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Articles by C Wu
Total Records ( 9 ) for C Wu
  L Zhang , G. D Eslick , H. H. X Xia , C Wu , N Phung and N. J. Talley

Background: Helicobacter pylori (H. pylori) is a cause of chronic gastritis and maybe responsible for functional dyspepsia in a subset of patients. Many risk factors, such as alcohol consumption and smoking, may contribute to the colonization and infection of H. pylori in humans. However, studies on the relationship between H. pylori infection and drinking or smoking have produced conflicting results. Objective: The aim of this study was to examine whether consumption of alcohol or smoking is associated with active H. pylori infection in functional dyspepsia patients. Methods: H. pylori infection was confirmed by CLOtest and histology on at least two biopsies. Active chronic gastritis was diagnosed using the updated Sydney system. In addition to gender and age, information on drinking and smoking habits was collected using a standard questionnaire. Functional dyspepsia was diagnosed according to the Rome II diagnostic criteria. Results: H. pylori infection was positive in 27.3% of the 139 functional dyspepsia patients. Both age and gender were not significantly associated with H. pylori infection. A multiple logistic model found that alcohol consumption (OR = 9.05, 95% CI: 1.05–77.98) and pathology (active gastritis) (OR = 595.39, 95% CI: 81.43–4353.33) were associated with H. pylori infection. Active gastritis was associated with alcohol consumption (OR = 2.89, 95% CI: 1.03–8.02), smoking (OR = 2.72, 95% CI: 1.22–6.05) and age (OR = 1.03, 95% CI: 1.01–1.06). Conclusions: In patients with functional dyspepsia, there is no significant association between active H. pylori infection and smoking. However, alcohol consumption appears to be associated with H. pylori infection.

  C Wu , D. K VanderVeen , A Hellstrom , C Lofqvist and L. E. H. Smith

Objective  To validate longitudinal postnatal weight gain as a method for predicting severe retinopathy of prematurity (ROP) in a US cohort.

Methods  Both ROP evaluations and weekly weight measurements from birth to postmenstrual week 36 for 318 infants were entered into a computer-based surveillance system, WINROP. This system signaled an alarm when the rate of weight gain decreased compared with control subjects. Infants were classified into 3 groups: (1) no alarm, (2) low-risk alarm, or (3) high-risk alarm. Maximum ROP for each infant was categorized as (1) no ROP (immature or mature vascularization), (2) mild ROP (stage 1 or 2 ROP in zone II or III, without plus disease), or (3) severe ROP (any prethreshold, any stage 3, or threshold ROP). A high-risk alarm identified infants at risk for developing severe ROP.

Results  A high-risk alarm occurred in 81 infants (25.5%) and detected all infants who developed severe ROP a median of 9 weeks before diagnosis. The remaining infants received no alarm or a low-risk alarm. None of these infants developed more than mild ROP.

Conclusions  Longitudinal postnatal weight gain may help predict ROP. In a US cohort, the WINROP system had a sensitivity of 100% and identified infants early who developed severe ROP. With further validation, WINROP has the potential to safely reduce the number of ROP examinations.

  H Wang , W Zhang , C Zhu , C Bucher , B. R Blazar , C Zhang , J. F Chen , J Linden , C Wu and Y. Huo

Background— Atherosclerosis is a chronic inflammatory disease of the arterial vessel wall. The A2A receptor (A2AR) plays a central role in many antiinflammatory effects of adenosine. However, the role of A2AR in atherosclerosis is not clear.

Methods and Results— The knockout of A2AR in apolipoprotein E–deficient (Apoe–/–/A2AR–/–) mice led to an increase in body weight and levels of blood cholesterol and proinflammatory cytokines, as well as the inflammation status of atherosclerotic lesions. Unexpectedly, Apoe–/–/A2AR–/– mice developed smaller lesions, as did chimeric Apoe–/– mice lacking A2AR in bone marrow–derived cells (BMDCs). The lesions of those mice exhibited a low density of foam cells and the homing ability of A2AR-deficient monocytes did not change. Increased foam cell apoptosis was detected in atherosclerotic lesions of Apoe–/–/A2AR–/– mice. In the absence of A2AR, macrophages incubated with oxidized LDL or in vivo–formed foam cells also exhibited increased apoptosis. A2AR deficiency in foam cells resulted in an increase in p38 mitogen–activated protein kinase (MAPK) activity. Inhibition of p38 phosphorylation abrogated the increased apoptosis of A2AR-deficient foam cells.

