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Biomedical subjects

Y Mizoguchi

Publications and source records attributed to Y Mizoguchi.

At least 73 records · Page 4Linked to original sources
PubMed1992

Increased 5-lipoxygenase activity in massive hepatic cell necrosis in the rat correlates with neutrophil infiltration.

Rats were treated with heat-killed Propionibacterium acnes and subsequent injection of a small amount of lipopolysaccharide after 7 days. After 24 hr most of the rats died of massive liver cell necrosis. Nonparenchymal liver cells were isolated from this liver injury model and incubated with arachidonic acid. Reverse-phase high-pressure liquid chromatography detected the 5-lipoxygenase metabolites (leukotriene B4 and 5-hydroxy-arachidonic acid), whereas these compounds were produced in negligible amounts when the rats were treated with P. acnes only. Immunohistochemical studies with 5-lipoxygenase antiserum revealed that the injured livers contained a large number of positively stained round cells with segmented nuclei, which were rarely found in the livers treated with P. acnes only. These positively stained cells were histologically identified as neutrophils. The results suggested that the increased 5-lipoxygenase activity in the injured rat liver is attributable to the infiltrating neutrophils rather than to nonparenchymal hepatic cells.

Animals↗
PubMed1992

Arachidonate metabolism in D-galactosamine or carbon tetrachloride-induced acute and chronic liver injuries in rats.

Arachidonate metabolism was examined in rats with experimentally induced acute and chronic liver injuries. Acute liver injury was induced by a single administration of D-galactosamine (D-Galn) and lipopolysaccharide (LPS) or carbon tetrachloride (CCl4). Chronic liver injury was produced by several administrations of CCl4 for 5 weeks. Non-parenchymal liver cells from rats with D-Galn/LPS-induced acute liver injury produced prominently leukotriene B4 and 5-hydroxy-arachidonic acid which were hardly synthesized by the normal rat liver. No apparent changes were observed in the arachidonate metabolism of the non-parenchymal cells of the acute CCl4-injured liver. In chronic liver injury, the production of 6-ketoprostaglandin F1 alpha, a stable metabolite of prostaglandin I2, by the non-parenchymal cell fraction was significantly enhanced in contrast with the fixed amount of the other arachidonate metabolites. These results suggested the arachidonate metabolism by non-parenchymal liver cells might change according to the pathogenesis of the liver disease.

Acute Disease↗
PubMed1992

Possible induction of fatty acid cyclo-oxygenase in lipopolysaccharide-stimulated rat Kupffer cells.

In response to stimulation with lipopolysaccharide, isolated rat Kupffer cells released increased amounts of prostaglandin E2, prostaglandin D2, 6-keto-prostaglandin F1 alpha, and thromboxane B2. There was a lag of 2-6 hours before a significant release of these metabolites into the medium was detected. Nonstimulated Kupffer cells converted exogenous arachidonic acid to prostaglandins and thromboxane B2, and a major product was prostaglandin D2. Twenty-four hours after stimulation with lipopolysaccharide, Kupffer cells produced approximately 7 times more prostaglandin E2 and 2 times more prostaglandin D2, 6-keto-prostaglandin F1 alpha; and thromboxane B2 than nonstimulated cells. Western immunoblotting of microsomal proteins prepared from the stimulated rat Kupffer cells showed a 70-kilodalton component that was immunoreactive with a polyclonal anticyclo-oxygenase antibody. The intensity of the band increased with the time of the lipopolysaccharide stimulation. These results suggest that the accelerated arachidonate metabolism in lipopolysaccharide-stimulated rat Kupffer cells might be attributed to an induction of the cyclo-oxygenase enzyme.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Enhancement of prostaglandin E2 production by liver macrophages (Kupffer cells) after stimulation with biological response modifiers.

PGE2 production by liver macrophages (Kupffer cells) activated by biological response modifiers was examined. Kupffer cells obtained from a normal rat liver possessed cyclooxygenase activity and produced TXB2, PGD2, and PGE2 from (1-14C)arachidonic acid. The major product was PGD2. When Kupffer cells were incubated in the presence of lipo-polysaccharide (LPS), OK-432, or heat-killed Propionibacterium acnes for 24 h, the amount of arachidonate cyclooxygenase products increased and the major product changed from PGD2 to PGE2. When liver macrophages including Kupffer cells were prepared from rats after an injection of LPS, OK-432, or heat-killed P. acnes, it was noticed that the number of cells obtained and PGE2 production increased compared with those of normal rat. These results suggested that PGE2 production by rat liver was induced when they were treated with biological response modifiers.

