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Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 307 records · Page 17Linked to original sources
PubMed1985

Diminished retrograde transport causes axonal dystrophy in the nucleus gracilis. Electron- and light-microscopic study.

To examine a possible cause of axonal dystrophy in the nucleus gracilis, dorsal root ganglion (DRG) neurons of rats were investigated by means of electron-microscopic autoradiography and horseradish peroxidase (HRP) tracing method. Following injections of tritiated amino acids into the L6 and S1 DRG, labeling was observed on the initial and halfway developed dystrophic terminals in the ipsilateral gracile nucleus. However, no grains or few, if any, were found on the well developed huge dystrophic endings. Compared with the thoracic and upper lumbar DRG, a decrease in velocity and amount of retrograde HRP transport was demonstrated in the lower lumbar and sacrococcygeal DRG neurons, especially of large cell diameter, irrespective of age of rats. These findings led us to conclude that the axonal dystrophy reflects a state of an anterograde overtransport of the axoplasm caused by a diminished retrograde transport which is specific to lower lumbar and sacrococcygeal DRG large neurons.

Animals↗
PubMed1985

Morphological aspects on pancreatic islets of non-obese diabetic (NOD) mice.

The pancreatic islets of female non-obese diabetic (NOD) mice (a model of insulin-dependent diabetes mellitus), have been examined by both light and electron microscopy. At about the age of 2 weeks, mononuclear cells began to infiltrate in or near the islets and some of these cells were in contact with the islet cells. Following this degeneration of islet B-cells took place, the process occurring in two ways. In many cells numerous secretory granules with extremely dense cores occupied the cytoplasm. Other cells, however, were filled with low-density secretory granules and the nuclei of these cells became pycnotic. After degeneration of B-cells, the islets were effaced by numerous mononuclear cells. With the onset of the diabetic state these mononuclear cells gradually disappeared, and thereafter small islets remained. By electron microscopy, retrovirus-like particles were observed in cisternae of the rough endoplasmic reticulum in islet B-cells at all stages. With an anti-retrovirus serum (goat anti-KiMSV-NIHxeno serum), positive immunofluorescence was observed in some pancreatic islet cells of NOD mice aged 1 day and 4, 6, 8, 9, 10 and 14 weeks. It is suggested that these virus particles may be intimately related to the inflammatory reaction occurring in the islets and to the development of diabetes mellitus.

Animals↗
PubMed1985

Decreased activities in mitochondrial inner membrane electron transport system in muscle from patients with Kearns-Sayre syndrome.

The present study shows biochemical data on skeletal muscle from 5 patients with Kearns-Sayre syndrome (KSS). Enzyme activities per muscle wet weight in the electron transport system of inner mitochondrial membrane were not significantly different in KSS from those in normal subjects except one patient with long duration of symptoms. On the other hand, mitochondrial contents were increased and enzyme activities per mitochondrial protein in the electron transport system were markedly decreased in the muscle of all cases. These results suggest that the decreased enzyme activity of the mitochondrial electron transport system in each mitochondrion may result in a compensatory increase in mitochondrial contents in the muscle of KSS.

Adolescent↗
PubMed1985

Morphological and biochemical studies on minocycline-induced black thyroid in rats.

The thyroid glands of the rats treated with 100 mg/kg/day of minocycline for 35 days showed black discoloration. In these thyroids, brown pigment granules were seen in the follicle epithelial cells, and they histochemically stained in the same manner as melanin. By electron microscopy, the deposition of the electron-dense material first occurred in lysosome-like granules and, with further administration, was observed also in the rough endoplasmic reticulum in some cells. Thin-layer chromatography showed that the Rf value of the extract from minocycline-treated rat thyroid was the same as that of the black substance obtained by mixing minocycline and 3% hydrogen peroxide but different from that of melanin. In minocycline-treated rats, the release of thyroxine (T4) from perifused thyroids was significantly less than that from control, and the analysis of iodoamino acids showed an increased monoiodotyrosine fraction. Thus, the pigment of thyroid in minocycline-treated rats was demonstrated to be a metabolic derivative of minocycline itself and minocycline may interfere with thyroid function in high-dose, long-term treatment.

Administration, Oral↗
PubMed1985

Unaltered stimulation of pituitary adrenocorticotrophin secretion by corticotrophin-releasing factor following sodium valproate administration in a patient with Nelson's syndrome.

A 53-year-old woman with Nelson's syndrome was treated with 600 mg sodium valproate daily. Her plasma ACTH was effectively decreased, whilst the response of plasma ACTH to corticotrophin-releasing factor (CRF) was unaltered. The result of the CRF test suggested that sodium valproate, at least in the present patient, acted at the hypothalamic level.

