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Biomedical subjects

N Inoue

Publications and source records attributed to N Inoue.

At least 505 records · Page 28Linked to original sources

[Inhibition of delta-aminolevulinic acid dehydratase by styrene and styrene oxide].

Effects of styrene and styrene oxide on delta-aminolevulinic acid dehydratase in rats were investigated, in vivo and in vitro. In the in vivo study, rats were exposed to styrene or styrene oxide intraperitoneally for seven days. delta-Aminolevulinic acid dehydratase in the erythrocyte was inhibited by both styrene and styrene oxide. The inhibition by styrene oxide had a clear dose-response relationship, but that by styrene did not. In the liver, however, these substances did not inhibit delta-aminolevulinic acid dehydratase. In the in vitro study, styrene oxide inhibited delta-aminolevulinic acid dehydratase both in the erythrocyte and in the liver, but styrene failed to inhibit it. These results suggest that styrene is metabolized to styrene oxide, and this metabolite inhibits delta-aminolevulinic acid dehydratase. It is also thought that the discrepancy of inhibition between the erythrocyte and the liver is due to a difference of distribution and metabolism of the substances.

Animals↗

[Effects of repeated inhalation-exposure to fenitrothion powder on blood cholinesterase activity in rats].

Effects of repeated exposure to Fenitrothion (Sumithion) powder on erythrocyte membrane acetylcholinesterase (AChE) and plasma cholinesterase (PChE) were studied. Rats (Wistar, male) were exposed to fenitrothion powder for 2 hrs/day, 5 days/week for up to 3 months. The suppression of AChE and PChE increased as the exposure period and exposure concentration increased, although no suppression of AChE was found after a single 4-hr exposure. The persistence of AChE inhibition after the termination of exposure increased with the increase of the exposure period and was longer than that of PChE. Therefore, the AChE activity seems to be useful in examining the response to the repeated exposure to fenitrothion powder.

Administration, Inhalation↗

A comparative immunohistochemical study of calcineurin and S-100 protein in mammalian and avian brains.

The cellular and topographic localization of calcineurin and S-100 protein was examined immunohistochemically in the mammalian and avian brain. Calcineurin immunoreactivity in both the avian and mammalian brain was located only in neuronal cells. S-100 protein was localized mainly in the glial and Schwann cells within the mammalian brain. However, in the avian brain, neuronal cells in certain regions such as the paleostriatum primitivum and the cerebellum, as well as other non-neuronal cells, exhibited S-100 protein immunoreactivity. A distinct difference was demonstrated in the macroscopic topographic distribution patterns of S-100 protein immunoreactivity between the mammalian and avian brains, while the patterns of calcineurin distribution were essentially identical. In addition, we provided calcineurin- and S-100 protein-immunocytochemical results for the turtle, frog and fish brain.

Animals↗

Antithrombin III concentrate in the treatment of fulminant hepatic failure.

Twenty-six patients with fulminant hepatic failure were treated with daily infusions of antithrombin III concentrate until recovery of consciousness or death. Seven patients were alive (group A), 7 survived 17 to 47 days after treatment (group B), and 12 died within 9 days (group C). Decreased plasma antithrombin III levels increased on the day after treatment, irrespective of the pretreatment levels in all patients. Continuous or temporary normalization was seen in all patients in groups A and B, but in only 5 in group C patients whose bleeding was extensive (p less than 0.05). An abrupt drop in peripheral platelet counts occurred when plasma antithrombin III levels were below normal. General bleeding accompanied this drop. These results suggest that maintained normal plasma antithrombin III levels are beneficial for prolonged survival time in fulminant hepatic failure, probably through controlling intravascular coagulation, and that antithrombin III infusion may be useful for such treatment.

Antithrombin III↗

Malignant ameloblastoma with pulmonary metastasis and hypercalcemia. Report of an autopsy case and review of the literature.

A case of malignant ameloblastoma with hypercalcemia in a 67-year-old Japanese woman is presented. The tumor of the maxilla was removed and diagnosed as a follicular ameloblastoma. The tumor recurred in the lower orbita-zygoma region, and multiple tumors of the lungs and hypercalcemia were detected eight months after the second operation. The recurrent tumor resembled the primary tumor but was less well differentiated. Autopsy revealed widespread lung metastasis of the malignant ameloblastoma, nephrocalcinosis, and sigmoid colon cancer. Histologic examination showed the metastatic ameloblastoma to be composed of nests and strands of basaloid and spindle-shaped cells surrounded by columnar cells arranged in palisade formation, with focal areas of squamous differentiation and occasional cystic degeneration. Only two cases of malignant ameloblastoma with hypercalcemia have previously been reported. This is the first case of malignant ameloblastoma with hypercalcemia and sigmoid colon cancer. In addition, prostaglandin E2 assay revealed that ameloblastoma produces prostaglandin E2, which results in hypercalcemia.

