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| 1 | Association of gene variants with susceptibility to type 2 diabetes among Omanis显示文摘AIM:To investigate the association of 10 known common gene variants with susceptibility to type 2diabetes mellitus(T2D)among Omanis.METHODS:Using case-control design,a total of992 diabetic patients and 294 normoglycemic Omani Arabs were genotyped,by an allelic discrimination assay-by-design TaqMan method on fast real time polymerase chain reaction system,for the following gene variants:KCNJ11(rs5219),TCF7L2(rs7903146),CDKAL1(rs10946398),CDKN2A/B(rs10811661),FTO(rs9939609 and rs8050136),IGF2BP2(rs4402960),SLC30A8(rs13266634)CAPN10(rs3792267)and HHEX(rs1111875).T2D patients were recruited from the Diabetes Clinic(n=243)and inpatients(n=749)at Sultan Qaboos Univesity Hospital(SQUH),Muscat,Oman.Adult control participants(n=294)were volunteers from the community and from those visiting Family Medicine Clinic at SQU,for regular medical checkup.The difficulty in recruiting Omani participants with no family history of diabetes was the main reason behind the small number of control participants in this study.Almost all volunteers questioned had a relativewith diabetes mellitus.Inspite of the small number of normoglycemic controls in this study,this sample was sufficient for detection of genes and loci for common alleles influencing T2D with an odds ratio of≥1.3reaching at least 80%power.Data was collected from June 2010 to February 2012.RESULTS:Using binary logistic regression analysis,four gene variants showed significant association with T2D risk:KCNJ11(rs5219,P=5.8×10^(-6),OR=1.74),TCF7L2(rs7903146,P=0.001,OR=1.46),CDKAL1(rs10946398,P=0.002,OR=1.44)and CDKN2A/B(rs10811661,P=0.020,OR=1.40).The fixation index analysis of these four gene variants indicated significant genetic differentiation between diabetics and controls{[KCNJ11(rs5219),P<0.001],[TCF7L2(rs7903146),P<0.001],[CDKAL1(rs10946398),P<0.05],[CDKN2A/B(rs10811661),P<0.05]}.The highest genotype variation%between diabetics and controls was found at KCNJ11(2.07%)and TCF7L2(1.62%).This study was not able to detect an association of T2D risk with gene variants of IGF2BP2(rs4402960),SLC30A8(rs13266634),CAPN10(rs3792267)and HHEX(rs1111875).Moreover,no association was found between FTO gene variants(rs9939609 and rs8050136)and T2D risk.However,T2D risk was found to be significantly associated with obesity(P=0.002,OR=2.22);and with the Waist-to-Hip ratio(n=532,P=1.9×10^(-7),OR=2.4),[among males(n=234,P=1.2×10^(-4),OR=2.0)and females(n=298,P=0.001,OR=6.3)].CONCLUSION:Results confirmed the association of KCNJ11(rs5219),TCF7L2(rs7903146),CDKAL1(rs10946398)and CDKN2A/B(rs10811661)gene variants with susceptibility to T2D among Omani Arabs. | Sawsan Al-Sinani Nicolas Woodhouse Ali Al-Mamari Omaima Al-Shafie Mohammed Al-Shafaee Said Al-Yahyaee Mohammed Hassan Deepali Jaju Khamis Al-Hashmi Mohammed Al-Abri Khalid Al-Rassadi Syed Rizvi Yengo Loic Philippe Froguel Riad Bayoumi | 2015 | World Journal of Diabetes2015，6，2： | 3 |
| 2 | SSJD15011600007878显示文摘 | María A. Mejía-Benítez Amélie Bonnefond Lo?c Yengo Marlène Huyvaert Aurélie Dechaume Jesús Peralta-Romero Miguel Klünder-Klünder Jaime García Mena Julia S. El-Sayed Moustafa Mario Falchi Miguel Cruz Philippe Froguel | 2015 | Diabetologia2015，，2： | 2 |
| 3 | Exercisetraining post - MI favorably modifies heart extracellular matrix inthe rat显示文摘 | Yengo CM Zimmerman SD McCormick RJ | 2012 | Med Sci Sports Exerc2012，44，6： | 1 |
| 4 | Contribution of 24 obesity-associated genetic variants to insulin resistance, pancreatic beta-cell function and type 2 diabetes risk in the French population 显示文摘 | Robiou-du-Pont S Bonnefond A Yengo L | 2013 | Int J Obes (Lond)2013，37，7： | 1 |
