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Biomedical subjects

I Murakami

Publications and source records attributed to I Murakami.

At least 91 records · Page 5Linked to original sources
PubMed1991

Recurrent malignant fibrous histiocytoma with expression of cytokeratin.

A case of locally recurrent malignant fibrous histiocytoma was documented in a 70-year-old man. He first noticed a subcutaneous nodule forty years previously. The tumor was surgically removed four times during the last four years with local recurrence on every occasion. In the recurrent tumors, the tumor cells almost completely replaced the whole dermis and invaded skeletal muscles. They were composed of pleomorphic spindle cells arranged in a storiform pattern and bizarre histiocytic cells, which were present principally in the deeper portions of the tumor. Both types of tumor cells showed marked nuclear atypicality. In the primary tumor, surrounding a large necrotic area, spindle-shaped cells were arranged in a storiform pattern. These tumor cells exhibited only mild nuclear atypia. The recurrent tumor was strongly positive for vimentin and alpha-1-antichymotrypsin. Most tumor cells were also weakly positive for KL1, a monoclonal antibody for keratin. A Western-blot analysis revealed the presence of two bands (62 and 69 Kd) reacting with KL1 in the fractions which were obtained from the tumor according to the method for keratin extraction.

Aged↗
PubMed1990

Interactive effects of etching and pre-oxidation on porcelain adherence to non-precious alloys: a guided planar shear test study.

Interactive effects of etching and pre-oxidation on porcelain adherence to non-precious alloys were studied by a guided planar shear bond test under non-cantilever conditions. The results indicated that electrolytic etching decreases bond strength, but that oxidation of etched surfaces restores the bond strength level. The results are explained by a hypothesis that depletion of critical elemental species occurs during etching. Potential replenishment of the lost elements during subsequent oxidation, although not confirmed, may assist in improving bond strength.

Acid Etching, Dental↗
PubMed1990

A human case of zoonotic onchocerciasis in Japan.

A 2-year-old girl living in southwestern Japan had a nodule of 2 months' duration on the left foot. A biopsy from the lesion showed transverse sections of a worm surrounded by granulomatous tissue. The worm was identified as an Onchocerca sp. from the morphological characteristics such as relatively thick cuticles, annular ridges on the cortical layer, and high somatic muscles. Positive serological tests using ELISA for Onchocerca gutturosa and Onchocerca volvulus supported the diagnosis. This was the first case of zoonotic Onchocerca infection detected in Japan. The clinicopathological aspects of zoonotic onchocerciasis of this case were discussed.

Child, Preschool↗
PubMed1990

Comparison of monoclonal antibodies reactive with lymphocyte subsets in routinely fixed paraffin-embedded material: flow cytometric analyses, immunoperoxidase staining and influence of fixatives.

We have attempted to clarify the characteristics of monoclonal antibodies (MAbs) detecting lymphocyte subsets in fixed materials. We examined by means of flow cytometric technique influences of fixatives and reactivity with malignant lymphomas (MLs). Specific markers for T-cells were UCHL1 and OPD4, which reacted especially with helper/inducer T-cells. MT1 recognized almost all of T-cells from peripheral blood and tonsils, but reacted with a part of B-MLs. As for B-cell markers, L26 was the most reliable marker for B-MLs. L26 and MB1 antigens could not be detected on living cells flow cytometrically. LN1 reacted with a part of T-cells as well as B-cells, but fluorescent intensity of the former was apparently stronger than that of the latter. Although LN2 antigen was located mainly in the cytoplasm close to the nuclear membrane immunohistochemically, it could be detected on living cells flow cytometrically. LN2 positive cells belonged to B-cells in peripheral blood and tonsils. When fixed for relatively short time, B5 and buffered formalin were better for examining MAbs than non-buffered formalin and ethanol.

Antibodies, Monoclonal↗
PubMed1988

Plasma glucose response after intravenous injection of tolbutamide in insulin-treated type I and type II diabetic patients.

