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Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 199 records · Page 11Linked to original sources
PubMed1989

[A case of facioscapulohumeral muscular dystrophy with sensorineural hearing loss and retinal angioma].

We report a sporadic case of 12 years old boy with facioscapulohumeral dystrophy (FSHD), sensorineural hearing loss and exudative angioma of bilateral retina. His hearing loss was noted at 9 years, followed by muscle weakness of his right upper extremity at 11 years. Complete neurological examination at 12 years revealed FSH type distribution of muscle weakness with high serum CK level (330 U/L), moderate sensorineural hearing loss and exudative angiomas of bilateral retina. The biopsy from biceps brachii muscle showed advanced dystrophic changes with a dense inflammatory cell infiltration predominating on perivascular distribution and type II fiber predominance. The features of infiltrating lymphocytic surface antigen seen in this case were compatible with those of FSHD rather than those of polymyositis. In the literature, the association of FSHD with hearing loss and retinal vessel abnormalities has been documented on 15 cases as an unusual form of FSHD. However, it has otherwise been noted that the associations of FSHD and hearing loss or retinal vessel abnormalities are unequivocally frequent, Whenever special attention has been made. Morphological examination with light and electron microscopies on the muscle specimen in this patient did not demonstrate any recognizable abnormality such as arterio-venous shunt or thickening of vessel wall basal lamina. However, it cannot be completely excluded that exudation around the abnormal vessel wall in the muscle may play an initial role in the pathogenesis of FSHD. Further morphological survey on vessel abnormalities may be necessary in the FSHD muscle.

Child↗
PubMed1989

Metabolic improvements associated with a reduction of abdominal visceral fat caused by a new alpha-glucosidase inhibitor, AO-128, in Zucker fatty rats.

The relationship between mesenteric fat accumulation and metabolic disorder was studied in genetically obese Zucker fatty rats. These animals had high levels of plasma glucose, triglyceride and total cholesterol as well as increased liver triglyceride in comparison with lean rats. In addition, portal free fatty acid (FFA) levels were also higher in fatty rats than in lean rats. Direct measurement of fat weight revealed a substantial increase of mesenteric as well as subcutaneous fat. The volume of mesenteric fat cells was greater than that of subcutaneous fat cells in Zucker fatty rats (1.67 +/- 0.49 nl versus 1.00 +/- 0.31 nl), although the mesenteric fat cell volume was less than half of the subcutaneous fat cell volume (0.05 +/- 0.02 nl versus 0.14 +/- 0.07 nl) in lean rats. An increase in mesenteric fat cell volume was thus more predominant than that of subcutaneous fat cells in the fatty rats. Administration of AO-128 (50 p.p.m./day), a new alpha-glucosidase inhibitor, caused a substantial reduction of mesenteric fat weight accompanied by a marked decrease in fat cell volume in Zucker fatty rats. The drug also caused a significant reduction of FFA levels in the portal vein in parallel with a marked reduction of triglyceride content in the liver. These observations indicate that the fat accumulation in the markedly enlarged mesenteric fat cells is related to the elevated levels of FFA in the portal vein, which in turn may cause metabolic disorders in the liver. A new alpha-glucosidase inhibitor improves these disorders, at least in part, by preventing an enlargement of mesenteric fat cells.

Adipose Tissue↗
PubMed1989

[Two patients with cervical diastematomyelia].

Two patients with cervical diastematomyelia are reported here. A nineteen year-old-man (patient 1) admitted to our hospital because of muscular weakness of right upper limb. He noted muscular atrophy of right upper limb at 16 years old, and then paresthesia was gradually aggravated in the ulnar side of the right hand. Physical examination showed muscular atrophy of right upper limb and hypesthesia in the right eight cervical and first thoracic dermatomes. The deep tendon reflexes were decreased in the right upper limb and were increased in the lower limb without pathological reflexes. In electromyographic examination, neurogenic motor units were observed in the upper right limb, dominantly in 1st interosseous muscle (between the fourth cervical and the first thoracic dermatome). Metrizamide computed tomographic (CT) myelography revealed sagittal splitting of the spinal cord from the third to the sixth cervical vertebra, producing two asymmetrical hemicords. A osseous or fibrous septum were not seen. The right hemicord was smaller than the left one. Patient 2 was a twenty-four-year-old woman. She visited our hospital because of muscular weakness of the right upper limb. In physical examination, there were the muscular atrophy of right hand and hypesthesia in the right eighth and first thoracic dermatomes. The deep tendon reflexes were decreased in the right upper limb and were increased in the right lower limb without pathological reflexes. The EMG studies revealed the neurogenic NMU in the right upper limb (between the fourth cervical and the first thoracic dermatome). Magnetic resonance imaging showed marked narrowing of the dural sac in flexion of the neck.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Glucagon-like peptide-1 (7-36 amide): a potent glucagonostatic and insulinotropic hormone.

