Search PubMed⌕ Search

Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 271 records · Page 15Linked to original sources
PubMed1986

Steroidogenic effect of ent-kaur-16-en-15 beta-ol (kaurenol) on isolated rat adrenal cells.

In an in vitro bioassay system for adrenocorticotropic hormone using isolated rat adrenal cells, kaurenol, a diterpene alcohol, stimulated corticosterone production and augmented the steroidogenic effect of adrenocorticotropin or forskolin, dose-dependently. Kaurenol had no effect on cyclic AMP production by the cells. The diterpene also had no stimulatory effect on the adrenal adenylate cyclase activity in a cell free system. The results suggest that this particular diterpene exerts a steroidogenic effect through a mechanism independent of cyclic AMP generation.

Adenylyl Cyclases↗
PubMed1986

Effects of the intravenous administration of magnesium sulfate on corrected serum calcium level and nephrogenous cyclic AMP excretion in normal human subjects.

The effect of intravenous magnesium sulfate infusion on corrected serum calcium level and parathyroid function assessed by determination of nephrogenous cAMP (NcAMP) excretion were studied in normal human subjects. Significant hypermagnesemia induced by the magnesium sulfate infusion for 120 minutes was accompanied by a gradual and progressive decrease in the corrected serum calcium level. NcAMP excretion fell rapidly, reaching a nadir between 60 and 120 minutes after the infusion began, and after that rose above the baseline excretion. Urinary calcium excretion gradually increased, reaching a peak between 120 and 180 minutes after the infusion began and then gradually decreased. Since magnesium was given as the sulfate, it is not clear whether these changes were attributable to magnesium or sulfate or both. As a control study, we performed intravenous sodium sulfate infusion. The sodium sulfate infusion caused slight hypocalcemia, slight hypercalciuria, and a significant increase in NcAMP excretion. These findings indicate that the hypocalcemia and the hypercalciuria caused by the magnesium sulfate infusion is mainly due to the effect of magnesium, and that the decrease in NcAMP excretion during the infusion is due to the effect of magnesium alone. We conclude that the hypocalcemia caused by the magnesium sulfate infusion is mainly due to the renal calcium loss, and that the inhibition of parathyroid function caused by hypermagnesemia may be only partially involved in the early phase of this hypocalcemia.

Adult↗
PubMed1986

Ultrastructural and immunocytochemical aspects of lymphocytic submandibulitis in the non-obese diabetic (NOD) mouse.

The submandibular glands of female non-obese diabetic (NOD) mice (22-26 weeks of age) were studied by light and electron microscopy. Mononuclear cells consisting mostly of lymphocytes were recognized in and among the acini and secretory ducts. Some parts of the secretory ducts and mucous acini surrounded by lymphocytes showed destructive changes. In the secretory ducts lymphocytes invaded the duct epithelial lining and the duct lumen was occluded by these cells. The duct epithelial cells in such lesions were extremely distorted and tonofilament bundles running in various directions were present in the cytoplasm. Lymphocytes were in close contact with the duct epithelial cells. In the mucous acini some acinar cells, which appeared to be compressed by the infiltrating lymphocytes, showed degenerative changes. Immunocytochemical study revealed that both T- and B-lymphocytes were involved, T-lymphocytes tending to occupy the center of the infiltrate, while B-lymphocytes occupied the periphery. Although autoantibody against duct epithelial cells was identified, damage to duct epithelial cells was not correlated with the presence of this antibody. The morphological changes in the submandibular gland of the NOD mouse are very similar to those reported in the salivary gland of patients with Sjögren's syndrome.

Animals↗
PubMed1986

A 31-year-old woman with homozygous familial hypercholesterolemia without significant lesions in the coronary arteries.

