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Biomedical subjects

S Shibata

Publications and source records attributed to S Shibata.

At least 829 records · Page 46Linked to original sources
PubMed1982

Membranous glomerulonephritis associated with eosinophilic lymphfolliculosis of the skin (Kimura's disease): report of a case and review of the literature.

A 48-year-old male, who had been suffering from eosinophilic lymphfolliculosis of the skin (Kimura's disease) for six years, developed the nephrotic syndrome. Renal biopsy revealed immunopathological and electron microscopic changes characteristic of membranous glomerulonephritis. A review of the literature disclosed a high frequency of renal involvement in Kimura's disease. Out of 175 reported cases of the disease, 21 (12%) were found to have proteinuria including 13 who had the nephrotic syndrome. Some of the patients were noticed to have proteinuria before the onset of the skin lesions, suggesting the existence of common etiological factor(s) capable of inducing both skin and kidney lesions.

Ear Neoplasms↗
PubMed1981

A third glycopeptide (nephritogenoside) isolated from the glomerular basement membrane.

A new glycopeptide was isolated from the glomerular basement membrane (GBM) of normal rats. Unlike already known glycopeptides, this glycopeptide has biological activity (nephritogenic activity) to induce glomerulonephritis when injected once into the footpads of homologous animals. A close relationship was found between the nephritogenic activity and the non-dialyzable glucose content of this glycopeptide. Thus the nephritogenic activity can be assessed quantitatively by estimating the content of "non-dialyzable glucose." Chemical purification of the nephritogenic glycopeptide involved the selective removal of inactive glycopeptide containing galactose, mannose, and N-acetyl-glucosamine (but no glucose). Trichloroacetic acid (TCA) treatment was a simple but highly effective procedure for selective removal of this inactive glycopeptide. The non-reducing terminus of the nephritogenic glycopeptide is alpha-D-glucopyranoside, and the glycopeptide reacts specifically with concanavalin A, even in the crude state. We propose that the nephritogenic glycopeptide is not an artifact produced during exhaustive proteolytic digestion, but a natural substance having a fixed molecular shape, even in the crude state, and whose union with GBM-proper can be easily broken by proteolytic digestion.

Animals↗
PubMed1981

Possible mechanism of the dual action of the new polypeptide (anthopleurin-B) from sea anemone in the isolated ileum and taenia caeci of the guinea-pig.

1 Anthopleurin-B (AP-B), a newly isolated polypeptide from a sea anemone (Anthopleura xanthogrammica) caused relaxation of the guinea-pig isolated ileum following a transient contraction at concentrations greater than 3 x 10(-9) M. 2 AP-B caused a tonic contraction followed by rhythmic relaxation of the guinea-pig isolated taenia caeci at a concentration of 3 x 10(-9) M or more. 3 The other polypeptides, anthopleurin-A (AP-A) from the same species of anthopleurin-C (AP-C) from Anthopleura elegantissima elicited similar effects but higher concentrations were required in both tissues. 4 These responses induced by AP-B in both tissues were abolished by treatment of each tissue with tetrodotoxin or incubation in a low-Na+ medium. 5 In the ileum, the AP-B-induced contraction was markedly inhibited by atropine but not by mecamylamine, whereas the AP-B-induced relaxation was not affected by phentolamine of guanethidine. 6 The AP-B-induced contraction of the taenia caeci was also inhibited by atropine, but not mecamylamine. However, in contrast to the ileum, the spontaneous relaxation of this tissue was completely abolished in the presence of phentolamine or guanethidine. 7 These results suggest that the AP-B-induced contractions of both tissues are mainly caused by acetylcholine (ACh) release from the cholinergic nerve terminals and that the AP-B-induced relaxation of the taenia caeci is due to the excitation of adrenergic nerves, while the relaxation of the ileum is mediated through non-adrenergic inhibitory mechanisms.

Animals↗
PubMed1981

Excitatory effect of a new polypeptide (anthopleurin-B) from sea anemone on the guinea-pig vas deferens.

1 Anthopleurin-B (AP-B, greater than 3 x 10(-9) M), a newly isolated polypeptide from sea anemone (Anthopleura xanthogrammica), caused powerful rhythmic contractions in the guinea-pig isolated vas deferens. The other polypeptides anthopleurin-A from A. xanthogrammica and anthopleurin-C from A. elegantissima, elicited similar effects but in higher concentrations ( less than 5 x 10(-8) M). Toxin II (10(-6) M) isolated from the sea anemone, Anemonia sulcata, had no effect. 2 The rhythmic contractions induced by AP-B were inhibited by phentolamine, bretylium, guanethidine, reserpine, 6-hydroxydopamine, tetrodotoxin (TTX) and verapamil. Mecamylamine, atropine, methysergide, chlorpheniramine, and indomethacin had no effect. 3 AP-B (10(-8) M approximately 10(-5) M) caused a dose-dependent increase in the amount of endogenous noradrenaline (NA) released from the vas deferens. AP-B (10-5M) increased the amount of NA released to approximately 310 times (12 micrograms/g tissue) that of untreated tissues. 4 The AP-B-induced release of NA was inhibited or abolished by TTX, verapamil, or incubation in Ca-free medium. 5 These results suggest that the AP-B-induced rhythmic contraction of the vas deferens is mediated through the release of NA from adrenergic nerve endings; AP-B is one of the most potent substances in stimulating NA release from the vas deferens.

Animals↗
PubMed1981

Electromechanical effects of anthopleurin-A (AP-A) on rabbit ventricular muscle: influence of driving frequency, calcium antagonists, tetrodotoxin, lidocaine and ryanodine.