Aged↗

The appearance of a highly digitalis-sensitive isoform of Na+,K+-ATPase during maturation in vitro of primary cultured rat cerebral neurons.

Immature neurons from the cerebra of 17-day rat fetuses were cultured, and changes in Na+, K+-ATPase activity of the cells were investigated during maturation in culture. The Na+, K+-ATPase activity of the particulate fraction from the cells increased during the course of culture, up to 0.38 +/- 0.01 (mumol/min/mg protein) (= 8.25 +/- 0.85 (mumol/min/mg DNA] by day 13 in culture. The values were more than 3 and 19 times those of the 17-day fetal cerebrum on the bases of protein and DNA, respectively. The enzyme in the immature neurons was mainly a weakly digitalis-sensitive form in terms of the inhibition pattern of the Na+,K+-ATPase activity by strophanthidin. Along with the maturation in vitro of the neurons, a highly digitalis-sensitive form of the enzyme was shown to appear and increase by the biphasic inhibition patterns of Na+,K+-ATPase activity by strophanthidin and of K+ uptake activity by ouabain. The enzyme activity of the highly sensitive form overwhelmed that of the weakly sensitive form by day 13 in culture. In cultured rat cerebral astrocytes, the enzyme was judged to be only the weakly digitalis-sensitive form from the simple inhibition patterns of the Na+,K+-ATPase and K+ uptake activities by digitalis.

Brain↗

Neuropsychological and neuropsychiatric findings in right hemisphere damaged patients.

We evaluated 46 patients with right hemisphere strokes for unilateral spatial neglect (USN), anosognosia, hemiasomatognosia, extinction, constructional disturbance, motor impersistence and organic mental syndrome. High correlations were found among the incidences of USN, anosognosia, hemiasomatognosia, extinction, motor impersistence and constructional disturbance. USN, hemiasomatognosia, motor impersistence, constructional disturbance and anosognosia tended to occur with large lesions. Organic personality syndrome was frequent (33%) and was more often associated with USN, anosognosia, hemiasomatognosia, extinction, constructional disturbance and motor impersistence than other psychiatric symptoms.

Aged↗

Localization of glycogen synthase in brain.

Antisera against glycogen synthase from canine brain were prepared and used for investigation of the localization of the enzyme in the brain. Antisera cross-reacted only with the 88-kilodalton protein that is the subunit of brain glycogen synthase. Immunoreactivity of glycogen synthase was universally distributed in all regions of the brain, although hippocampus, cerebral cortex, caudatoputamen, and cerebellar cortex had relatively high immunoreactivity. Light microscopic examination revealed that the immunoreactivity was found in all cell types, such as neurons in several regions, astrocytes, ependymal cells surrounding the ventricle, oligodendrocytes, and epithelial cells of the choroid plexus in the ventricle. Immunoreactive intensity was more prominent in neurons than glial cells. Immunostaining may be a useful tool for investigation of the state of glycogen metabolism under normal and pathological conditions.

Animals↗

Nerve growth factor induces Na+,K+-ATPase in a nerve cell line.

The effects of nerve growth factor (NGF) on induction of Na+,K+-ATPase were examined in a rat pheochromocytoma cell line, PC12h. Na+,K+-ATPase activity in a crude particulate fraction from the cells increased from 0.37 +/- 0.02 (n = 19) to 0.55 +/- 0.02 (n = 20) (means +/- SEM, mumol Pi/min/mg of protein) when cultured with NGF for 5-11 days. The increase caused by NGF was prevented by addition of specific anti-NGF antibodies. Epidermal growth factor and insulin had only a small effect on induction of Na+,K+-ATPase. A concentration of basic fibroblast growth factor three times higher than that of NGF showed a similar potency to NGF. The molecular form of the enzyme was judged as only the alpha form in both the untreated and the NGF-treated cells by a simple pattern of low-affinity interaction with cardiotonic steroids: inhibition of enzyme activity by strophanthidin (Ki approximately 1 mM) and inhibition of Rb+ uptake by ouabain (Ki approximately 100 microM). As a consequence, during differentiation of PC12h cells to neuron-like cells, NGF increases the alpha form of Na+,K+-ATPase, but does not induce the alpha(+) form of the enzyme, which has a high sensitivity for cardiotonic steroid and is a characteristic form in neurons.

