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Biomedical subjects

T Imamura

Publications and source records attributed to T Imamura.

At least 505 records · Page 28Linked to original sources
PubMed1988

A nation-wide study of atherosclerosis in infants, children and young adults in Japan.

This paper reports the results of a nation-wide cooperative study of atherosclerosis in young, first generation Japanese with ages ranging from 1 month to 39 years, who were autopsied between 1978 and 1982 in hospitals distributed over the entire archipelago of Japan. Atherosclerotic lesions in 2320 aortas, 1620 coronary arteries and 344 cerebral arteries were classified into fatty streaks, fibrous plaques and complicated lesions and were then quantificated with the point-counting method. Atherosclerosis of aortas, coronary arteries and cerebral arteries, determined by surface involvement (SI) of atherosclerotic lesions and atherosclerotic index (AI), increased with age; the severest were seen in aortas, and then, with decreasing severity, in the coronary and cerebral arteries. Fatty streaks preceded the other lesions and accounted for the largest portion of the lesions in aortas and coronary arteries. Fibrous plaques and complicated lesions developed in the later decades of life. The patients with collagen diseases had a greater severity of aortic atherosclerosis in the 2nd and 3rd decades of life, than those without such disorders. Correlation of antemortem clinical data with SI and AI of each artery were analyzed, using simple correlation analysis and multiple regression analysis. Age, serum cholesterol and blood pressure were significantly and positively correlated with SI and AI of aortas and coronary arteries. Serum cholesterol was more strongly correlated with the extent of fatty streaks than was mean blood pressure and vice versa with that of fibrous plaques. Atherosclerosis of cerebral arteries, however, showed a significant correlation only with the factor of mean blood pressure. Therefore the susceptibility to risk factors varies with the artery in cases of early lesions of atherosclerosis in young Japanese.

Adolescent↗
PubMed1988

Protective effect of alpha-human atrial natriuretic polypeptide (alpha-hANP) on chemical-induced pulmonary edema.

It has been established that alpha-hANP, the newly discovered peptide extracted from human cardiac atria, has potent natriuretic and hypotensive actions. Our present investigation is the first to demonstrate that alpha-hANP is capable of protecting against pulmonary edema caused by various chemicals, using isolated perfused guinea pig lung system. Lungs were perfused via pulmonary artery with Krebs-Ringer bicarbonate buffer at 5.0 ml/min, and wet weight of lungs and perfusion pressure of pulmonary artery (Pa) were monitored. Bolus injection of Triton-X or CHAPS into cannulated pulmonary artery produced edema as indicated by a massive increase in wet weight and a slight increase in Pa. Constant infusion of alpha-hANP through pulmonary artery at 200 ng/ml was effective in causing decrease in wet weight of lung. Perfusion of lung with paraquat or PGF2 alpha, and repeated bolus injection of arachidonic acid or PGE2 caused elevation in both wet weight of lung and Pa. The treatment with alpha-hANP similar to that described above also protected against edema caused by paraquat or arachidonic acid. Bolus administration of epinephrine induced a slight increase in wet weight and Pa, and alpha-hANP was effective in decreasing the elevated lung wet weight and Pa of lungs. Infusion or bolus administration of alpha-hANP into control lungs increased cGMP level in outflow perfusate as well as in lung tissue significantly. In lungs with edema which were induced by Triton-X or paraquat, there was a slight increase in cGMP level in Triton-X treated and no increase in paraquat treated lung tissues. In either cases, was there any increase in cGMP level in perfusate. The specific binding study of [125I]alpha-hANP revealed that the lack of increase in cGMP was not due to a loss of receptor in Triton-X or paraquat treated lungs. Thus our study demonstrated that alpha-hANP had a direct anti-edematic action(s) in lung which was not secondary to the systemic natriuretic and/or hypotensive action(s).

Animals↗
PubMed1988

Morphogenesis of O,O,S-trimethyl phosphorothioate-induced pulmonary injury in mice.