Cardiovascular complications were examined in a 31-year-old woman with homozygous familial hypercholesterolemia (FH) (LDL receptor defective type), who had had no clinical symptoms of coronary artery disease. She had delivered 2 children without any cardiac complications, and her exercise electrocardiogram showed no positive findings for ischemic heart disease. Coronary angiography showed no significant arterial lesions, and left ventriculography revealed good contraction of the left ventricle (ejection fraction: 67%). This is considered to be a very rare case of homozygous FH without significant lesions in the coronary arteries. This might be attributed at least in part to her dietary regimen consisting of a very low fat and low calorie diet, to the residual LDL receptor activity or to the low value of prothrombin time.

Adult↗
PubMed1986

Influence of endogenous hyperinsulinism on high density lipoprotein2 level in type 2 (non-insulin-dependent) diabetes mellitus and impaired glucose tolerance.

We determined the insulin response to an oral glucose ingestion and levels of serum lipoproteins in 25 untreated patients with type 2 diabetes mellitus, in 26 subjects with impaired glucose tolerance (IGT), and in 35 non-diabetic control subjects. The three groups had similar compositions with respect to age and sex distribution. The levels of VLDL triglyceride in the subjects with type 2 diabetes or IGT were higher than those in controls. Serum HDL- and HDL2 cholesterol were significantly decreased in type 2 diabetics, and the subjects with IGT showed a similar tendency. Serum apolipoprotein A-II levels were lower in the male subjects with type 2 diabetes or IGT than in controls. Insulin response, i.e., sum of immunoreactive insulin (IRI) levels at basal, 30, 60, 90 and 120 min after a 75-g oral glucose load, negatively correlated to HDL- and HDL2 cholesterol levels (r = -0.396, P less than 0.05; r = -0.482, P less than 0.001, respectively), and positively correlated to VLDL triglyceride values (r = 0.485, P less than 0.001) in the male subjects with type 2 diabetes or IGT. In the female subjects, fasting plasma IRI values significantly correlated to HDL cholesterol (r = -0.496, P less than 0.05). There was a significant negative correlation between the concentrations of HDL2 cholesterol and VLDL triglyceride. These data show that lipoprotein metabolism, not only in type 2 diabetics, but also in IGT tends to show changes such as decreased HDL2 cholesterol and increased VLDL triglyceride levels, and which might be related to the hypersecretion of endogenous insulin.

Adult↗
PubMed1986

The role of hepatic triglyceride lipase in the metabolism of intermediate-density lipoprotein--postheparin lipolytic activities determined by a sensitive, nonradioisotopic method in hyperlipidemic patients and normals.

With a view to elucidating the physiologic role of hepatic triglyceride lipase (H-TGL), we studied the relationship between the activity of H-TGL and the concentrations of the lipids of ultracentrifugally separated lipoprotein fractions in sera from 81 cases of primary hyperlipidemia, 5 of hypothyroidism, and 31 normal subjects. The activity of H-TGL in postheparin plasma was determined by the sensitive, nonradioisotopic method that was recently developed by us. In the entire group of subjects including the normals, the activity of H-TGL had a significant inverse correlation with the concentration of the cholesterol (r = -0.443, P less than 0.001) and phospholipid (r = -0.433, P less than 0.001) of intermediate density lipoprotein (IDL). When the patients were divided into subgroups according to the phenotype of hyperlipidemia, it was found that the correlation was more significant in type IIb (r = 0.695, P less than 0.001) or type IV + V (r = -0.664, P less than 0.0001). In the five cases of hypothyroidism, the mean IDL cholesterol level was high (28.3 +/- 12.3 mg/dL) and the H-TGL activity was very low (4.6 +/- 4.5 mumol/h/mL). The H-TGL activity was also significantly correlated with the ratio of high density lipoprotein-2 to high density lipoprotein-3 cholesterol (r = 0.351, P less than 0.001) in the entire group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Interaction of famotidine with rat liver microsomes, a study showing less inhibition of drug metabolism than with cimetidine.