To estimate the residual beta-cell function, plasma glucose and C-peptide response to an intravenous injection of tolbutamide were observed in seven Type I (insulin dependent) and nine Type II (non-insulin dependent) diabetic patients on insulin therapy. Fasting plasma glucose in the patient was controlled below 11 mmol/l by conventional insulin therapy, and 1 g of tolbutamide was intravenously injected. In the serum C-peptide response following tolbutamide injection, seven of nine Type II diabetics showed the peak values of serum C-peptide more than 0.3 nmol/l from 20 min to 60 min after the load, and Type I diabetics gained the peak values less than 0.3 nmol/l except one patient. The decrease of plasma glucose within 60 min after tolbutamide injection was more than 20% of the basal level in eight of nine Type II diabetics, and in all of seven Type I diabetics the decrease did not exceed 15%. Both serum C-peptide and plasma glucose after tolbutamide load responded differently between Type I and Type II diabetics on insulin therapy, and it was thought that tolbutamide load-glucose response test may be a useful method to estimate the residual beta-cell function in the diabetics.

Adult↗
PubMed1987

Effect of beta-hydroxybutyrate and acetoacetate on insulin and glucagon secretion from perfused rat pancreas.

To elucidate the physiological significance of ketone bodies on insulin and glucagon secretion, the direct effects of beta-hydroxybutyrate (BOHB) and acetoacetate (AcAc) infusion on insulin and glucagon release from perfused rat pancreas were investigated. The BOHB or AcAc was administered at concentrations of 10, 1, or 0.1 mM for 30 min at 4.0 ml/min. High-concentration infusions of BOHB and AcAc (10 mM) produced significant increases in insulin release in the presence of 4.4 mM glucose, but low-concentration infusions of BOHB and AcAc (1 and 0.1 mM) caused no significant changes in insulin secretion from perfused rat pancreas. BOHB (10, 1, and 0.1 mM) and AcAc (10 and 1 mM) infusion significantly inhibited glucagon secretion from perfused rat pancreas. These results suggest that physiological concentrations of ketone bodies have no direct effect on insulin release but have a direct inhibitory effect on glucagon secretion from perfused rat pancreas.

3-Hydroxybutyric Acid↗
PubMed1987

Effect of hyperglycemia on serum T4 and T3 levels in rats.

In order to elucidate the effect of hyperglycemia on serum thyroid hormone levels, serum T4 and T3 concentrations were measured in rats with continuous intravenous glucose infusion. 30% glucose solution was infused into the left jugular vein at a rate of 1 ml/hr for 12 hr, and serum glucose level was maintained at 400 mg/dl. Serum T4 levels were slightly but not significantly decreased and serum T3 levels were significantly decreased by infusion of glucose for 12 hr. The ratio of serum T3 to T4 was not significantly changed in rats with glucose infusion. These results suggest an inhibitory effect of hyperglycemia on thyroid hormone release.

Animals↗
PubMed1987

Effect of intestinal factors on extraction of insulin in perfused rat liver.

To study the direct effect of intestinal factors on hepatic extraction of insulin, an investigation was made into the extraction of insulin from isolated rat liver perfused with portal venous effluent (PVE) obtained from the isolated perfused rat intestine. Rat intestine was perfused with Krebs-Ringer bicarbonate medium for 45 min, and the PVE was collected from glucose-, lipid-, or NaCl-treated and untreated control intestines. The PVE, after adjustment of its glucose (180 mg/dl) and insulin (200 microU/ml) concentrations, was used as the perfusing medium for the liver of a different rat. The liver was perfused without recirculation with the PVE not containing insulin for 15 min and then perfused with the PVE containing insulin for the next 30 min. Insulin removal from liver perfused with PVE from lipid- or NaCl-treated intestine (52.6 +/- 5.4 or 46.6 +/- 4.1%) was similar to that from comparable controls (49.7 +/- 2.8 or 48.2 +/- 2.9%), respectively. However, that from glucose-treated intestine (39.7 +/- 6.2%) was significantly (P less than 0.01) lower than that from control intestine (51.1 +/- 2.5%). These results indicate that an intestinal factor secreted after glucose ingestion significantly reduces hepatic extraction of insulin and that at least a part of the incretin phenomenon is due to a decreased hepatic extraction of insulin after oral glucose administration.

Animals↗
PubMed1987

Aspects of metal-ceramic bonding.

Despite many problems associated with ceramometal crowns of any alloy composition, their continued widespread use attests to their clinical effectiveness. This is due to the very positive aspects of many of their properties.

Dental Alloys↗
PubMed1986

Effect of thyrotropin on conversion of T4 to T3 in perfused rat liver.