1 Anthopleurin-A (AP-A 5 x 10(-9) M, 1 x 10(-8) M) caused a prolongation of action potential duration (APD) and an increase of contractile force in rabbit isolated ventricular muscle preparations.2 The prolongation of APD and the positive inotropic effect of AP-A (1 x 10(-8) M) were augmented by lowering the driving frequency from 2.0 to 0.2 Hz, resulting in an apparent negative staircase of contractile force in this frequency range. When the preparation was driven at an extremely low frequency (0.017 Hz), AP-A did not increase the contractile force, but caused a considerable prolongation of APD.3 Verapamil (1 x 10(-6) M) and nifedipine (1 x 10(-6) M) had no apparent influence on the APD prolongation by AP-A (5 x 10(-9) M, 1 x 10(-8) M). The positive inotropic effect of AP-A was also relatively well maintained even in the presence of these calcium antagonistic drugs when the preparation was driven at a lower frequency (0.2 Hz).4 Tetrodotoxin (TTX 2 x 10(-6) M) and lidocaine (1 x 10(-4) M) markedly inhibited both the APD prolongation and the positive inotropic effect of AP-A (1 x 10(-8) M).5 In the presence of ryanodine (2 x 10(-6) M), an agent which is known to interfere with calcium release from the intracellular activator pool, AP-A (1 x 10(-8) M) failed to cause its positive inotropic effect in spite of the marked prolongation of APD.6 These results suggest that the effects of AP-A on cardiac muscle are primarily mediated by the fast sodium inward current. Thus, delayed inactivation of sodium inward current may cause APD prolongation, and probably induces an alteration of intracellular calcium kinetics reflected by an increase of contractile force.

Action Potentials↗
PubMed1981

A comparative study of the relaxing effect of nitroprusside and verapamil on human umbilical vessels.

Relaxing effects of nitroprusside and verapamil on the resting or K-stimulated tension and 45Ca uptake in human umbilical vessels were investigated. Both nitroprusside and verapamil reduced the resting and K-stimulated tensions in a dose-dependent manner. Nitroprusside was much more effective than verapamil in reducing resting tension. However, verapamil caused a greater relaxation of the K-induced contraction than nitroprusside. In a Ca2+-free medium, K+ still caused a small and sustained contraction. Nitroprusside abolished the contraction in the Ca2+-free medium, which verapamil failed to inhibit. Neither nitroprusside nor verapamil affected the resting 45Ca uptake measured by a lanthanum method. The K-induced increase in 45Ca uptake was inhibited by verapamil, but not by nitroprusside. The results suggest that nitroprusside unlike verapamil does not act as a Ca2+ influx inhibitor resulting in the relaxation of human umbilical vessels.

Calcium↗
PubMed1981

Pharmacological sequential trials for the fractionation of components with hypoglycemic activity in alloxan diabetic mice from ginseng radix.

Three methods of fractionation of ginseng radix (Panax ginseng C.A. MEYER) components for a survey of hypoglycemic principle in alloxan diabetic mice were conducted and three groups of hypoglycemic principle in alloxan diabetic mice were conducted and three groups of components tested; fat-soluble components, ginseng saponins and a third component with hypoglycemic activity. Pharmacological sequential trials of the fractionation yielded a most active fraction which was about 100-fold more effective than the original water-soluble extract of the ginseng radix. The ED50 value was 0.4 mg/kg in lowering the blood level of glucose in alloxan diabetic mice. It was demonstrated that some ginseng fractions inhibited epinephrine-induced transient hyperglycemia in mice, increased glycogen content in rat liver, decreased the blood level of acetone bodies in alloxan diabetic mice, and inhibited the release of free fatty acid from rat epididymal fat pad. The results showed that hypoglycemic components existed in a new component of ginseng radix which is different from saponin.

Animals↗
PubMed1981

Effects of electroconvulsive shock on mouse-killing behavior (muricide) in olfactory bulbectomized rats.

We investigated the influence of electroconvulsive shock (ECS), regarded to possess an antidepressant effect clinically, on muricide in olfactory bulbectomized rats (OB rats). Muricide in these rats was markedly inhibited by ECS treatment. Five and 10 min after the termination of ECS-induced convulsions, muricide was inhibited by 100%. Even after intervals of 20 and 60 min, inhibition rates of 80% and 30% were obtained, respectively. ECS-induced muricide inhibition was remarkably antagonized by pretreatment with the alpha-blocker phenoxybenzamine but not by pretreatment with the beta-blocker sotalol. ECS-induced suppression of muricide was potentiated by repeated ECS treatment once daily for 10 days. After several applications of ECS treatment, muricide was inhibited in muricide tests done 24 hours after ECS treatment; this state persisted for up to 10 days thereafter. The results of this experiment demonstrated that ECS treatment specifically inhibited muricide in OB rats and further suggested that the cerebral noradrenergic alpha-receptor system plays an important role in this ECS-induced inhibition of muricide. Similar findings in the case of antidepressant administration, inhibition of muricide was potentiated by chronic ECS treatment. Specific inhibition of muricide in OB rats by antidepressants indicated that this phenomenon may serve as an animal model for the evaluation of antidepressant activity. Our results reiterate the usefulness of muricide in OB rats as an excellent experimental model for the assessment of antidepressant activity.

Aggression↗
PubMed1981

Hemoglobin Yusa (beta 21 (B3) Asp leads to Tyr), a new abnormal hemoglobin found in Japan.

An electrophoretically slowly moving hemoglobin variant, Hb Yusa, was found in a 48-year-old man, his younger sister and mother. No clinical or hematological abnormalities were seen in the individuals heterozygous for this mutant gene. Structural studies of this abnormal hemoglobin showed a new type substitution of beta 21 (B3) Asp leads to Tyr. The percentage of the abnormal hemoglobin in the hemolysate was 40.8. The hemoglobin had neither instability nor functional abnormality.

Amino Acids↗