Animals↗
PubMed1992

Calcium-dependent prostaglandin biosynthesis by lipopolysaccharide-stimulated rat Kupffer cells.

Isolated rat Kupffer cells produced and released prostaglandin (PG) E2, 6-keto-PGF1 alpha, and thromboxane B2 (TXB2) in response to lipopolysaccharide (LPS) stimulation. This elevation of PGE2, 6-keto-PGF1 alpha and TXB2 in the medium was not observed when cells were cultured in the absence of extracellular calcium or in the presence of an extracellular calcium chelator, EGTA. An intracellular calcium antagonist, TMB-8, also suppressed the production of PGE2, 6-keto-PGF1 alpha and TXB2 in a concentration-dependent manner. The intra-cellular calcium concentration of Kupffer cells elevated early after the addition of LPS determined by the use of fura-2 and a fluorescence microscopy. Moreover, calmodulin inhibitors, W-7 and W-13, apparently inhibited the production of PGF2, 6-keto-PGF1 alpha and TXB2. All these results suggest that LPS-induced PG production by stimulated rat Kupffer cells may be regulated by a calcium-calmodulin pathway.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Choleretic effects of alpha-iridodiol on experimentally induced intrahepatic cholestasis.

When a lymphokine, the cholestatic factor, was intravenously injected into rats through a mesenteric vein, a remarkable reduction in bile flow was observed. Using this experimentally induced intrahepatic cholestasis model, we studied the choleretic effects of alpha-iridodiol, an iridoid compound. When alpha-iridodiol was administered 30 min before, at the same time, or 30 min after injection of the cholestatic factor, the reductions in bile flow and bile acid excretion were significantly inhibited. Remarkable choleretic effects were also noted when it was administered to normal rats. These results suggested that alpha-iridodiol may be effective in the treatment of intrahepatic cholestasis.

Animals↗
PubMed1992

Effect of Gomisin A (TJN-101) on liver regeneration.

We studied the effect of TJN-101, a lignan component of Schisandra fruits (Schisandrae fructus), on liver regeneration after partial hepatectomy. TJN-101 was given orally to male Wistar rats 30 min before partial hepatectomy. The mitotic index and the level of DNA synthesis increased after partial hepatectomy and their increase was significantly enhanced by TJN-101. Ornithine decarboxylase (ODC) activity increased in the early stages of liver regeneration and it was also significantly enhanced by TJN-101. Besides, TJN-101 enhanced the increase in hepatic putrescine. These results suggest that TJN-101 stimulates liver regeneration after partial hepatectomy by enhancing ODC activity, which is an important biochemical event in the early stages of liver regeneration.

Animals↗
PubMed1992

Circulating immune complex levels measured by new ELISA kits utilizing monoclonal anti-C1q and anti-C3d antibodies correlate with clinical activities of SLE but not with those of RA.

The authors studied sera from both patients with SLE and from those with RA to evaluate clinical usefulness and significance of circulating immune complexes (CIC) detected with new ELISA kits utilizing monoclonal anti-C1q and anti-C3d antibodies. CIC values of patients with SLE significantly correlated to severity of disease activities evaluated by clinical symptoms and laboratory tests, especially for serum complement levels. Since substances detected with the ELISA kits were closely related to serum complement components, it was determined that a direct relationship exists between clinical activities and CIC values appearing in SLE patients with hypocomplementemia. In RA patients, CIC values did not correlate to clinical activities evaluated by Lansbury's index, anatomical bone damage with X-ray or functional assessment of activities of daily living, but did significantly correlate to levels of IgM-RF, serum IgG concentrations and some markers of systemic inflammation. Detection of IC after fractionation of RA sera revealed a broad range of molecular sizes detectable with the ELISA kits, which indicated that CIC in vivo were heterogenic and complicated in formation, degradation and interaction with serum complements.

Adult↗
PubMed1992

[Cancer of the kidney mimicking renal multilocular cyst].

