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Biomedical subjects

A Baba

Publications and source records attributed to A Baba.

At least 271 records · Page 15Linked to original sources
PubMed1985

An inhibitory factor against monocyte spreading in the sera of patients with systemic lupus erythematosus.

The effect of the sera of patients with systemic lupus erythematosus (SLE) on monocyte function was studied using cell spreading as an indicator. Monocyte spreading induced by exogenous stimuli was shown to be inhibited by SLE sera. Gel filtration of SLE sera on Sephadex G-200 revealed that the factor responsible for this inhibition had a molecular weight of about 50,000. Pretreatment of monocytes with the inhibitory factor led to suppression of cell spreading induced by subsequent stimulation, but this hyporeactivity was reversible. Spreading of monocytes was rapidly aborted by the addition of this inhibitory factor. Thus, the inhibitory factor appeared to affect monocyte itself, but its effect seemed to be transient.

Cell Adhesion↗
PubMed1985

Irreversible inhibition of calcium uptake in synaptosomes by quinacrine mustard: relationship to labeling sites of quinacrine mustard.

The sites of interaction of quinacrine with synaptic membranes were labeled with quinacrine mustard. Quinacrine mustard had an inhibitory effect on depolarization-induced calcium uptake by synaptosomes similar to that of quinacrine. The inhibition of depolarization-induced calcium uptake by quinacrine was reduced by 70% after washing, whereas that by quinacrine mustard was not affected. Fluorescence electrophoretograms of the quinacrine mustard-treated synaptic membranes showed that quinacrine mustard specifically labeled two proteins, with corresponding molecular weights of about 37,000 and 32,000.

Animals↗
PubMed1984

Sexual dimorphism of the fifth component of mouse complement.

Sexual dimorphism of mouse complement component 5 (C5) was detected by isoelectric focusing of desialated ethylenediamine tetraacetic acid (EDTA)-plasma on agarose gel, followed by immunofixation with anti-mouse C5. Male plasma displayed two C5 bands, basic and acidic, while female plasma had only a basic C5 band. In all mouse strains tested except C5-deficient strains, the identical patterns of the dimorphism were obtained. The basic and acidic C5 were antigenically and hemolytically indistinguishable from each other. In the neonatal mice of both sexes, the basic C5 was observed at the same levels, but the acidic C5 was only slightly detected. Injection of testosterone into mice resulted in an appearance of the acidic C5 in females and its increase in males. By contrast, injection of estradiol decreased the acidic C5. These results indicate that the expression of the acidic C5 is under the control of testosterone.

Animals↗
PubMed1984

Effect of taurine on a benzodiazepine-GABA-chloride ionophore receptor complex in rat brain membranes.

Taurine at 10 mM had no effect on basal binding of [3H]diazepam to the membranes, while it significantly inhibited a GABA-stimulated binding of [3H]diazepam in cerebral cortex, hippocampus, but not in cerebellum. The inhibition by taurine in the presence of GABA (1 microM to 1 mM) was not competitive. At low concentrations (0.04 to 0.2 nM) the binding of [3H]propyl-beta-carboline-3-carboxylate, a ligand exhibiting higher affinity for type I than type II benzodiazepine receptors, was not enhanced by GABA, while the binding of higher concentrations (0.5 nM) was. This GABA enhancement of [3H]propyl-beta-carboline-3-carboxylate binding was also selectively blocked by taurine. Pentobarbital increased the binding of [3H]diazepam in a medium containing chloride and this effect was potentiated by taurine at 1-10 mM. These findings may be relevant to the modulatory role of taurine in the central nervous system.

Animals↗
PubMed1984

Modulation by unsaturated fatty acids of norepinephrine- and adenosine-induced formation of cyclic AMP in brain slices.

The effect of linoleic acid on the formation of cyclic AMP in the slices of guinea pig cerebral cortex was examined. Treatment of the slices with linoleic acid resulted in an increase of basal and of norepinephrine-stimulated formation of cyclic AMP. The stimulatory effect on the basal level of cyclic AMP was not specific for linoleic acid: the potency of the fatty acid was related to the magnitude of unsaturation. In contrast, the enhancement of norepinephrine-stimulated formation of cyclic AMP seemed relatively specific for linoleic acid and arachidonic acid. Linoleic acid markedly enhanced the stimulated formation of cyclic AMP by histamine and adenosine, as well that by norepinephrine, without affecting that by excitatory amino acids and veratridine. Theophylline, adenosine deaminase, and 2'-deoxyadenosine antagonized the effect of linoleic acid. Linoleic acid enhanced the maximum responses to norepinephrine and adenosine without altering the ED50 values for these agonists. When linoleic acid-treated slices were washed with Krebs-Ringer containing defatted bovine serum albumin, both enhancement of the response to norepinephrine and the amount of [14C]linoleic acid incorporated in a free form significantly diminished.

