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Biomedical subjects

N Ono

Publications and source records attributed to N Ono.

At least 217 records · Page 12Linked to original sources
PubMed1985

Role of the central muscarinic receptor of prostaglandin I2 in cardiovascular function in rat.

The effects of injection of prostaglandin (PG) I2 into the cerebral ventricle on cardiovascular responses and their modification by intracerebroventricular (i.c.v.) pretreatment with several drugs were studied in male Wistar rats under urethane anesthesia. When injected into the ventricle, PG I2 (50 nmol/kg) caused a decrease in blood pressure and an increase in heart rate which were of short duration and were significantly inhibited by i.c.v. pretreatment with drugs, such as atropine (0.4 mumol/kg) and diphenhydramine (1 mumol/kg), having an anticholinergic effect. The similar effects induced by intravenous (i.v.) injection of PG I2 (5 nmol/kg) were not inhibited by i.v. pretreatment with these drugs. These results suggest that PG I2 play a role in regulation of cardiovascular function through central muscarinic acetylcholine receptors.

Animals↗
PubMed1985

Ultrashort-loop positive feedback of corticotropin (ACTH)-releasing factor to enhance ACTH release in stress.

Previous experiments have shown that intraventricular injection of ovine corticotropin (ACTH)-releasing factor (oCRF) in doses too low to elevate plasma ACTH by direct action on the pituitary does not lower plasma ACTH, suggesting that the peptide lacks a negative ultrashort-loop feedback action to suppress its own release under resting conditions. The present study was performed to determine whether oCRF has any action to alter CRF release in stress. The peptide was injected into the third ventricle or external jugular vein of freely moving ovariectomized female rats 5 min prior to application of ether stress. When oCRF was injected into the third ventricle in doses of 500 pg (0.1 pmol) or less, there was no significant alteration in plasma ACTH prior to ether stress; however, there was a significantly enhanced increase in plasma ACTH 2 and 5 min after ether stress applied 5 min after intraventricular injection of oCRF at doses of 50 (0.01 pmol) or 150 pg (0.03 pmol). These results suggest that the peptide acts on structures adjacent to the third ventricle to augment stress-induced CRF release. To rule out the possibility that the sensitivity of the pituitary itself to CRF increases dramatically following stress, 10 or 100 ng of oCRF was injected i.v. These doses produced a significant dose-related increase in plasma ACTH at 2, 5, or 15 min. In other groups receiving the same doses of oCRF and ether stressed 5 min later, plasma ACTH was significantly higher 2 or 5 min after ether stress when compared with plasma ACTH in ether-stressed saline-injected animals. However, in contrast with the results of intraventricular injection of oCRF, the release of ACTH was no greater than that obtained by summing the independent effects of exogenous oCRF and the CRF released by stress. We conclude that CRF may have a positive ultrashort-loop feedback action to enhance stress-induced ACTH release and that this enhancement is not due to increased sensitivity of anterior pituitary corticotrophs to CRF.

Adrenocorticotropic Hormone↗
PubMed1985

Effects of intravenous and intraventricular injection of antisera directed against corticotropin-releasing factor on the secretion of anterior pituitary hormones.

To determine the physiological significance of corticotropin-releasing factor (CRF) in the control of pituitary hormone secretion, highly specific antibodies directed against the peptide were injected either intravenously or intraventricularly (third ventricle) and the effect on plasma levels of pituitary hormones was determined before and after application of ether stress for 1 min. The intravenous injection of CRF antiserum (0.5 ml) did not significantly alter basal corticotropin (ACTH) levels in freely moving ovariectomized rats but largely blocked the increase in plasma ACTH resulting from ether stress. These antibodies had no effect on the ether-induced decline in plasma growth hormone (GH), and they failed to modify plasma luteinizing hormone levels. In a second experiment, CRF antiserum (3 microliter) or normal rabbit serum was injected into the third ventricle. A blood sample was drawn 24 hr later and immediately thereafter another injection of CRF antiserum or normal rabbit serum was made. There was no modification in the level of any of the hormones 24 hr after the first injections, and they were similar in CRF antiserum and normal rabbit serum-injected animals. After imposition of ether stress, the response of plasma ACTH was nearly completely blocked by the intraventricular CRF antiserum, but the degree of blockade was slightly less than that obtained by intravenous injection. The decline in plasma GH after ether stress was blocked by the intraventricular CRF antiserum. There was no effect of the intraventricular injection of the antiserum on the levels of the other pituitary hormones. The results with intravenous injection of the antisera indicate that CRF plays an extremely important but probably not completely indispensable role in the release of ACTH after ether stress. The results of the intraventricular injection of the antiserum suggest strongly that endogenous CRF may also modify its own release in response to stress, augmenting it by a positive ultrashort loop feedback, and that the antisera against the peptide blocked this action; however, an action at the pituitary of these intraventricularly injected antibodies cannot be completely ruled out. The blockade of the stress-induced suppression of GH release by the CRF antibodies suggests that CRF released intrahypothalamically during ether stress brings about an alteration in the hypothalamic control of GH secretion such that the stress-induced inhibition of GH release is blocked.