Conclusion— Inactivation of A2AR, especially in BMDCs, inhibits the formation of atherosclerotic leisons, suggesting that A2AR inactivation may be useful for the treatment of atherosclerosis.

  C Wu , Z Hu , D Yu , L Huang , G Jin , J Liang , H Guo , W Tan , M Zhang , J Qian , D Lu , T Wu , D Lin and H. Shen

Recent three genome-wide association studies have mapped a lung cancer susceptibility locus to chromosome 15q25 in Caucasians. However, the reported risk single nucleotide polymorphisms (SNPs) are extremely rare in Asians, arguing against any of these being causative variants. This study sought to identify other variants on 15q25 associated with lung cancer susceptibility in Chinese. Two-stage case-control studies were conducted in subjects derived from both Northern and Southern China. The first-stage, consisting of 576 cases and 576 controls, was to discover novel risk variants using a haplotype-tagging SNP approach, and these variants were then replicated in the second-stage, consisting of 2,989 cases and 2,880 controls. Associations were estimated by logistic regression models, and function of the variants was examined by biochemical assays. We found that the three risk SNPs reported in Caucasians were not associated with lung cancer risk in Chinese. However, we identified four novel SNPs (rs2036534C>T, rs667282C>T, rs12910984G>A, and rs6495309T>C) that were associated with significantly increased lung cancer risk and smoking behavior, which were all confirmed in the replication analyses [odds ratios (95% confidence intervals) in the dominant model: 1.39 (1.23–1.57; P = 2.3 x 10–7), 1.52 (1.35–1.71; P = 2.0 x 10–12), 1.44 (1.28–1.63; P = 2.7 x 10–9), and 1.43 (1.27–1.61; P = 2.6 x 10–9), respectively]. We characterized the rs6495309T>C change in the CHRNA3 promoter as a functional variant because it affected the Oct-1 binding ability, resulting in increased CHRNA3 expression. These results support 15q25 as a susceptibility region for lung cancer in Chinese but underscore the difference in genetic markers among different ethnic populations. [Cancer Res 2009;69(12):5065–72]

  F Liu , C Wu and X. Lin

Droste [CRYPTO’96] proposed a construction of threshold visual cryptography scheme (TVCS) under the visual cryptography model of Naor and Shamir, i.e. the visual cryptography model with the underlying operation OR. In this article, we give three extensions of TVCS. First, we prove that the TVCS proposed by Droste which was based on the OR operation is still a valid TVCS under the XOR operation, and then we propose a method to further reduce its pixel expansion. We then propose an interesting construction of TVCS with all shares being concolorous. Finally, we give a construction of threshold extended visual cryptography scheme (TEVCS) with the underlying operation OR or XOR. All of our schemes can be applied to the visual cryptography model introduced by Tuyls et al. (First Int. Conf. Security in Pervasive Computing 2004, International Patent with Application No.: PCT/IB2003/000261).

  Y Liu , Y Wang , C Wu and P. Zheng

The majority of the Lafora's disease (LD) is caused by defect in the EPM2A gene, including missense and nonsense mutations and deletions. These defects mainly occur in the carbohydrate-binding domain, and how these mutations cause neuronal defects is under active investigation. Here, we report that the mutant proteins encoded by all missense mutations and most deletions tested are unstable, insoluble and ubiquitinated, and are accumulated in aggresome-like structures. The effect of apparent ‘gain-of-function’ mutations can be corrected by co-transfection of wild-type EPM2A cDNA, which is consistent with the recessive nature of these mutations in LD patients. In a neuronal cell line, these mutant aggregates exacerbate endoplasm reticulum (ER) stress and make the cells susceptible to the apoptosis induced by ER stressor, thapsigargin. The chemical chaperon, 4-phenylbutyrate, increased the mutant solubility, reduced the ER stress and dulled the sensitivity of mutant neuronal cells to apoptosis induced by thapsigargin and the mutant laforin proteins. The increased sensitivity to ER stress-induced apoptosis may contribute to LD pathogenesis.