Two cases of multilocular cystic adenocarcinoma of the kidney are presented. Although ultrasonography (US) and x-ray computed tomography (CT) are generally considered to be excellent diagnostic methods for renal cystic lesions, in the 2 cases reported here they failed to give the correct diagnosis. These unusual cases altered us to the possibility that the capabilities of modern diagnostic imaging techniques can lead to a false sense of security regarding the prognosis. To our knowledge, there are no reliable clinical features which distinguish multilocular cystic adenocarcinoma from multilocular cystic nephroma.

Adenocarcinoma↗
PubMed1992

[Prognostic significance of echogenic lesion within small hepatocellular carcinoma].

To evaluate prognostic significance of echogenic lesion within small hepatocellular carcinoma (SHCC, less than or equal to 2 cm in diameter), clinical and pathological findings of 32 cases with SHCC containing echogenic lesion (echogenic SHCC) were compared with those of 55 cases with non-echogenic SHCC. Compared with the non-echogenic SHCC group, the frequency of clinical stage I was significantly higher, and there were significantly more cases with solitary tumor relative to cases with multiple tumors in the echogenic SHCC group. Histologically, the incidence of the HCC composed of well-differentiated tumor cells corresponding to Edmondson's grade I was significantly higher in the echogenic SHCC group than in the non-echogenic SHCC group. Although HCCs tended to become progressively less differentiated with increasing tumor sizes in the both groups, the process of cellular change appeared to proceed more slowly in the echogenic SHCC group. Survival rate after tumor detection was 73% at three years, 56% at five years and 48% at seven years and nine years in the echogenic SHCC group, while it was 46% at three years, 42% at five years and 0% at seven years in the non-echogenic SHCC group. The present results showed that the presence of echogenic lesion within SHCC could be useful prognostic indicator.

Aged↗
PubMed1992

[Disseminated varicella-zoster virus infection without vesicles in a patient with malignant lymphoma].

A 76-year-old man was diagnosed as having malignant lymphoma (non-Hodgkin's lymphoma, diffuse medium cell-sized, B cell type). He was treated with CHOP therapy but with no response. In the terminal stage, he had continuous high temperature despite the administration of anti-bacterial and anti-fungal agents. Paralytic ileus, liver and pancreas dysfunction, and gastrointestinal bleeding developed. No skin eruptions occurred throughout the clinical course. He died on day 36 of treatment. Postmortem examination revealed foci of hemorrhagic necrosis containing many multinuclear giant-cells some of which with intranuclear inclusion bodies (Cowdry type A), in the liver, pancreas, gastrointestinal tract, bone marrow and other organs. Electron microscopy showed viral particles in the cytoplasm but not the nuclei of infected cells which were covered with a capsule, which was characteristic of varicella-zoster virus infection. Cells of the above organs were positive for immunohistochemical staining using antivaricella-zoster antibodies. The multiorgan failure seen in the terminal stage was considered to be due to disseminated varicella-zoster infection.

Aged↗
PubMed1992

Analysis of proliferating hepatocytes using a monoclonal antibody against proliferating cell nuclear antigen/cyclin in embedded tissues from various liver diseases fixed in formaldehyde.

The authors studied histochemically the morphologic features of proliferating hepatocytes positive for proliferating cell nuclear antigen (PCNA/cyclin) to analyze the process of liver regeneration in embedded tissues fixed with formaldehyde using an anti-PCNA/cyclin monoclonal antibody. In liver specimens from patients with acute viral hepatitis (AVH) and confluent necrosis, many small basophilic hepatocytes surrounding large clear hepatocytes were positively stained in the areas next to the confluent necrosis. Therefore these small hepatocytes may be daughter cells derived from large clear hepatocytes that probably enter the mitotic cell cycle repeatedly to repair a large necrotic area. In the case of AVH with spotty necrosis, the positively stained hepatocytes were scattered around the necrotic foci. In the liver specimens from patients with chronic active hepatitis, most of the positively stained hepatocytes were located next to the necrotic area. As for cirrhosis of the liver, the number of hepatocytes positive for PCNA/cyclin varied greatly in different pseudolobules, and in the specimens of hepatocellular carcinoma (HCC), the HCC cells positive for PCNA/cyclin were detected throughout the cancer nests.

