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Biomedical subjects

I Niki

Publications and source records attributed to I Niki.

At least 55 records · Page 3Linked to original sources
PubMed1988

Insulin release by glucose anomers in a rat model of non-insulin-dependent diabetes.

The effects of the alpha and beta anomers of D-glucose on insulin release were studied in a rat model of non-insulin-dependent diabetes, which was induced by streptozotocin injection at 2 days of age. Glucose tolerance of the streptozotocin-treated rats at 8-10 weeks of age was mildly diabetic. Insulin release from the isolated perfused pancreas of the diabetic rats in response to 10 mmol/l alpha-D-glucose was markedly impaired, while insulin response to 10 mmol/l beta-D-glucose in the diabetic pancreas was only slightly reduced as compared to that in the control pancreas.

Animals↗
PubMed1988

Possible involvement of diacylglycerol-activated, Ca2+-dependent protein kinase in glucose memory of the rat pancreatic B-cell.

Exposure to high concentrations of glucose potentiates insulin release from the pancreatic B-cell stimulated by various secretagogues after an interval under basal condition. We studied the role of diacylglycerol-activated, Ca2+-dependent protein kinase (protein kinase C) in this priming effect of glucose in rat pancreatic islets, using 12-O-tetradecanoyl phorbol-13-acetate (TPA), 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7),N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004) and forskolin. The priming effect of glucose was mimicked by 10 nmol/l of TPA, an activator of protein kinase C, but not by 5 mumol/l of forskolin, which increases cAMP via activating adenylate cyclase. When pancreatic islets were exposed to glucose (10 mmol/l) together with 50 mumol/l of H-7, an inhibitor of protein kinase C, the secretory response to glucose (10 mmol/l) after a 30-min interval was significantly reduced compared with that in the islets previously exposed to 10 mmol/l glucose alone. In contrast, this was not the case for HA-1004, its inhibitory activity against protein kinase C being less potent than H-7. These findings suggest that protein kinase C may play an important role in the priming effect of glucose on the pancreatic B-cell.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Prostaglandins affect the central nervous system to produce hyperglycemia in rats.

The influence of prostaglandins (PG) on central nervous system regulation of blood sugar homeostasis was studied in rats. Substances were injected into the third cerebral ventricle of anesthetized rats while rectal temperature and hepatic venous plasma glucose concentration were recorded. Stereotaxic microinjection of PGD2, E1, E2, and F2 alpha produced hyperglycemia and hyperthermia. The relative order of potency in hyperglycemia, PGF2 alpha greater than D2 greater than E1 greater than E2, was not consistent with that of hyperthermia, PGE2 greater than F2 alpha greater than E1 greater than D2, which suggests that hyperglycemia was a primary, not secondary, response to hyperthermia. Injection of PGF2 alpha caused a dose dependent (5-200 micrograms) increase in the hepatic venous plasma glucose level. Neither the injection of PGF2 alpha (50 micrograms) into the cortex nor into the systemic vein caused hyperglycemia. The injection of PGF2 alpha into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norephinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through the femoral vein completely prevented the increase of glucagon after administration of PGF2 alpha, although the increase of plasma glucose level was still observed. PGF2 alpha-induced hyperglycemia did not occur in adrenodemedullated rats. Intravenous injection of naloxone or propranolol did not affect the hyperglycemia, but phentolamine significantly prevented the hyperglycemic effect of PGF2 alpha. These results suggest that intraventricular PGF2 alpha affects the central nervous system to produce hyperglycemia by increasing epinephrine secretion from the adrenal medulla.

Alprostadil↗
PubMed1979

Noninvasive recording of His-Purkinje activity in patients with complete atrioventricular block. Clinical application of an "automated discrimination circuit".

In seven patients with complete atrioventricular (AV) block, His bundle electrograms (HBEs), standard ECG recordings, bipolar esophageal ECGs and highly amplified, filtered, bipolar chest lead ECGs were simultaneously recorded. The filtered chest lead ECG was averaged to determine His-Purkinje activity (HPA). A simplified device, the "automated discrimination circuit," was used to selectively eliminate the superimposed atrial and ventricular potentials that are characteristic of complete AV block and unsuitable for signal averaging. The processed chest lead ECG was amenable to conventional techniques of signal averaging. In four patients with block proximal to the AV node diagnosed by HBE, there was no activity after the P wave in the surface-averaged ECGs. HPA was consistently recorded before the QRS in the surface-averaged ECG. The measurements of the HV and HPA-V intervals were very close, with a difference of less than 2 msec. Three patients with block distal to the His bundle by HBE showed a loss of electrical potential before the QRS in the surface-averaged ECG, but had a consistent HPA after the P waves. The P-HPA intervals coincided well with PH intervals, with a maximal difference of 5 msec.

Action Potentials↗
PubMed1977

[Clinical studies on endoscopic electromyogram of gastric cancer (author's transl)].

Endoscopic gastroelectromyograms were obtained from 8 patients with gastric cancer, which was located at the gastric antrum. These cancers include 6 cases of advanced cancers and 2 cases of early cancers with mucosal invasion. On healthy volunteers, the gastroelectromyograms from the gastric antrum showed spike bursts with equal intervals. On the other hand, in the patients with advanced cancers on which muscular layer was completely destroyed by the cancerous invasion, the gastroelectromyograms from the cancerous lesion showed no spike bursts. However, in the patients with mucosal cancers in which the cancerous invasion destroyed neither muscular membrane nor muscular layer, the gastroelectromyogram from the cancerous lesion showed spike bursts similar to those of healthy volunteers. From these results, it is proved that the deeper cancerous invasion disturbed the local motility at the cancerous lesion. In future, endoscopic lead of gastroelectromyogram will become useful for the diagnosis of the degree of cancerous invasion and infiltration.

Adenocarcinoma↗