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Articles by W Huang
Total Records ( 12 ) for W Huang
  N. S Balakathiresan , S Bhattacharyya , U Gutti , R. P Long , C Jozwik , W Huang , M Srivastava , H. B Pollard and R. Biswas
 

Cystic fibrosis (CF) is due to mutations in the CFTR gene and is characterized by hypersecretion of the proinflammatory chemokine IL-8 into the airway lumen. Consequently, this induces the highly inflammatory cellular phenotype typical of CF. Our initial studies revealed that IL-8 mRNA is relatively stable in CF cells compared with those that had been repaired with [WT]CFTR (wild-type CFTR). Relevantly, the 3'-UTR of IL-8 mRNA contains AU-rich sequences (AREs) that have been shown to mediate posttranscriptional regulation of proinflammatory genes upon binding to ARE-binding proteins including Tristetraprolin (TTP). We therefore hypothesized that very low endogenous levels of TTP in CF cells might be responsible for the relative stability of IL-8 mRNA. As predicted, increased expression of TTP in CF cells resulted in reduced stability of IL-8 mRNA. An in vitro analysis of IL-8 mRNA stability in CF cells also revealed a TTP-induced enhancement of deadenylation causing reduction of IL-8 mRNA stability. We conclude that enhanced stability of IL-8 mRNA in TTP-deficient CF lung epithelial cells serve to drive the proinflammatory cellular phenotype in the CF lung.

  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.

  S Zhang , J Lu , X Zhao , W Wu , H Wang , Q Wu , X Chen , W Fan , H Chen , F Wang , Z Hu , L Jin , Q Wei , H Shen , W Huang and D. Lu
 

Checkpoint kinase (CHEK) 2, a tumor suppressor gene, plays an essential role in the DNA damage checkpoint response cascade. We first investigated two polymorphisms in the proximal promoter of the CHEK2 gene and evaluated their associations with the risk of lung cancer in a case–control study using 500 incident lung cancer cases and 517 cancer-free controls. We found that CHEK2 rs2236141 –48 G > A was significantly associated with lung cancer risk (P = 0.0018). Similar results were obtained in a follow-up replication study in 575 lung cancer patients and 589 controls (P = 0.042). Quantitative polymerase chain reaction showed that individuals with the G allele had lower levels of CHEK2 transcripts in peripheral blood mononuclear cells and normal lung tissues. The –48 G->A variant eliminated a methylation site and thereby relieve the transcriptional repression of CHEK2. Therefore, this polymorphism affected downstream transcription through genetic and epigenetic modifications. Luciferase reporter assays demonstrated that the major G allele significantly attenuated reporter gene expression when methylated. Electrophoretic Mobility shift assays and surface plasmon resonance revealed that the methylated G allele increased transcription factor accessibility. We used in vivo chromatin immunoprecipitation to confirm that the relevant transcription factor was Sp1. Using lung tissue heterozygous for the G/A single-nucleotide polymorphism, we found that Sp1 acted as a repressor and had a stronger binding affinity for the G allele. These results support our hypothesis that the CHEK2 rs2236141 variant modifies lung cancer susceptibility in the Chinese population by affecting CHEK2 expression.

  P Wiesner , S. H Choi , F Almazan , C Benner , W Huang , C. J Diehl , A Gonen , S Butler , J. L Witztum , C. K Glass and Y. I. Miller
 

Rationale: Oxidized low-density lipoprotein (LDL) is an important determinant of inflammation in atherosclerotic lesions. It has also been documented that certain chronic infectious diseases, such as periodontitis and chlamydial infection, exacerbate clinical manifestations of atherosclerosis. In addition, low-level but persistent metabolic endotoxemia is often found in diabetic and obese subjects and is induced in mice fed a high-fat diet.

Objective: In this study, we examined cooperative macrophage activation by low levels of bacterial lipopolysaccharide (LPS) and by minimally oxidized LDL (mmLDL), as a model for subclinical endotoxemia-complicated atherosclerosis.

