Flame propagation in a closed deformable channel

Izhevsk. Translated from Fizika Goreniya i Vzryva, Vol. 26, No. 3, pp. 27–33, May–June, 1990.     

Volumetric (PVT) and Calorimetric (C V VT) Measurements for Pure Methanol in the Liquid Phase

Volumetric (PVT) and calorimetric (C _V VT) properties of pure methanol were measured in the liquid phase with a twin-cell adiabatic calorimeter. Temperatures were measured in a range from 314 to 411 K, densities between 699.3 and 775.6 kgm^–3, and pressures to 20 MPa. The calorimetric cell (70 cm³ capacity) was surrounded by adiabatic thermal shielding (high vacuum). The sample pressures were measured by means of a quartz crystal transducer to within an uncertainty of about ±7 kPa. The relative uncertainty of C _V was estimated to be 2%, with a coverage factor k = 2, by combining the various sources of experimental uncertainty using a root-sum-of-squares formula. The results for pure methanol were compared with other recent measurements performed with a second high-temperature, high-pressure adiabatic calorimeter. Deviations of less than 3% were found between the earlier C _V data and the present results for pure methanol. The uncertainty of the density measurements was estimated to be 0.2% (k = 2). The measured densities and isochoric heat capacities were compared with values calculated with an IUPAC equation of state. Agreement of density was within 0.088% and that for isochoric heat capacity was within 0.95%. Values of vapor pressure were determined by extrapolating experimental P–T data to the saturated temperature along a fixed isochore. In the temperature range of this study, decomposition of methanol was not observed.     

Type of hydrocarbon activation and nature of active sites of base catalysts in methane oxidative dehydrodimerization

Methane activation on magnesium-oxide-cased catalysts for methane dehydrodimerization has been studied. As found, the rate of dehydrodimerization changes proportionally with the concentration of base sites on the catalytic surface. The activation of methane results in the formation of the methyl anion, as ascertained by IR-Fourier spectroscopy. The dehydrodimerization rates have been compared with the concentration of one-electron sites and the rate of the CH₄---CD₄ isotope exchange. Based on the data obtained a new mechanism of methane dehydrodimerization has been proposed; at the first reaction step a fast heterolytic dissociation of methane on base sites takes place. The rate-determining step is that of the metal-methyl dissociation leading to the formation of the methyl radical which determines a high activation energy of methane dehydrodimerization on oxide catalysts.     

Watanabe rabbits with heritable hypercholesterolaemia: a model of atherosclerosis

Many factors play important roles in the development of atherosclerotic lesions. The leading risk factor for atherosclerosis is familial hypercholesterolaemia (FH). FH is a genetic disease characterized by a deficiency of receptors for low density lipoprotein (LDL) on the plasmalemma of endothelial cells, a high level of serum LDL, and early development of atherosclerosis and skin xanthoma. Watanabe and colleagues have developed a line of rabbits with unprovoked hypercholesterolaemia, increased blood level of LDL, pronounced atherosclerosis and skin xanthoma. These Watanabe Heritable Hyperlipidaemic (WHHL) rabbits possess an inheritable mutation of one gene, similar to that in human FH. The morphogenesis of atherosclerosis in patients with FH is characterized by multifocal deposit of lipids in the stromal cells of thymus, spleen, skin, interstitial and parenchymatous cells of kidneys and the presence of some single foam cells in aorta. The manifestation of atherosclerotic lesions in WHHL rabbits increases progressively with age but the presence of atherosclerotic lesions in newborn WHHL rabbits suggest that the process may commence in utero. Moreover, the main mass of plasma cholesterol in WHHL rabbits is first found in LDL and to a lesser degree in lipoproteins of intermediate density. This is contrary to diet-induced atherosclerosis in rabbits where the main mass of serum cholesterol is found in very low density beta-lipoproteins. Thus the distribution of cholesterol among lipoprotein fractions differs from that in WHHL rabbits. Atherosclerotic damage of arteries in WHHL rabbits goes through several stages. During the progression of intimal damage, lipid and foam cell deposits are found in the internal surface together with developing plaques and increased content of lipids in the tunica media. Calcification often follows this process. The main factors initiating atherosclerosis in WHHL rabbits are adhesion of leukocytes and platelets to endothelial cells and the accumulation of lipids in the aortic wall. The deposits of lipids in macrophages and intimal smooth muscle cells in WHHL rabbits occurs mostly at the expense of cytoplasmic neutral lipid particles with some accumulation in lysosomes. Hypertension as a risk factor increases the area of atherosclerotic damage in all arterial vessels in WHHL rabbits, particularly in the thoracic and abdominal aorta. Morphogenesis of the development of atherosclerosis in WHHL and diet-induced atherosclerosis in rabbits was similar, but differs from rats with heritable hypercholesterolaemia. Damage or loss of endothelial cells can predispose the atherosclerotic vessels to vasospasm and can leave vessels unprotected against vasoconstrictor stimuli. The development of the WHHL model has not only given insight into the mechanisms of development of familial hypercholesterolaemia but has also provided a model for assessing various therapeutic approaches for the prevention and treatment of atherosclerosis.