Menopause increases the risk for women independent of age. Prior to menopause, the risk of Coronary Artery Disease (CAD) for women lags behind the risk for men. After menopause, women have similar risks of CAD as men of the same age. The functional and morphological alteration in endothelial cells is critical to atherosclerotic process. After menopause, marked decline in Estrogen and Nitric Oxide (NO) levels takes place. Estrogen exerts its various CAD protective actions by arterial endothelium sex steroid receptors. Nitric oxide released from vascular endothelium is one of most known versatile molecules and has a role in almost every biological system. Nitric oxide inhibits various key steps in development of atherosclerosis via inhibition of platelet activity and smooth muscle cell proliferation. Further presence of Endothelial Nitric Oxide Synthase (eNOS) gene polymorphism Glu298Asp may provide additional insult by decreasing NO levels adding to the CAD risk. Hence, postmenopausal women those who presents with eNOS Glu298Asp polymorphic gene may have higher CAD risk.
Les informations fournies dans la section « Synopsis » peuvent faire référence à une autre édition de ce titre.
Menopause increases the risk for women independent of age. Prior to menopause, the risk of Coronary Artery Disease (CAD) for women lags behind the risk for men. After menopause, women have similar risks of CAD as men of the same age. The functional and morphological alteration in endothelial cells is critical to atherosclerotic process. After menopause, marked decline in Estrogen and Nitric Oxide (NO) levels takes place. Estrogen exerts its various CAD protective actions by arterial endothelium sex steroid receptors. Nitric oxide released from vascular endothelium is one of most known versatile molecules and has a role in almost every biological system. Nitric oxide inhibits various key steps in development of atherosclerosis via inhibition of platelet activity and smooth muscle cell proliferation. Further presence of Endothelial Nitric Oxide Synthase (eNOS) gene polymorphism Glu298Asp may provide additional insult by decreasing NO levels adding to the CAD risk. Hence, postmenopausal women those who presents with eNOS Glu298Asp polymorphic gene may have higher CAD risk.
Dr. Pradeep has obtained his MD Biochemistry from Lady Hardinge Medical College, Delhi, India in 2007. He has been awarded many times for his research in “Postmenopausal Women CAD Risk”. Dr. Jayashree has supervised the role of Nitric Oxide in various diseases extensively. Vandana Dabla has expertise in Total Quality Management and Statistics.
Les informations fournies dans la section « A propos du livre » peuvent faire référence à une autre édition de ce titre.
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Taschenbuch. Etat : Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Menopause increases the risk for women independent of age. Prior to menopause, the risk of Coronary Artery Disease (CAD) for women lags behind the risk for men. After menopause, women have similar risks of CAD as men of the same age. The functional and morphological alteration in endothelial cells is critical to atherosclerotic process. After menopause, marked decline in Estrogen and Nitric Oxide (NO) levels takes place. Estrogen exerts its various CAD protective actions by arterial endothelium sex steroid receptors. Nitric oxide released from vascular endothelium is one of most known versatile molecules and has a role in almost every biological system. Nitric oxide inhibits various key steps in development of atherosclerosis via inhibition of platelet activity and smooth muscle cell proliferation. Further presence of Endothelial Nitric Oxide Synthase (eNOS) gene polymorphism Glu298Asp may provide additional insult by decreasing NO levels adding to the CAD risk. Hence, postmenopausal women those who presents with eNOS Glu298Asp polymorphic gene may have higher CAD risk. N° de réf. du vendeur 9783848484201
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