Amino acid sequence surrounding the lipoic acid cofactor of bovine kidney 2-oxoglutarate dehydrogenase complex

The 2-oxoglutarate dehydrogenase complex was succinylated using 2-oxo[5-14C]glutarate in the presence of N-ethylmaleimide to label the lipoic acid cofactor of the transuccinylase (E2) component. Following peptic digestion, 14C-lipoate-containing peptides were purified and subjected to automated Edman degradation and amino acid analysis. The amino acid sequence surrounding the lipoyllysine residue is reported.     

Angiotensin II-induced vascular smooth muscle cell hypertrophy: PDGF A-chain mediates the increase in cell size

We report here that angiotensin II-mediated hypertrophy of vascular smooth muscle cells (VSMC) exhibits PDGF A-chain-and -pathways. Secretion of PDGF A-chain is required for the increase in cell size, but not for the increase in protein synthesis. Angiotensin II stimulates a hypertrophic growth response in VSMC characterized by increases in cell size and protein synthesis, but not cell number. Because angiotensin II-stimulated VSMC hypertrophy has been associated with increased PDGF A-chain expression, we studied its role in the hypertrophic response by inhibiting PDGF A-chain expression with hydrocortisone or anti-PDGF antibody. Hydrocortisone (1 μM for 48 h) inhibited basal protein synthesis by 47%, but angiotensin II-stimulated protein synthesis was enhanced (111% increase after hydrocortisone treatment vs. 25% increase in control). In contrast, hypertrophy, as measured by cell size, was completely inhibited. Although hydrocortisone had no effect on early growth signals stimulated by angiotensin II (e.g., activation of protein kinase C, stimulation of Na⁺/H⁺ exchange, and c-fos and c-myc expression), it significantly decreased angiotensin II-stimulated secretion of PDGF-like material into the medium from 0.4 to 0.1 ng/ml/24 h (p < 0.01). However, the time course for PDGF secretion (maximal at 16–24 h) was significantly slower than the time course for angiotensin II-stimulated protein synthesis (maximal at 4–12 h). To block the action of PDGF A-chain selectively, VSMC were treated with anti-PDGF A-chain antibody. The antibody completely inhibited the angiotensin II-stimulated increase in cell size, but it had no significant effect on protein synthesis at early times (<8 h). These findings demonstrate two pathways involved in angiotensin II-stimulated VSMC hypertrophy: an increase in cell size dependent on PDGF A-chain and an increase in protein synthesis independent of PDGF A-chain. © 1993 Wiley-Liss, Inc.     

THE INFLUENCE OF SODIUM, POTASSIUM AND LANTHANUM ON AMINO ACID RELEASE FROM SPINAL–MEDULLARY SYNAPTOSOMES

Abstract— The effects of electrical pulses and raised potassium on glycolysis and the release of the putative transmitter amino acids glutamate, aspartate, glycine and GABA from spinal medullary synaptosomes is studied and compared with effects on glutamine, alanine and serine. The actions of ouabain, p -hydroxymercuribenzoate ( p -HMB), lanthanum chloride and lowered sodium levels on the release of all the amino acids is examined. All agents caused a change in the pattern of release of the amino acids, mostly, producing an increase, but only lanthanum, p -HMB and lowered sodium prevented the stimulus-induced release.     

Review of the taxonomy of the Calanidae (Copepoda) and the limits to the genus Calanus

Conflicting systems of classifying the Calanidae (Brodsky, 1972; Bradford & Jillett, 1974) are analysed and a preferred system recommended. Brodsky's system, based on characters with assumed adaptive and functional significance is rejected as is his claim to have produced a phylogenetic scheme. Bradford & Jillett's system, based on a variety of characters, results in a coherent classification which aims to be neutral concerning phylogenetic relationships among genera. Species of Calanoides, Calanus, Nannocalanus, and Neocalanus are surveyed and the need for further taxonomic work is assessed.