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Articles by W Chen
Total Records ( 14 ) for W Chen
  C Peng , W Chen , Y Han , T Sanders , G Chew , J Liu , E Hawrot , C Chi and C. Wang
 

As part of continuing studies of the identification of gene organization and cloning of novel -conotoxins, the first 4/4-conotoxin identified in a vermivorous Conus species, designated Qc1.2, was originally obtained by cDNA and genomic DNA cloning from Conus quercinus collected in the South China Sea. The predicted mature toxin of Qc1.2 contains 14 amino acid residues with two disulfide bonds (I-III, II-IV connectivity) in a native globular configuration. The mature peptide of Qc1.2 is supposed to contain an N-terminal post-translationally processed pyroglutamate residue and a free carboxyl C-terminus. This peptide was chemically synthesized and refolded for further characterization of its functional properties. The synthetic Qc1.2 has two interconvertible conformations in aqueous solution, which may be due to the cis-trans isomerization of the two successive Pro residues in its first Cys loop. Using the Xenopus oocyte heterologous expression system, Qc1.2 was shown to selectively inhibit both rat neuronal 3β2 and 3β4 subtypes of nicotinic acetylcholine receptors with low potency. A block of ~63% and 37% of the ACh-evoked currents was observed, respectively, and the toxin dissociated rapidly from the receptors. Compared with other characterized -conotoxin members, the unusual structural features in Qc1.2 that confer to its receptor recognition profile are addressed.

  C Peng , W Chen , T Sanders , G Chew , J Liu , E Hawrot and C. Chi
 

-Conotoxins are small disulfide-constrained peptides that act as potent and selective antagonists on specific subtypes of nicotinic acetylcholine receptors (nAChRs). We previously cloned two -conotoxins, Mr1.1 from the molluscivorous Conus marmoreus and Lp1.4 from the vermivorous Conus leopardus. Both of them have the typical 4/7-type framework of the subfamily of -conotoxins that act on neuronal nAChRs. In this work, we chemically synthesized these two toxins and characterized their functional properties. The synthetic Mr1.1 could primarily inhibit acetylcholine (ACh)-evoked currents reversibly in the oocyte-expressed rat 7 nAChR, whereas Lp1.4 was an unexpected specific blocker of the mouse fetal muscle 1β1 receptor. Although their inhibition affinities were relatively low, their unique receptor recognition profiles make them valuable tools for toxin-receptor interaction studies. Mr1.1 could also suppress the inflammatory response to pain in vivo, suggesting that it should be further investigated with respect to its molecular role in analgesia and its mechanism or therapeutic target for the treatment of pain.

  M Zhang , N Congdon , L Li , Y Song , K Choi , Y Wang , Z Zhou , X Liu , A Sharma , W Chen and D. S. C. Lam
 

Objective  To study the effect of myopia and spectacle wear on bicycle-related injuries in rural Chinese students. Myopia is common among Chinese students but few studies have examined its effect on daily activities.

Methods  Data on visual acuity, refractive error, current spectacle wear, and history of bicycle use and accidents during the past 3 years were sought from 1891 students undergoing eye examinations in rural Guangdong province.

Results  Refractive and accident data were available for 1539 participants (81.3%), among whom the mean age was 14.6 years, 52.5% were girls, 26.8% wore glasses, and 12.9% had myopia of less than –4 diopters in both eyes. More than 90% relied on bicycles to get to school daily. A total of 2931 accidents were reported by 423 participants, with 68 requiring medical attention. Male sex (odds ratio, 1.55; P < .001) and spectacle wear (odds ratio, 1.38; P = .04) were associated with a higher risk of accident, but habitual visual acuity and myopia were unassociated with the crash risk, after adjusting for age, sex, time spent riding, and risky riding behaviors.

Conclusion  These results may be consistent with data on motor vehicle accidents implicating peripheral vision (potentially compromised by spectacle wear) more strongly than central visual acuity in mediating crash risk.

