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Biomedical subjects

I Mori

Publications and source records attributed to I Mori.

At least 19 recordsLinked to original sources
PubMed1992

Growth hormone (GH)-dependent hepatic GH receptors in the Japanese eel, Anguilla japonica: effects of hypophysectomy and GH injection.

Control mechanisms of growth hormone (GH) receptors in the eel liver were examined by following the time course of changes in total (MgCl2-treated membranes) and free (untreated membranes) GH-binding sites after hypophysectomy and replacement therapy with homologous GH. Both total and free binding sites decreased significantly 1 week after hypophysectomy. Scatchard analysis indicated that the reduction in GH receptors was primarily due to a decrease in the number of binding sites, rather than to a change in binding affinity. When recombinant eel GH was injected intramuscularly into hypophysectomized eels (2 micrograms/g body wt), plasma GH concentration increased to a maximal value after 10 hr and decreased to the initial level by 72 hr. Free binding sites decreased to a minimal value 24 hr after the injection and returned to the initial level after 72 hr. The reduction in free binding sites seems to be due to occupation of GH receptors. Total binding sites increased gradually to almost twofold over those of the controls 5 days after the injection, the increase being due to an increase in the binding capacity. GH appears to be importantly involved in inducing and maintaining its own receptors in the eel liver.

Analysis of Variance↗
PubMed1992

Immunofluorescent antibody response to lactic dehydrogenase virus in different strains of mice.

The development of antibody against lactic dehydrogenase virus in five strains of mice (NZB x NZWF1, BALB/c, C.B-17, ICR and C.B-17 scid or SCID mice) was examined by indirect immunofluorescence (IIF) of infected liver sections. IIF antibody appeared 1 to 3 weeks and rose progressively 2 to 4 weeks after infection in four strains of mice (NZB x NZWF1, BALB/c, C.B-17 and ICR mice). SCID mice did not develop antibody. These results suggest that IIF may be applicable for detecting LDV infection in many other ordinary strains of mice.

Animals↗
PubMed1992

Reperfusion after a two-hour period of pulmonary artery occlusion causes pulmonary necrosis.

The role of reperfusion injury in the progression to necrosis in pulmonary embolism was evaluated. To simulate this condition, we used a technique that enables occlusion and reopening of the pulmonary arterial branch supplying the right upper lobe in conscious rats. The rats were divided into five groups: the occlusion group (n = 12), in which the pulmonary artery (PA) branch was occluded without reperfusion; the reperfusion group (n = 12), in which the PA branch was reopened after a 2-h period of occlusion; and the reperfusion-SOD (n = 9), reperfusion-IM (n = 8), or reperfusion-IA-SOD (n = 6) groups, in which superoxide dismutase (SOD), indomethacin (IM), or inactivated SOD (IA-SOD), respectively, was administered during reperfusion. The lungs were removed 24 h after the PA occlusion, and histologic examination was performed. In the occlusion group, the alveolar structure of the right upper lobe was well preserved, and there was no erythrocyte or leukocyte accumulation. The only significant changes compared with the control lobe was the appearance of wavy internal elastic lamina of the PA and slight neutrophil adherence to the endothelial cells. In contrast, the right upper lobe of the reperfusion group disclosed numerous foci of hemorrhagic necrosis, with disrupted alveoli and leukocyte accumulation in all cases. With SOD treatment, the changes compatible with hemorrhagic necrosis were attenuated to the level of the control lobes. However, neither IM nor IA-SOD decreased these changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Inhibitory effects of hyaluronan on [14C]arachidonic acid release from labeled human synovial fibroblasts.

The effects of hyaluronan (HA) on the release of arachidonic acid (AA) from phospholipids induced by bradykinin in synovial fibroblasts of osteoarthritic patients were examined. HA inhibited [14C]AA release from prelabeled synovial cells stimulated with and without bradykinin 1 hr after incubation with HA and thereafter. The inhibitory effects of HA on [14C]AA release were dependent on the concentration and molecular weight of HA. However, inhibition of [14C]AA release by HA was not merely due to the viscosity of HA. The [14C]AA release induced by calcium-ionophore A23187 was also inhibited by HA with a high molecular weight. In addition, HA did not affect [14C]AA uptake by the cells. Our results suggest that HA with a high molecular weight elicits anti-inflammatory effects, at least in part, by inhibiting AA release in inflamed joints.

Arachidonic Acid↗
PubMed1992

Binding of asparaginase to mouse monocytes.

We have demonstrated that biotinylated asparaginase binds to mouse monocytes. Also, asparaginase bound to peritoneal exudate, resident, splenic, bone marrow and pulmonary macrophages, but not to neutrophils or lymphocytes. Labelled asparaginase binding to peritoneal exudate macrophages was inhibited by 20-fold excess of unlabelled asparaginase. The binding of asparaginase to monocytes from mice injected with lactic dehydrogenase virus (LDV) or carrageenan was decreased. This decreased binding following treatment with LDV or carrageenan was reversed when mice were treated with diethylstilboestrol. In-vivo asparaginase clearance in mice infected with LDV was impaired as compared with that in uninfected mice. Neither strain nor age differences affected the binding to monocytes. The results suggest that the ability of asparaginase to bind to monocytes in vitro may reflect clearance function in vivo.