Glucagon-like peptide-1 (GLP-1) (1-37) and the fraction derived from it, GLP-1 (7-36 amide), are peptides encoded by the preproglucagon gene and possibly co-secreted with enteroglucagon. When added at a 25-nM concentration, GLP-1 (7-36 amide) decreased the release of glucagon from the perfused rat pancreas from 68.5 +/- 9.0 pg/ml to 41.5 +/- 11.5 pg/ml at 2 min in the presence of 11.2 mM glucose (P less than 0.01), and from 196.0 +/- 32.5 pg/ml to 87.0 +/- 23.5 pg/ml at 5 min in the presence of 2.8 mM glucose (P less than 0.05). Insulin levels increased from 12.6 +/- 3.0 microU/ml to 48.9 +/- 14.0 microU/ml at 10 min in the presence of 11.2 mM glucose (P less than 0.05) and from 2.0 +/- 0.4 microU/ml to 8.2 +/- 2.3 microU/ml at 2 min in the presence of 2.8 mM glucose (P less than 0.05). Glucagon and insulin release were not affected significantly by GLP-1 (1-37), irrespective of glucose concentration. We suggest that GLP-1 (7-36 amide) rather than enteroglucagon may be the true physiologic gut hormone and that it may act as 'incretin' in the enteroinsular axis. We suggest further that the glucagonostatic and insulinotropic activities of this peptide are unique and might be important in islet-cell function.

Animals↗
PubMed1988

Selective reduction of cholesterol in HDL2 fraction by probucol in familial hypercholesterolemia and hyperHDL2 cholesterolemia with abnormal cholesteryl ester transfer.

Long-term treatment with probucol induced marked regression of xanthoma in patients with both homozygous and heterozygous familial hypercholesterolemia despite a substantial accompanying decrease in high-density lipoprotein (HDL) cholesterol. Furthermore, a close correlation was found between the extent of the regression and the reduction of HDL cholesterol, which suggests that the probucol-induced decrease in HDL may not be an atherogenic change, but may reflect a favorable change for lipoprotein metabolism. The present study also evaluated the effects of probucol on HDL metabolism in patients with familial hyperHDL2 cholesterolemia who had extremely high levels of HDL cholesterol ranging from 130 to 280 mg/dl. Premature corneal opacities were present in 2 patients, 1 of whom also had coronary artery disease despite high HDL cholesterol levels. In the 2 cases, the net transfer of cholesteryl ester from HDL to very low density lipoprotein and LDL was impaired, and low hepatic triglyceride lipase activity was observed, but cholesteryl ester transfer protein was not deficient. Administration of probucol to these patients caused a marked reduction of serum cholesterol, which was accounted for exclusively by a reduction in the HDL2 fraction. The size of the HDL2 particles, which had been much larger, decreased to normal, and the net transfer rate of cholesteryl ester was normalized. In the other 3 cases of hyperHDL2 cholesterolemia, the cholesteryl ester transfer activity was completely deficient. Unlike its effect in the first 2 cases, probucol did not cause any change in lipid and apoprotein in the 3 patients with complete deficiency of cholesteryl ester transfer activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Carrier Proteins↗
PubMed1988

Trophic effect of glucagon-(1-21)-peptide on the isolated rat ileal mucosal cells.

The trophic effect of glucagon-(1-21)-peptide on rat ileal epithelial cells was studied in vitro. Glucagon-(1-21)-peptide stimulated [3H]thymidine incorporation of mucosal cells significantly in a dose-dependent manner. Then glucagon-related peptides which have common sequences with glucagon-(1-21)-peptide were also tested. The biological potencies to augment [3H]-thymidine uptake were closely related with their amino-acid residues of N-terminal region. The result suggests that the N-terminal amino-acid sequence of glucagon molecule plays an important role in intestinal cell growth.

Amino Acid Sequence↗
PubMed1988

Resistance of the peripheral nerve to ischemia in diabetic patients--an electrophysiological study.

We studied the effect of ischemia on the excitability of the sensory fibers of the median nerve in 43 patients with non-insulin-dependent diabetes mellitus (NIDDM) by a double stimulation method. Ischemia caused significantly less reduction of nerve excitability in patients with poor glycemic control and in patients diseased for 5 years or longer than in the normal control group. Hyperexcitability after ischemia was markedly greater than normal among short-term, poorly controlled diabetics, and markedly less pronounced among long-term, poorly controlled diabetics. In many diabetic patients with normal conduction velocity or without sensory disturbance, post-ischemic hyperexcitability was remarkable. A study of nerve excitability may be useful as one means of detecting early-stage disturbance of the diabetic peripheral nerve.

Adult↗
PubMed1988

Localization of cytochrome P-450 in the colonic mucosa of 3-methylcholanthrene-pretreated and untreated rats. An immunohistochemical study.

