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Biomedical subjects

Y Kishida

Publications and source records attributed to Y Kishida.

At least 37 records · Page 2Linked to original sources
PubMed1996

Role of Na(+)-Ca2+ exchanger in agonist-induced Ca2+ signaling in cultured rat astrocytes.

We have previously demonstrated that activation of the Na(+)-Ca2+ exchanger in the reverse mode causes Ca2+ influx in astrocytes. In addition, we showed that the exchange activity was stimulated by nitric oxide (NO)/cyclic GMP and inhibited by ascorbic acid. The present study demonstrates that the Na(+)-Ca2+ exchanger is involved in agonist-induced Ca2+ signaling in cultured rat astrocytes. The astrocytic intracellular Ca2+ concentration ([Ca2+]i) was increased by L-glutamate, noradrenaline (NA), and ATP, and the increases were all attenuated by the NO generator sodium nitroprusside (SNP). SNP also reduced the ionomycin-induced increase in [Ca2+]i. The NA-induced Ca2+ signal was also attenuated by S-nitroso-L-cysteine and 8-bromo cyclic GMP, whereas it was enhanced by 3,4-dichlorobenzamil, an inhibitor of the Na(+)-Ca2+ exchanger. Treatment of astrocytes with antisense, but not sense, deoxynucleotides to the sequence encoding the Na(+)-Ca2+ exchanger enhanced the ionomycin-induced increase in [Ca2+]i and blocked the effects of SNP and 8-bromo cyclic GMP in reducing the NA-induced Ca2+ signal. Furthermore, the ionomycin-induced Ca2+ signal was enhanced by removal of extracellular Na+ and pretreatment with ascorbic acid. These findings indicate that the Na(+)-Ca2+ exchanger is a target for NO modulation of elevated [Ca2+]i and that the exchanger plays a role in Ca2+ efflux when [Ca2+]i is raised above basal levels in astrocytes.

Adenosine Triphosphate↗
PubMed1996

Ca2+ depletion facilitates taurine release in cultured rat astrocytes.

Removal of external Ca2+ facilitated endogenous taurine release in cultured rat astrocytes. The stimulated release was not affected by furosemide, sucrose, tetrodotoxin and 3,4-dichlorobenzamil, but partially inhibited by nifedipine. Omission of external Na+ increased basal taurine release, and the effects of Na+ removal and Ca2+ depletion on the release were additive. The Na(+)-free condition did not affect Ca2+ paradox-induced cell death in astrocytes. These findings suggest that Ca2+ depletion facilitates taurine release in a mechanism independent of volume and the Na+ gradient and that the release is not involved in Ca2+ paradox-induced delayed cell toxicity in astrocytes.

Amiloride↗
PubMed1995

Ability of prolonged interferon treatment to suppress relapse after cessation of therapy in patients with chronic hepatitis C: a multicenter randomized controlled trial.

The aim of this study was to determine whether 12 months course of interferon alfa (IFN-alpha) therapy could improve the beneficial effect of IFN in chronic hepatitis C. Eighty-eight patients were treated with natural IFN-alpha for either 28 weeks (45 cases) or 52 weeks (43 cases). Sustained response was achieved in 15 (33.3%) of 45 cases treated for 28 weeks and in 23 (53.5%) of 43 cases treated for 52 weeks. Transient response with relapse of alanine transaminase (ALT) after completion of therapy was observed in 13 cases (28.9%) treated for 28 weeks and in 4 cases (9.3%) treated for 52 weeks. Thus, ALT relapse was suppressed by prolonged IFN treatment. No response was found in 17 cases (37.8%) treated for 28 weeks and in 16 cases (37.2%) treated for 52 weeks, indicating that approximately 38% of the patients with chronic hepatitis C were resistant to IFN therapy even with prolonged treatment. The rate of sustained response was significantly higher in patients with type 2a or 2b than in those with type 1b. Even in type 1b cases, it was higher in the 52-week treatment group than in the 28-week treatment group, and the rate of transient response was lower in the 52-week treatment group, indicating that relapse in type 1b cases was suppressed by prolonged IFN therapy. IFN therapy was not effective for patients with advanced liver fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Prevalence of hepatitis C virus in family members of patients with hepatitis C.

