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Biomedical subjects

S Morisawa

Publications and source records attributed to S Morisawa.

At least 73 records · Page 4Linked to original sources
PubMed1990

An antibody to S1 proteins from rat liver.

S1 proteins (A, B, C and D) are a group of nuclear proteins, isolated by lowering pH to 4.9 of the reaction supernatant of hepatocyte nuclei that had been mildly digested with DNase I. Protein B, apparently ubiquitous in vertebrate cells, was prepared from rat liver and used to immunize a rabbit. The raised antiserum specifically reacted with S1 proteins; it reacted not only with protein B, but also with C and D. Immunoblotting demonstrated that these proteins occurred exclusively in the nucleus, being absent in the cytosol, microsome and mitochondrial fractions. Indirect immunofluorescence of liver tissue sections confirmed their nuclear localization, and further showed that the antibody selectively stained extranucleolar regions of the cell nucleus. These findings suggest that the anti-S1 antibody is specific to S1 proteins and may be useful for their structural and functional studies.

Animals↗
PubMed1990

Effect of gomisin A (TJN-101) on the arachidonic acid cascade in macrophages.

It has been reported that leukotrienes (LTs) may play a role in inflammatory liver diseases, and several inhibitors of LTs show an inhibitory effect on experimental liver injuries. In this study, the effect of Gomisin A (TJN-101), which is a lignan component of schisandra fruits, on the arachidonic acid cascade in macrophages was examined to explain the mechanisms of the inhibitory effect of TJN-101 on liver injuries. The production of leukotriene B4 was suppressed by treatment with TJN-101, while the activity of 5-lipoxygenase was not affected. The release of arachidonic acid from macrophages stimulated with fMet-Leu-Phe or the Ca++ ionophore A23187 was suppressed by treatment with TJN-101. The activity of phospholipase A2 was not affected by treatment with TJN-101. These results suggested that TJN-101 produces an inhibitory effect on the biosynthesis of LTs by preventing the release of arachidonic acid, and it was thought that the preventive effect on the arachidonic acid cascade may be partially associated with the inhibitory effect of TJN-101 on liver injuries.

Animals↗
PubMed1990

The postnatal development of the mouse pericardium; the time and mechanism of formation of pericardial pores.

The mouse pericardium is a continuous serous membrane, up to postnatal day 6 (P6), that consists of pericardial and pleural mesothelia with sparse connective tissue sandwiched in between. This study shows that on P7 the pericardium becomes fenestrated, and the pericardial and pleural cavities become continuous. We found that the number of pores per pericardium increased continuously with the advance of age and reached as many as 3000 on P21. Transmission electron microscopy of the pericardium revealed various structures of the pericardial and pleural mesothelia that may relate to the formation of the pericardial pores. The pericardial and pleural mesothelia were adjoined with cytoplasmic processes that extended toward the base of the opposing mesothelium. As a result of the adjoinment, a pair of U-shaped folds were formed. The two U-shaped folds were connected with tight junctions at their apices, and separation of these junctions may give rise to the pericardial pores.

Animals↗
PubMed1990

Distribution of valves in the great saphenous vein; its clinical implications.

The number and distribution of valves were examined in 26 great saphenous veins. The number of valves per vein ranged from 3 to 11 with an average of 6.7. The valves tended to be concentrated in two segments; one within 10 cm from the sapheno-femoral junction, and the other between 35 cm and 45 cm from the sapheno-femoral junction. More than 55% of the valves were located in these two segments. This fact should be taken into account when obtaining vein segments in graft operations.

Adult↗
PubMed1990

Possible involvement of platelet-activating factor in the induction of liver cell injury.

In order to examine whether the platelet-activating factor (PAF) plays a role in the induction of liver cell injury, the effects of a PAF antagonist were studied in an experimental model of mice with acute liver cell injury induced by intravenous injection of heat-killed Propionibacterium acnes (P. acnes) and lipopolysaccharide. As a result, an intravenous injection of the PAF antagonist was shown to improve the histological changes in the liver, reducing the degree of focal tissue necrosis. In addition, liver adherent cells isolated from normal mice and from those pretreated with P. acnes were shown to produce PAF by stimulation with calcium ionophore A 23187. These results suggested that PAF produced by liver adherent cells may be involved in the induction of liver cell injury.

Animals↗
PubMed1990

[The protective effects of glucagon and insulin in an experimental massive hepatic cell necrosis model].

When heat-killed Propionibacterium acnes was intravenously injected into mice and seven days later, a small amount of gram-negative lipopolysaccharide (LPS) was also intravenously injected, most of them died of massive hepatic cell necrosis. However, then glucagon (0.5 mg/kg body weight) and insulin (0.5 units/kg body weight) or glucagon (0.5 mg/kg body weight) individually were administered during this experimental induction of massive hepatic cell necrosis, the survival rate of mice increased and serum transaminase levels improved. Also, the histological changes of the liver improved remarkably. But, insulin (0.5 units/kg body weight) individually was not effective in an experimental massive cell necrosis model. These results suggested that glucagon and insulin was effective in our experimental massive hepatic cell necrosis model.

