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21篇 您的检索式:作者名="Verseyden"
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1ATG16L1 and NOD2 polymorphisms enhance phagocytosis in monocytes of Crohn's disease patients显示文摘AIM:To investigate if the presence of relevant genetic polymorphisms has effect on the effectual clearance of bacteria by monocytes and granulocytes in patients with Crohn’s disease(CD).METHODS:In this study,we assessed the differential responses in phagocytosis by measuring the phagocytic activity and the percentage of active phagocytic monocytes and granulocytes in inflammatory bowel disease patients as well as healthy controls.As both autophagy related like 1(ATG16L1)and immunityrelated guanosine triphosphatase gene are autophagy genes associated with CD and more recently nucleo-tide-binding ligomerization domain-containing protein2(NOD2)has been identified as a potent inducer of autophagy we genotyped the patients for these variants and correlated this to the phagocytic reaction.The genotyping was done with restriction fragment length polymorphisms analysis and the phagocytosis was determined with the pHrodo?Escherichia coli Bioparticles Phagocytosis kit for flowcytometry.RESULTS:In this study,we demonstrate that analysis of the monocyte and granulocyte populations of patients with CD and ulcerative colitis showed a comparable phagocytic activity(ratio of mean fluorescence intensity)between the patient groups and the healthy controls.CD patients show a significantly higher phagocytic capacity(ratio mean percentage of phagocytic cells)compared to healthy controls(51.91%±2.85%vs 37.67%±7.06%,P=0.05).The extend of disease was not of influence.However,variants of ATG16L1(WT:2.03±0.19 vs homozygoot variant:4.38±0.37,P<0.009)as well as NOD2(C-ins)(heterozygous variant:42.08±2.94 vs homozygous variant:75.58±4.34(P=0.05)are associated with the phagocytic activity in patients with CD.CONCLUSION:Monocytes of CD patients show enhanced phagocytosis associated with the presence of ATG16L1 and NOD2 variants.This could be part of the pathophysiological mechanism resulting in the disease.Simone CS Wolfkamp Caroline Verseyden Esther WM Vogels Sander Meisner Kirsten Boonstra Charlotte P Peters Pieter CF Stokkers Anje A te Velde 2014World Journal of Gastroenterology2014,20,10:2
2Effects of atorvastatin on fasting and postprandial complement component 3 response in familial combined hyperlipidemia显示文摘VERSEYDEN C MEIJSSEN S van DIJK H 2003J Lipid Res2003,44,11:1
3Postprandial recmitment of neutrophils may contribute to endothelial dysfunction显示文摘Van Ostrom AJ Sijmonsma TP Verseyden C 2003J Lipid Res2003,44,:1
4Haematopoietic stem cells and endothelial progenitor cells in healthy men: effect of aging and training 显示文摘Thijssen DH Vos JB Verseyden C 2006Aging Cell2006,5,6:1
5Fibrin and activated platelets cooperatively guide stem cells to a vascular injury and promote differentiation towards an endothelial cell phenotype显示文摘de Boer HC Verseyden C Ulfman LH 2006Arterioscler Thromb Vasc Biol2006,26,7:1
6Postprandial recruitment of neutrophils may contribute to endothelial dysfunction显示文摘Van-Oostrom A J Sijmonsma T P Verseyden C 2003J Lipid Res2003,44,3:1
7Delayed and exaggerat- ed postprandial complement component 3 response in familial com- bined hyperlipidemia 显示文摘Meijssen S van-Dijk H Verseyden C 2002Arterioscler Thromb Vasc Biol2002,22,5:1
8Haematopoietic stem cells and endothelial progenitor cells in healthy men:effect of aging and training显示文摘Thijssen DHJ Vos JB Verseyden C 0,,:1
9Delayed and exaggerated postprandial complement component 3 response in familial combined hyperlipidemia显示文摘Meijssen S van Dijk H Verseyden C Erkelens DW Cabezas MC 2002Arterioscler Thromb Vasc Biol2002,22,5:1
10Delayed and exaggerated postprandial complement component 3 response in familial combined hyperlipidemia显示文摘Meijssen S van Dijk H Verseyden C 2002Arterioscler Thromb Vasc Biol2002,22,:1
11Delayed and exaggerated postprandial complement component 3 response in familial combined hyperlipidemia显示文摘Meijssen S van Dijk H Verseyden C 2002Arterioscler Thromb Vasc Biol2002,22,5:1
12Fibrin and activa- ted platelets cooperatively guide stem cells to a vascular injury and promote differentiation towards an endothelial cell phenotype 显示文摘de Boer HC Verseyden C Ulfman LH 2006Arterioscler Thromb Vase Biol2006,26,7:1
13Fibrin and Activated Platelets Cooperatively Guide Stem Ceils to a Vascular Injury and Promote Differentiation Towards an Endothelial Cell Phenotype显示文摘H C de Boer C Verseyden L H Ulfman 2006Arterioscler Thromb Vasc Bio12006,26,:1
14Postprandial recruitment of neutrophils may contribute to endothelial dysfunction显示文摘van Oostrom AJ Sijmonsma TP Verseyden C Jansen EH de Koning EJ Rabelink TJ 2003J Lipid Res2003,44,:1
15Delaye and exaggerated postprandial complement component 3 response in familial combined hyperlipidemia显示文摘Meijssen S Van Dijk H Verseyden C 2002Arterioscler Thromb Vase Biol2002,22,5:1
16Effects of atorvastatin on fasting and postprandial complement component 3 response in familial combined hyperlipidemia显示文摘Verseyden C Meijssen S van Dijk H 2003J Lipid Res2003,44,:1
17Postprandial recruitment of neutrophils may contribute to endothelial dysfunction显示文摘van Oostrom AJ Sijmonsma TP Verseyden C 2003J Lipid Res2003,44,3:1
18Haematopoietic stem ceils and endothelial progenitor ceils in healthy men: effect of aging and training显示文摘Thijssen DH Vos JB Verseyden C van Zonneveld AJ Smits P Sweep FC Hopman MT de Boer HC 2006Aging Cell2006,5,6:1
19Delayed and exaggerated postprandial complement component 3 response in familial combined hyperlipidemia 显示文摘Meijssen S van Dijk H Verseyden C 2002Arterioscler Thromb Vasc Biol2002,22,5:1
20Addition of glucose to an oral fat load reduces post-prandial free fatty acids and prevents the postprandial increase in complement component 3 显示文摘VAN OOSTROM A J VAN DIJK H VERSEYDEN C 2004Am J Clin Nutr2004,79,3:1
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