The purpose of this study was to establish and characterize an experimental model in mice that examined the pulmonary effects of O,O,S-trimethyl phosphorothioate (OOS-TMP), a contaminant present in commercially important organophosphorus insecticides. Characterization of the model will allow the delineation of comparative effects between species and its possible extrapolation to man, and provide an additional experimental animal species satisfactory for mechanistic-oriented studies on OOS-TMP and related compounds. The morphogenesis of pulmonary injury induced by OOS-TMP was studied in mice by light and transmission electron microscopy. Weanling female C57BL/Ka mice received OOS-TMP dissolved in corn oil by intraperitoneal injection and were studied at intervals from 6 to 168 hr after treatment. Morphologic changes were observed in Clara cells only at the initial time period examined. Injury of pulmonary parenchymal cell populations, including the endothelium and type I alveolar epithelium, occurred after morphologic changes indicative of severe cell injury and necrosis in Clara cells. Endothelial cell injury was accompanied by significant increases in wet lung weight and percentage lung water content. Type I alveolar epithelial cell injury and loss resulted in a bare basal lamina, followed by attenuation, hypertrophy, and hyperplasia of type II alveolar epithelial cells. The results of this study document the successful establishment of a mouse experimental model of OOS-TMP-induced pulmonary toxicity. It is concluded that the Clara cell was the initial and most severely affected pulmonary cell population in mice receiving OOS-TMP. The administration of OOS-TMP in mice also results in marked morphologic alterations in the pulmonary parenchyma that were accompanied by significant changes in lung weight and composition.

Animals↗
PubMed1988

Evaluation of long-term cultured endothelial cells as a model system for studying vascular ageing.

Long-term cultures of human umbilical endothelial cells were examined for changes in cell growth, cell density, cell volume, occurrence of multinucleated cells, prostacyclin production and negative charge of the cell surface during in vitro cellular ageing. The changes observed were consistent with the previously described changes in vascular endothelial cells during in vivo ageing. Therefore, we conclude that cumulative cell division is deeply involved in in vivo ageing of endothelial cells and that this in vitro system is suitable for investigating in vivo ageing of vascular endothelial cells.

Aging↗
PubMed1988

The carpal bones in congenital hand anomalies: a radiographic study in patients older than ten years.

Abnormalities of the carpal bones in 192 anomalous hands of 154 patients older than 10 years were examined. Judging from the time of appearance of the pisiform, there was no delay of carpal bone maturation in these anomalies. There were differences between the carpal bones of three distinct groups: which included central polydactyly, syndactyly, and typical cleft hand; the group which included radial and ulnar deficiency, and the group which included symbrachydactyly and transverse defect. This suggests that there were differences between these groups in the timing and degree of injury to the limb bud or the hand plate in the course of development. It is thought that the first group originates from maldistribution of mesenchymal tissue of the limb bud (or of the apical ectodermal ridge), the second group from defects of that tissue, and the last group from defects of the mesenchymal tissue of the hand plate.

Adolescent↗
PubMed1988

Revascularization of digits after prolonged warm ischemia.

Four cases of digit revascularization after prolonged warm ischemia are presented. Amputation injuries occurred in the summer, with the average temperature above 23 degrees C. The average warm ischemia time was 24 hr (range: 20 to 30 hr) from injury to the time of establishment of arterial inflow. Complete survival was achieved in three cases and partial survival in one case. Previously, eight to ten hours were believed an acceptable limit for warm ischemia; however, this study indicates that successful revascularization is still possible, even after a much longer period of time.

Adult↗
PubMed1988

Changes in arterial norepinephrine concentration following intravenous administration in dogs with lung edema.

Arterial concentrations of given norepinephrine (NE) were measured after bolus administration in dogs with normal lungs and in those with oleic acid-induced lung edema. In both groups, the peak NE concentration was given by blood samples taken 30 sec after injection and the concentration showed a decreasing tendency thereafter. NE concentrations were always greater in the lung edema group than in the control group and a longer period was needed for NE concentrations to return to the baseline level. This delay in the clearance of NE from the circulation might reflect a diminished uptake by the pulmonary endothelium. This phenomenon may be used for the diagnosis of pulmonary endothelial injury.

Animals↗
PubMed1988

Severe diabetes induced in subtotally depancreatized dogs by sustained hyperglycemia.

