Effects of unstirred layers or transport number discontinuities on the transient and steady-state current-voltage relationships of membranes

The effects of current-induced electrolyte accumulation and depletion on the electrical properties of a two-layered membrane system have been examined. The membrane consisted of a charged, ion permselective layer and an uncharged, non-selective layer. The model was designed to reveal the properties of membranes possessing long pores with ionic charges at one end or of ion-selective membranes bounded by highly unstirred aqueous layers. Electrolyte concentration profiles in the inert layer and their time-dependent changes were obtained from solutions of the diffusion equation under the condition of constant current. The profiles were then used to calculate the voltage developed across the membrane at various times after the current is switched on. The theoretical results are presented in the form of i-V curves with reduced coordinates that can be used to obtain time-current-voltage relationships for membranes of the type considered having any thickness of the non-selective layer and bathed in any concentration of any 1:1 electrolyte. Experimental results on a model composite membrane were in good agreement with calculations that assume that ion transport occurs only under the influence of electrical potential and concentration gradients, suggesting that in such systems, the combined effects of convection, osmosis, electro-osmosis, and concentration-dependence of diffusion coefficients, activity coefficients, and transference numbers are small. Voltage fluctuations in the form of periodic spikes were observed experimentally at the limiting current density (the current density at which the electrolyte concentration at one surface of the selective layer goes to 0). These phenomena were not seen when the current was in the direction leading to accumulation of electrolyte in the non-selective (unstirred) layer. Such composite membranes can exhibit S-shaped and N-shaped i-V curves under ramp-voltage and ramp-current clamps, respectively.     

Trichinosis causing extensive ventricular mural endocarditis with superimposed thrombosis. Evidence that severe eosinophilia damages endocardium

Clinical and morphologic observations are described in a 46 year old woman with fatal trichinosis. Attention is called to the occurrence of extensive ventricular endocardial damage with superimposed thrombosis; Evidence is presented to indicate that the most likely cause of the endocardial damage is the associated eosinophilia. The mechanism by which eosinophils damage endocardium, however, remains obscure.     

Leucine and isoleucine as in vitro precursors for lipid synthesis by rat aorta

The in vitro conversion of¹⁴C-labeled leucine, isoleucine, and pyruvate to specific lipids was compared in rat aorta, diaphragm, and fat pad. Total lipid specific radioactivity from all precursors was greatest in aorta. The ratio of label incorporated into polar lipids vs. neutral lipids by aorta was generally several-fold that incorporated by muscle and fat pad. The labeling of sterols in the aorta from¹⁴C-leucine and pyruvate was equivalent. It is concluded that leucine may be a substantial precursor to polar lipids and to sterols in rat aorta. This paper was presented in part at the 1974 Biochemistry and Biophysics Meeting of the Fed. Am. Soc. Exp. Biol.     

Studies on the mechanism of action of halofenate

This paper reviews most of the preclinical studies on the mode of action of halofenate, an established hypolipidemic-hypouricemic agent in man. In yeast cultures and in isolated rat adipocytes, halofenate was found to inhibit the conversion of pyruvate to acetyl CoA. While pyruvate dehydrogenase was inhibited in vitro, halofenate also inhibited the activity of various other isolated enzymes. In rats maintained on halofenate in the diet (0.02–0.10%) for 2–14 days, there were 20–40% decreases in plasma cholesterol, trigly cerides, phospholipids, and free fatty acids. Inhibition of liver HMG-CoA reductase does not appear to account for the hypocholesterolemic effect, and activation of mitochondrial α-glycerophosphate dehydrogenase does not explain the hypotriglyceridemic action. Kinetic measurements of the serum appearance and disappearance of triglycerides in drug-treated rats suggest that the hypotriglyceridemic activity is due to a net inhibition of hepatic triglyceride synthesis. Reduction of very low density lipoprotein (VLDL) and high density lipoprotein (HDL) levels in rats with sucrose-induced hyperlipidemia and normalization of the altered apolipoprotein profiles are in accord with the effects of halofenate on plasma triglyceride and cholesterol levels. The reduced insulin-to-glucagon ratio observed in Zucker obese hyperlipemic rats is also consistent with halofenate's hypotriglyceridemic activity. Preliminary experiments in rats on the mechanism of its hypoglycemic activity, observed in some diabetic hyperlipidemic patients, indicate that halofenate acts differently than conventional oral hypoglycemic agents. Some, but not all, of the effects of halofenate were observed with clofibrate at two to ten times higher levels. The list of literature references on halofenate cited in this paper is not a complete one. Since 1970, there have been over 100 publications on halofenate of which 20 relate to mechanism of action studies in laboratory animals or man. Fifty are primarily concerned with clinical hypolipemic and hypouricemic activity and the balance on other aspects of its properties.     

trans-6-hexadecenoic acid in the spadefishChaetodipterus faber

Fatty acid methyl esters were prepared from spadefish (Chaetodipterus faber) liver oil and were analyzed by open tublar gas chromatography. The unusual fatty acidtrans-6-hexadecenoic acid was identified as a major monoenoic component by reductive ozonolysis and by mass spectrometry of the di-trimethylsilyl ether. Very minor amounts of 7-methyl-7-hexadecenoic acid were found.