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Biomedical subjects

Y Hirano

Publications and source records attributed to Y Hirano.

At least 235 records · Page 13Linked to original sources
PubMed1989

Heparin and heparan sulfate partially inhibit induction of acetylcholine receptor accumulation by nerve in Xenopus culture.

It has been demonstrated that ACh receptors in Xenopus nerve-muscle cultures migrate in the membrane to the nerve contact area during junction formation (Anderson et al., 1977) and that "diffusion trapping" is the major mechanism for nerve-induced receptor accumulation (Kidokoro and Brass, 1985; Kuromi et al., 1985; Kidokoro et al., 1986). A crucial remaining question is how the nerve induces the trap for randomly diffusing ACh receptors. In this study we examined the effect of various glycosaminoglycans in the culture medium on the nerve-induced receptor accumulation and found that heparin and heparan sulfate partially inhibited nerve-induced receptor accumulation, but similar molecules, chondroitin sulfate type A and type C, did not. By chemical modification of heparin we also showed that N-sulfate residues and a large-molecular-weight molecule are essential for this inhibitory effect. Heparin did not affect ACh receptor clustering (hot-spot formation) in myocytes cultured without nerve. By changing the time and duration of heparin application, we found that heparin was effective in inhibiting nerve-induced receptor accumulation only when it was present in the culture medium during the period that neurites are actively forming contact with muscle membrane.

Animals↗
PubMed1989

[Alteration of prostaglandin metabolism in alcoholic liver disease: its association with platelet dysfunction after chronic alcohol ingestion].

Recently, hepatic microcirculation has been focused on as an important pathogenic factor in progression of alcoholic liver disease (ALD). Therefore, blood levels of several prostaglandins, which are associated with organ microcirculation, were determined in various liver diseases, including ALD. Blood thromboxane B2 (TXB2) level was significantly increased in ALD, when compared to other types of liver diseases, whereas both 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) and prostaglandin E were not changed. These consequences resulted in the imbalance of 6-keto PGF1 alpha to TXB2, which might promote platelet aggregation and blood vessel contraction. Indeed, the increase of beta-thromboglobulin and platelet factor 4 in blood was observed in ALD. Furthermore, in ALD, the rate of arachidonate-induced platelet aggregation was prominently enhanced, and malondialdehyde production in platelet, which was well correlated with blood TXB2 levels, significantly increased. Thus, the present study may indicate that, in ALD, hyper-aggregability of platelet is produced, because of the derangement of prostaglandin metabolism and platelet dysfunction.

Adult↗
PubMed1989

[Usefulness of partial splenic embolization (PSE) in hepatocellular carcinomas showing a risk of gastrointestinal bleeding after transcatheter arterial embolization (TAE)].

We have examined 103 patients with a hepatocellular carcinoma (HCC) who were treated by transcatheter arterial embolization (TAE) with a partial splenic embolization (PSE) (n = 5) or without a PSE (n = 98). It was found that gastrointestinal (GI) bleeding after TAE occurred in 10 (10.2%) out of the 98 TAE patients and within 10 days after the TAE. In these GI bleeding after TAE patients, the platelet counts were significantly low and marked splenomegaly was seen. It also was found that there was a risk of GI bleeding after TAE in cases showing thrombocytopenia (less than 50,000/microliters) and marked splenomegaly with a splenic index of more than 50. In 5 patients with a high risk of GI bleeding, for whom a PSE was performed, the platelet counts were markedly increased even four weeks after the TAE. The survival rate of TAE patients given a PSE was significantly higher than in TAE patients manifesting a risk of GI bleeding. From these results, it would seem that TAE patients given a PSE is the better therapy for HCC patients manifesting a risk of GI bleeding.

Carcinoma, Hepatocellular↗
PubMed1989

[A case of metastatic liver cell carcinoma in the abdominal wall due to direct skin invasion from protruding liver tumor].

A case of a hepatocellular carcinoma with a metastasis to abdominal wall is reported. The patient was a 52-year-old man who, in December, 1982, had been found to have a 16 x 13 cm of tumor in the right lobe of the liver. He received transcatheter arterial embolization (TAE) several times and a hepatic segmentectomy twice. He survived more than six years until his death on January, 17, 1989. A subcutaneous tumor that had appeared in May, 1988 had gradually increased in size and was found to have reached 6 x 5.5 x 2.5 cm on autopsy. The tumor had connected directly with the liver tumor.

Abdominal Muscles↗
PubMed1989

[An experimental study on the severe type of alcoholic liver disease--a pathogenetic role of potentiated activation of complement system by endotoxin after chronic ethanol consumption].

Endotoxemia frequently appears in severe type of alcoholic liver disease. However, we have little knowledge how endotoxin influences the progression of alcoholic liver injury. Thus, to study the causal mechanism for the progression to the severe type of alcoholic liver diseases, endotoxin (0.2 mg/100 g BW, E. Coli O26:B6) was intravenously injected in chronic ethanol-fed rats and controls, and then, rats were sacrificed after 16 hours of endotoxin treatment. The elevation of serum GOT and GPT activities induced by endotoxin was significantly higher in chronic ethanol-fed rats than controls, and these biochemical changes were well correlated with the grade of necrosis of liver histology. Furthermore, in chronic ethanol-fed rats, endotoxin treatment tremendously increased blood BUN and creatinine levels and produced the degeneration of renal tubuli with neutrophil infiltration into glomerulus. These experimental findings are very similar to the severe type of alcoholic liver disease. On the other hand, endotoxin significantly decreased serum values of CH50 in chronic ethanol-fed rats, but not in controls. Such alterations of CH50 induced by endotoxin were well correlated with the several parameters indicating the injury of liver and kidney. Therefore, the present study may indicate that chronic ethanol ingestion aggravates endotoxin-induced organ injury, and that the activation of complement system may associate with such progression of organ injury.