  A. L Van Dyke , M. L Cote , A. S Wenzlaff , W Chen , J Abrams , S Land , C. N Giroux and A. G. Schwartz
 

Studies on the relationships between inflammatory pathway genes and lung cancer risk have not included African-Americans and have only included a handful of genes. In a population-based case-control study on 198 African-American and 744 Caucasian women, we examined the association between 70 cytokine and cytokine receptor single-nucleotide polymorphisms (SNPs) and risk of non–small cell lung cancer (NSCLC). Unconditional logistic regression was used to estimate odds ratios and 95% confidence intervals in a dominant model adjusting for major risk factors for lung cancer. Separate analyses were conducted by race and by smoking history and history of chronic obstructive pulmonary disease among Caucasians. Random forest analysis was conducted by race. On logistic regression analysis, IL6 (interleukin 6), IL7R, IL15, TNF (tumor necrosis factor), and IL10 SNP were associated with risk of non–small cell lung cancer among African-Americans; IL7R and IL10 SNPs were also associated with risk of lung cancer among Caucasians. Although random forest analysis showed IL7R and IL10 SNPs as being associated with risk for lung cancer among African-Americans, it also identified TNFRSF10A SNP as an important predictor. On random forest analysis, an IL1A SNP was identified as an important predictor of lung cancer among Caucasian women. Inflammatory SNPs differentially predicted risk for NSCLC according to race, as well as based on smoking history and history of chronic obstructive pulmonary disease among Caucasian women. Pathway analysis results are presented. Inflammatory pathway genotypes may serve to define a high risk group; further exploration of these genes in minority populations is warranted. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1829–40)

  W Chen , Y Luo , L Liu , H Zhou , B Xu , X Han , T Shen , Z Liu , Y Lu and S. Huang
 

Cryptotanshinone (CPT), a natural compound isolated from the plant Salvia miltiorrhiza Bunge, is a potential anticancer agent. However, little is known about its anticancer mechanism. Here, we show that CPT inhibited cancer cell proliferation by arresting cells in G1-G0 phase of the cell cycle. This is associated with the inhibition of cyclin D1 expression and retinoblastoma (Rb) protein phosphorylation. Furthermore, we found that CPT inhibited the signaling pathway of the mammalian target of rapamycin (mTOR), a central regulator of cell proliferation. This is evidenced by the findings that CPT inhibited type I insulin-like growth factor I– or 10% fetal bovine serum–stimulated phosphorylation of mTOR, p70 S6 kinase 1, and eukaryotic initiation factor 4E binding protein 1 in a concentration- and time-dependent manner. Expression of constitutively active mTOR conferred resistance to CPT inhibition of cyclin D1 expression and Rb phosphorylation, as well as cell growth. The results suggest that CPT is a novel antiproliferative agent. Cancer Prev Res; 3(8); 1015–25. ©2010 AACR.

  C. G Magnussen , J Koskinen , W Chen , R Thomson , M. D Schmidt , S. R Srinivasan , M Kivimaki , N Mattsson , M Kahonen , T Laitinen , L Taittonen , T Ronnemaa , J. S. A Viikari , G. S Berenson , M Juonala and O. T. Raitakari
  Background—

The clinical utility of identifying pediatric metabolic syndrome (MetS) is controversial. This study sought to determine the status of pediatric MetS as a risk factor for adult subclinical atherosclerosis (carotid intima-media thickness [cIMT]) and type 2 diabetes mellitus (T2DM) and compare and contrast this prediction with its individual components.

Methods and Results—

Using data from the population-based, prospective, observational Bogalusa Heart and Cardiovascular Risk in Young Finns studies, we examined the utility of 4 categorical definitions of youth MetS and their components in predicting adult high cIMT and T2DM among 1781 participants aged 9 to 18 years at baseline (1984 to 1988) who were then examined 14 to 27 years later (2001–2007) when aged 24 to 41 years. Youth with MetS were at 2 to 3 times the risk of having high cIMT and T2DM as adults compared with those free of MetS at youth. Risk estimates with the use of high body mass index were similar to those of MetS phenotypes in predicting adult outcomes. Comparisons of area under the receiver operating characteristic curve and net reclassification index suggested that prediction of adult MetS, high cIMT, and T2DM in adulthood with the use of youth MetS was either equivalent or inferior to classification based on high body mass index or overweight and obesity.

Conclusions—

Youth with MetS are at increased risk of meaningful adult outcomes; however, the simplicity of screening for high BMI or overweight and obesity in the pediatric setting offers a simpler, equally accurate alternative to identifying youth at risk of developing adult MetS, high cIMT, or T2DM.

  N Sawhney , R Anousheh , W Chen and G. K. Feld
  Background—

There has been growing concern that linear ablation is associated with an increased risk of iatrogenic arrhythmias in patients undergoing ablation for atrial fibrillation (AF). Therefore, we compared circumferential pulmonary vein ablation plus left atrial linear ablation (CPVA+LALA) with segmental pulmonary vein isolation (PVI)in patients with paroxysmal AF.