Chronic clamping of plasma glucose levels at greater than or equal to 250 mg/dl in four partially depancreatized but previously nondiabetic dogs was followed within 2 wk by persistent hyperglycemia and glycosuria of less than or equal to 500 g/day, ketonuria, and weight loss. Three of the four dogs required daily insulin injections to control these catabolic manifestations. There was no evidence of spontaneous improvement of the severe diabetic state during the 39-69 days of observation after discontinuation of intravenous glucose infusion. Impairment of intravenous glucose tolerance, loss of the insulin response to glucose and arginine, fasting hyperglucagonemia, exaggerated glucagon responsiveness to arginine, and a significant reduction in sensitivity to insulin were characteristic of all diabetic dogs. Morphometric analysis of the endocrine pancreas revealed a profound reduction in the number and size of identifiable islets of the hyperglycemic dogs compared with islets from their own pancreases resected months earlier and with those from pancreatic remnants of eight subtotally depancreatized control dogs that had not been subjected to chronic hyperglycemic clamping. The reduction in number and size of islets of the hyperglycemic dogs was largely the consequence of depletion of insulin-containing cells and was similar to that of dogs with long-standing alloxan-induced diabetes. In the eight control dogs, clinical evidence of diabetes did not develop during a follow-up period of 193-296 days. In this group, there was no evidence of diminution of intravenous glucose tolerance, of the insulin response to glucose or arginine, or of insulin sensitivity as determined by an acute hyperinsulinemic hyperglycemic clamp. The number and size of islets and number of beta-cells in pancreatic remnants from these dogs did not differ morphometrically from those of the pancreatic segment that had been resected. We conclude that in subtotally depancreatized but nondiabetic dogs, maintenance of constant hyperglycemia of greater than or equal to 250 mg/dl by means of intravenous glucose infusion causes a severe, persistent, and often insulin-requiring diabetic state that does not occur in the absence of the hyperglycemia.

Animals↗
PubMed1988

The lca as an onco-fetal gene: its expression in human fetal liver.

The lca-transforming DNA was isolated from human hepatocellular carcinomas. This gene has no homology with known transforming DNA from human sources, and its role in neoplastic tissue formation has been left unanswered. In this communication, we report that RNAs prepared from human fetal livers hybridize to the lca DNA probe. The RNA is 1.8 kilobase in size and appears in the fetal liver only for a limited period during its development, viz. 19 weeks through 24 weeks of gestation. No other tissues carry detectable levels of the lca messenger RNA. Fetal hepatocytes at 5 weeks of gestation showed no transcripts of lca, but upon culturing for 2 more weeks in vitro, the cells became producers of the lca messenger RNA. These results suggest that the lca plays some role in the proliferative stage of the liver.

Carcinoma, Hepatocellular↗
PubMed1987

Recombinant interferon beta and gamma in the treatment of adult T-cell leukemia.

Adult T-cell leukemia (ATL) is one of the most difficult diseases to treat because of severe underlying immune deficiency and metabolic disturbance. Interferon has potent antiviral, antiproliferative, and immunomodulating properties, and therefore, this may be a good agent to treat such immune deficient patients with peripheral T-cell leukemia. During a period from April 1984 to August 1985, six patients were treated with interferon-beta (IFN-beta), and interferon-gamma (IFN-gamma) was given to five patients. Three patients achieved partial remission by IFN-beta administration with a response duration of 1, 1.5, and 12 months respectively, whereas one complete remission and two partial responses were experienced by IFN-gamma treatment with 4, 4, and 2 months of response. Side effects of IFN-beta were similar to those of IFN-gamma including fever, chills, fatigue, mild hematologic depression, and transient hepatic enzyme abnormalities. These promising results warrant further well-designed clinical trials including combination with other agents or modalities of treatment.

Adult↗
PubMed1987

A phosphorothionate isomer protects against the pneumotoxicity caused by O,O,S-trimethyl phosphorothioate.

