OR, 0.8; 95% CI, 0.7-1.0). When analyzed together, a rare haplotype (4.4%) with both rs11644561 A and rs11643630 G was found to have a significantly reduced risk of breast cancer (OR, 0.6; 95% CI, 0.4-0.8). In addition, rare allele homozygotes for rs243865 (–1306 C/T) tended to have an increased risk of breast cancer (OR, 1.4; 95% CI, 0.9-2.4). Together, these findings support a role for MMP-2 genetic variation in breast cancer susceptibility. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1770–6)

  Y Zheng , S Vertuani , S Nystrom , S Audebert , I Meijer , T Tegnebratt , J. P Borg , P Uhlen , A Majumdar and L. Holmgren

Rationale: We have previously shown that angiomotin (Amot) is essential for endothelial cell migration during mouse embryogenesis. However, 5% of Amot knockout mice survived without any detectable vascular defects. Angiomotin-like protein 1 (AmotL1) potentially compensates for the absence of Amot as it is 62% homologous to Amot and exhibits similar expression pattern in endothelial cells.

Objective: Here, we report the identification of a novel isoform of AmotL1 that controls endothelial cell polarization and directional migration.

Methods and Results: Small interfering RNA–mediated silencing of AmotL1 in mouse aortic endothelial cells caused a significant reduction in migration. In confluent mouse pancreatic islet endothelial cells (MS-1), AmotL1 colocalized with Amot to tight junctions. Small interfering RNA knockdown of both Amot and AmotL1 in MS-1 cells exhibited an additive effect on increasing paracellular permeability compared to that of knocking down either Amot or AmotL1, indicating both proteins were required for proper tight junction activity. Moreover, as visualized using high-resolution 2-photon microscopy, the morpholino-mediated knockdown of amotl1 during zebrafish embryogenesis resulted in vascular migratory defect of intersegmental vessels with strikingly decreased junction stability between the stalk cells and the aorta. However, the phenotype was quite distinct from that of amot knockdown which affected polarization of the tip cells of intersegmental vessels. Double knockdown resulted in an additive phenotype of depolarized tip cells with no or decreased connection of the stalk cells to the dorsal aorta.

Conclusions: These results cumulatively validate that Amot and AmotL1 have similar effects on endothelial migration and tight junction formation in vitro. However, in vivo Amot appears to control the polarity of vascular tip cells whereas AmotL1 mainly affects the stability of cell–cell junctions of the stalk cells.

  W Zheng , W Wen , Y. T Gao , Y Shyr , Y Zheng , J Long , G Li , C Li , K Gu , Q Cai , X. O Shu and W. Lu

Most of the genetic variants identified from genome-wide association studies of breast cancer have not been validated in Asian women. No risk assessment model that incorporates both genetic and clinical predictors is currently available to predict breast cancer risk in this population.


We analyzed 12 single-nucleotide polymorphisms (SNPs) identified in recent genome-wide association studies mostly of women of European ancestry as being associated with the risk of breast cancer in 3039 case patients and 3082 control subjects who participated in the Shanghai Breast Cancer Study. All participants were interviewed in person to obtain information regarding known and suspected risk factors for breast cancer. The c statistic, a measure of discrimination ability with a value ranging from 0.5 (random classification) to 1.0 (perfect classification), was estimated to evaluate the contribution of genetic and established clinical predictors of breast cancer to a newly established risk assessment model for Chinese women. Clinical predictors included in the model were age at menarche, age at first live birth, waist-to-hip ratio, family history of breast cancer, and a previous diagnosis of benign breast disease. The utility of the models in risk stratification was evaluated by estimating the proportion of breast cancer patients in the general population that could be accounted for above a given risk threshold as predicted by the models. All statistical tests were two-sided.


Eight SNPs (rs2046210, rs1219648, rs3817198, rs8051542, rs3803662, rs889312, rs10941679, and rs13281615), each of which reflected a genetically independent locus, were found to be associated with the risk of breast cancer. A dose–response association was observed between the risk of breast cancer and the genetic risk score, which is an aggregate measure of the effect of these eight SNPs (odds ratio for women in the highest quintile of genetic risk score vs those in the lowest = 1.85, 95% confidence interval = 1.58 to 2.18, Ptrend = 2.5 x 10–15). The genetic risk score, the waist-to-hip ratio, and a previous diagnosis of benign breast disease were the top three predictors of the risk of breast cancer, each contributing statistically significantly (P < .001) to the full risk assessment model. The model, with a c statistic of 0.6295 after adjustment for overfitting, showed promise for stratifying women into different risk groups; women in the top 30% risk group accounted for nearly 50% of the breast cancers diagnosed in the general population.


A risk assessment model that includes both genetic markers and clinical predictors may be useful to classify Asian women into relevant risk groups for cost-efficient screening and other prevention programs.

  Y Zheng , X. W He , Y. H Ying , J. F Lu , S. B Gelvin and H. X. Shou

We expressed the Arabidopsis thaliana histone AtHTA1 in rice under the control of the maize ubiquitin promoter. Transformation efficiencies of rice plants that constitutively expressed AtHTA1 were 28–44% higher than calli containing an empty vector control. Furthermore, co-infection of rice calli with a vector containing AtHTA1 and another vector with the target gene increased transformation by 27–50%. Thus, expression of AtHTA1 either transiently or in stably transformed cells improved rice transformation efficiency.

  W Yuan , J Xie , C Long , H Erdjument Bromage , X Ding , Y Zheng , P Tempst , S Chen , B Zhu and D. Reinberg

The presence of histone H3 lysine 36 methylation (H3K36me) correlates with actively transcribed genes. In yeast, histone H3K36me mediated by KMT3 (also known as Set2) recruits a histone deacetylase complex, Rpd3s, to ensure the fidelity of transcription initiation. We report the purification of human KMT3a (also known as HYPB or hSet2) complex and the identification of a novel, higher eukaryotic specific subunit, heterogeneous nuclear ribonucleoprotein L (HnRNP-L). Interestingly, although KMT3a has intrinsic activity in vitro, HnRNP-L is essential in vivo. Moreover, KMT3a generates mono-, di-, and trimethylated products in vitro, but RNA interference against KMT3a or HnRNP-L down-regulates exclusively the H3K36me3 mark in vivo.

  G Pickert , C Neufert , M Leppkes , Y Zheng , N Wittkopf , M Warntjen , H. A Lehr , S Hirth , B Weigmann , S Wirtz , W Ouyang , M. F Neurath and C. Becker

Signal transducer and activator of transcription (STAT) 3 is a pleiotropic transcription factor with important functions in cytokine signaling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. We demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IECs). Studies in genetically engineered mice showed that epithelial STAT3 activation in dextran sodium sulfate colitis is dependent on interleukin (IL)-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC-specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis, and pathways associated with wound healing in IECs. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22–dependent mucosal wound healing.

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