Methods and Results—

Sixty-six consecutive patients with paroxysmal AF were prospectively randomly assigned to receive PVI versus CPVA+LALA (consisting of encircling lesions around the pulmonary veins), a roof line, and a mitral isthmus line with documentation of bidirectional mitral isthmus block. All patients were seen at 1, 3, 6, and every 12 months after ablation, with 14-day continuous ECG monitoring every 6 months. At 16.4±6.3 months after 1 ablation procedure, 19 patients (58%) remained free of atrial arrhythmias after PVI versus 17 patients (51%) after CPVA+LALA (P=0.62). After PVI, 14 patients had recurrent paroxysmal AF, whereas after CPVA+LALA, 8 patients had recurrent AF, 6 had atypical left atrial flutter (LAFL), and 2 had both AF and LAFL (P=0.32 between PVI versus CPVA+LALA for AF but P=0.002 for LAFL). Twenty-eight patients (85%) remained arrhythmia-free after 1.3±0.5 PVI procedures versus 28 patients (85%) after 1.4±0.6 CPVA+LALA procedures (P=NS). Fluoroscopy time was longer after CPVA+LALA versus PVI (91 versus 73 minutes, P=0.04).

Conclusions—

As an initial ablation approach in patients with paroxysmal AF, more LAFL occurred after CPVA+LALA and fluoroscopy times were longer compared with segmental PVI.

  J Li , H Huang , L Sun , M Yang , C Pan , W Chen , D Wu , Z Lin , C Zeng , Y Yao , P Zhang and E. Song
 

Purpose: We aim to examine miR-21 expression in tongue squamous cell carcinomas (TSCC) and correlate it with patient clinical status, and to investigate its contribution to TSCC cell growth, apoptosis, and tumorigenesis.

Experimental Design: MicroRNA profiling was done in 10 cases of TSCC with microarray. MiR-21 overexpression was quantitated with quantitative reverse transcription-PCR in 103 patients, and correlated to the pathoclinical status of the patients. Immunohistochemistry was used to examine the expression of TPM1 and PTEN, and terminal deoxynucleotidyl transferase–mediated dUTP labeling to evaluate apoptosis. Moreover, miR-21 antisense oligonucleotide (ASO) was transfected in SCC-15 and CAL27 cell lines, and tumor cell growth was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, adherent colony formation, and soft agar assay, whereas apoptosis was determined by Annexin V assay, cytochrome c release, and caspase 3 assay. Tumorigenesis was evaluated by xenografting SCC-15 cells in nude mice.

Results: MiR-21 is overexpressed in TSCC relative to adjacent normal tissues. The level of miR-21 is reversely correlated with TPM1 and PTEN expression and apoptosis of cancer cells. Multivariate analysis showed that miR-21 expression is an independent prognostic factor indicating poor survival. Inhibiting miR-21 with ASO in TSCC cell lines reduces survival and anchorage-independent growth, and induces apoptosis in TSCC cell lines. Simultaneous silencing of TPM1 with siRNA only partially recapitulates the effect of miR-21 ASO. Furthermore, repeated injection of miR-21 ASO suppresses tumor formation in nude mice by reducing cell proliferation and inducing apoptosis.

Conclusions: miR-21 is an independent prognostic indicator for TSCC, and may play a role in TSCC development by inhibiting cancer cell apoptosis partly via TPM1 silencing.

  D Yamaji , R Na , Y Feuermann , S Pechhold , W Chen , G. W Robinson and L. Hennighausen
 

Mammary alveologenesis is abrogated in the absence of the transcription factors STAT5A/5B, which mediate cytokine signaling. To reveal the underlying causes for this developmental block, we studied mammary stem and progenitor cells. While loss of STAT5A/5B did not affect the stem cell population and its ability to form mammary ducts, luminal progenitors were greatly reduced and unable to form alveoli during pregnancy. Temporally controlled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the luminal progenitor population and rescued alveologenesis in a reversible fashion in vivo. Thus, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells.

