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Biomedical subjects

C Hirayama

Publications and source records attributed to C Hirayama.

At least 55 records · Page 3Linked to original sources
PubMed1990

An association between alpha 1-antitrypsin phenotype and chronic liver disease.

The phenotypes of alpha-1-antitrypsin have been analyzed by isoelectric focusing on polyacrylamide gels in 232 healthy Japanese blood donors and in 240 Japanese patients with chronic liver diseases: 69 with chronic active hepatitis, 122 with liver cirrhosis, 41 with hepatocellular carcinoma and 8 with primary biliary cirrhosis. The liver cirrhosis patients had a gene frequency of 0.07 for P1*M3, which was significantly higher (P less than 0.01) than that (0.03) in blood donors. The gene frequency of P1*M3 was significantly increased in cryptogenic liver cirrhosis (P less than 0.05), and there was a tendency toward an increased frequency of P1*M3 in post-transfusion groups, and in primary biliary cirrhosis. There were also tendencies toward increased frequencies of P1*M3 in cryptogenic and post-transfusion groups of patients with chronic active hepatitis. The present study indicates that P1*M3 is a genetic or predisposing factor for chronic liver diseases, especially for cryptogenic and/or non A-non B viral chronic liver disease and also for primary biliary cirrhosis.

Carcinoma, Hepatocellular↗
PubMed1990

[15N]glycine metabolism in normal and cirrhotic subjects.

Following a single oral dose of 10 mg/kg of [15N]glycine, plasma [15N]glycine kinetics and urinary 15N excretion were measured in 12 cirrhosis patients and in 6 control subjects. Cirrhosis patients were divided into two groups of 6 patients with and without a history of hepatic encephalopathy designated as group II and group I, respectively. Thirty minutes after oral administration of labeled glycine, the plasma concentration of [15N]glycine was significantly higher in both cirrhosis groups than that in the control group (P less than 0.05 and P less than 0.01). The elimination constant of plasma [15N]glycine slightly decreased in group II, but not significantly. Urinary 15N excretion did not differ among the three groups, but the rate of urinary ammonia 15N in urinary 15N was significantly increased in group II (P less than 0.05). The whole-body protein flux did not differ among the three groups, but whole-body protein breakdown was significantly increased in group II cirrhosis patients (P less than 0.05). These findings indicated that the kinetics of glycine were substantially altered in severe cirrhosis patients. Because hepatic uptake and oxidation of glycine was well maintained even in group II, increased endogenous protein breakdown seemed to be responsible for hyperglycinemia and also for the negative nitrogen balance seen in this group.

Female↗
PubMed1990

Effects of chronic administration of somatostatin analogue SMS 201-995 on the progression of chronic renal failure in subtotal nephrectomized rats.

The recent study has demonstrated the presence of somatostatin (SRIF) secretory cells in the rat glomerulus. Because of the polyvalent actions of this peptide, SRIF may play some roles in the evolution of chronic renal failure. The present study evaluated the effects of a long acting SRIF analogue, SMS 201-995 on the progression of renal failure in 3/4 nephrectomized (NPX) rats. Animals were divided into four groups; (1) normal control (C) (n = 9), (2) NPX-C (n = 10), (3) NPX treated with SMS 201-995 (0.5 micrograms/day) (NPX-0.5) (n = 9) and (4) NPX with SMS 201-995 (5.0 micrograms/day) (NPX-5.0) (n = 9). This drug was subcutaneously given daily for 6 weeks. Periodic observations were done at 0, 3 and 6 weeks. Both hematocrit and systolic blood pressure showed significant fall and rise, respectively, in NPX rats compared with C at 3 and 6 weeks. Also both serum creatinine and blood urea nitrogen in these groups elevated significantly at 3 and 6 weeks compared with C. Not significant changes were observed in the 24-h urine volume among the NPX rats. At 6 weeks, the urinary protein excretion in NPX-5.0 was significantly less than those in NPX-C and NPX-0.5 rats. Urinary sodium excretion in NPX-5.0 was significantly lower than that in NPX-C. Histologic examination of the kidney showed less proliferation of mesangial cells in NPX-5.0 than NPX-C. These results suggest that SMS 201-995 may limit the rate of progression of chronic renal failure in this experimental model.