Methods and Results: We found that both in vitro and in vivo, mmLDL and LPS (Kdo2-LipidA) cooperatively activated macrophages to express proinflammatory cytokines Cxcl2 (MIP-2), Ccl3 (MIP-1), and Ccl4 (MIP-1β). Importantly, the mmLDL and LPS cooperative effects were evident at a threshold LPS concentration (1 ng/mL) at which LPS alone induced only a limited macrophage response. Analyzing microarray data with a de novo motif discovery algorithm, we found that genes transcribed by promoters containing an activator protein (AP)-1 binding site were significantly upregulated by costimulation with mmLDL and LPS. In a nuclear factor–DNA binding assay, the cooperative effect of mmLDL and LPS costimulation on c-Jun and c-Fos DNA binding, but not on p65 or p50, was dependent on mmLDL-induced activation of extracellular signal-regulated kinase (ERK) 1/2. In addition, mmLDL induced c-Jun N-terminal kinase (JNK)-dependent derepression of AP-1 by removing nuclear receptor corepressor (NCoR) from the chemokine promoters.

Conclusions: The cooperative engagement of AP-1 and nuclear factor (NF)-B by mmLDL and LPS may constitute a mechanism of increased transcription of inflammatory cytokines within atherosclerotic lesions.

  C Lee , Q Teng , W Huang , R Zhong and Z. H. Ye
 

Xylan is the second most abundant polysaccharide in dicot wood. Unraveling the biosynthetic pathway of xylan is important not only for our understanding of the process of wood formation but also for our rational engineering of wood for biofuel production. Although several glycosyltransferases are implicated in glucuronoxylan (GX) biosynthesis in Arabidopsis, whether their close orthologs in woody tree species are essential for GX biosynthesis during wood formation has not been investigated. In fact, no studies have been reported to evaluate the effects of alterations in secondary wall-associated glycosyltransferases on wood formation in tree species. In this report, we demonstrate that PoGT47C, a poplar glycosyltransferase belonging to family GT47, is essential for the normal biosynthesis of GX and the normal secondary wall thickening in the wood of the hybrid poplar Populus alba x tremula. RNA interference (RNAi) inhibition of PoGT47C resulted in a drastic reduction in the thickness of secondary walls, a deformation of vessels and a decreased amount of GX in poplar wood. Structural analysis of GX using nuclear magnetic resonance (NMR) spectroscopy demonstrated that the reducing end of GX from poplar wood contains the tetrasaccharide sequence, β-d-Xylp-(1->3)--l-Rhap-(1->2)--d-GalpA-(1->4)-d-Xylp, and that its abundance was significantly decreased in the GX from the wood of the GT47C-RNAi lines. The transgenic wood was found to yield more glucose by cellulase digestion than the wild-type wood, indicating that the GX reduction in wood reduces the recalcitrance of wood to cellulase digestion. Together, these results provide direct evidence demonstrating that the PoGT47C glycosyltransferase is essential for normal GX biosynthesis in poplar wood and that GX modification could improve the digestibility of wood cellulose by cellulase.

  W Huang , Q Liu , S. G Rhee and L. Zhang
 

The empirical evidence on the cross-sectional relation between idiosyncratic risk and expected stock returns is mixed. We demonstrate that the omission of the previous month's stock returns can lead to a negatively biased estimate of the relation. The magnitude of the omitted variable bias depends on the approach to estimating the conditional idiosyncratic volatility. Although a negative relation exists when the estimate is based on daily returns, it disappears after return reversals are controlled for. Return reversals can explain both the negative relation between value-weighted portfolio returns and idiosyncratic volatility and the insignificant relation between equal-weighted portfolio returns and idiosyncratic volatility. In contrast, there is a significantly positive relation between the conditional idiosyncratic volatility estimated from monthly data and expected returns. This relation remains robust after controlling for return reversals.

 
 
 
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