Jean-Charles Fruchart, Bart Staels, Patrick Duriez (auth.),'s Atherosclerosis, Hypertension and Diabetes PDF

By Jean-Charles Fruchart, Bart Staels, Patrick Duriez (auth.), Grant N. Pierce PhD, FACC, Makoto Nagano MD, PhD, Peter Zahradka PhD, Naranjan S. Dhalla PhD, MD (Hon), DSc (Hon) (eds.)

ISBN-10: 1441992324

ISBN-13: 9781441992321

ISBN-10: 1461348501

ISBN-13: 9781461348504

This quantity is dedicated to atherosclerosis, high blood pressure, and diabetes, 3 of crucial sickness stipulations on this planet this present day. dietary intervention, ldl cholesterol reducing brokers, lipids themselves, relatively oxidized LDL, protein amendment through ADP-ribose, bone marrow research, endothelial mobilephone disorder, angiotensin, and the function of an infection and irritation are all mentioned within the context of atherosclerotic cardiovascular disease.

The high blood pressure part specializes in components which may be liable for hypertension, comparable to genetic predisposition, vascular hyperplasia and transforming, insulin resistance, neurological points resembling hypothalamic peptides. additionally mentioned are the potential contributions of the mobile functionality of the endothelium, foodstuff, kidney disorder, leptin, and the mind. Novel routes of drug supply for therapy of high blood pressure can be a focus.

The possibility elements and mechanisms accountable for diabetic vascular and cardiac disorder are mentioned. Lipid profile alterations and fibrinolysis in diabetic sufferers is certain, in addition to adipogenesis, diabetic cardiomyopathy, power metabolism within the diabetic center, vanadate in its place to insulin, insulin resistance mechanisms, and neurotransmitters as objectives for the prevention of heart problems and diabetes.

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Macrophages cultured with native LOL-No uptake of LOL by macrophages. macrophages leads to altered surface markers which leads to increased uptake of oxidized LOL leading to atherosclerosis. 2 Conversion of native LDL to OX-LDL Macrophages were cultured with native LOL, there was no uptake of LOL by macrophages (Fig. 11). When exposed to oxidants, native LOL was converted to rninimaily modified LOL (MM/LOL) and the morphology of macrophages was slightly altered with the result that few lipid particles (stained by oil '0' Red) were seen in macrophage ceils (Fig.

Diminished very low density lipoprotein fractional catabolic rate associated with increased apo CIII and reduced apo E on the particles. J Clin Invest 90:18891900. 27. Aalto-Setala K, Weinstock PH, Bisgaier CL, Wu L, Smith JD, Breslow J1. 1996. Further characterization of the metabolie properties of triglyceride- rich lipoproteins from human and mouse apoCIII transgenic mice. J Lipid Res 37:1802-1811. 28. Ebara T, Ramakrishnan R, Steiner G, Shachter NS. 1997. Chylomicronemia due to apolipoprotein CIII overexpression in apolipoprotein E-null mice.

Chlamydia Pneumoniae as an Atherogenic Agent 25 10. Paigen B, Morrow A, Brandon C, Mitchell D, Holmes P. 1985. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis 57:65-73. 11. Ishibashi S, Brown MS, Goldstein JL, Gerard RD, Hammer RE, Herz). 1993. Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery. J Clin Invest 92:883-893. 12. Zhang SH, Reddick RL, Piedrahita JA, Maeda N. 1992. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E.

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Atherosclerosis, Hypertension and Diabetes by Jean-Charles Fruchart, Bart Staels, Patrick Duriez (auth.), Grant N. Pierce PhD, FACC, Makoto Nagano MD, PhD, Peter Zahradka PhD, Naranjan S. Dhalla PhD, MD (Hon), DSc (Hon) (eds.)

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