Interaction of famotidine with rat liver microsomes and its effect on drug metabolism in vitro were studied. Famotidine interacted with liver microsomes obtained from untreated, phenobarbital-pretreated and 3-methylcholanthrene-pretreated rats to produce characteristic type II spectral changes with peaks at 423-426 nm and troughs at 387-390 nm. The spectral dissociation constants were in the range of 0.84-0.94 mM. Famotidine inhibited aminopyrine N-demethylase activity to a much lesser extent than did cimetidine. The extent of inhibition at a concentration of 5 mM of famotidine was from 12 to 18% for the microsomes from the rats with different pretreatments. In contrast, 5 mM of cimetidine inhibited the activity 80, 59 and 80% in the microsomes from untreated, phenobarbital-pretreated and 3-methylcholanthrene-pretreated rats, respectively. Both famotidine and cimetidine inhibited aminopyrine N-demethylase in a mixed-type manner for the microsomes from phenobarbital-pretreated rats, with inhibition constants of 4.7 and 0.7 mM, respectively. These results demonstrate that famotidine is an in vitro inhibitor of microsomal drug metabolism in rats but is much less inhibitory than cimetidine.

Aminopyrine N-Demethylase↗
PubMed1986

Inhibition of pentagastrin-stimulated gastric acid secretion by intraileal administration of bile and elevation of plasma concentrations of gut glucagon-like immunoreactivity in anesthetized dogs.

The effects of intraileal administration of bile on gastric acid secretion stimulated by a submaximal dose of intravenous pentagastrin infusion and on plasma concentrations of gut glucagon-like immunoreactivity (gut GLI) were studied in anesthetized dogs. Gastric acid secretion was measured for a 2-h period at 15-min intervals before and after intraluminal instillation of test solutions. 100 ml of canine bladder bile diluted to 10% in saline evoked a significant inhibition (20%) of gastric acid secretion. The inhibition of gastric acid secretion was accompanied by an elevation of plasma concentration of gut GLI, whereas saline instillation (in controls) caused no responses. Although the inhibition of gastric acid secretion and the elevation of plasma gut GLI are parallel phenomena, gut GLI can be reasonably postulated as one of the candidate mediators of bile-induced inhibition of gastric acid secretion, since its structurally related peptides, pancreatic glucagon, glicentin and oxyntomodulin have been reported as inhibitors of gastric acid secretion.

Animals↗
PubMed1986

Expression of human gastrin gene in normal and gastrinoma tissues.

The complete sequence of the human gastrin gene is reported here. This gene consists of three exons. Nine Alu family sequences are found within the gene and in the surrounding region. S1 mapping study showed that the transcription of gastrin gene starts at 60, 57, or 55 bp upstream from the 3' end of the first exon. The mechanism of mRNA synthesis in a gastrinoma tissue was studied to clarify the ectopic production of gastrin. It was found that mRNA synthesis starts from the same three transcriptional start points. Southern blotting profiles for normal gastric antrum and gastrinoma DNA were indistinguishable from each other within the 18-kb region containing the gastrin gene, showing that no genomic rearrangements are associated with the gastrinoma formation. Thus, the overproduction of gastrin in this tumor is likely to be due to an aberrant expression control system of the cell, rather than a change in the control region of the gastrin gene.

Amino Acid Sequence↗
PubMed1986

Analysis of debromination of 1,2-dibromoethane by cytochrome P-450-linked hydroxylation systems as observed by bromide electrode.

Debromination of 1,2-dibromoethane (DBE) by a rabbit liver microsomal preparation and a reconstituted cytochrome P-450 enzyme system was investigated. The reaction was performed in our newly constructed reaction vessel, in which a bromide electrode was installed. During the reaction, the liberated bromide ion was continuously measured by the bromide electrode, and the amount was recorded. In the microsomal preparation, the DBE-debromination rate per nmol cytochrome P-450 was enhanced by phenobarbital-pretreatment of rabbits compared with the untreated microsomes, whereas it was diminished by 3-methylcholanthrene-pretreatment. The debromination reaction was reconstituted in a purified enzyme system containing phenobarbital-inducible rabbit liver microsomal cytochrome P-450 (P-450PB), NADPH-cytochrome P-450 reductase, and NADPH. The optimum conditions required the presence of dilauroylphosphatidylcholine and cytochrome b5. Cytochrome b5 was found not to be an obligatory component for the DBE-debromination in the reconstituted system, but it stimulated the activity about 3.4-fold. Preincubation of the reconstituted mixture with guinea pig anti-cytochrome P-450PB antiserum markedly inhibited the debromination reaction.