Animals↗
PubMed1990

Collagenase and collagenolytic cathepsin in normal and fibrotic rat liver.

Collagenase and collagenolytic cathepsin activities in normal and carbon tetrachloride-induced fibrotic livers of rats were simultaneously determined at 35 and 25 degrees C for 18 h, using the same 14C-labeled neutral soluble collagen as a substrate. Collagenolytic cathepsin had higher activity under the assay conditions at both 35 and 25 degrees C than collagenase in normal and fibrotic livers. On sodium dodecyl sulfate-polyacrylamide slab gel electrophoresis, the collagen was visibly degraded by collagenolytic cathepsin, but not by collagenase. These results indicate that, unlike collagenase, collagenolytic cathepsins exist as active forms in the rat liver, and can participate in the degradation of collagens, especially of soluble collagens including procollagens.

Animals↗
PubMed1989

Fasting plasma caffeine level in cirrhotic patients: relation to plasma levels of catecholamines and renin activity.

Fasting plasma caffeine concentrations, plasma levels of catecholamines and plasma renin activity were measured in patients with cirrhosis and control patients without hepatic dysfunction. A careful dietary history showed no significant difference in caffeine consumption (mean +/- S.E.) among 46 cirrhotics (86 +/- 7 mg per day) vs. 34 control patients (91 +/- 8 mg per day). Fasting plasma caffeine concentrations, however, were significantly higher (7.68 +/- 1.42 micrograms per ml) in cirrhotics than in controls (1.01 +/- 0.20 micrograms per ml) (p less than 0.01). Fasting plasma caffeine concentrations in cirrhotics varied significantly with Child's criteria, namely Child's A patients (2.06 +/- 0.38 micrograms per ml); Child's B patients (6.92 +/- 1.86 micrograms per ml), and Child's C patients (17.70 +/- 3.65 micrograms per ml) (p less than 0.001). In 44 cirrhotics, fasting plasma caffeine concentrations were compared with plasma levels of catecholamines and plasma renin activity. Plasma epinephrine concentrations were normal; however, plasma norepinephrine concentrations were increased in six cirrhotics, and plasma renin activities were increased in 28 cirrhotics. After a 3-day caffeine abstinence, plasma caffeine concentration and renin activity were significantly decreased (p less than 0.01), and high plasma norepinephrine levels were also decreased in 12 cirrhotics. Plasma caffeine concentration, renin activity and norepinephrine level did not change in a control group of cirrhotics who continued to receive caffeine for 3 days (n = 6). After abstinence from caffeine, the decrease of fasting plasma caffeine concentration correlated well with the decrease of plasma renin activity (r = +0.746, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

A multicenter randomized controlled clinical trial of Shosaiko-to in chronic active hepatitis.

The efficacy of Shosaiko-to (SST) on 222 patients with chronic active hepatitis was studied in a double-blind multicenter clinical study. One hundred and sixteen patients received SST in a daily oral dose of 5.4 g for 12 weeks, followed by the same dose for a further 12 weeks. One hundred and six patients received a placebo containing 0.5 g of SST for 12 weeks, followed by a cross-over to SST for a further 12 weeks. Among the liver tests, serum AST and ALT values decreased significantly with the administration of SST. The difference of the mean value between the SST group and the placebo group was significant after 12 weeks. In patients with chronic active type B hepatitis, a tendency towards a decrease of HBeAg and an increase of Anti-HBe antibodies was also observed. No remarkable side effects were noticed.