| 5 | Exercise Training Post-MI Favorably Modifies Heart Extracellular Matrix in the Rat显示文摘 | CHRISTOPHER M. YENGO SCOTT D. ZIMMERMAN RICHARD J. McCORMICK D. PAUL THOMAS | 2012 | Medicine & Science in Sports & Exercise2012，，6： | 1 |
| 6 | Bio-chemical and bioinformatic analysis of the myosin-XIX mo- tor domain 显示文摘 | ADIKES R C UNRATH W C YENGO C M | 2013 | Cytoskeleton ( Hoboken )2013，70，5： | 1 |
| 7 | Kinetic mechsnism of blebbistatin inhibi- tion of nonmuscle myosin Iib显示文摘 | Rarsamurthy B Yengo CM Straight AF | 2004 | Biochemistry2004，43，14： | 1 |
| 8 | Contribution of 24 obesity-associated genetic variants to insulin resistance, pancreatic beta-cell function and type 2 diabetes risk in the French population显示文摘 | Robiou-du-Pont S Bonnefond A Yengo L | 2013 | Int J Obes (Lend)2013，37，： | 1 |
| 9 | Nonmuscle myosin Ⅱ regulates migration but not contraction in rat hepatic stellate cells显示文摘AIM: To identify and characterize the function of non-mu-scle myosin Ⅱ (NMM Ⅱ) isoforms in primary rat hepatic stellate cells (HSCs).METHODS: Primary HSCs were isolated from male Spra-gue-Dawley rats by pronase/collagenase digestion. Total RNA and protein were harvested from quiescent and culture-activated HSCs. NMM Ⅱ isoform (Ⅱ-A, Ⅱ-B and Ⅱ-C) gene and protein expression were measured by RealTime polymerase chain reaction and Western blot analyses respectively. NMM Ⅱ protein localization was visualized in vitro using immunocytochemical analysis. For in vivo assessment, liver tissue was harvested from bile duct-ligated (BDL) rats and NMM Ⅱisoform expression determined by immunohistochemistry. Using a selective myosin Ⅱ inhibitor and siRNA-mediated knockdown of each isoform, NMM Ⅱ functionality inprimary rat HSCs was determined by contraction and migration assays.RESULTS: NMM Ⅱ-A and Ⅱ-B mRNA expression was increased in culture-activated HSCs (Day 14) with sig-niflicant increases seen in all pairwise comparisons (Ⅱ-A: 12.67 ± 0.99 (quiescent) vs 17.36 ± 0.78 (Day 14), P < 0.05; Ⅱ-B: 4.94 ± 0.62 (quiescent) vs 13.90 ±0.85 (Day 14), P < 0.001). Protein expression exhibited similar expression patterns (Ⅱ-A: 1.87 ± 2.50 (quiescent) vs 58.64 ± 8.76 (Day 14), P < 0.05; Ⅱ-B: 1.17 ± 1.93 (quiescent) vs 103.71 ± 21.73 (Day 14), P < 0.05). No signif icant differences were observed in NMM Ⅱ-C mRNA and protein expression between quiescent and activated HSCs. In culture-activated HSCs, NMM Ⅱ-A and Ⅱ-B merged with F-actin at the cellular periphery and throughout cytoplasm respectively. In vitro stud-ies showed increased expression of NMM Ⅱ-B in HSCs activated by BDL compared to sham-operated animals. There were no apparent increases of NMM Ⅱ-A and Ⅱ-C protein expression in HSCs during hepatic BDL injury. To determine the contribution of NMM Ⅱ-A and Ⅱ-B to migration and contraction, NMM Ⅱ-A and Ⅱ-B expres-sion were downregulated with siRNA. NMM Ⅱ-A and/or Ⅱ-B siRNA inhibited HSC migration by approximately 25% compared to scramble siRNA-treated cells. Conversely, siRNA-mediated NMM Ⅱ-A and Ⅱ-B inhibition had no signif icant effect on HSC contraction; however, contraction was inhibited with the myosin Ⅱ inhibitor, blebbistatin (38.7% ± 1.9%).CONCLUSION: Increased expression of NMM Ⅱ-A and Ⅱ-B regulates HSC migration, while other myosin Ⅱclasses likely modulate contraction, contributing to development and severity of liver f ibrosis. | Cathy C Moore Ashley M Lakner Christopher M Yengo Laura W Schrum | 2011 | World Journal of Hepatology2011，3，7： | 1 |
| 10 | 父母2型糖尿病病史,转录因子7类似物2变异体和低胰岛素分泌与高血压发生相关显示文摘胰岛素分泌和高血压发生之间的关系尚未明确。研究人员假设,父母糖尿病史和转录因子7类似物2(transcription factor 7-like2,TCF7L2)rs7903146基因多态性与高血压发生相关。同时研究人员对另一个独立的队列进行分析,评估低胰岛素分泌与高血压发生的关系。 | Bonnet F Roussel R Natali A Cauchi S Petrie J Laville M Yengo L Froguel P Lange C Lantieri O Marre M Balkau B Ferrannini E 刘莉 叶鹏 | 2013 | 中华高血压杂志2013，21，9： | 0 |
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