Adrenocorticotropic Hormone↗
PubMed1985

T-cell abnormalities in patients with idiopathic thrombocytopenic purpura: the presence of OKT4+8+ cells.

40 patients with idiopathic thrombocytopenic purpura (ITP) were studied for T-cell abnormalities using a panel of monoclonal antibodies (McAbs). These patients showed a tendency to have a decreased OKT4+:OKT8+ ratio compared with normal subjects and a significant increase was observed in OKT10-positive cells in ITP patients. Further analyses were made utilizing McAbs of different subclasses in combination (BMA040 mouse IgG1 McAb, helper/inducer T and BMA081 mouse IgG2 McAb, suppressor/cytotoxic T). An increased proportion of cells reactive with both BMA040 and BMA081 McAbs (double-labelled cells) was demonstrated in patients with ITP compared with the normal controls. Furthermore, there was an inverse correlation between the proportion of "double-labelled cells" and the platelet counts. These data suggest that abnormalities of the T-cell subsets in the peripheral blood may play an important role in the pathogenesis of ITP.

Adolescent↗
PubMed1985

Noninvasive study of left ventricular performance in obese patients: influence of duration of obesity.

We studied the performance of the left ventricle in 35 obese patients by means of noninvasive methods, including echocardiography, carotid arterial pulse tracing, and phonocardiography. Patients were divided into two groups according to the duration of obesity: group 1 included patients who had been obese for less than 15 years, and group 2 comprised patients who had been obese for more than 15 years. There were no differences in the degree of obesity and cellularity of adipose tissue between two groups. Left ventricular dimension and wall thickness, stroke volume, and cardiac output were significantly greater in both groups of obese patients than in nonobese control subjects. Group 2 had a significantly increased end-diastolic dimension index (DdI, calculated as end-diastolic dimension/cube root of body surface area), stroke index (SI), and radius/wall thickness ratio (R/Th) of the left ventricle compared with group 1. Multiple regression analysis showed that DdI, SI, and R/Th correlated significantly with the duration of obesity. We conclude that alterations of cardiac performance in obese patients with left ventricular enlargement and wall thickening is attributed not only to the excess of body weight but also to the duration of obesity.

Adolescent↗
PubMed1985

Excess purine degradation in exercising muscles of patients with glycogen storage disease types V and VII.

To investigate purine catabolism in exercising muscles of patients with muscle glycogen storage disease, we performed ischemic forearm exercise tests and quantitated metabolites appearing in cubital venous blood. Two patients with glycogen storage disease type V and three with glycogen storage disease type VII participated in this study. Basal lactate concentrations lowered in every patient with glycogen storage disease type V or type VII. Two patients with glycogen storage disease type VII, who had markedly elevated concentrations of serum uric acid (14.3 and 11.9 mg/dl, respectively), showed high basal concentrations of ammonia (118 and 79 mumol/liter, respectively; 23 +/- 4 mumol/liter in healthy controls) and of hypoxanthine (23.4 and 20.4 mumol/liter, respectively; 2.0 +/- 0.4 mumol/liter in healthy controls). Other patients showed near normal measurements of these metabolites. After forearm exercise, ammonia, inosine, and hypoxanthine levels increased greatly in every patient studied, in contrast with the lack of increase in lactate levels. The incremental area under the concentration curves for venous ammonia was 13-fold greater in the glycogen storage disease group than in controls (1,120 +/- 182 vs. 83 +/- 26 mumol X min/liter). The incremental areas of inosine and hypoxanthine were also greater in the glycogen storage disease group (29.2 +/- 7.2 vs. 0.4 +/- 0.1 and 134.6 +/- 23.1 vs. 14.9 +/- 3.2 mumol X min/liter, respectively). The incremental areas of ammonia in controls and in glycogen storage disease patients strongly correlated with those of hypoxanthine (r = 0.984, n = 11, P less than 0.005). These findings indicated that excess purine degradation occurred in the exercising muscles of patients with glycogen storage disease types V and VII, and suggested that the ATP pool in the exercising muscles may be deranged because of defective glycogenolysis or glycolysis.

Adult↗
PubMed1985

Inhibitory effect of iopanoic acid on the thyrotropin-stimulated release of cyclic adenosine 3',5'-monophosphate and of 3,5,3'-triiodothyronine from perifused rat thyroids.