Adult↗
PubMed1989

Urinary hydroxyproline and hydroxylysine excretions in relation to hepatic hydroxyproline content in chronic liver disease.

In patients with or without various chronic liver diseases, the total urinary excretion of hydroxyproline and hydroxylysine and the hepatic content of hydroxyproline were examined. In 7 patients without liver disease, the urinary excretion of hydroxyproline and hydroxylysine were 10.3 +/- 1.5 and 1.31 +/- 0.21 mmol/mol creatinine, respectively, and the hepatic content of hydroxyproline was 4.9 +/- 0.6 mumol/g of wet liver. In 33 patients with liver disease, the urinary excretion of hydroxyproline and hydroxylysine and the hepatic content of hydroxyproline were increased in proportion to the severity of liver disease. The hepatic content of hydroxyproline showed a significant correlation with the urinary excretion of hydroxyproline and hydroxylysine (r = +0.406 and r = +0.531, respectively). These results suggest that the study of urinary hydroxyproline and hydroxylysine excretion may yield useful information on the metabolism of hepatic collagen in chronic liver disease. Moreover, urinary hydroxylysine excretion seemed to be a better index of hepatic collagen metabolism than urinary hydroxyproline excretion; perhaps urinary hydroxylysine excretion is not much affected by dietary collagen intake.

Adult↗
PubMed1989

Lack of effect of indomethacin and captopril on protein-induced glomerular hyperfiltration in normal subjects.

We examined the possible roles of renal prostaglandins, renin-angiotensin and the kallikrein-kinin system in protein-induced glomerular hyperfiltration in normal subjects. The normal subjects were divided into three groups, i.e., control, indomethacin-treated and captopril-treated groups. Protein loading (0.6 g/kg BW as protein) resulted in a significant increase in glomerular filtration rate (GFR) from a baseline of 98 +/- 8 ml/min/1.73 M2 to 135 +/- 13 (P less than 0.01) in the control group. In both the indomethacin and captopril groups, significant elevations of GFR were observed after the test meal. The urinary kallikrein excretions after the meal were not significantly different from those for preloading in all groups. These results suggest that renal prostaglandins, renin-angiotensin and the kallikrein-kinin system may be less involved in protein-induced glomerular hyperfiltration in normal subjects.

Adult↗
PubMed1989

Effect of renal prostaglandins on survival in patients with liver cirrhosis.

To assess the effect of renal prostaglandins on the prognosis of liver cirrhosis, we studied the relationship between the effect of prostaglandin synthetase inhibition by indomethacin on glomerular filtration rate (GFR) and effective renal plasma flow (RPF) and survival in 30 patients with liver cirrhosis. After indomethacin administration, GFR dropped significantly from 86 +/- 2 ml/min to 73 +/- 3 ml/min (p less than 0.01) and RPF from 421 +/- 10 to 349 +/- 14 ml/min (p less than 0.01). Survival was not correlated with baseline GFR or RPF, but was correlated with changes in both GFR and RPF after indomethacin administration (p less than 0.01). The cumulative survival rate from 1 to 7 yr was significantly higher (p less than 0.01) in patients with a decrease in GFR of less than or equal to 15% after indomethacin administration than in patients with a decrease in GFR of more than 15%. Findings for changes in RPF after indomethacin administration were similar. These results suggest that the augmentation of prostaglandin inhibition by indomethacin is associated with a poor prognosis of liver cirrhosis. It may be involved in the depletion of renal prostaglandins to maintain renal hemodynamics in patients with liver cirrhosis.

Female↗
PubMed1988

Chromatographic resolution of dipeptide enantiomers and diastereomers on chiral stationary phases from poly(L-leucine) or poly(L-phenylalanine).

Two types of chiral stationary phase, polymer-bonded and non-bonded, containing poly(L-leucine) and poly(L-phenylalanine) were prepared. These stationary phases gave higher enantioselectivity for the optical resolution of various derivatives of leucylphenylalanine methyl ester by liquid chromatography than did poly(L-alanine) and poly(L-glutamate).