Animals↗
PubMed1992

Lactic dehydrogenase virus infection prevents development of anti-nuclear antibody in (NZB x NZW)F1 mice; role of prostaglandin E2 and macrophage Ia antigen expression.

Persistent lactic dehydrogenase virus (LDV) infection prevents the development of antinuclear antibody (ANA) in (NZB x NZW)F1 mice. To assess the suppressive mechanisms, we focused on the role of the E series of prostaglandin(PGE), since previously we have shown enhanced production of PGE by macrophages from chronically LDV-infected mice. Treatment with PGE2 suppressed ANA titres more markedly in non-infected mice than in LDV-infected mice. Indomethacin enhanced ANA titres more markedly in LDV-infected mice than in non-infected mice. The number of Ia antigen positive(Ia+) macrophages was less in LDV-infected mice than in uninfected mice. The number of Ia+ macrophages was decreased in non-infected mice by PGE2 treatment and increased in LDV-infected mice by indomethacin treatment. These results suggest that the low ANA production in LDV-infected (NZB x NZW)F1 mice may be related to the decreased number of Ia+ macrophages and that one of the factors responsible for suppression of Ia+ macrophages may be the enhanced PGE2 production in the LDV-infected mice.

Animals↗
PubMed1992

Enhanced clearance of lactic dehydrogenase-5 in severe combined immunodeficiency (SCID) mice: effect of lactic dehydrogenase virus on enzyme clearance.

The lactic dehydrogenase (LDH) level in plasma and the clearance of LDH in C.B-17 scid (severe combined immunodeficiency; SCID) mice were compared with those in C.B-17 or BALB/cCrSlc mice with or without lactic dehydrogenase virus (LDV) infection. The resting enzyme level in SCID mice showed little difference from that in C.B-17 or BALB/cCrSlc mice. The degree of increased plasma LDH level in SCID mice was lower than that in C.B-17 and BALB/cCrSlc mice after LDV infection. To assess the mechanisms of decrease in LDH elevation in SCID mice infected with LDV, virus replication was compared in SCID and BALB/cCrSlc mice. The infectivity titre of plasma in SCID mice was higher (more than 10 times) than that in BALB/cCrSlc mice. Moreover, the percentage of virus antigen positive Kupffer cells was higher in SCID mice than that in BALB/cCrSlc mice. The level of endogenous LDH release as a result of carbon tetrachloride treatment was similar in the SCID and BALB/cCrSlc mice. The clearance rate of endogenous LDH was greater in SCID mice than in BALB/cCrSlc mice with or without LDV infection. The rate of clearance of intravenously injected porcine LDH-5, but not porcine LDH-1, was enhanced in SCID mice as compared with that in BALB/cCrSlc mice. Furthermore, carbon clearance was higher in SCID mice than that in BALB/cCrSlc mice. These results suggest that the smaller increase of plasma LDH after infection might be due, at least in part, to the enhanced LDH-5 clearance function by macrophages in SCID mice.

Animals↗
PubMed1979

Evaluation of phentolamine as a provocative test for idiopathic hypertrophic subaortic stenosis.

Intravenous injection of phentolamine potentially offers a better provocative test for aortic left ventricular outflow tract obstruction than do Valsalva's maneuver, inhalation of isoproterenol, or of amyl nitrite. In hemodynamic studies, phentolamine enhanced myocardial contractility, and decreased afterload with only induction of slight tachycardia. Phentolamine (5 mg.) was administered intravenously to five patients who had idiopathic hypertrophic subaortic stenosis, and 35 patients who had valvular dysfunctions, after which echocardiographic and phonocardiographic recordings were performed. Recordings were of high quality despite changing hemodynamics. Systolic pressures fell an average of 20 mm. Hg; no pressure fell below 90 mm. Hg; there was no notable increase in heart rate. In the five patients with typical idiopathic hypertrophic subaortic stenosis, the amyl nitrite increased the obstructive index from 39.6 +/- 12 to 51 +/- 18.9 (P less than 0.05); whereas, phentolamine increased the obstructive index to 69.8 +/- 25.6 (P less than 0.015). After a 2 week course of oral administration of 80 mg. of propranolol daily, and then either inhalation of amyl nitrite or injection of phentolamine, there was no change from the mean resting obstructive index. Phentolamine appears to be a safe, simple and specific diagnostic agent, and more potent than amyl nitrite in eliciting dynamic obstruction in IHSS; phentolamine and amyl nitrite do not affect the obstructive index in patients with beta blockade.

Amyl Nitrite↗
PubMed1978

Psychosomatic aspects of the effect of conjugated estrogens in patients with postoperative ovarian deficiency syndrome.

Fifty-three uterine cancer patients who complained of the syndrome dur to vasomotor manifestations or psychosomatic response after ovariectomy were given Premarin tablets, 1.25 mg per day or placebo for 3 weeks and improvement in their complaints was compared from the psychosomatic aspects by the double-blind method. Premarin was significantly more effective than placebo (P less than 0.001) in the psychologically normal patients. On the other hand, no difference in the effectiveness of these drugs were found in the psychologically abnormal patients (P = 0.119). According to the self evaluation by the patients, Premarin was significantly more effective than placebo (P less than 0.05) in the psychologically normal patients. However, there was no difference in the effects of these agents in the psychologically abnormal patients.

Adult↗