Immunohistochemical localization of cytochrome P-450 in the colonic mucosa of 3-methylcholanthrene-pretreated and untreated rats was studied by indirect fluorescent antibody staining technique. A polyclonal antibody for cytochrome P-450MC purified from hepatic microsomes of 3-methylcholanthrene-pretreated rats was used for this experiment. A strong immunofluorescence was found to be localized in the cytoplasm of the surface epithelium of the mucosa in the colon of 3-methylcholanthrene-pretreated rats. A faint immunofluorescence was also observed in the epithelium of untreated rats. 7-Ethoxycoumarin O-deethylase activity of colonic microsomes was significantly enhanced by 3-methylcholanthrene-pretreatment in parallel with an increase in the intensity of immunostaining for cytochrome P-450MC in Western blotting analysis. This is the first report on the localization of cytochrome P-450 in the colonic mucosa.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1988

Marked secretion of pyruvate in human duodenal juice stimulated with pancreozymin or secretin.

Pyruvate and lactate in duodenal aspirates were investigated to determine whether they are excreted from human pancreas as substrates for alkaline secretion as is bicarbonate. Secretion of these acids was compared with that of another organic acid, citrate, which is thought to be excreted in close relationship to digestive enzymes. All acids were assayed in the fluid obtained from 11 subjects without pancreatic diseases, before and after sequential intravenous injections of 1 unit/kg pancreozymin and 1 unit/kg secretin. Pyruvate concentrations were markedly increased by each stimulation, especially by secretin, and the cumulative excretions of pyruvate and bicarbonate after secretin stimulation were significantly correlated among the subjects. In contrast, lactate concentrations, although high just after administration of pancreozymin, declined to a considerable extent following each injection, rather similar to those of protein or citrate. These data suggest that pyruvate may be secreted from human pancreatic duct cells similar to bicarbonate secretion through mechanisms related to alkaline secretion.

Adult↗
PubMed1988

Lipid composition of platelets from patients with atherosclerosis: effect of purified eicosapentaenoic acid ethyl ester administration.

Although eicosapentaenoic acid (EPA) has been shown to have beneficial effects in the prevention of atherosclerosis, the mechanism by which these effects occur is not entirely clear. We investigated the lipid composition of platelets in paired subjects with and without atherosclerotic disease, either hypercholesterolemic (low density lipoprotein [LDL] cholesterol [Chol] greater than or equal to 170 mg/dl) or normocholesterolemic (LDL-Chol less than 170 mg/dl). Platelets from patients with atherosclerotic disease had a lower phosphatidylcholine (PC)/Chol ratio, when compared with those from patients without atherosclerotic disease, irrespective of LDL-Chol levels. Eleven patients with atherosclerotic disease were treated with purified EPA ethyl ester (1.8 g/day), and changes in lipid composition of platelets were investigated. Plasma levels of total Chol and LDL-Chol decreased significantly after EPA administration. The phospholipid (PL)/Chol ratio and the PC/Chol ratio in platelets from patients with atherosclerotic disease increased significantly after 4-10 wk EPA treatment. The EPA content in platelets increased, while the arachidonic acid (AA) content decreased. EPA-induced changes in the PL/Chol and the PC/Chol ratios of platelets, as well as fatty acyl chain shifts, may be related to the beneficial effects in preventing atherosclerosis, possibly by increase in the membrane fluidity.

Adult↗
PubMed1988

Ionophore A23187 inhibits the release of thyrotropin-stimulated 3, 5, 3'-triiodothyronine from perifused rat thyroid glands.

We have studied the effect of ionophore A23187 on the release of T3 and cAMP from perifused rat thyroid glands and on the morphological changes of the follicle epithelial cells. Ionophore A23187 at a concentration of 5 microM significantly inhibited TSH-stimulated T3 release. Depletion of Ca2+ in the infusion buffer completely abolished the inhibitory effect of ionophore A23187 on TSH-stimulated T3 release. In the presence of TSH and 3-isobutyl-1-methylxanthine, ionophore A23187 at 5 microM did not significantly affect either the release of cAMP during a 3-h perifusion or the cAMP content in the thyroid tissues after 1-h perifusion. By electron microscopy, the follicle epithelial cells of the rat thyroid tissues showed marked responses to TSH after 3-h stimulation. By the addition of 5 microM ionophore A23187, the ultrastructural changes such as phagocytotic uptake of luminal colloid and the formation of intracellular colloid droplets were rarely observed in spite of the presence of TSH. The present study indicates that ionophore A23187 at a concentration of 5 microM inhibits both TSH-induced morphological changes of the follicle epithelial cells and TSH-stimulated T3 release without reducing cAMP level stimulated by TSH in rat thyroid glands.

Animals↗