Download PDF by Ronald R. Watson: AIDS and Heart Disease

By Ronald R. Watson

ISBN-10: 0203021894

ISBN-13: 9780203021897

ISBN-10: 0824741153

ISBN-13: 9780824741150

The 1st connection with gather the most recent learn and studies at the remedy and pathogenesis of middle disorder in AIDS sufferers, this reference makes an attempt to enhance the analysis, administration, and treatment of HIV-associated middle failure by way of learning the lengthy results of immunosuppression and opportunistic and viral an infection, in addition to cofactors affecting middle affliction similar to drug-related cardiotoxicity, cocaine abuse, and dietary deficiencies on cardiac functionality.

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Extra resources for AIDS and Heart Disease

Sample text

We activated endothelial cells with tat protein, lipopolysaccharide (LPS), or IL-1 β and measured oxidation of nonfluorescent 2′,7′dichlorohydrofluorescein (DCHF) to dichlorofluorescein (DCF), which emits fluorescence. The fluorescence microplate reader was used to monitor fluorescence. The results are shown in Figure 5. 05 compared to control). Endothelial dysfunction, monocyte activation, and worsening of vascular disease may follow production of ROS. This may be accentuated by nutritional deficiencies of antioxidants in patients infected with HIV.

Found that by itself gp120 could enhance monocyte adhesion to endothelial cells, a phenomenon crucial to early atherogenesis (75). However, this adhesive event was blocked by the addition of morphine and anadamide to the cell cultures. This suggested the involvement of nitric oxide, since both drugs induce production of nitric oxide (NO), which prevents monocyte adherence, perhaps by reducing expression of the adhesion molecule VCAM-1 on endothelial surfaces. In summary, gp120, a soluble product of HIV infection, can alter endothelial function in several ways, including induction of apoptosis, activating cytokine expression by mononuclear cells, enhancing adhesiveness of mononuclear cells to endothelium, and increasing endothelial permeability.

The oxidation of dihydrohydrochlorofluorescein to dicholorofluorescein was assessed using a fluorescent plate reader. 05 compared to control. levels of plasma glutathione, ascorbate, and vitamin E as well as increased plasma levels of lipid peroxidation products. The decrease in antioxidant nutrients is related to the severity of the disease (96). We activated endothelial cells with tat protein, lipopolysaccharide (LPS), or IL-1 β and measured oxidation of nonfluorescent 2′,7′dichlorohydrofluorescein (DCHF) to dichlorofluorescein (DCF), which emits fluorescence.

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AIDS and Heart Disease by Ronald R. Watson


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