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Biomedical subjects

Y Mizoguchi

Publications and source records attributed to Y Mizoguchi.

At least 109 records · Page 6Linked to original sources
PubMed1990

Interferon gamma stimulates prostaglandin E2 production by mouse Kupffer cells.

When mononuclear phagocytes, including Kupffer cells, are activated by various agents, they synthesize and release arachidonic acid metabolites, prostaglandins (PGs) and leukotrienes (LTs). In this study, we examined the effect of in vitro Kupffer cell activation with recombinant murine IFN gamma on PGE2 and LTB4 secretion. IFN gamma enhanced PGE2 secretion, and this effect of IFN gamma was stronger than that of IL-1 or TNF. Moreover, IFN gamma promoted LTB4 release especially in the absence of PGs. On the other hand, dexamethasone and indomethacin inhibited and, EGTA and TMB-8, which reduce intracellular Ca++ Levels, blocked IFN gamma induced PGE2 production, which suggested that the activation of phospholipase A2 and cyclooxygenase in Kupffer cells requires the elevation of intracellular Ca++ levels.

Animals↗
PubMed1990

Synthesis of eicosanoids by Propionibacterium acnes-elicited liver adherent cells and their effect on production of interleukin 1 and tumor necrosis factor.

When heat-killed Propionibacterium acnes (P. acnes) is intravenously injected into rats or mice, liver adherent cells including macrophages and Kupffer cells increase in number and they synthesize various kinds of biologically-active materials. We studied the production of eicosanoids and the cytokines, interleukin 1 (IL-1) and tumor necrosis factor (TNF), by P. acnes-elicited liver adherent cells and the regulatory mechanisms of eicosanoids in the synthesis of cytokines. As a result, P. acnes-elicited liver adherent cells synthesized not only prostaglandin (PG) E2, 6-keto-PGF1 alpha, thromboxane B2 and leukotriene B4, but also IL-1 and TNF. In addition, PGE2 and PGI2 suppressed the production of these cytokines. These results suggested that there are auto-regulatory mechanisms in production of cytokines in the liver.

Animals↗
PubMed1990

Changes in leukotrienes and prostaglandins in the liver tissue of rats in the experimental massive hepatic cell necrosis model.

When heat-killed Propionibacterium acnes is intravenously injected into rats followed by an intravenous injection of a small amount of Gram-negative lipopolysaccharide (LPS) 7 days later, massive hepatic cell necrosis is induced and most of the rats die within 24 hours of LPS injection. Using this experimental model, we studied the changes in the levels of leukotrienes (LTs) and prostaglandins (PGs) in the liver tissue and bile of rats with experimentally-induced massive hepatic cell necrosis. Both the levels of LTs and PGs in the liver tissue and LTs in the bile increased before the microscopic appearance of hepatic cell necrosis. These results suggest that arachidonic acid metabolites may play an important role in the induction of liver cell injury.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Immunocytochemical studies on cholestatic factor in human liver with or without cholestasis.

The localization of the cholestatic factor (CF) was immunocytochemically investigated in liver biopsy specimens obtained from patients with various liver diseases. CF was detected in seven of nine patients with drug-induced liver injury, three of four with acute viral hepatitis, three of five with alcoholic liver injury and in the two patients with autoimmune hepatitis. Fourteen of these 15 CF-positive patients had jaundice in their clinical courses. CF was stained diffusely in the cytoplasm of hepatocytes throughout the lobules in a granular pattern. Electron-microscopically, it was localized on the ribosomes and polysomes as well as on the filamentous structures around the bile canaliculi. However, CF was not detected in liver specimens from normal controls and patients with primary biliary cirrhosis and extrahepatic biliary obstruction. These findings suggest that CF plays an important role in intrahepatic cholestasis in various liver diseases.

Adult↗
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

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

[Interferon-alpha/beta receptors in patients with chronic HBV infection].

We analyzed the binding of 125I-labelled IFN-alpha to peripheral blood mononuclear cells in 19 healthy controls, 25 asymptomatic HBV carriers (AsC), and 69 patients with HBs antigen positive chronic liver disease (CLD). Histological examination showed that of the 69 patients with CLD, 14 had chronic persistent hepatitis (CPH), 46 had chronic active hepatitis (CAH), 9 had liver cirrhosis (LC). The mean number of IFN-alpha/beta receptor sites per cell totaled 1270 +/- 340 in the healthy controls, 1440 +/- 290 in AsC, and 1600 +/- 480 in CLD (with 1770 +/- 480 in CPH, 1580 +/- 490 in CAH, and 1420 +/- 410 in LC). HBV carriers had more IFN-alpha/beta receptor sites than the healthy controls (AsC: P less than 0.1, CLD: P less than 0.01). In CLD, patients with LC tended to have fewer IFN-alpha/beta receptor sites than those with CPH or CAH. The number of IFN-alpha/beta receptor sites in CLD was correlated with the HBe antigen titer (P less than 0.01), and activity of HBV-DNA polymerase (P less than 0.05). These results were suggested that IFN-alpha/beta receptor sites was higher at the HBV carrier state, and correlated with viral replication.