Animals↗
PubMed1989

[Experimental Candida albicans chorioretinitis].

The long term (12 months) clinical and histopathological features of experimental chorioretinitis induced by intravenous injection of Candida albicans (5-10 x 10(6) spores) in pigmented rabbits were reported. Nine of 26 animals developed bilateral and 11 of 26 animals unilateral chorioretinal lesions. The lesions were round, yellow-white spots initially growing with a fluffy border, and breaking into the vitreous body. Finally, the lesions became chorioretinal scars with bridging strands in the vitreous body. Histologically, the initial lesions were subretinal microabscesses of pseudoeosinophils with PAS-positive spores, then macrophages invaded and typical granuloma with epithelioid and multinucleated giant cells developed. One year after the inoculation, focal chorioretinal scars with vitreous strands were found.

Animals↗
PubMed1988

Biochemical changes before and during oral calcium tolerance test in calcium stone formers.

116 normocalcemic and 8 primary hyperparathyroid (PHPT) patients with calcium (Ca) nephrolithiasis and 10 normal controls underwent 1 g of oral Ca tolerance test following 4 days of Ca restricted diet (400 mg/day). On the basis of urinary Ca/creatinine (Cr) ratio obtained by the test, the 116 patients with normocalcemic nephrolithiasis were divided into 3 groups (normocalciuric nephrolithiasis; NN, absorptive hypercalciuria; AH, renal hypercalciuria; RH) according to our criteria which were slightly modified from Pak et al. Changes in urinary Ca/Cr ratio, and those in serum Ca and phosphorus (P), tubular maximum reabsorption of phosphate/glomerular filtration rate (TmPO4/GFR), nephrogenous adenosine 3',5'-monophosphate (NcAMP) and plasma immunoreactive parathyroid hormone (iPTH) were determined. As a result, the 116 patients were divided into 82NN, 13AH and 21RH. In general, a rise in serum Ca and fall in NcAMP were seen first, followed by rises in urinary Ca/Cr ratio, serum P and TmPO4/GFR although the changes were small. The group PHPT showed abnormality in the changes of TmPO4/GFR, NcAMP and plasma iPTH. The former one decreased constantly during the test and the latter two did not fall to within the normal range, suggesting parathyroid autonomy or abnormal suppressibility. Regarding the normal controls, all the changes were smallest among the 5 groups and clear parathyroid suppression was not observed while it was seen in the groups NN, AH and RH. In conclusion, oral Ca tolerance test is useful not only to separate NN, AH and RH, but also for the diagnosis of PHPT by demonstrating parathyroid autonomy or abnormal suppressibility assessed by NcAMP and/or TmPO4/GFR.

Administration, Oral↗
PubMed1988

Barium-induced automatic activity in isolated ventricular myocytes from guinea-pig hearts.

1. A suction-pipette whole-cell clamp technique was applied to single ventricular myocytes isolated from guinea-pig hearts, in order to investigate the ionic mechanism underlying Ba2+-induced automatic activity. 2. The application of 0.1 mM or less Ba2+ to the myocytes caused a depolarization of the resting membrane potential without inducing spontaneous activity. The stimulated action potential showed a prolonged repolarization phase followed by an after-hyperpolarization. 3. Concentrations of Ba2+ of 0.2 mM or greater produced further depolarization of the resting membrane potential and induced spontaneous activity. Spontaneous activity developed from the slow diastolic depolarization preceded by after-hyperpolarizations of spontaneous or stimulated action potentials. 4. Under voltage-clamp conditions, a decaying outward or inward current in response to hyperpolarizing clamp steps from depolarized potentials appeared in the presence of Ba2+. The Ba2+-induced current decay showed a faster time course with increasing hyperpolarizing clamp pulses and reversed its polarity at around -90 mV, the presumed equilibrium potential for K+ (EK). In the late current-voltage (I-V) relation, Ba2+ almost eliminated the inward-rectifying property. These effects on the cardiac membrane are consistent with a time- and voltage-dependent blocking action of Ba2+ on inward-rectifying K+ currents as reported for other excitable tissues. 5. The concentration- and voltage-dependence of the steady-state block of the inward rectifying K+ current (IK1) was fitted by a simple model assuming 1:1 binding of Ba2+ to a site within the membrane. The apparent dissociation constant at the holding potential of 0 mV (K(0] was 0.3 mM, and the parameter for the membrane potential dependence of Ba2+ blockade (mu) was approximately 0.5. 6. A computer model of the ventricular action potential proposed by Beeler & Reuter (1977) was modified, based on the recent experiments using single cardiac myocytes. The modifications include (1) the current-voltage relationship of IK1, (2) time courses of activation and inactivation of the Ca2+ current (ICa), (3) the activation voltage range for the delayed outward K+ current (IK). 7. The time- and voltage-dependent blocking action of Ba2+ on IK1, including the experimentally determined values for K(0) and mu, were incorporated into the modified version of the action potential model. The computer model reproduced an after-hyperpolarization at doses of Ba2+ lower than 0.1 mM and automatic activity at doses higher than 0.15 mM.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