Animals↗
PubMed1990

The enhancement of liver injury by lipopolysaccharide in an experimental drug-induced allergic hepatitis model.

When guinea pigs sensitized with trinitrophenylated (TNPed) liver protein 1 (LP1) were intravenously injected with TNPed isolated hepatocytes, remarkable hepatic cell injury was induced 24 hours later. In this experimental model, drug-induced allergic liver injury was induced by using trinitrobenzen sulfonic acid (TNBS) as the hapten and LP1 as the carrier. When these sensitized guinea pigs were intravenously injected with 10 micrograms of lipopolysaccharide (LPS) along with TNPed isolated hepatocytes, serum AST and ALT levels were remarkably higher than those of the guinea pigs not injected with LPS. Hepatic cell necrosis was also more extensive, and some bleeding was observed. Although none of the guinea pigs died even after 24 hours, when 50 micrograms of LPS was injected, many of the guinea pigs started to die and the survival rate was 5% at 24 hours. These results suggested that LPS enhanced liver injury in this experimental drug-induced allergic liver injury model.

Animals↗
PubMed1990

[Serotonin and tryptamine metabolism in the acute hepatic failure model--changes in tryptophan and its metabolites in the liver, brain, kidney and serum].

When trinitrophenylated (TNP) hepatocytes and lipopolysaccharide (LPS) are intravenously injected into TNP-liver protein sensitized guinea pigs, massive hepatic cell necrosis was induced in most of mice. Using this experimental acute hepatic failure model, the tryptophan metabolism in the liver, brain, kidney and serum was studied. As a result, the tryptophan level was remarkably high in all three organs and serum, and the metabolism of both the tryptamine pathway and serotonin pathway was induced. Also, in the brain, the tryptamine metabolism was more induced compared to the serotonin. These results suggest that the metabolites of tryptophan may be involved in this acute hepatic failure model.

Acute Disease↗
PubMed1989

Control by hyperthermia of ornithine decarboxylase in Ehrlich ascites tumor cells.

The effect of hyperthermia on the activity and the messenger RNA levels of ornithine decarboxylase (ODC), which has a rapid rate of turnover in cultured cells, was studied in Ehrlich ascites tumor cells. When the cells were incubated at 42 degrees C, elevation of ODC activity by a change of the medium was prevented. Total RNA was isolated from cells treated at 37 degrees C or 42 degrees C, and the relative abundance of the ODC mRNA was measured by Northern blot analysis. These levels in heat-treated cells were comparable to those in control cells. Inhibition by hyperthermia was reversible. The recovery was suppressed by cycloheximide but not by actinomycin D. In hyperthermic-treated cells, the biological half-life of ODC was 14 min, which was the same time as for cells cultured at 37 degrees C. These results suggest that hyperthermic treatment of Ehrlich ascites tumor cells suppressed ODC induction during translation, not during transcription or after translation.

Animals↗
PubMed1989

Unesterified long-chain fatty acids inhibit thyroid hormone binding to the nuclear receptor. Solubilized receptor and the receptor in cultured cells.

Unesterified long-chain fatty acids strongly inhibited thyroid hormone (T3) binding to nuclear receptors extracted from rat liver, kidney, spleen, brain, testis and heart. Oleic acid was the most potent inhibitor, attaining 50% inhibition at 2.8 microM. Oleic acid similarly inhibited the partially purified receptor and enhanced dissociation of the preformed T3-receptor complex. The fatty acid acted in a soluble form and in a competitive manner for the T3-binding sites, thereby reducing the affinity of the receptor for T3. The affinity of the receptor for oleic acid (Ki) was 1.0 microM. In HTC rat hepatoma cells in culture, fatty acids added to the medium reached the nucleus and inhibited nuclear T3 binding; oleic acid being the most potent. T3 binding of the cells was reversibly restored in fresh medium free of added fatty acids. Oleic acid did not affect all the T3-binding sites in the HTC cells: one form (80%) was inhibited and the other was not and these two forms were commonly present in all rat tissues examined. Thus, fatty acids inhibited the solubilized nuclear receptor as well as a class of nuclear T3-binding sites in cells in culture.

Animals↗
PubMed1989

Synergistic inhibition of DNA synthesis in Ehrlich ascites tumour cells by a combination of unsaturated fatty acids and hyperthermia.

Wide attention has been given to hyperthermia as a new measure for cancer treatment. Clinical trials of hyperthermia, as they possess antitumour activity on some occasions. When cells were incubated with oleic we examine if fatty acids exert a synergistic effect on Ehrlich ascites tumour cells when combined with hyperthermia, as they possess antitumour activity on some occasions. When cells were incubated with oleic acid and linoleic acid (unsaturated fatty acids) at 37 degrees C, the DNA synthesis of cells was significantly inhibited. Palmitic and stearic acids, which are saturated fatty acids, did not suppress DNA synthesis. Hyperthermic treatment without the presence of fatty acids at 42 degrees C for 1 h decreased DNA synthesis to 62% of the control level of 37 degrees C. The combination of an unsaturated fatty acid and hyperthermia synergistically suppressed DNA synthesis. When the cells were incubated in serum-free medium containing 0.1% albumin, unsaturated fatty acids were more effective in inhibiting DNA synthesis. However, saturated fatty acids had little or no effect on DNA synthesis in control or hyperthermia-treated cells. These results indicate that unsaturated fatty acids are useful for enhancing the inhibitory effect of hyperthermia on DNA synthesis, which may increase the in vitro antitumour effects of hyperthermia.