Adrenal Gland Neoplasms↗

Increment of calmodulin in proportion to enhancement of non-nicotinic responses after preganglionic stimulation of the dog cardiac sympathetic ganglia.

The possible involvement of calmodulin in ganglionic function was investigated. Drugs were given directly into the cardiac sympathetic ganglia through the right subclavian artery (i.a.), unless otherwise stated. Positive chronotropic responses to angiotensin II (0.1 and 0.2 micrograms) were enhanced after repetitive high frequency preganglionic stimulation to the right stellate ganglion. After the stimulation, positive chronotropic responses to bethanechol (2.5, 5 and 10 micrograms), but not those to dimethylphenylpiperazinium (2.5, 5 and 10 micrograms), also were enhanced. The enhancement of response to angiotensin II was not affected by i.v. pretreatment with hexamethonium (40 mg/kg) plus atropine (1 mg/kg) or nifedipine (1 mg/kg). Responses to angiotensin II were not enhanced by A23187 (0.3 mg). The enhanced response to angiotensin II after the stimulation was reduced by the calmodulin antagonists, trifluoperazine (0.1, 0.2 and 0.4 mg) and by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (0.5, 1 and 2 mg), but not by promethazine (1 mg) and N-(6-aminohexyl)-1-naphthalenesulfonamide (0.5, 1 and 2 mg). The enhanced response to bethanechol after the stimulation also was inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide. Pretreatment with N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide before the stimulation prevented development of the enhancement in responses to the peptide. The inhibition of endogenous protein synthesis by cycloheximide, 2.5 or 5 mg/kg i.v. 6 hr before surgical procedures, strongly inhibited development of the enhancement in responses to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

[Transmitral blood flow velocity patterns evaluated by pulsed Doppler echocardiography in diagnosing transient myocardial ischemia].

To evaluate the influences of transient myocardial ischemia on transmitral blood flow velocity patterns, pulsed Doppler echocardiography was performed during coronary artery occlusion in 10 anesthetized open-chest dogs, and also during esophageal pacing or the administration of dipyridamole in 79 patients with coronary artery disease (CAD), and in 19 control subjects. During occlusion of the coronary artery, an abrupt decrease in the peak velocity of the rapid filling wave (R) was noted within one min simultaneously with rapid decrease of % wall thickening in the ischemic regions. The peak velocity of atrial filling was augmented compensatorily. Although the transmitral blood flow velocity pattern did not change in the controls with esophageal pacing, changes similar to those which were obtained during experimental studies were demonstrated in CAD patients. There were no significant differences between transmitral blood flow velocity patterns of patients with multivessel disease and those with single vessel disease. Ischemic changes in transmitral blood flow velocity patterns were not demonstrated in patients with mitral regurgitation. Sublingual nitroglycerin normalized post-pacing abnormal blood flow velocity patterns. In contrast, after the intravenous administration of 0.56 mg/kg of dipyridamole, R and A were increased and the A/R ratio was unchanged both in CAD patients and the control groups. Deceleration time, or the half time, was prolonged during both provocation tests in CAD patients, and these changes were transient and were restored within several min. Furthermore, they were noted more frequently than was the development of ST depression on ECG, or chest pain. These findings indicate that the transmitral blood flow velocity patterns obtained by pulsed Doppler echocardiography are useful for detecting transient myocardial ischemia, though they have limitations in diagnosing the extent of coronary artery disease.

Animals↗

Effects of chronic inhalation of ethylene oxide on lipid peroxidation and glutathione redox cycle in rat liver.

The chronic effects of ethylene oxide (EO) on hepatic metabolism were investigated. Both reduced and oxidized forms of glutathione in liver were not changed during chronic exposure to EO for 13 weeks. On the other hand, increased levels of malondialdehyde were detected at 6 weeks and at the end of exposure periods, as compared with those of control livers. The activity of glutathione reductase was decreased at 6 and 13 weeks and therefore in inverse proportion to the lipid peroxide, although the reduced form of glutathione did not decrease probably due to the increase of de novo synthesis. These results indicate that EO treatment enhances lipid peroxidation and also affects glutathione redox cycle, but glutathione did not play a causative role in the induction of lipid peroxidation under the present conditions.

Administration, Inhalation↗