  C Wang , D. C Popescu , C Wu , J Zhu , W Macklin and Y. Wang

We describe a novel fluorescent dye, 3-(4-aminophenyl)-2H-chromen-2-one (termed case myelin compound or CMC), that can be used for in situ fluorescent imaging of myelin in the vertebrate nervous system. When administered via intravenous injection into the tail vein, CMC selectively stained large bundles of myelinated fibers in both the central nervous system (CNS) and the peripheral nervous system (PNS). In the CNS, CMC readily entered the brain and selectively localized in myelinated regions such as the corpus callosum and cerebellum. CMC also selectively stained myelinated nerves in the PNS. The staining patterns of CMC in a hypermyelinated mouse model were consistent with immunohistochemical staining. Similar to immunohistochemical staining, CMC selectively bound to myelin sheaths present in the white matter tracts. Unlike CMC, conventional antibody staining for myelin basic protein also stained oligodendrocyte cytoplasm in the striatum as well as granule layers in the cerebellum. In vivo application of CMC was also demonstrated by fluorescence imaging of myelinated nerves in the PNS. (J Histochem Cytochem 58:611–621, 2010)

  C Wu , L Yan , C Depre , S. K Dhar , Y. T Shen , J Sadoshima , S. F Vatner and D. E. Vatner

Cytochrome c oxidase (COX) is composed of 13 subunits, of which COX I, II, and III are encoded by a mitochondrial gene. COX I and II function as the main catalytic components, but the function of COX III is unclear. Because myocardial ischemia affects mitochondrial oxidative metabolism, we hypothesized that COX activity and expression would be affected during postischemic cardiomyopathy. This hypothesis was tested in a monkey model following myocardial infarction (MI) and subsequent pacing-induced heart failure (HF). In this model, COX I protein expression was decreased threefold after MI and fourfold after HF (P < 0.05 vs. sham), whereas COX II expression remained unchanged. COX III protein expression increased 5-fold after MI and further increased 10-fold after HF compared with sham (P < 0.05 vs. sham). The physiological impact of COX III regulation was examined in vitro. Overexpression of COX III in mitochondria of HL-1 cells resulted in an 80% decrease in COX I, 60% decrease in global COX activity, 60% decrease in cell viability, and threefold increase in apoptosis (P < 0.05). Oxidative stress induced by H2O2 significantly (P < 0.05) increased COX III expression. H2O2 decreased cell viability by 47 ± 3% upon overexpression of COX III, but only by 12 ± 5% in control conditions (P < 0.05). We conclude that ischemic stress in vivo and oxidative stress in vitro lead to upregulation of COX III, followed by downregulation of COX I expression, impaired COX oxidative activity, and increased apoptosis. Therefore, upregulation of COX III may contribute to the increased susceptibility to apoptosis following MI and subsequent HF.

  D. M Kuang , Q Zhao , C Peng , J Xu , J. P Zhang , C Wu and L. Zheng

Macrophages (M) are prominent components of solid tumors and exhibit distinct phenotypes in different microenvironments. We have recently found that tumors can alter the normal developmental process of M to trigger transient activation of monocytes in peritumoral stroma. We showed that a fraction of monocytes/M in peritumoral stroma, but not in cancer nests, expresses surface PD-L1 (also termed B7-H1) molecules in tumors from patients with hepatocellular carcinoma (HCC). Monocytes activated by tumors strongly express PD-L1 proteins with kinetics similar to their activation status, and significant correlations were found between the levels of PD-L1+ and HLA-DRhigh on tumor-infiltrating monocytes. Autocrine tumor necrosis factor and interleukin 10 released from activated monocytes stimulated monocyte expression of PD-L1. The PD-L1+ monocytes effectively suppressed tumor-specific T cell immunity and contributed to the growth of human tumors in vivo; the effect could be reversed by blocking PD-L1 on those monocytes. Moreover, we found that PD-L1 expression on tumor-infiltrating monocytes increased with disease progression, and the intensity of the protein was associated with high mortality and reduced survival in the HCC patients. Thus, expression of PD-L1 on activated monocytes/M may represent a novel mechanism that links the proinflammatory response to immune tolerance in the tumor milieu.

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