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Biomedical subjects

T Kariya

Publications and source records attributed to T Kariya.

At least 55 records · Page 3Linked to original sources
PubMed1991

Albumin mRNA expression in human liver diseases and its correlation to serum albumin concentration.

The expression of albumin mRNA in human liver samples was investigated in order to understand the molecular mechanism of albumin gene expression in various liver diseases. Albumin mRNA in acute hepatic failure and decompensated liver cirrhosis was reduced significantly compared to normal control liver (P less than 0.05). Serum albumin concentration is closely correlated with albumin mRNA content (r = 0.895, P less than 0.01). These data suggest that albumin concentration is mainly regulated at albumin mRNA level in the liver despite the presence of other regulatory mechanisms and that expression of albumin mRNA level is correlated with disease severity. But in several cases there was a discrepancy between albumin mRNA level and severity of liver disease, so further investigation of the regulatory factors of albumin gene expression should be performed.

Albumins↗
PubMed1991

Prevalence of chronic liver diseases and anti-HCV antibodies in different districts of Saga, Japan.

The authors examined the contribution of Hepatitis C Virus (HCV) to the morbidity of chronic liver diseases (CLD) in selected districts of Saga, Japan, one group with low (L) and the other with a high (H) mortality rate of CLD. Age and sex-matched epidemiological studies showed an extremely high morbidity of CLD in the H-district (5.3%) and a low one in the L-districts (2.1%). Randomized selected studies of anti-HCV antibodies showed an extremely high frequency of 10.8% in the H-district and a frequency of 4.6% in the L-district. In addition, the number of subjects with both CLD and positive anti-HCV antibodies was significantly higher in subjects older than the fifth decade, in the H-district. The high prevalence of HCV may be related to the high morbidity and mortality rate of CLD in these districts of Japan.

Adult↗
PubMed1991

[Statistical survey of prosthetic restorations--outline and single crowns, cast cores and inlays].

This is a report on the statistical classification of the prosthetic restorations placed in out-patients of the Tokyo Medical and Dental University Hospital. The data were collected from the laboratory records during the period of January to June of 1986. The results are summarized as follows: 1. The total number of the prosthetic restorations placed in the outpatients were 7355, and 56% of these were covered by the health insurance. 2. Of the total restorations, 29.6% were cast cores, 18.2% were inlays and 17.2% were crowns. Post crowns, jacket crowns and partial veneer crowns were very few, being only 0.3%, 0.4% and 0.5%, respectively. 3. Approximately 50% of the prosthetic restorations were single crowns. 4. Compared to the record from about 20 years ago, the number as well as the ratio of the crowns including the facing crowns was approximately doubled. On the contrary, the number of jacket and post crowns has remarkably decreased. 5. With regard to the single anterior prosthetic restorations, the majority were the porcelain fused to metal crowns which were not popular 20 years ago.

Crowns↗
PubMed1990

Effects of various inhibitors on platelet activation induced by TP 82, a CD 9 monoclonal antibody.

TP 82, a monoclonal antibody against CD 9 antigen, induced human platelet activation at concentrations higher than 0.4 microgram/mL in terms of aggregation, release of intracellular granule contents, production of arachidonic acid metabolites, and elevation of the intracellular Ca2+ concentration. The effects of a competitive inhibitor of ADP, acetylsalicylic acid, EGTA, and GRGDSP which blocks fibrinogen binding to IIb/IIIa complex suggested that each of released ADP, thromboxane A2, extracellular Ca2+, and close cell contact acts together to potentiate platelet activation induced by TP 82. While each of these inhibitors severely suppressed platelet activation induced by lower concentrations of the antibody (less than or equal to 0.8 microgram/mL), that induced by higher concentrations (greater than or equal to 3.2 micrograms/mL) was only partially blocked. Intracellular Ca2+ elevation was totally dependent upon the production of thromboxane A2, regardless of the antibody concentrations.

Adenosine Diphosphate↗
PubMed1990

Mastoparan, a wasp venom, activates platelets via pertussis toxin-sensitive GTP-binding proteins.

Mastoparan induced limited release of serotonin from intact human platelets, while neither intracellular calcium ion elevation nor arachidonic acid mobilization was observed. Cytolysis induced by mastoparan was negligible in the concentration range that induced serotonin release. In digitonin-permeabilized cells, mastoparan induced Ca(++)-independent release of serotonin and Ca(++)-dependent arachidonic acid release. Both serotonin release and arachidonic acid release were reduced by pertussis toxin, suggesting that platelet activation induced by mastoparan is mediated by GTP-binding proteins.

Arachidonic Acids↗
PubMed1990

Ionomycin, a Ca++ ionophore, increases platelet volume independently of the Na+/H+ exchanger.