Animals↗
PubMed1986

A primary extranodal lymphoma associated with IgM-kappa paraproteinaemia: different secretory capacities of cutaneous and circulating lymphoma cells.

We report a patient with non-Hodgkin's lymphoma of small lymphocytic type with IgM-kappa monoclonal gammopathy who developed extranodal involvement with orbital and nasal manifestations, followed by generalized subcutaneous nodules. Immunological study disclosed that the peripheral blood and the subcutaneous nodule were both involved in a common monoclonal proliferation of B cells at various stages of differentiation, including secretory cells which accounted for the serum paraprotein. The secretory capacity was far greater in the peripheral blood than in the subcutaneous tissue. These clinical and immunological manifestations might reflect the physiological behaviour of a particular B cell subset which shows a preference for mucocutaneous sites to secrete IgM in the peripheral blood.

Female↗
PubMed1986

Hyperlipoproteinaemia in primary gout: hyperlipoproteinaemic phenotype and influence of alcohol intake and obesity in Japan.

Serum lipoprotein profiles were investigated in 108 male patients with primary gout before treatment to elucidate the prevalence of each individual phenotype of coexisting hyperlipoproteinaemia and pathogenic factors responsible for it. The mean serum triglyceride (TG) and total cholesterol (TC) levels in the patients with gout were 2.10 +/- 0.14 mmol/l and 5.26 +/- 0.10 mmol/l (mean +/- SEM) respectively, which were significantly higher (p less than 0.01 and p less than 0.05 respectively) than the levels in age matched controls without gout (1.30 +/- 0.07 mmol/l and 4.77 +/- 0.08 mmol/l respectively). Serum high density lipoprotein cholesterol (HDL-C) values were slightly decreased in patients with gout compared with controls (1.24 +/- 0.08 mmol/l v 1.40 +/- 0.03 mmol/l, p less than 0.05). Hyperlipoproteinaemia was seen in 61 patients (56%), of whom patients with type IIa, IIb, and IV hyperlipoproteinaemia formed 13, 15, and 69% respectively. Thus the prevalence of type IV hyperlipoproteinaemia was high in primary gout as compared with primary hyperlipoproteinaemia with primary hyperlipoproteinaemia (69% v 43%, p less than 0.01). The independent and relative influences of clinical data of the patients upon the concentrations of serum lipids were assessed by stepwise multiple regression analysis. Two major predictors of serum TG level were alcohol intake (p less than 0.01) and serum uric acid level (p less than 0.05). The most significant predictive variable was alcohol intake, but its influence was judged to be small (r2 = 0.067). None of the other variables, including obesity index, had any significant influence. The relationships between any of these variables and serum TC or HDL-C levels were not significant. In addition, serum lipid levels were investigated in patients with neither obesity (defined as 120% or more of ideal body weight) nor a history of alcohol intake. Their serum TG and TC concentrations were also significantly higher than the respective control levels. Thus hyperlipoproteinaemia in primary gout its unlikely to be secondary to excess alcohol intake or obesity, or both. Instead, it may result from genetic factors such as a combined hyperlipidaemic trait.

Adult↗
PubMed1986

Renal hypouricaemia in a patient with 48,XXYY syndrome.

Studies on hypouricaemia observed in a patient with 48,XXYY syndrome revealed an abnormality in renal urate handling. His renal urate clearance was abnormally increased. Inosine administration and provocative tests using probenecid and pyrazinamide identified an isolated renal tubular abnormality with increased urate secretion. Since the serum urate in his brother with a normal sex chromosome constitution was also low, the association of renal hypouricaemia and 48,XXYY syndrome in this patient is probably coincidental. Although the brother was not investigated, these siblings may be a previously unreported case of familial hypouricaemia due to isolated renal hypersecretion.

Adult↗