Carrier State↗
PubMed1990

[Hereditary stomatocytosis of the hydrocytosis type: a report of one family and red cell membrane studies].

A case of hereditary stomatocytosis with hemolytic anemia, increased autohemolysis, increased osmotic fragility, and shortened erythrocyte survival is reported. The erythrocytes were abnormally permeable to sodium and potassium; the sodium concentration of the erythrocytes was high, and the potassium level was low. This case was different from the first reported Japanese case of hereditary stomatocytosis of the hydrocytosis type in the Na(+)-K+ ATPase and Mg+ ATPase activity. In the first reported Japanese case, these activities were within normal limits, but in this case, they were increased. The findings indicate that membrane transport in hereditary stomatocytosis of the hydrocytosis type may vary from case to case.

Aged↗
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

[Evaluation of left ventricular function after Jatene's operation for transposition of the great arteries--influence of age at repair].

The postoperative left ventricular function (LV) of Jatene's operation for transposition of the great arteries (TGA) was evaluated by angiocardiography and echocardiography in 39 patients. In 16 patients repaired at less than 3 months of age, left ventricular endodiastolic volume (LVEDV) was significantly decreased at the angiography 2 months after repair: form 215 +/- 685% normal of preoperative LVEDV to 120 +/- 14% normal postoperatively (p less than 0.05) in 7 patients with simple TGA (Group IA), and from 220 +/- 64% normal to 130 +/- 33% normal (p less than 0.05) in 8 patients associated with ventricular septal defect (Group IIA). On the other hand, among 24 patients repaired at 3 or more months of age, 19 patients with simple TGA (Group IB) showed the significant increase of LVEDV (from 159 +/- 40% normal to 183 +/- 23% normal, p less than 0.05), and 5 patients associated with ventricular septal defect (Group IIB) showed no remarkable change (from 208 +/- 96% normal to 193 +/- 23% normal). There was no significant difference of postoperative pulmonary artery (PA) wedge pressure among the four groups. Postoperative left ventricular diastolic dimension (LVDd) revealed the tendency of normalization in all groups during the first postoperative year. Group IA and IIA completed the normalization of LVDd in 2 months and Group IIB in 6 months after the repair. However, LVDd in Group IB could not decrease to normal range even in 12 months after repair. There was a significant correlation between postoperative LVDd and the age at PA banding in 14 patients of Group IB, who had the preparatory PA banding for LV training.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1989

Recurrent parotid gland enlargement as an initial manifestation of Sjögren syndrome in children.

Recurrent parotid gland enlargement is a common disorder in children, while that of auto-immune aetiology is rare. Three children with recurrent parotid swelling had autoantibodies including antinuclear antibody, anti-SS-A (Sjögren syndrome-A), SS-B (Sjögren syndrome-B) antibodies and rheumatoid factor, abnormal sialograms and lymphocytic infiltration of salivary glands, which were consistent with Sjögren syndrome. Initially, all three lacked symptoms of keratoconjunctivitis sicca. During follow up, two patients developed xerostomia and were diagnosed as having primary Sjögren syndrome. Recurrent parotid enlargement appears to be important as an initial manifestation of Sjögren syndrome in children.

Adolescent↗
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

Implications of hyperechoic lesions in small hepatocellular carcinoma.

Of 34 solitary small hepatocellular carcinomas (HCC) 2 cm in diameter or less, 13 with hyperechoic lesions were observed serially by sonography, and 11 of these were examined histologically. Serial examination showed that hypoechoic areas appeared at the periphery of or within, the hyperechoic tumor, and that these areas expanded more with tumor growth than the hyperechoic areas as if compressing or displacing the existing hyperechoic areas. Histologically, the hyperechoic lesions were composed mostly of well-differentiated cancer cells containing fat droplets, whereas the hypoechoic lesions were composed of cancer cells without fat droplets. In the two tumors that were formed almost completely of cancer cells showing fatty metamorphosis, cancer cells without fat droplets proliferated mainly in the periphery of the tumor. These findings suggest that, in hyperechoic HCC, cancer cells with fat droplets appear in the early stage of HCC, and probably change into concer cells without fat droplets by the time that a certain tumor size is reached, with gradual displacement by the latter type of cell during tumor growth.

Biopsy↗
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↗