To investigate the prevalence of hepatitis C virus in the family members of patients with hepatitis C, we examined antibody to hepatitis C virus with a second-generation enzyme-linked immunosorbent assay and viral RNA with a combined assay of reverse transcription and polymerase chain reaction in sera. Among 219 (75 spouses, 110 children, and 34 others), 26 (12%) were antibody positive. The positive rate of antibody to hepatitis C virus was significantly higher than that of the control group (2.0%) and of volunteer blood donors in our district (1.5%), and it increased with age. In particular, the positive rate of antibody to hepatitis C virus among spouses was high (24%). Among family members with elevated ALT, 59% were antibody positive, which was significantly higher than that of the control group (11%). Of the 26 who were antibody positive, 21 (81%) had viral RNA, whereas of the 70 who were antibody negative, only one (1.4%) had viral RNA. These data suggest that hepatitis C virus was transmitted by the infrafamilial route during long duration of contact with patients or sexual transmission. In family members, hepatitis C viral infection is the main cause of liver disorder, and many who were antibody-positive with a second-generation enzyme-linked immunosorbent assay had viremia in the sera.

Adolescent↗
PubMed1993

Pulmonary venoocclusive disease in a patient with systemic lupus erythematosus.

A 26-year-old woman with systemic lupus erythematosus (SLE) developed dyspnea and hypoxemia on exertion. She died from rapidly progressive respiratory failure. Autopsy revealed right ventricular hypertrophy and occlusion of the pulmonary veins compatible with pulmonary venoocclusive disease (PVOD). Although PVOD has been reported in patients with suspected collagen vascular disease, this appears to be the first reported case of PVOD occurring in a patient with SLE.

Adult↗
PubMed1991

Management of congenital diaphragmatic hernia by extracorporeal membrane oxygenation (ECMO).

The purpose of this study was to evaluate the efficacy of extracorporeal membrane oxygenation (ECMO) for patients with congenital diaphragmatic hernia (CDH). Ten patients whose mortality was predicted to be more than 80% with previous therapeutics, were selected to use ECMO over the past five years. Patients were placed on ECMO by cannulating the right jugular vein and the right carotid artery. ECMO was started at 34.3 hours after birth on an average, and the average time on ECMO was 96.3 hours. Seven patients (70%) survived, and six out of them are in good health without any sequelae. In particular, all five patients whose pathological condition needing ECMO was persistent fetal circulation (PFC), survived. Therefore we believe ECMO is highly beneficial to overcome the condition of PFC. The survival rate of CDH patients under 24 hours of age in our hospital is 76.2% (16/21 cases) over the last 5 years, and it has improved compared with 57.1% (12/21 cases) before then. The fact that some of the critical patients who were lethal with conventional management, have been successfully treated by ECMO, played a great role in this improvement.

Child Development↗
PubMed1991

[Research and development of pravastatin].

The attempts to find a potent inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase which catalyzes the rate limiting step of cholesterol biosynthesis were started from 1971. The first potent inhibitor, ML-236B (compactin), was found from the culture broth of Penicillium citrinum. Among many derivatives of ML-236B, pravastatin sodium (hereafter refer to pravastatin) was finally selected because of its potency and tissue selectivity. Since pravastatin has a hydroxyl group at 6 beta position in the skeleton of decaline of ML-236B, the microbial hydroxylation was adopted for the production of pravastatin. Streptomyces carbophilus was finally chosen as a potent converter with the formation of a lesser amount of by-products. For the sake of industrial production of pravastatin, many devices and improvements were performed for selecting high potent strains and for culturing conditions both with ML-236B and pravastatin. Pravastatin strongly inhibited the sterol synthesis in freshly isolated rat hepatocytes, but only weakly inhibited in the cells from nonhepatic tissues. This selective inhibition of pravastatin in sterol synthesis was further confirmed by ex vivo and in vivo experiments by using rats and mice. Pravastatin markedly reduced serum cholesterol levels in dogs, monkeys and rabbits, including Watanabe heritable hyperlipidemic (WHHL) rabbits, an animal model for familial hypercholesterolemia. Pravastatin showed the preventive effect on the development of coronary atherosclerosis and xanthoma in young WHHL rabbits in consequence of maintaining the serum cholesterol levels low. In the clinical trials, pravastatin significantly reduced serum cholesterol and low density lipoprotein cholesterol levels, whereas inversely increased high density lipoprotein cholesterol levels.