Using a perifusion system, we studied the effect of iopanoic acid, an iodinated contrast agent used in oral cholecystography, on the release of cAMP, T3, T4, and rT3 from perifused rat thyroid pieces. A 0.1 mg/ml iopanoic acid solution significantly inhibited the TSH-stimulated release of cAMP (without iopanoic acid, 8175 +/- 373; with iopanoic acid, 5169 +/- 355 fmol/mg thyroid X 3 h, mean +/- SE) and T3 (without iopanoic acid, 971 +/- 32; with iopanoic acid, 659 +/- 32 pg/mg thyroid X 3 h) in the presence of 3-isobutyl-1-methylxanthine. T4 and rT3 releases were not significantly affected. Inhibition of TSH-stimulated T3 release by iopanoic acid was also observed at a concentration of 0.01 mg/ml. Propylthiouracil completely abolished the inhibitory effect of iopanoic acid on TSH-stimulated cAMP release but not on TSH-stimulated T3 release. TSH-stimulated cAMP release was augmented by iodide at a concentration of 1 X 10(-3) M in the presence of 3-isobutyl-1-methylxanthine but suppressed by iodide at a concentration of 1 X 10(-5) M. TSH-stimulated T3 release was suppressed slightly at both concentrations of iodide. These results suggest that iopanoic acid may have an inhibitory effect on the TSH-stimulated cAMP and T3 release from perifused rat thyroids. This effect can probably be attributed to the iodide contained in the agent and to the inhibited intrathyroidal conversion of T4 to T3.

1-Methyl-3-isobutylxanthine↗
PubMed1985

Primary cortisol resistance accompanied by a reduction in glucocorticoid receptors in two members of the same family.

This report describes studies of a man suspected of having primary cortisol resistance. This conclusion is based on his high plasma cortisol levels and high 24-h urinary 17-hydroxycorticosteroid and cortisol excretion, plus the fact that he had no manifestations of Cushing's syndrome. Among family members tested, his mother also had hypercortisolemia. Both mother and son had high levels of unbound plasma cortisol, but their plasma ACTH concentrations were within the normal range. Both were partially resistant to dexamethasone adrenal suppression, and both had mild hypertension without hypokalemia. To study this apparent end-organ resistance to cortisol, we examined the glucocorticoid receptors in peripheral mononuclear cells. Using whole cell assays, glucocorticoid receptors in both patients were found to have reduced total binding capacity. We conclude that these two patients, members of the same family, have primary cortisol resistance accompanied by a reduced number of glucocorticoid receptors.

17-Hydroxycorticosteroids↗
PubMed1985

Improvement of abnormal pyruvate metabolism and cardiac conduction defect with coenzyme Q10 in Kearns-Sayre syndrome.

In a patient with Kearns-Sayre syndrome, concentration of coenzyme Q10, a component of the mitochondrial electron transport system, was decreased in serum and in the mitochondrial fraction of skeletal muscle. Serum concentrations of lactate and pyruvate were abnormally high, especially after exercise or oral glucose loading. Levels of folic acid in plasma and CSF were decreased. ECG showed a first-degree atrioventricular block. After administration of coenzyme Q10 60 to 120 mg daily for 3 months, serum levels of lactate and pyruvate became normal, with improvement of atrioventricular block and ocular movements.

Adult↗
PubMed1985

Forskolin stimulation of 3, 5, 3'-triiodothyronine release from perifused rat thyroids.

In a perifusion system in the presence of 3-isobutyl-1-methylxanthine, forskolin stimulated secretion of not only cAMP but also 3, 5, 3'-triiodothyronine (T3) from rat thyroid glands. The increases in both cAMP and T3 were dose-dependent at forskolin concentrations of 2.0 X 10(-7)M to 2.0 X 10(-5)M. After perifusion for 4 h, tissue concentrations of cAMP also increased as a result of forskolin treatment. Since forskolin is regarded as a specific activator of the cAMP generating system, this observed forskolin stimulation of T3 secretion from perifused rat thyroid glands indicates that cAMP is involved in regulating thyroid hormone secretion.

1-Methyl-3-isobutylxanthine↗
PubMed1985

Tubuloreticular inclusions and paired cisternae induced in human lymphocytes cultured with Staphylococcus aureus Cowan 1.

Tubuloreticular inclusions (TRI) and paired cisternae (PC) were induced in lymphocytes of normal individuals after incubation with Staphylococcus aureus Cowan 1. TRI were initially detected in lymphoid cells on day 2 (48-h culture). The frequency of TRI-positive cell sections on day 5 increased about twofold over those on days 2-4. On day 7, TRI were predominantly seen in lymphoplasmacytoid cells or plasmacytoid cells, with an incidence of up to 18% of sections. The regions in these cells were most extensive and anastomosed with the cisternae of adjacent well-developed rough endoplasmic reticulum (RER). TRI formation appears not to be essential for mitogen-induced B-cell differentiation to plasmacytoid cells, because pokeweed mitogen (PWM) failed to induce TRI. The diverse expressions of TRI induction between these two mitogens may be due to a difference in B-cell activation mechanisms. Paired cisternae were observed in a great majority of mitotic cells at various stages. These were encountered most frequently on day 4. PC were also seen in the PWM-stimulated culture. Our observations suggest that PC formation may be related to new formation of RER as well as to reconstruction of the nuclear envelope.