The present study was undertaken to elucidate the direct effect of thyrotropin (TSH) on the conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) in the isolated perfused rat liver. The liver was perfused without recirculation with a synthetic medium containing 10 micrograms/dl T4 and the effect of constant infusion of bovine TSH (125 or 250 microU/ml) on the conversion of T4 to T3 was examined. T4 uptake in the perfused liver was not changed by the addition of TSH. The release of T3 (10.3 +/- 1.4 ng/g/30min, mean +/- SD), tissue T3 production (99.5 +/- 21.4 ng/g/30min), net T3 production (102.6 +/- 20.2 ng/g/30min), and the conversion rate of T4 to T3 (14.8 +/- 3.5%) in the liver perfused with 250 microU/ml TSH were significantly higher than those in controls (8.1 +/- 1.2 ng/g/30min, 69.0 +/- 6.8 ng/g/30min, 69.9 +/- 6.1 ng/g/30min, and 10.0 +/- 0.8%), respectively. These results suggest that TSH may directly enhance hepatic conversion of T4 to T3 in rats in vitro.

Animals↗
PubMed1986

Effect of glibenclamide on thyroid hormone metabolism in rats.

This study was undertaken to elucidate the effect of glibenclamide, one of sulfonylurea drugs, on thyroid hormone metabolism in vivo and on the conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) in the isolated perfused rat liver and kidney. Glibenclamide (0.2 mg/kg body weight) was intraperitoneally administered to normal and streptozotocin-induced (50 mg/kg) diabetic rats for 14 days. The liver and kidney of normal rats were perfused for 30 minutes with a synthetic medium containing 20 micrograms/dl T4 and glibenclamide (200 or 400 ng/ml), and production of T3 in the tissues was measured by radioimmunoassay. Serum T4 and T3 levels in control and streptozotocin-induced diabetic rats were not changed by daily intraperitoneal glibenclamide administration. The production of T3 (111 +/- 40 and 95 +/- 16 ng/g/30 min, mean +/- SD) and the conversion rate of T4 to T3 (11.1 +/- 2.9 and 10.2 +/- 2.3%) in the liver perfused with glibenclamide (200 and 400 ng/ml) were not significantly different from those in controls (109 +/- 41 ng/g/30 min and 12.8 +/- 5.4%). And those (120 +/- 33 and 99 +/- 19 ng/g/30 min, and 3.5 +/- 0.6 and 2.5 +/- 0.4%) in the kidney perfused with glibenclamide (200 and 400 ng/ml) were similar to those in controls (98 +/- 33 ng/g/30 min and 3.0 +/- 1.5%).

Animals↗
PubMed1986

Secretion and degradation of insulin and glucagon in carbon tetrachloride-induced liver injury rats.

To elucidate the mechanism of hyperinsulinemia and hyperglucagonemia in liver diseases, secretion of insulin and glucagon from perfused pancreas and extraction of insulin and glucagon by perfused liver were investigated in carbon tetrachloride inhalated liver injury rats. Fasting plasma insulin and glucagon levels and insulin and glucagon levels after arginine injection (0.25 g/kg) in liver injury rats were significantly higher than those in control rats. Glucagon levels after glucose injection (0.5 g/kg) were slightly increased in the liver injury group. Insulin responses to 16.7 mM glucose and 10 mM arginine from perfused pancreas were similar in liver injury rats and control rats. Glucagon response to 10 mM arginine from perfused pancreas was also similar in liver injury rats and control rats. Insulin extraction by perfused liver in liver injury rats (45 +/- 9%) was significantly (P less than 0.05) lower than that (64 +/- 11%) in control rats, and glucagon extraction by perfused liver was also significantly (P less than 0.05) decreased in liver injury rats (57 +/- 8%) compared with controls (73 +/- 9%). It is concluded that in carbon tetrachloride-induced liver injury rats, hyperinsulinemia and hyperglucagonemia may be dependent on decreased insulin and glucagon extraction by the liver.

Animals↗
PubMed1986

Conversion of T4 to T3 in perfused liver of rats with carbontetrachloride-induced liver injury.

