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Biomedical subjects

H Ishida

Publications and source records attributed to H Ishida.

At least 883 records · Page 49Linked to original sources
PubMed1985

Prevention of supersensitivity-like phenomena in rat vas deferens by colchicine.

Rat vas deferens has been shown to become supersensitive to alpha-adrenergic agonists on brief treatment with epinephrine (Epi-treatment). Epi-treatment increased the contractile response and the number of alpha-adrenoceptors in the tissue. The application of colchicine (2.5 mM) during Epi-treatment prevented the supersensitivity-like phenomena and increase in number of alpha-adrenoceptors. Vinblastine (10 microM) also counteracted the effect of Epi-treatment but cytochalasin B (100 microM) and strychnine (2.5 mM) did not. It is suggested that the supersensitivity-like phenomena induced in rat vas deferens by Epi-treatment were due to a change in microtubular components of the membrane.

Animals↗
PubMed1985

Congenital bile duct dilatation--possibly an hereditary condition.

A female patient underwent resection of a large choledochal cyst and hepaticojejunostomy when she was 11 years old at Tokyo Medical and Dental University Hospital. Her mother, 48 years old, also had congenital bile duct dilatation (CBD) with cancer. The mother had an anomalous pancreatico-biliary ductal junction. To investigate the possibility of a genetic link, family members of another three consecutive CBD cases were examined for bile duct dilatation and anomalous pancreatico-biliary junction. Endoscopic retrograde choledocho-pancreatography (ERCP) revealed an anomalous pancreatico-biliary ductal junction, without bile duct dilatation in the mother of a 17-year-old CBD patient. Two familial occurrences of CBD had been reported in the Japanese literature. Their combinations were; a father--a daughter and two sisters, respectively. Considering that the sex ratio of CBD is one male to 2.6 females, our results suggest that CBD or anomalous pancreatico-biliary ductal junction may be 1) an X-linked dominant trait or 2) autosomal dominant trait with relatively low penetrance in males. Since anomalous pancreatico-biliary ductal junction does not necessarily develop into bile duct dilatation, more familial investigations on pancreatico-biliary ductal junction and bile duct dilatation are essential to clarify the genetic contribution to CBD.

Adolescent↗
PubMed1985

Diabetic osteopenia and circulating levels of vitamin D metabolites in type 2 (noninsulin-dependent) diabetes.

The degree of diabetic osteopenia and serum vitamin D metabolite levels were measured in 168 type 2 (noninsulin-dependent) diabetic patients. Based on six indices obtained by microdensitometry, we found the bone mass in 26.2% of diabetic patients to be clearly decreased and in 11.9% to be severely decreased. Our direct method of analysis of bone mass shows that diabetic osteopenia differs from typical osteoporosis in character. In addition, serum 24,25-dihydroxyvitamin D was significantly decreased (P less than 0.01), but 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were similar to those of controls.

Absorptiometry, Photon↗
PubMed1985

Assays for cholesterol 7 alpha-hydroxylase and 12 alpha-hydroxylase using high performance liquid chromatography.

Rapid and accurate assay methods for cholesterol:NADPH oxidoreductase (EC 1.14.13.17, 7 alpha-hydroxylating) and 7 alpha-hydroxy-4-cholesten-3-one 12 alpha-hydroxylase (enzyme not yet registered) are described. 7 alpha-Hydroxylase utilizes the endogenous cholesterol of liver microsomes as substrate. The reaction products were separated by high performance liquid chromatography monitored at 214 nm. Much higher activity was obtained with the method compared to literature values, which were obtained using externally added radioactive cholesterol as the substrate. The 12 alpha-hydroxylase activity was measured using non-radioactive steroid as the substrate. The reaction products were separated by the chromatography and detected at 240 nm. Comparable activities were obtained by this method compared to those that were obtained using radioactive substrate.

Animals↗
PubMed1985

Comparison of somatostatin-28 and somatostatin-14 clearance by the perfused rat liver.

The hepatic clearances of somatostatin (SS)-28 and SS-14 by the perfused rat liver were compared, using a recirculating, plasma-free, erythrocyte-containing perfusion system. The disappearance rate constant, half time, clearance, and hepatic extraction ratio when 1.2 nM SS-28 was added to the perfusate were 0.0221 +/- 0.0051 min-1, 36.6 +/- 7.6 min, 0.34 +/- 0.08 mL/min, and 17.2 +/- 3.9%, respectively. The corresponding values obtained when SS-14 was added to the perfusate were 0.0405 +/- 0.0022 min-1, 17.3 +/- 1.0 min, 0.71 +/- 0.05 mL/min, and 35.4 +/- 2.6%, respectively. The differences between the SS-28 and SS-14 indices were all statistically significant. In addition, the perfusates with SS-28 added were eluted on Sephadex G-25 fine columns and somatostatinlike immunoreactivity (SLI) was determined. No SS-14 was found in perfusate containing SS-28 at both 5 and 30 min after the beginning of the perfusion. To investigate whether or not the liver plays an important role in the clearance of SS-28 or the conversion of SS-14 in vivo, the plasma disappearance of 2 micrograms SS-28 was compared in the whole rat and the functionally hepatectomized model. The half time of plasma SS-28 was 1.43 +/- 0.12 min in the whole rat, significantly shorter than the 2.20 +/- 0.14 min in the hepatectomized model. Gel filtration of plasma extract samples at 0.5 min after the SS-28 injection showed two major peaks of SLI: a first peak corresponding to SS-28 and a second peak coeluted in the position of SS-14 in both the whole rat and the hepatectomized model. At 4 min after the SS-28 injection, the first peak disappeared and only a small second peak was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Vagal regulation of GRP, gastric somatostatin, and gastrin secretion in vitro.