Cells, Cultured↗
PubMed1985

Nicotinamide prevents lymphocytic infiltration in submandibular glands but not the appearance of anti-salivary duct antibodies in non-obese diabetic (NOD) mice.

Previously we have shown that nicotinamide prevents spontaneously occurring diabetes associated with insulitis in non-obese diabetic (NOD) mice. In this study we injected nicotinamide (0.5 mg/g) or saline (0.01 ml/g) into female NOD mice daily during a period between 4 and 16 weeks of age. At the end of the treatment, periductal and perivascular lymphocytic infiltration in submandibular glands was observed in 91% of saline-injected control mice and 36% of nicotinamide-injected mice (P less than 0.01). No significant difference was observed in the prevalence of anti-salivary duct antibodies or antinuclear antibodies between the nicotinamide group and the saline group. Nicotinamide may alter cell-mediated, but not humoral, immunity to salivary gland cells, resulting in the prevention of submandibulitis.

Animals↗
PubMed1985

Predominance of T lymphocytes in pancreatic islets and spleen of pre-diabetic non-obese diabetic (NOD) mice: a longitudinal study.

We examined sequential changes in the subsets of mononuclear cells infiltrating the pancreatic islets and splenic lymphocytes in pre-diabetic non-obese diabetic (NOD) mice, an animal model for type I diabetes, using immunofluorescent techniques. In the pancreas, a predominant infiltration by activated T lymphocytes, including helper inducer and cytotoxic suppressor T cells, was observed in the early stage of insulitis. Natural killer cells were also detected in the lesions. Immunoglobulin bearing cells tended to increase in number with the progression of insulitis. T lymphocytes were localized close to islet cells, while immunoglobulin bearing cells appeared adjacent to blood vessels and around T cell clusters. Immunoglobulin deposition or Ia expression on islet cells was not observed. The percentage of splenic T lymphocytes was markedly increased in the initial stage of insulitis as compared with control ICR mice and this elevated proportion of T cells continued throughout the observation period. As for splenic T cell subsets, cytotoxic suppressor T cells were increased in NOD mice. These results suggest that T lymphocytes play an important role in the initiation of insulitis long before the onset of overt diabetes. Moreover, NOD mice seem to have characteristic immunological features different from the BB rat or a reported case with human type I diabetes.

Animals↗
PubMed1985

Changes in serum levels of pancreatic isoamylase, lipase, trypsin, and elastase 1 after endoscopic retrograde pancreatography.

To compare the behavior of pancreatic enzymes in the circulation, serum levels of pancreatic isoamylase activity, lipase activity, immunoreactive trypsin (IRT), and immunoreactive elastase 1 (IRE) were measured in the same serum samples taken serially from 29 subjects undergoing endoscopic retrograde pancreatography (ERP). A striking correlation between the maximal increments of serum pancreatic enzyme levels after ERP and the degrees of opacification of pancreatic duct system was observed, except in 6 subjects with chronic pancreatitis. In 13 out of 19 subjects whose main pancreatic duct (MPD) and branches were opacified, serum pancreatic enzyme levels reached a peak within 2 hours after ERP and decreased thereafter. The mean maximal rise of serum levels of lipase, IRT, pancreatic isoamylase, and IRE in the 13 subjects was 32, 21, 10, and 4 times the basal value, respectively. A delay of peaking in serum levels of pancreatic isoamylase and IRE as compared with those of lipase and IRT was observed in the 13 subjects. The mean disappearance half-time of serum lipase, IRT, pancreatic isoamylase, and IRE in the 13 subjects was 2.8, 4.6, 8.0 and 16.0 hours, respectively.

Adolescent↗
PubMed1985

Release of vasoactive intestinal peptide by intraduodenal infusion of HCl or fat and intramuscular injection of neostigmine in man.

A highly sensitive radioimmunoassay system for plasma vasoactive intestinal peptide (VIP) was developed to examine the effect of intraduodenal infusion of HCl or fat on the plasma VIP levels in healthy subjects, and the effect of intramuscular injection of neostigmine in patients with irritable bowel syndrome (IBS). Intraduodenal infusion of 100 ml of 0.1 N HCl or 10 g fat caused a significant rise in plasma VIP level. Neostigmine (12.5 micrograms/kg) produced a significant rise in plasma VIP level, and the plasma VIP response to neostigmine was significantly greater in the IBS group than in the normal group. These results suggest that VIP might play a role in the pathophysiology of IBS.

Adult↗