Adrenocorticotropic Hormone↗
PubMed1985

Influenza virus A/Kumamoto haemagglutinin induces type I, III, and IV hypersensitivity in mice.

Influenza virus A/Kumamoto haemagglutinin was found to induce type I, III, and IV hypersensitivity in mice. MRL/Mp-I pr/lpr (MRL/l) mice are known to be lower responders to, and poor inducers of, interleukin-2 (IL-2). Recombinant IL-2 was found to augment the type III reaction in BALB/c mice and to suppress the reaction in MRL/I mice in vivo. Cyclophosphamide 100 mg/kg had a selective suppressive effect on the suppressor T cells responsible for type IV reaction, and subsequently the delayed type hypersensitivity (DTH) was augmented. Higher doses of cyclophosphamide suppressed both suppressor and effector T cells in DTH, and subsequently the DTH was suppressed markedly. This experimental model system employing viral haemagglutinin may provide a new screening method for the development of immunomodulators.

Animals↗
PubMed1984

Intrahypothalamic action of corticotrophin-releasing factor (CRF) to inhibit growth hormone and LH release in the rat.

The effects of intravenous or intraventricular injection of synthetic ovine corticotrophin-releasing factor (oCRF) on plasma levels of anterior pituitary hormones were studied in conscious, ovariectomized (OVX) female rats and compared with the actions of the peptide on dispersed anterior pituitary cells from OVX female rats incubated in the presence of CRF. Third ventricular injection of oCRF in freely moving rats caused a significant increase in plasma levels of ACTH in a dose-related manner with a minimal effective dose of less than 0.5 micrograms (0.1 nmol). The effect was observable at 5 min after injection and persisted for the 60 min duration of the experiment. In contrast, growth hormone levels were significantly depressed within 15 min with a minimal effective intraventricular dose of 0.5 micrograms. The suppression persisted for the duration of the experiment but there was no additional effect of the higher dose of 5 micrograms. Plasma LH levels were also lowered by the highest dose of 5 micrograms (1.0 nmol) of oCRF, with the first significant lowering at 30 min. Lower doses had no effect on plasma LH. Plasma TSH levels were not significantly altered. Control injections of the 0.9% NaCl diluent were without effect on the levels of any of the hormones. Intravenous injection of similar doses of oCRF had no effect on plasma levels of GH or LH. The ACTH-releasing action of the oCRF preparation was confirmed by in vitro incubation of the peptide with dispersed anterior pituitary cells for 2 h. A dose-related release of ACTH occurred in doses ranging from 0.1-10 nM, but there were no effects on the release of the other anterior pituitary hormones. The results suggest that oCRF may act within the hypothalamus to suppress the release of GH and to a lesser extent LH. The stimulation of ACTH release following intraventricular CRF is presumably related to its uptake by portal blood vessels with delivery to the pituitary and stimulation of the corticotrophs.

Adrenocorticotropic Hormone↗
PubMed1984

Synthesis of flagellin and hook subunit protein in flagellar mutants of Escherichia coli K12.

We have examined Escherichia coli K12 flagellar mutants affected in each of 29 different loci for the synthesis of flagellin and hook subunit protein. Immune precipitation experiments were employed by treating cell extracts with antiserum against each protein. Flagellin was synthesized in mutants defective in genes flaS , flaT, flaU and flbC . The flaE and flaZ mutants produced small amounts of flagellin, while all the other mutants failed to produce any detectable amount of flagellin. Hook subunit protein was found in most mutants including those defective in genes flaA , flaB , flaC, flaD , flaE , flaG , flaH , flaL , flaM , flaN , flaO , flaP, flaQ , flaR , flaS , flaT, flaU , flaV , flaW , flaX, flaY , flaZ , flbA , flbC , flbD , and hag but not in mutants of flaK , flaI , and flbB . The results conform to the predictions made by our previous indirect gene fusion study ( Komeda 1982).