To evaluate the effect of hepatocellular damage on thyroid hormone metabolism, the conversion of T4 to T3 in the perfused liver of rats with carbontetrachloride (CCl4)-induced liver injury was investigated. The liver was perfused non-recyclically with a synthetic medium containing 10 micrograms/dl T4 for 30 min, and the T3 production and the conversion of T4 to T3 were examined. The serum T3 level was significantly (P less than 0.05) lower in liver-injury rats (72 +/- 9 ng/dl) compared with controls (88 +/- 10 ng/dl). The uptake of T4 (4.15 +/- 0.85 micrograms/g/30 min), net T3 production (180 +/- 48 ng/g/30 min), and conversion rate of T4 to T3 (4.4 +/- 0.9%) in the perfused liver of liver-injury rats were similar to the values (3.78 +/- 0.66 micrograms/g/30 min, 191 +/- 31 ng/g/30 min, and 5.0 +/- 1.0%) in control rats, whereas the release of T3 (12.7 +/- 3.2 ng/g/30 min) in the effluent in injured livers was significantly (P less than 0.05) lower than that (16.9 +/- 3.0 ng/g/30 min) in control livers. We concluded that in CCl4-induced liver-injury rats, the low serum T3 level may partly be due to the decreased release of T3 from liver cells after conversion of T4 to T3 rather than to a decreased conversion of T4 to T3.

Alanine Transaminase↗
PubMed1986

Decreased glucose production from maltose in perfused kidney of streptozotocin diabetic rats.

To elucidate the role of renal maltase in the metabolism of circulating maltose, glucose production from maltose was investigated in perfused kidney of normal and streptozotocin (STZ) diabetic rats. The kidney was perfused with 150 mg/dl maltose for 30 min and perfusate maltose and glucose were measured. Perfusate glucose concentration in the kidney of control rats gradually increased during perfusion. That in the kidney of diabetic rats was significantly lower than that in controls. Perfusate maltose concentration in the kidney of diabetic rats was significantly higher than that in controls. These results suggest that circulating maltose may enter kidney cells and subsequently metabolized to glucose, and that maltose uptake and glucose production were decreased in the kidney of STZ diabetic rats.

Animals↗
PubMed1985

Effect of TSH on conversion of T4 to T3 in perfused rat kidney.

This study was undertaken to elucidate the effect of thyrotropin (TSH) on the conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) in the isolated perfused rat kidney. The kidney was perfused with a synthetic medium containing 20 micrograms/dL T4 and the effect of constant infusion of bovine TSH (125 or 250 microU/mL) on the conversion of T4 to T3 was investigated. T4 uptake in the perfused kidney was not changed by the addition of TSH. However, the release of T3 (89 +/- 11 ng/g/30 min, mean +/- SD), tissue T3 (190 +/- 23 ng/g/30 min), net T3 production (227 +/- 37 ng/g/30 min), and the conversion rate of T4 to T3 (9.5 +/- 1.6%) in the kidney perfused with 250 microU/mL TSH were significantly (P less than 0.005) greater than those in controls (63 +/- 9, 143 +/- 15, 152 +/- 36 ng/g/30 min, and 6.3 +/- 1.9%), respectively. Degradation rate of T3 in perfused rat kidney was not changed by the addition of 250 microU/mL TSH. These results suggest that TSH may directly affect renal iodothyronine-monodeiodinating activity in rats in vitro.

Animals↗
PubMed1985

Effect of diabetes on triiodothyronine and reverse triiodothyronine production in the perfused rat liver and kidney.

This study was undertaken to elucidate the effect of diabetes on the conversion of T4 to T3 and rT3 in the isolated, perfused rat liver and kidney. The livers and kidneys from streptozocin (STZ)-induced (50 mg/kg i.p. 2 wk before killing) diabetic rats with or without T4 (30 micrograms/kg s.c. daily) treatment were perfused for 30 min with a synthetic medium containing T4 (6 micrograms/dl), and production of T3 and rT3 in the tissues was measured by radioimmunoassay. The production of T3 (111 +/- 38 ng/g/30 min, mean +/- SD) and conversion rate of T4 to T3 (19.7 +/- 5.8%) in the liver of diabetic rats without T4 treatment and those (124 +/- 41 ng/g/30 min and 21.6 +/- 4.9%) in the liver of diabetic rats with T4 treatment were significantly lower than those of controls (196 +/- 48 ng/g/30 min and 30.6 +/- 5.2%), respectively. The production of rT3 and conversion rate of T4 to rT3 in the liver of diabetic rats with or without T4 treatment were similar to those of controls. The production of T3 and rT3, and conversion rate of T4 to T3 and T4 to rT3, in the kidney of diabetic rats with or without T4 treatment were not significantly different from those of controls. These results suggest that the liver is far more important than the kidney in the overall reduction in the T4 to T3 conversion that occurs in diabetic rats.

Animals↗