A Ca++-ionophore, ionomycin, increased the volume of human platelets suspended in a Ca++-containing buffer. This change in cell volume was dependent upon ionomycin and extracellular Ca++ concentrations, suggesting that the volume change occurs when the intracellular Ca++ reaches a certain level (greater than uM as determined by aequorin method). The ionomycin-induced volume increase was suppressed by replacement of extracellular Na+ with membrane-impermeable N-methyl-D-glucamine or Cs+, but not with Li+, K+, or Rb+. Ethylisopropylamiloride, a potent inhibitor of the Na+/H+ exchanger, had only weak inhibitory effect, and the apparent Km for Na+ was approximately 350 mM, which is much larger than that of the Na+/H+ exchanger. It is suggested that certain mechanisms other than the Na+/H+ exchanger are responsible for ionomycin-induced volume increase.

Blood Platelets↗
PubMed1990

Synthesis and cardiotonic activity of novel biimidazoles.

A series of substituted 2,2'-bi-1H-imidazoles and related analogues was synthesized and evaluated for inotropic activity. Structure-activity relationship studies based on a nonclassical bioisosteric approach indicated the necessity of a cyano group on one of the imidazole rings to obtain the desired pharmacological profile. 4(5)-Cyano-2,2'-bi-1H-imidazole (15a) was the most potent inotropic agent in the series. It produced a 25% increase in left ventricular dP/dt at 0.16 mg/kg iv (ED25% = 0.16 mg/kg) and increased left ventricular contractile force 60% at 1 mg/kg iv in anesthetized dogs. Compound 15a is a good inhibitor of type IV cyclic nucleotide phosphodiesterase isolated from dog heart having a potency similar to that of amrinone. Neither 5'-cyano-2,4'-bi-1H-imidazole (44) nor 4-cyano-2,4'-bi-1H-imidazole (48) demonstrated inotropic activity. In addition, the two possible 1,1'-dimethylcyano-2,2'-bi-1H-imidazoles (24 and 25) were inactive, indicating that an acidic NH as well as a cyano group are essential for inotropic activity.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1990

MDL 27,032 [4-propyl-5-(4-pyridinyl)-2(3H)-oxazolone], an active site-directed inhibitor of protein kinase C and cyclic AMP-dependent protein kinase that relaxes vascular smooth muscle.

MDL 27,032 [4-propyl-5-(4-pyridinyl)-2(3H)-oxazolone] is a novel vasodilator whose mechanism of action has not been elucidated. We investigated whether smooth muscle relaxation by MDL 27,032, in vitro, may involve an alteration in the activity of protein kinase C, cyclic AMP (cAMP)-dependent protein kinase or myosin light chain kinase by investigating the effects of MDL 27,032 on cyclic nucleotide phosphodiesterases (PDEs) and protein kinase activities. Strips of dog femoral artery or saphenous vein contracted with phorbol 12-myristate 13-acetate (PMA) were relaxed by 100 microM concentrations of MDL 27,032, as well as by other known inhibitors of PDEs [3-isobutyl-1-methylxanthine and papaverine], myosin light chain kinase (W-7) and protein kinase C (H-7 and polymyxin B). In contrast to 3-isobutyl-1-methylxanthine and papaverine, MDL 27,032 was either inactive or weak as an inhibitor of purified PDE types I, II, IVa and IVb. Similarly, it was a weak inhibitor of myosin light chain kinase. However, MDL 27,032 was a significantly more potent inhibitor of protein kinase C and cAMP-dependent protein kinase in cytosolic extracts of dog vein. Kinetic experiments utilizing purified rat brain protein kinase C revealed that inhibition with MDL 27,032 was competitive with Mg(++)-ATP (Ki 24 microM) and noncompetitive with phospholipid, diacylglycerol, PMA, calcium or substrate proteins. Inhibition of the catalytic subunit of cAMP-dependent protein kinase was also competitive with Mg(++)-ATP (Ki 14.3 microM). Similar results were obtained with MDL 27,032 and H-7 on both enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

GABAB receptors are up-regulated by chronic treatment with lithium or carbamazepine. GABA hypothesis of affective disorders?

The effects of lithium and carbamazepine on GABAA and GABAB receptors were examined. The binding of [3H]muscimol and [3H](-)-baclofen to synaptic membranes from rat brain was used to label GABAA and GABAB receptors, respectively. Neither the [3H]muscimol nor the [3H](-)-baclofen binding site was displaced by lithium or carbamazepine even at a concentration of 100 microM. A single treatment with either of these drugs did not induce any change in [3H]muscimol and [3H](-)-baclofen binding sites in the frontal cortex and hippocampus. [3H](-)-Baclofen binding sites were up-regulated in the hippocampus but not in the frontal cortex following chronic treatment with lithium or carbamazepine. These results suggest that one common mechanism of action of lithium and carbamazepine is mediated by GABAB receptors and that GABA is involved in the pathophysiology of affective disorders.

Animals↗