Bacterial Proteins↗
PubMed1984

Bacteriophage chi sensitivity and motility of Escherichia coli K-12 and Salmonella typhimurium Fla- mutants possessing the hook structure.

The production of hook protein and flagellin in 29 Fla- mutants of Escherichia coli K-12 was determined by the complement fixation assay. Six mutants produced hook protein, and four of them also produced flagellin. A flaE mutation was introduced into these fla mutants carrying the hook structure. All of these mutants made polyhooks and were used as hosts for a newly isolated host-range mutant of chi phage that has a high affinity for the hook structure. All except one mutant produced significant amounts of progeny phages. A flaD flaE double mutant was that exception which did not yield significant amounts of progeny by the phage propagation method. All of the flaE double mutants produced comparable amounts of polyhooks, and no qualitative difference was detected between chi-sensitive and chi-insensitive mutants by the complement fixation assay. Accordingly, it was thought that the polyhook of the flaD flaE mutant had a mechanical defect for chi phage infection. This assumption was confirmed by tethered-cell experiments; the flaD flaE mutant did not rotate. These results are well explained by a proposed regulation pathway of flagellar genes. flaE mutants can express other genes which govern the final step of the flagellar morphogenesis, whereas flaD mutants cannot rotate, possibly because the mocha operon is not expressed. The results obtained in E. coli were also found to be applicable to Salmonella typhimurium.

Bacterial Proteins↗
PubMed1984

[A case report of primary double cancer of the stomach and choledochus].

We encountered a relatively rare case of primary double cancer arising simultaneously from both the stomach and choledochus in a 72-year-old woman with obstructive jaundice. The patient was admitted to Saiseikai Shigaken Hospital, and was diagnosed as having both early gastric cancer at the lesser curvature of the antrum and cancer of the choledochus. She underwent curative pancreato-duodenectomy with extended gastrectomy. One of the resected tumors was histopathologically diagnosed as a well differentiated, tubular adenocarcinoma of the stomach with invasion reaching as deep as the submucosa. The other tumor was a moderately differentiated, tubular adenocarcinoma of the choledochus with lymph node metastases (hepatic, retroligamentic, paracholedochal, and posterior and superior pancreaticoduodenal lymph nodes). Our review of the literature suggests that the incidence of primary double malignancies is on the increase.

Adenocarcinoma↗
PubMed1984

[Primary malignant lymphoma of the spleen in a long surviving patient and review of the literature].

A case of primary malignant lymphoma of the spleen is presented. The tumor was successfully removed and eight years after the surgery, the patient died without any recurrence of the malignant lymphoma. A review of the literature, with special reference to prognosis is also presented. Long-term follow-up is necessary in patients with primary malignant lymphoma of the spleen who have been curatively operated because the malignant lymphoma of the spleen may in fact be a metastatic lesion from nodal and extranodal lymphomas, or may be a partial lesion from a multicentrically originating lymphoma.

Humans↗
PubMed1983

Central effects of prostaglandin F2 alpha on the cardiovascular system in the rat.

Effects on blood pressure and heart rate of prostaglandin (PG) F2 alpha administered into a lateral cerebral ventricle (i.c.v.) were investigated in urethane anesthetized rats. PG F2 alpha at doses ranging from 2.4 to 47.4 micrograms caused dose-dependent pressor and positive chronotropic actions, but did not exert such actions at a dose of 47.4 micrograms in spinal rats. The cardiovascular actions of PG F2 alpha were reduced by intravenous (i.v.) pretreatment with hexamethonium (2 mg/kg). In addition, the pressor action was blocked by phentolamine (5 mg/kg i.v.) and the positive chronotropic action by propranolol (0.2 mg/kg i.v.). PG F2 alpha (47.4 micrograms) and norepinephrine (2 micrograms/kg) injected i.v. induced transient pressor and positive chronotropic actions. This pressor action of norepinephrine was almost completely eliminated but that of PG F2 alpha was only partially inhibited by phentolamine (5 mg/kg i.v.), while the positive chronotropic actions were unaffected. The results suggest that PG F2 alpha accelerates the cardiovascular functions by stimulating the peripheral sympathetic tone through its central action.

Animals↗