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Articles by Q. Xu
Total Records ( 4 ) for Q. Xu
  X Luo , W. Y Tsai and Q. Xu
 

By embedding the missing covariate data into a left-truncated and right-censored survival model, we propose a new class of weighted estimating functions for the Cox regression model with missing covariates. The resulting estimators, called the pseudo-partial likelihood estimators, are shown to be consistent and asymptotically normal. A simulation study demonstrates that, compared with the popular inverse-probability weighted estimators, the new estimators perform better when the observation probability is small and improve efficiency of estimating the missing covariate effects. Application to a practical example is reported.

  A Zampetaki , L Zeng , A Margariti , Q Xiao , H Li , Z Zhang , A. E Pepe , G Wang , O Habi , E deFalco , G Cockerill , J. C Mason , Y Hu and Q. Xu
 

Background— Histone deacetylase 3 (HDAC3) is known to play a crucial role in the differentiation of endothelial progenitors. The role of HDAC3 in mature endothelial cells, however, is not well understood. Here, we investigated the function of HDAC3 in preserving endothelial integrity in areas of disturbed blood flow, ie, bifurcation areas prone to atherosclerosis development.

Methods and Results— En face staining of aortas from apolipoprotein E-knockout mice revealed increased expression of HDAC3, specifically in these branching areas in vivo, whereas rapid upregulation of HDAC3 protein was observed in endothelial cells exposed to disturbed flow in vitro. Interestingly, phosphorylation of HDAC3 at serine/threonine was observed in these cells, suggesting that disturbed flow leads to posttranscriptional modification and stabilization of the HDAC3 protein. Coimmunoprecipitation experiments showed that HDAC3 and Akt form a complex. Using a series of constructs harboring deletions, we found residues 136 to 206 of HDAC3 to be crucial in this interaction. Enforced expression of HDAC3 resulted in increased phosphorylation of Akt and upregulation of its kinase activity. In line with these findings, knockdown of HDAC3 with lentiviral vectors (shHDAC3) led to a dramatic decrease in cell survival accompanied by apoptosis in endothelial cells. In aortic isografts of apolipoprotein E-knockout mice treated with shHDAC3, a robust atherosclerotic lesion was formed. Surprisingly, 3 of the 8 mice that received shHDAC3-infected grafts died within 2 days after the operation. Miller staining of the isografts revealed disruption of the basement membrane and rupture of the vessel.

Conclusions— Our findings demonstrated that HDAC3 serves as an essential prosurvival molecule with a critical role in maintaining the endothelial integrity via Akt activation and that severe atherosclerosis and vessel rupture in isografted vessels of apolipoprotein E-knockout mice occur when HDAC3 is knocked down.

  A. E Pepe , Q Xiao , A Zampetaki , Z Zhang , A Kobayashi , Y Hu and Q. Xu
 

Rationale: Nuclear factor erythroid 2-related factor (Nrf)3, a member of the cap ‘N’ collar family of transcription factors that bind to the DNA-antioxidant responsive elements, is involved in reactive oxygen species balancing and in muscle precursor migration during early embryo development.

Objective: To investigate the functional role of Nrf3 in smooth muscle cell (SMC) differentiation in vitro and in vivo.

Methods and Results: Nrf3 was upregulated significantly following 1 to 8 days of SMC differentiation. Knockdown of Nrf3 resulted in downregulation of smooth muscle specific markers expression, whereas enforced expression of Nrf3 enhanced SMC differentiation in a dose-dependent manner. SMC-specific transcription factor myocardin, but not serum response factor, was significantly upregulated by Nrf3 overexpression. Strikingly, the binding of SRF and myocardin to the promoter of smooth muscle differentiation genes was dramatically increased by Nrf3 overexpression, and Nrf3 can directly bind to the promoters of SMC differentiation genes as demonstrated by chromatin immunoprecipitation assay. Moreover, NADPH-derived reactive oxygen species production during SMC differentiation was further enhanced by Nrf3 overexpression through upregulation of NADPH oxidase and inhibition of antioxidant signaling pathway. In addition, Nrf3 was involved in the endoplasmic reticulum stressor induced SMC differentiation.

Conclusion: Our findings demonstrate for the first time that Nrf3 has a crucial role in SMC differentiation from stem cells indicating that Nrf3 could be a potential target for manipulation of stem cell differentiation toward vascular lineage.

  X.S. Wu , W.B. Bao , J.T. Shu , Q. Xu , X.Y. Zhang , W. Han and G.H. Chen
  This study was designed to investigate the effect of Adenylosuccinate Lyase (ADSL) gene on Inosine Monophosphate content (IMP) in chicken. The chickens used for the study included exogenous Recessive White chicken and Chinese indigenous chicken breeds such as Silkies, Baier, Tibetan and Xiaoshan chickens. A pair of primer was designed to detect exon 2 of ADSL gene by PCR-SSCP and mutation detected was directly sequenced. A synonymous mutation at 3484 bp in exon 2 was substituted C/T SNP. In five chicken breeds, three genotypes TT, CT and CC were observed in exon 2. Muscle IMP content of individuals with TT genotype in exon 2 had significantly higher than those with CT and CC genotypes (p<0.05). In exon 2, Recessive White, Xiaoshan and Baier chickens were in Hardy-Weinberg equilibrium (p>0.05) and Silkies and Tibetan chickens were significant departure from Hardy-Weinberg equilibrium (p<0.01).
 
 
 
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