The effects of second-hand smoke on biological processes important in atherogenesis

BACKGROUND: Atherosclerosis is the leading cause of death in western societies and cigarette smoke is among the factors that strongly contribute to the development of this disease. The early events in atherogenesis are stimulated on the one hand by cytokines that chemoattract leukocytes and on the other hand by decrease in circulating molecules that protect endothelial cells (ECs) from injury. Here we focus our studies on the effects of "second-hand" smoke on atherogenesis. METHODS: To perform these studies, a smoking system that closely simulates exposure of humans to second-hand smoke was developed and a mouse model system transgenic for human apoB(100 )was used. These mice have moderate lipid levels that closely mimic human conditions that lead to atherosclerotic plaque formation. RESULTS: "Second-hand" cigarette smoke decreases plasma high density lipoprotein levels in the blood and also decreases the ratios between high density lipoprotein and low density lipoprotein, high density lipoprotein and triglyceride, and high density lipoprotein and total cholesterol. This change in lipid profiles causes not only more lipid accumulation in the aorta but also lipid deposition in many of the smaller vessels of the heart and in hepatocytes. In addition, mice exposed to smoke have increased levels of Monocyte Chemoattractant Protein–1 in circulation and in the heart/aorta tissue, have increased macrophages in the arterial walls, and have decreased levels of adiponectin, an EC-protective protein. Also, cytokine arrays revealed that mice exposed to smoke do not undergo the switch from the pro-inflammatory cytokine profile (that develops when the mice are initially exposed to second-hand smoke) to the adaptive response. Furthermore, triglyceride levels increase significantly in the liver of smoke-exposed mice. CONCLUSION: Long-term exposure to "second-hand" smoke creates a state of permanent inflammation and an imbalance in the lipid profile that leads to lipid accumulation in the liver and in the blood vessels of the heart and aorta. The former potentially can lead to non-alcoholic fatty liver disease and the latter to heart attacks

Liquid−Liquid and Liquid−Liquid−Solid Equilibrium of the Poly(ethylene glycol) Dimethyl Ether 2000 + Sodium Sulfate + Water System

The phase diagram for the poly(ethylene glycol) dimethyl ether (PEGDE) + Na2SO4 + H2O system at 298.15 K using PEGDE with a molar mass of 2000 was determined. Compositions of the liquid−liquid and the liquid−liquid−solid equilibria were determined using calibration curves of refractive index of the solutions, and atomic absorption (AA) and X-ray diffraction analyses were made on the solids. The solid phase in equilibrium with the biphasic region was anhydrous Na2SO4. An empirical nonlinear three-parameter expression developed by Merchuk was used for reproducing the experimental binodal data at T = (288.15, 298.15, 308.15, and 318.15) K, and the fitting parameters were obtained for the corresponding temperatures. The effects of temperature on the binodal curve were also studied, and it was observed that the area of the biphasic region increased slightly with an increase in temperature. The experimental tie-line compositions at the aforementioned temperatures were fitted to both the Othmer−Tobias and Bancroft and Setschenow-type equations. Correlation coefficients for all equations are reported.</p