Adenosine↗
PubMed1983

Inhibition by quinacrine of depolarization-induced acetylcholine release and calcium influx in rat brain cortical synaptosomes.

The effects of quinacrine on depolarization-induced [3H]acetylcholine (ACh) release and 45Ca2+ influx were examined in rat brain cortical synaptosomes. Quinacrine significantly reduced the stimulated release of [3H]ACh by high K+ and veratridine without affecting the spontaneous efflux from the preloaded synaptosomes. Quinacrine had no effect on ionophore A23187-induced release of [3H]ACh from the synaptosomes. Quinacrine (100 microM) markedly diminished the stimulated Ca2+ influx by veratridine and high K+ but not that by "Na+-free." Trifluoperazine, a potent calmodulin antagonist, inhibited both Ca2+ influx and ACh release induced by the depolarizing agents. Inhibitory potencies of the two drugs on ACh release and Ca2+ influx were compared with the antagonism of calmodulin by two drugs, suggesting that the inhibition of depolarization-induced Ca2+ influx and ACh release by these drugs could not be explained by the antagonism of calmodulin.

Acetylcholine↗
PubMed1983

Inhibition by Diazepam and γ-Aminobutyric Acid of Depolarization-Induced Release of [¹⁴C]Cysteine Sulfinate and [³H]Glutamate in Rat Hippocampal Slices.

Effects of diazepam and γ-aminobutyric acid-related compounds on the release of [¹⁴C]cysteine sulfinate and [³H]glutamate from preloaded hippocampal slices of rat brain were examined by a superfusion method. Diazepam markedly inhibited the release of cysteine sulfinate and glutamate evoked either by high K⁺ or veratridine without affecting that of other neurotransmitter candidates, e.g., γ-aminobutyric acid, acetylcholine, noradrenaline, and dopamine; IC₅₀ values for the release of cysteine sulfinate and glutamate were about 20 and 7 μM, respectively. γ-Aminobutyric acid (1 to 10 μM) and muscimol (100 μM) significantly reduced high K⁺-stimulated release of glutamate. Bicuculline, which had no effect on the release at a concentration of 50 μM by itself, antagonized the inhibitory effects of diazepam and γ-aminobutyric acid on glutamate release. Similar results were obtained with the release of cysteine sulfinate except that a high concentration (100 μM) of γ-aminobutyric acid was required for the inhibition. These results indicate the modulation by γ-aminobutyric acid innervation of the release of excitatory amino acids in rat hippocampal formation, and also suggest that some of the pharmacological effects of diazepam may be a consequence of inhibition of excitatory amino acid transmission.

Animals↗
PubMed1982

Solubilization of adenylate cyclase of brain membranes by lipid peroxidation.

Adenylate cyclase in the membrane fractions of bovine and rat brains, but not in rat liver plasma membranes, was solubilized by treatment with Fe2+ (10 microM) plus dithiothreitol (5 mM). Solubilization of the enzyme by these agents was completely prevented by simultaneous addition of N,N'-diphenyl-p-phenylenediamine (DPPD), an inhibitor of lipid peroxidation. Ascorbic acid also solubilized the enzyme from the brain membranes. Lipid peroxidation of the brain membranes was characterized by a selective loss of phosphatidylethanolamine. Solubilization of membrane-bound enzymes by Fe2+ plus dithiothreitol was not specific for adenylate cyclase, because phosphodiesterase, thiaminediphosphatase and many other proteins were also solubilized. Solubilized adenylate cyclase had a high specific activity and was not activated by either NaF, 5'-guanylyl imidodiphosphate (Gpp[NH]p) or calmodulin. These results suggested that lipid peroxidation of the brain membranes significantly solubilized adenylate cyclase of high specific activity.

Adenylyl Cyclases↗
PubMed1982

Cysteine sulfinic acid in the central nervous system: uptake and release of cysteine sulfinic acid by a rat brain preparation.

Uptake and release of cysteine sulfinic acid by synaptosomal fractions (P2) and slices of rat cerebral cortex were investigated. The P2 fraction had a Na+-dependent high-affinity uptake system for cysteine sulfinic acid (Km, 12 microM), which was restricted to the synaptosomes. High-affinity uptake of cysteine sulfinic acid was competitively inhibited by glutamate, aspartate, and cysteic acid. None of the various centrally acting drugs tested specifically inhibited this transport system. Release of [14C]cysteine sulfinic acid from preloaded cortical slices or P2 fractions was examined by a superfusion method, which avoided reuptake of released [14C]cysteine sulfinic acid. High K+ (56 mM) and veratridine (10 microM) stimulated the release of cysteine sulfinic acid from slices and the P2 fraction in a partly Ca2+-dependent manner. Diazepam at concentrations of 10 and 100 microM markedly inhibited the stimulated release, but not the spontaneous release, by cortisol slices. On the contrary, it had no effect on the stimulated release of cysteine sulfinic acid from the P2 fraction.

Animals↗