Animals↗
PubMed1989

An experimentally-induced acute hepatic failure model in various strains of mice.

When BALB/cAJc1 mice are intravenously injected with heat-killed Propionibacterium acnes (P. acnes) followed by an intravenous injection of lipopolysaccharide (LPS) 7 days later, massive necrosis is induced in the liver tissue and most of the mice die within 24 hours of LPS injection. Using this experimental model, acute hepatic failure was induced in various strains of mice and the difference in the response was studied. As a result, as in BALB/cAJc1 mice, acute hepatic failure was also induced in BALB/cAJc1-nu, AKR/J, C3H/HeNJc1, C57BL/6NJc1 and DDy mice. However, as an exception, hepatic cell necrosis was hardly seen and the survival rate was remarkable high in C3H/HeJ mice, which genetically do not respond to LPS stimulation. These results indicate that for this experimental induction of acute hepatic failure, macrophages must be activated by the two-step stimulation of P. acnes and LPS.

Acute Disease↗
PubMed1989

Estradiol receptors in the cytosol of peripheral blood mononuclear cells in hepatitis B virus carriers treated with interferon-alpha.

Estradiol receptors in the cytosol of peripheral blood mononuclear cells and the effects of interferon-alpha (IFN-alpha) on estradiol receptors were studied in asymptomatic hepatitis B virus (HBV) carriers, patients with chronic hepatitis B and normal controls. The level of estradiol receptors in the cytosol of mononuclear cells was significantly lower in asymptomatic HBV carriers and patients with chronic hepatitis B, compared to normal controls. This low level of cytosol estradiol receptors in patients with chronic hepatitis B was increased by the administration of IFN-alpha. In addition, when peripheral blood mononuclear cells from patients with chronic hepatitis B were incubated with IFN-alpha in vitro, the level of cytosol estradiol receptors also increased by increasing the concentration of IFN-alpha. We previously reported that the response of mononuclear cells to estrogen is impaired in HBV carriers, and our present results suggested that this may be due to the low level of estradiol receptors in the cytosol of mononuclear cells.

Carrier State↗
PubMed1989

Effects of bile acids on liver cell injury by cultured supernatant of activated liver adherents cells.

When heat-killed Propionibacterium acnes (P. acnes) is intravenously injected into mice followed by an intravenous injection of a small amount of lipopolysaccharide (LPS) 7 days later, most of the mice die of massive hepatic cell necrosis within 24 hours of LPS injection. In addition, when the liver adherent cells including Kupffer cells are separated from the mice 7 days after P. acnes injection and incubated in vitro with LPS, remarkable activity of the cytotoxic factor is found in the culture supernatant. This cytotoxic factor is thought to cause liver injury. Using this experimental model, the effects of various bile acids on liver cell injury were studied. As a result, ursodeoxycholic acid and dehydrocholic acid suppressed liver cell injury induced by the cytotoxic factor. However, cholic acid, deoxycholic acid and chenodeoxycholic acid did not have any hepatocytoprotective effects.

Animals↗
PubMed1989

Two mechanisms of spermidine/spermine N1-acetyltransferase-induction.

The changes in activity of spermidine/spermine N1-acetyltransferase (SAT), a rate-limiting enzyme in polyamine degradation, were investigated to understand the mechanism of the induction of this enzyme in bovine lymphocytes. The activity of SAT was induced by stimulation with phytohemagglutinin (PHA), calcium ionophore A23187, sodium n-butyrate, or methylglyoxal bis(guanylhydrazone) (MGBG). When the cells were treated with a combination of PHA with either MGBG or butyrate, the increase in SAT was synergistic. However, the treatment of cells with both PHA and A23187 did not cause more induction of the enzyme activity than the stimulatory effects of each agent alone. The elevation in SAT caused by PHA or A23187 was inhibited by the simultaneous addition of 25 microM H-7, a protein kinase C inhibitor; the induction of the enzyme activity by MGBG or butyrate was slightly enhanced in the presence of H-7. In cells treated with a high concentration of O-tetradecanoylphorbol 13-acetate, which results in the breakdown of protein kinase C, PHA and A23187 did not give the maximum response, and MGBG slightly enhanced the enzyme activity. Dibutyryl cyclic AMP inhibited PHA-induced enzyme activity, but it stimulated MGBG- or butyrate-induced activity. Exposure to PHA or A23187 but not to MGBG or butyrate significantly increased the ornithine decarboxylase activity and DNA synthesis. These results showed that there were two different mechanisms of SAT induction. One is dependent on protein kinase C. The other one is independent of protein kinase C and is enhanced by cyclic AMP.

1-Methyl-3-isobutylxanthine↗