Chromatography, Liquid↗
PubMed1988

Homogeneous immunoassay based on dihexadecyl-dimethylammonium bilayer membranes.

We describe a rapid, highly sensitive, simple immunoassay based on cationic bilayer membranes prepared from dihexadecyl-dimethylammonium bromide. This detergent was dispersed in water to give a slightly turbid solution which contained lamellar (not vesicular) bilayer membranes with a gel to liquid crystal phase transition (Tc, 28 degrees C). An anionic hapten (N,N'-bis(2,4-dinitrophenyl)-L-lysine) combined electrostatically with this cationic membrane to induce aggregation of membranes, making the solution turbid. This aggregation was suppressed by antibodies to the hapten. The aggregation rate was rapid at a temperature above Tc, and the amount of antibodies was quantified by measuring absorbance or light scattering of the aqueous solution with a detection limit of 0.1 ng/ml of the antibodies. Anionic and zwitterionic bilayer membranes from di(tetradecyl)phosphate and phosphocholine derivatives, respectively, were less sensitive as detectors of the hapten-antibody reaction. Ionic interactions between cationic bilayer membranes and anionic haptens are important for successful assay performance.

Agglutination↗
PubMed1988

Free and small peptide-bound [14C]hydroxyproline synthesis in rat liver in vitro in CCl4-induced hepatic fibrosis.

To clarify the process of free and small peptide-bound hydroxyproline synthesis in hepatic fibrogenesis, we measured the in vitro synthesis of [14C]hydroxyproline in the 67% ethanol soluble fraction in rat liver slices, together with hepatic protein-bound [14C]hydroxyproline synthesis. In control rat liver, the amount of free and small peptide-bound [14C]hydroxyproline synthesized was 13.1 +/- 2.6 10(-4) x dpm/g liver/3 hr. In the CCl4-treated rat liver, where the hepatic hydroxyproline content was increased 4.6-fold, the protein-bound [14C]hydroxyproline synthesis was significantly increased 1.5-fold, but free and small peptide-bound [14C]hydroxyproline synthesis was decreased into 70%. There was a significant inverse correlation between free and small peptide-bound [14C]hydroxyproline synthesis, and hepatic hydroxyproline content. These results suggest that the combination of an increase in collagen synthesis and a decrease in free and small peptide-bound [14C]hydroxyproline synthesis contributes to rapid accumulation of collagen in hepatic fibrosis.

Animals↗
PubMed1988

Hypogonadism in liver cirrhosis: implication in altered amino acid metabolism in muscle.

To investigate the relationship between hypogonadism and altered amino acid metabolism in patients with liver cirrhosis, we measured the basal levels of plasma testosterone, estradiol, and free amino acids, plus urinary 3-methylhistidine excretion, in 16 control and 19 cirrhotic patients. The concentration of plasma testosterone correlated significantly with that of plasma branched-chain amino acids, and inversely with urinary 3-methylhistidine excretion. This suggests that hypogonadism causes a disturbance in amino acid metabolism at least partly related to an augmented muscle protein turnover.

Amino Acids↗
PubMed1988

Vitamin B6 status in cirrhotic patients in relation to apoenzyme of serum alanine aminotransferase.

Plasma levels of pyridoxal-5'-phosphate (PLP) in cirrhotic patients were significantly lower than in control subjects. However, the plasma total pyridoxal level and urinary 4-pyridoxic acid excretion were not decreased in non-alcoholic patients but in alcoholic patients. In the latter, the percentage of apo alanine aminotransferase was not related to the plasma PLP level, but was significantly correlated with plasma total pyridoxal level and urinary 4-pyridoxic acid excretion. We conclude that alcoholic cirrhotic patients have vitamin B6 deficiency, which is at least responsible for low serum alanine aminotransferase activity.

Alanine Transaminase↗