  Y He , Y Li , Z Peng , H Yu , X Zhang , L Chen , Q Ji , W Chen and R. Wang
 

A prominent feature of the rodent Muc3 SEA module is the precursor cleavage event that segregates the O-glycosylated N-terminal fragment and transmembrane domain into the noncovalently attached heterodimer. There are seven potential N-glycosylation sites that occur in a cluster in the SEA module of Muc3. However, it is unknown if these sites are modified or what the function of these N-glycans may be in the SEA module. Our data show that the proteolytic cleavage of the rodent Muc3 SEA module was partially prevented by treatment with tunicamycin, an inhibitor of N-glycosylation. Each single mutant of the seven N-glycosylation sites (N1A, N2A, N3A, N4A, N5A, N6A, and N7A) and multiple mutants, including double (N34A) and triple (N345A) mutants, and mutants with four (N3457A), five (N34567A), six (N134567A and N234567A), seven (N1234567A) mutations, confirmed that all seven of these potential sites are N-glycosylated simultaneously. The proteolytic cleavage of the SEA module was not affected when it lacked only one, two, or three N-glycans, but was partially inhibited when lacking four, five, and six N-glycans. In all, 2%, 48%, 85%, and 73% of the products from N3457A, N34567A, N134567A, and N234567A transfectants, respectively, remained uncleaved. The proteolytic cleavage was completely prevented in the N1234567A transfectant, which eliminated all seven N-glycans in the SEA module. The interaction of the heterodimer was independent of the N-glycans within the rodent Muc3 SEA module. Thus, the N-glycosylation pattern constituted a control point for the modulation of the proteolytic cleavage of the SEA module.

  P Liu , W Chen , H Zhu , B Liu , S Song , W Shen , F Wang , S Tucker , B Zhong and D. Wang
  Objective

The purpose of this study was to specifically investigate the clinicopathological role of expression of vascular endothelial growth factor-C (VEGF-C) as well as the correlation with clinical outcomes in esophageal squamous cell carcinomas (ESCCs).

Methods

Seventy-three patients with ESCC resected in our institute were included in this study. Formalin-fixed paraffin-embedded specimens were stained for VEGF-C and the correlation between the staining, its clinicopathological parameters and its prognostic power were analyzed statistically.

Results

Of the 73 ESCC patients studied, 39 cases (53.4%) were strongly positive for VEGF-C. Six cases (8.2%) were negative and 28 cases (38.4%) revealed unclear weak reactions. All 34 cases were included in the negative group (46.6%). VEGF-C expression correlated with histological grade (P = 0.005), depth of tumor invasion (pT) (P = 0.021), lymph node metastasis (pN) (P = 0.002) and lymphatic invasion (P = 0.008). The median overall survival of 39 patients who had positive staining for tumor cell VEGF-C and 34 patients who had negative staining were 10.4 months (95% CI, 6.9–13.9 months) and 28.5 months (95% CI, 12.6–44.4 months), respectively (P = 0.003). In univariate analysis by log-rank test, histological grade, pN, stage, lymphatic invasion and VEGF-C were significant prognostic factors (P = 0.047, 0.007, 0.018, 0.002 and 0.003, respectively.). In multivariate analysis, high VEGF-C expression (P = 0.0451) maintained its independent prognostic influence on overall survival, as well as pN status (P = 0.0029).

Conclusions

Expression of VEGF-C is related to histological grade, pT, pN and lymphatic invasion, and is a prognostic indicator for ESCC.

  P Zhao , M Dai , W Chen and N. Li
 

Cancer is the leading death cause in urban China and the second one in rural China. Lung cancer is the most common cancer, followed by stomach cancer, liver cancer, esophageal cancer and colorectal cancer. Cancer Control Programs in China focus on prevention, early diagnosis and treatment. The prevention program includes an anti-smoking campaign and immunization against hepatitis B for infants and children under the age of 15. Screening for breast and cervix cancers is among efforts for the early detection and treatment. Public education and the promotion of healthy lifestyles have been actively carried out.

  K. M Wojtanik , K Edgemon , S Viswanadha , B Lindsey , M Haluzik , W Chen , G Poy , M Reitman and C. Londos
 

We investigated the role of LMNA in adipose tissue by developing a novel mouse model of lipodystrophy. Transgenic mice were generated that express the LMNA mutation that causes familial partial lipodystrophy of the Dunnigan type (FPLD2). The phenotype observed in FPLD-transgenic mice resembles many of the features of human FPLD2, including lack of fat accumulation, insulin resistance, and enlarged, fatty liver. Similar to the human disease, FPLD-transgenic mice appear to develop normally, but after several weeks they are unable to accumulate fat to the same extent as their wild-type littermates. One poorly understood aspect of lipodystrophies is the mechanism of fat loss. To this end, we have examined the effects of the FPLD2 mutation on fat cell function. Contrary to the current literature, which suggests FPLD2 results in a loss of fat, we found that the key mechanism contributing to the lack of fat accumulation involves not a loss, but an apparent inability of the adipose tissue to renew itself. Specifically, preadipocytes are unable to differentiate into mature and fully functional adipocytes. These findings provide insights not only for the treatment of lipodystrophies, but also for the study of adipogenesis, obesity, and insulin resistance.

 
 
 
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