The effect of electrical stimulation of the vagus nerves on the release of immunoreactive gastrin-releasing peptide (GRP), gastrin, and somatostatin was investigated using the isolated perfused rat stomach. Electrical stimulation (10 Hz, 1 ms duration, 10 V) of the peripheral end of the subdiaphragmatic vagal trunks produced a significant increase in both GRP and gastrin but a decrease in somatostatin. The infusion of atropine sulfate at a concentration of 10(-5) M augmented GRP release and reversed the decrease in somatostatin release in response to vagal stimulation to an increase above basal levels. However, the gastrin response to vagal stimulation was not affected by atropine. The infusion of hexamethonium bromide at a concentration of 10(-4) M significantly suppressed GRP release but did not affect gastrin secretion in response to vagal stimulation. On the other hand, the somatostatin response to vagal stimulation was completely abolished by hexamethonium. These findings lead us to conclude that the intramural GRP neurons might play an important role in the regulation of gastrin as well as somatostatin secretion and that somatostatin secretion may be controlled not only by a cholinergic inhibitory neuron but also by a noncholinergic, e.g., peptidergic stimulatory neuron, both of which may be regulated through preganglionic vagal fibers via nicotinic receptors. In addition, because the infusion of 10(-7) M GRP suppressed the somatostatin secretion, we suggest that either GRP should be excluded from the list of candidates for the noncholinergic stimulatory neurotransmitter for somatostatin secretion or that there are different mechanisms of action for endogenous and exogenous GRP.

Animals↗
PubMed1985

Forskolin induces supersensitivity of the amylase secretory response of rat parotid tissue.

The stimulatory effect of forskolin on amylase secretion was studied by pretreating rat parotid tissue with forskolin for 10 min, incubating it in medium without forskolin for 10 min, and then treating it with forskolin again. Pretreatment with 10 microM forskolin for 10 min resulted in increased amylase secretion and enhanced accumulation of cyclic AMP in the tissue during the second incubation with forskolin. In the presence of colchicine or vinblastine, the enhancement in cyclic AMP accumulation during the second incubation with forskolin was prevented, but the increased amylase secretion remained unchanged. The increased amylase secretion was counteracted only in the presence of concanavalin A. On the other hand, increased amylase secretion induced by isoproterenol (IPR) pretreatment was counteracted by colchicine, vinblastine, concanavalin A or strychnine. These data suggest that the total amount of cyclic AMP in the tissue does not have any essential role in the supersensitivity of the amylase secretory response, and that the supersensitivity induced by forskolin differs from that induced by IPR.

Amylases↗
PubMed1985

Effects of insulin on altered mineral and vitamin D metabolism in streptozotocin-induced diabetes.

In order to ascertain whether or not abnormal mineral and vitamin D metabolism in diabetes can be reversed by insulin therapy, plasma calcium, ionized calcium, phosphorus, parathyroid hormone (PTH) and vitamin D metabolites were measured in control, streptozotocin (STZ) diabetic and insulin-treated diabetic rats. Blood glucose levels in diabetic rats treated with insulin decreased to normal. The low plasma calcium and ionized calcium levels in diabetic rats were found to be normal in insulin-treated diabetic rats. An elevated PTH level was observed in the diabetic group, but it was at normal levels in the insulin-treated diabetic group. Plasma 25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)2D) in the diabetic group were decreased compared to those in control rats, but these were also fully restored to control levels by insulin therapy. However, plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) levels in the untreated diabetic group tended to be lower than in controls, and the values in insulin-treated rats were significantly decreased compared to the control group. The ratio of 1,25(OH)2D to 25(OH)D in diabetic rats was higher than in controls, but it was decreased after insulin therapy and was significantly lower than in the control group. It is suggested, therefore, that the negative calcium balance and decreased 25(OH)D and 24,25(OH)2D levels are derived from the metabolic derangement due to the insulin deficiency. Furthermore, insulin seems to suppress the conversion of 25(OH)D to 1,25(OH)2D in experimental diabetes in vivo.

Animals↗