O,O,S-Trimethyl phosphorothioate (OOS-TMP), an impurity in many organophosphorus insecticides, causes pneumotoxicity in rats at low doses (20 mg/kg) resulting in increases in bronchopulmonary lavage lactate dehydrogenase (LDH) activity and morphological alterations of bronchiolar epithelium. Coadministration of the nontoxic isomer, O,O,O-trimethyl phosphorothioate (OOO-TMP), at 1% of the toxicant dose, has been found to protect against the increase in LDH levels and morphological changes in bronchioles caused by OOS-TMP. Since OOO-TMP appears to require metabolic activation for pneumotoxicity, the effects of OOO-TMP on pulmonary and hepatic P-450 content and P-450-mediated monooxygenases were examined as a possible biochemical mechanism of antagonism. Oral treatment with OOO-TMP (0.5, 1.0, and 4.0 mg/kg) decreased pulmonary P-450 levels by 23 to 50% at 2 and 6 hr, while no changes were detected in hepatic P-450 levels. Lung microsomal 7-ethoxycoumarin O-deethylase (7-Ec) was inhibited by 71 to 100%, while liver 7-Ec was inhibited by 26 to 52%. p-Nitroanisole demethylase activity was decreased 22 to 47% following treatment with the two highest dose levels of OOO-TMP. These results further support the view that the lung is a target organ of delayed toxicity produced by OOS-TMP, and that the antagonistic effect of OOO-TMP is due to alterations in the metabolic activation processes of OOS-TMP in the lung and/or liver.

Animals↗
PubMed1987

Caseins are cross-linked through their ester phosphate groups by colloidal calcium phosphate.

Artificial casein micelles were prepared by adding 30 mM calcium, 22 mM phosphate and 10 mM citrate to sodium caseinate solutions, and the content of the casein aggregates cross-linked by colloidal calcium phosphate was determined by high-performance gel chromatography on a TSK-GEL G4000SW column in the presence of 6 M urea. The content of the casein aggregates cross-linked by colloidal calcium phosphate in artificial whole casein micelles was 48% of total casein, and their relative casein composition determined by high-performance ion-exchange chromatography was 53.1% for alpha s1-casein, 15.8% for alpha s2-casein, 31.1% for beta-casein and 0% for kappa-casein. The order of cross-linking by colloidal calcium phosphate agreed with that of the ester phosphate content of casein constituents. The content of the casein aggregates cross-linked by colloidal calcium phosphate was higher in alpha s1-kappa-casein micelles than in beta-kappa-casein micelles. kappa- and gamma-caseins and dephosphorylated alpha s1-casein were not cross-linked by colloidal calcium phosphate. Although kappa-casein was not cross-linked, chemically phosphorylated kappa-casein, of which the average phosphate content was 8.5 per molecule, was cross-linked. It is concluded that caseins are cross-linked through their ester phosphate groups by colloidal calcium phosphate.

Animals↗
PubMed1987

Heparan sulfate and heparin as a potentiator or a suppressor of growth of normal and transformed vascular endothelial cells.

The effects of glycosaminoglycans (GAGs), especially heparan sulfate, on human and porcine vascular endothelial cell growth in the presence of 10% fetal bovine serum (FBS) or so-called heparin-binding growth factors, acidic FGF (aFGF) or basic FGF (bFGF), were investigated in a series of studies in order to clarify their role in cell proliferation. The promotion of normal cell growth by aFGF was suppressed by heparan sulfate but enhanced by heparin, while growth promotion by bFGF was suppressed by both GAGs. Chondroitin sulfate and hyaluronic acid showed no significant suppression of promotion, even at much higher concentrations. The growth of spontaneously transformed cells was enhanced by heparan sulfate or heparin in the presence of 10% FBS or aFGF, while growth promotion in the presence of bFGF was suppressed by both GAGs. From these results, we concluded that heparan sulfate and heparin are not always functional analogs and that in some cases they exert opposite actions on the modulation of normal endothelial cell growth. The findings that heparan sulfate enhanced the growth of transformed cells but suppressed the growth of normal cells in the presence of 10% FBS or aFGF were consistent with those of our previous studies on human fibroblasts, confirming the occurrence of some common alterations in the signal transduction system or cell surface upon cellular transformation. The role of heparan sulfate in the modulation of endothelial cell proliferation in vivo is also discussed.

Cell Division↗