Animals↗
PubMed1990

Fv-1 restriction of endogenous feline C-type RD114 virus genome phenotypically mixed with ecotropic murine leukemia viruses.

Endogenous feline leukemia RD114 virus genome rendered capable of infecting mouse cells by phenotypic mixing with an ecotropic murine leukemia virus (MuLV) exhibited the Fv-1 restriction pattern of the ecotropic murine virus. However, RD114 genomes phenotypically mixed with ecotropic MuLV showed one-hit dose-response kinetics, even when titrated with murine cells with the restricted Fv-1 phenotype.

AKR murine leukemia virus↗
PubMed1989

Mutational analysis of the human immunodeficiency virus vpr open reading frame.

Mutations were introduced by recombinant DNA techniques into the vpr open reading frame of an infectious molecular clone of human immunodeficiency virus type 1. The effect of these changes on the replicative and cytopathologic properties of the virus recovered from transfected cells was studied in several human CD4+ lymphocyte cell lines. In all cases, mutant viruses were infectious and cytopathic. However, when a low-input dose was used, mutants grew significantly more slowly than the wild-type virus. The growth kinetics of vpr mutants were distinct from those of vif and vpu mutants.

Cytopathogenic Effect, Viral↗
PubMed1985

Purification of phenylalanine hydroxylase from human adult and foetal livers with a monoclonal antibody.

Phenylalanine hydroxylase from adult and foetal livers was purified by single step monoclonal antibody affinity chromatography. From adult and foetal livers, about 1280- and 1450-fold purified enzymes were obtained with 37% and 23% yield, respectively. Sodium dodecyl sulfate polyacrylamide gel electrophoresis of the resultant adult enzyme showed an essentially single band with an apparent molecular weight of 49K. On the other hand, two subunits (molecular weights 52K and 49K) were observed from the foetal enzyme. Molecular weights of the native adult and foetal enzymes as determined on Sepharose CL-6B column chromatogram were 150K and 160K, respectively. It was clear that adult and foetal liver phenylalanine hydroxylases were different proteins having different subunit molecular weights.

Adult↗
PubMed1983

Effect of acute and chronic ethanol consumption on hepatic tissue oxygen tension in rats.

In vivo hepatic tissue oxygenation was investigated in chronically ethanol-treated rats using micro oxygen electrode and reflectance spectrophotometry. Effect of acute ethanol administration was also studied. Hepatic oxygen tension of rats treated with ethanol chronically (daily ethanol intake, 9-12 g/kg for 9 months) was very low as compared with that of normal rats, the decrease being comparable to that of rats treated with carbon tetrachloride. The hepatic oxygen tension in normal controls shortly after ethanol ingestion increased from basal level (median, 23 mmHg) to 40-70 mmHg, while in chronically ethanol-treated rats, the hepatic oxygen tension decreased transiently, followed by a gradual increase, but it still remained low. In CCl4-treated rats, the hepatic oxygen tension decreased further after the ethanol ingestion. It is concluded that chronic ethanol consumption in rats resulted in hepatic hypoxia with decreased liver blood flow and volume. Also acute ethanol administration does not induce hepatic hypoxia in normal rats, while in rats with injured liver it induces hypoxia.

Alcoholism↗
PubMed1978

Cadmium toxicity and liver mitochondria. I. Different effects of cadmium administered in vivo to adult, young, and ethionine-fed rats.

The changes in liver mitochondrial respiratory activities and cytochrome concentrations were investigated when cadmium chloride was administered orally to adult, young, and ethionine-fed rats. Following a seven-day administration of 30 ppm cadmium in drinking water, adult rats showed no change, while young rats and ethionine-fed rats exhibited a marked increase in mitochondrial respiration with concomitant decrease of respiratory control index and P/O ratio. The concentrations of cytochromes aa3, b, and c + c1 in liver mitochondria were unchanged in adult rats, but increased significantly in ethionine-fed rats. In young rats receiving cadmium the liver mitochondrial protein increased with a slight change in the cytochrome concentration in mitochondria. It was further found that in adult rats a higher concentration (300 ppm) of cadmium in drinking water was toxic to the liver mitochondrial functions. Thus, the effect of oral administration of cadmium on the liver mitochondrial function depends on the condition of the animals.

Aging↗