By E.Z. Fisman, A. Tenenbaum, J.S. Borer
The superiority of weight problems, metabolic syndrome and diabetes - 3 hyperlinks of an analogous >atherothrombotic chain' - has reached pandemic proportions world wide. accordingly, our civilization is at conflict opposed to a threatening enemy: cardio-diabetes. numerous self sustaining physiological methods underlie the clustering of cardio-diabetes, together with valuable weight problems, insulin resistance, dyslipidemia, irritation, impaired glucose tolerance, and high blood pressure. Early detection is of overwhelming value for public overall healthiness. The advanced and intimate courting among heart problems and diabetes from easy technological know-how to medical and healing matters is mentioned during this notable publication. starting with molecular, biochemical, inflammatory and mobile facets, this e-book keeps with histological and pathophysiological concerns, info specific difficulties in particular metabolic and scientific settings, and at last analyzes a number of features of scientific pharmacology targeting the optimum administration of mixed dyslipidemia and non-insulin antidiabetic treatment in cardiac diabetic sufferers. This booklet could be a achieve in wisdom for each heart specialist, diabetologist, professional in inner drugs, nutritionalist, normal medical professional and clinical pupil.
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Extra resources for Cardiovascular Diabetology: Clinical, Metabolic and Inflammatory Facets (Advances in Cardiology)
86]. an ACE inhibitor in hypercholesterolemic coronary artery disease patients (fig. 5) . Although the method of evaluating endothelial responses by measurements on the brachial artery is noninvasive and easily repeated, without any risk to the patient, it is time consuming and needs skilled and patient operators [77, 125]. With just a small displacement of the transducer the results are altered. Some automated systems have shown a reduction in the variation between operators [77, 126, 127].
Wells L, Vosseller K, Hart GW: Glycosylation of nucleocytoplasmic proteins: signal transduction and O-GlcNAc. Science 2001;291:2376–2378. Du XL, Edelstein D, Dimmeler S, Ju Q, Sui C, Brownlee M: Hyperglycemia inhibits endothelial nitric oxide synthase activity by posttranslational modification at the Akt site. J Clin Invest 2001;108:1341–1348. Du XL, Edelstein D, Rossetti L, Fantus IG, Goldberg H, Ziyadeh F, Wu J, Brownlee M: Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation.
The endothelial cell membranes contain Esper/Vilariño/Machado/Paragano 22 specialized ion channels, such as Ca2ϩ-activated Kϩ channels, which open in response to shear stress . The effect is to hyperpolarize the endothelial cell, increasing the driving force for Ca2ϩ entry and activating the enzyme NOS-III and the subsequent generation of NO . Nitrates given in any way are NO donors, unconfined NO into the circulation directly releasing cGMP in the smooth muscle cell and causing a vasodilatation that is not dependent on the endothelial response, and for this reason it is called endothelium-independent vasodilatation.
Cardiovascular Diabetology: Clinical, Metabolic and Inflammatory Facets (Advances in Cardiology) by E.Z. Fisman, A. Tenenbaum, J.S. Borer