Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet adherence and aggregation on vessel walls are the first crucial steps in thrombogenesis and atherosclerosis. Whether platelets can be activated on damaged endothelial cells or their activation is achieved only when subendothelial structures are exposed was controversially discussed in the past. Recently, an electron-microscopic study has revealed an amorphous electron-dense substance (AEDS) after endothelial cell damage and has discussed its role as a possible trigger of thrombogenesis. The aim of the present study is to elucidate the role and origin of this substance and to investigate the influence which inhibitors of platelet function (acetylsalicylic acid), coagulation (heparin), stimulation of fibrinolysis (streptokinase) and addition of factor VIII (AHF) have on AEDS.
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PMID:Influence of heparin, aspirin, streptokinase and factor VIII (AHF) on amorphous electron-dense substance, a mediator of platelet and thrombus adhesion in vivo. 311 26

Epidemiological studies demonstrated the importance of postprandial hyperglycemia on the progression of atherosclerosis. However, whether treatment of postprandial hyperglycemia by insulin or insulin secretagogues has a beneficial effect on atherosclerosis has not been elucidated. To elucidate the effects of reduction of postprandial rise of blood glucose by insulin and nateglinide on monocyte adhesion to endothelial cells, we used non-obese type 2 diabetic Goto-Kakizaki (GK) rats fed twice daily, as a model of repetitive postprandial hyperglycemia. We investigated the effects of insulin injection and nateglinide administration just before each meal for 12 weeks on monocyte adhesion to endothelial cells. By setting the doses of insulin and nateglinide, both treatment significantly reduced postprandial hyperglycemia without significant reduction of HbA1c. Nateglinide also reduced serum insulin level just after 1 h meal. Both nateglinide and insulin therapy reduced the number of monocytes adherent to the aortic endothelial layer. Nateglinide, but not insulin, reduced intimal thickness of the thoracic aorta. While increased serum insulin level might be regarded as a factor responsible for the progression of atherosclerosis, our data showed that treatment with pre-meal insulin or nateglinide, which reduces postprandial hyperglycemia, reduced monocyte adhesion to endothelial cells.
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PMID:Insulin and nateglinide reduce monocyte adhesion to endothelial cells in Goto-Kakizaki rats exhibiting repetitive blood glucose fluctuation. 1699 77