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Articles by Y. C Wang
Total Records ( 3 ) for Y. C Wang
  A Moran , D Gu , D Zhao , P Coxson , Y. C Wang , C. S Chen , J Liu , J Cheng , K Bibbins Domingo , Y. M Shen , J He and L. Goldman

Background— The relative effects of individual and combined risk factor trends on future cardiovascular disease in China have not been quantified in detail.

Methods and Results— Future risk factor trends in China were projected based on prior trends. Cardiovascular disease (coronary heart disease and stroke) in adults ages 35 to 84 years was projected from 2010 to 2030 using the Coronary Heart Disease Policy Model–China, a Markov computer simulation model. With risk factor levels held constant, projected annual cardiovascular events increased by >50% between 2010 and 2030 based on population aging and growth alone. Projected trends in blood pressure, total cholesterol, diabetes (increases), and active smoking (decline) would increase annual cardiovascular disease events by an additional 23%, an increase of approximately 21.3 million cardiovascular events and 7.7 million cardiovascular deaths over 2010 to 2030. Aggressively reducing active smoking in Chinese men to 20% prevalence in 2020 and 10% prevalence in 2030 or reducing mean systolic blood pressure by 3.8 mm Hg in men and women would counteract adverse trends in other risk factors by preventing cardiovascular events and 2.9 to 5.7 million total deaths over 2 decades.

Conclusions— Aging and population growth will increase cardiovascular disease by more than a half over the coming 20 years, and projected unfavorable trends in blood pressure, total cholesterol, diabetes, and body mass index may accelerate the epidemic. National policy aimed at controlling blood pressure, smoking, and other risk factors would counteract the expected future cardiovascular disease epidemic in China.

  X. B Wang , L. Y Wu , Y. C Wang and N. Y. Deng

Palmitoylation is an important hydrophobic protein modification activity that participates many cellular processes, including signaling, neuronal transmission, membrane trafficking and so on. So it is an important problem to identify palmitoylated proteins and the corresponding sites. Comparing with the expensive and time-consuming biochemical experiments, the computational methods have attracted much attention due to their good performances in predicting palmitoylation sites. In this paper, we develop a novel automated computational method to perform this work. For a sequence segment in a given protein, the encoding scheme based on the composition of k-spaced amino acid pairs (CKSAAP) is introduced, and then the support vector machine is used as the predictor. The proposed prediction model CKSAAP-Palm outperforms the existing method CSS-Palm2.0 on both cross-validation experiments and some independent testing data sets. These results imply that our CKSAAP-Palm is able to predict more potential palmitoylation sites and increases research productivity in palmitoylation sites discovery. The corresponding software can be freely downloaded from

  Y. C Wang , X. B Hu , F He , F Feng , L Wang , W Li , P Zhang , D Li , Z. S Jia , Y. M Liang and H. Han

Dendritic cells (DCs) are professional antigen presenting cells to initiate immune response against pathogens, but mechanisms controlling the maturation of DCs are unclear. Here we report that, in the absence of recombination signal binding protein-J (RBP-J, the transcription factor mediating Notch signaling), lipopolysaccharide-stimulated monocyte-derived DCs are arrested at a developmental stage with few dendrites, low major histocompatibility complex II (MHC II) expression, and reduced motility and antigen presentation ability. RBP-J null DCs had lower expression of CXCR4. Transduction with a CXCR4-expressing lentivirus rescued developmental arrest of RBP-J-deficient DCs. Activation of Notch signaling in DCs up-regulated CXCR4 expression and increased the outgrowth of dendrites and the expression of MHC II. These effects were abrogated by a CXCR4 inhibitor. Therefore, Notch signaling is essential for DCs to transit from a dendritelowMHC IIlow immature state into a dendritehighMHC IIhigh mature state, during the lipopolysaccharide-induced DC maturation, most likely through the up-regulation of CXCR4.

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