Antibodies, Monoclonal↗
PubMed1992

Immunocytochemical identification of proliferative hepatocytes using monoclonal antibody to proliferating cell nuclear antigen (PCNA/cyclin). Comparison with immunocytochemical staining for DNA polymerase-alpha.

The authors investigated whether immunocytochemical staining with a monoclonal antibody to proliferating cell nuclear antigen (PCNA/cyclin) could be used to identify proliferative hepatocytes in frozen sections fixed in a mixture of periodate, lysine, and 2% paraformaldehyde. Paraffin sections also were used, which were fixed in 10% formaldehyde. Specimens of liver tissue were obtained from 27 patients with various hepatic diseases. Hepatocytes that were positive for PCNA/cyclin were observed in both types of substrate specimens. In acute hepatitis and chronic active hepatitis, most hepatocytes that were labeled for PCNA/cyclin were located near necrotic foci. However, in cirrhosis, they were detected most often near fibrotic septa; the number of immunoreactive cells varied greatly in different areas of tissue sections in such cases. In hepatocellular carcinoma, many PCNA/cyclin-positive tumor cells were seen throughout the neoplasms. Hepatocytes that were positive for DNA polymerase-alpha showed a similar distribution pattern in serial sections of study cases.

Adult↗
PubMed1992

Importance of direct hepatocytolysis by liver macrophages in experimental fulminant hepatitis.

When lipopolysaccharide was administered to mice that had been injected with heat-killed Propionibacterium acnes, most of them died of massive liver necrosis. Previously, we demonstrated that a soluble hepatocytotoxic factor released by liver adherent cells fully activated by both P. acnes and lipopolysaccharide was attributable to the late stage of this severe liver injury. In this report, we focused on the hepatocytolysis by these liver adherent cells in a cell-cell interaction manner. Shortly after stimulation with lipopolysaccharide, the P. acnes-elicited liver adherent cells almost completely killed the hepatocytes prepared from both normal syngeneic mice and P. acnes-treated ones. Since P. acnes-elicited liver adherent cells also proved to produce various kinds of cytokines in a short time, the role of cytokines in this liver injury was analyzed. Only TNF-alpha enabled the P. acnes-elicited liver adherent cells to kill hepatocytes prepared from the same mice, but none from the normal ones. These results suggest that the liver adherent cells accumulated and partly stimulated by P. acnes-treatment might rapidly lyse the autologous hepatocytes once triggered by lipopolysaccharide and that the TNF-alpha these liver adherent cells produced might upregulate their own hepatocytotoxic ability.

Acute Disease↗
PubMed1992

Study on the mechanism of an experimental immunological intrahepatic cholestasis model.

Tuberculin-sensitized guinea pigs were intravenously injected with heat-killed Propionibacterium acnes followed by an intravenous injection of purified protein derivatives 7 day later, resulting in the induction of intrahepatic cholestasis. Using this experimental model, the following results were obtained: (1) Both uptake and release of bile acid were inhibited in the hepatocytes prepared from the cholestasis guinea pigs. (2) The results of the erythritol clearance method indicated that the decrease in bile flow observed in the cholestasis guinea pigs was mostly attributable to the reduced bile excretion from the canaliculi. (3) The decrease in the formation of bile acid independent bile flow was the cause of the decrease in bile flow observed in the cholestasis guinea pigs. (4) There was no change in the permeability of the interhepatocellular tight junction in the cholestasis guinea pigs.

Animals↗
PubMed1992

[Successful surgical treatment by Konno aortoventriculoplasty in 2 cases of congenital aortic valvular stenosis].

Konno's aortoventriculoplasty was performed in two children aged 6 years and 10 years old with congenital aortic valvular stenosis. One had previous aortic valvotomy at 21 days of age. Preoperative peak systolic pressure gradients between the left ventricle and the aorta were 120 and 140 mmHg, respectively. The original diameter of the aortic valve ring were 12 mm and 16 mm and one had supra-annular aortic stenosis whose diameter was 7 mm. The 19 mm and 23 mm SJM prosthetic valves were inserted in the subcoronary position. The postoperative course was uneventful. Their ECG showed sinus rhythm with complete right bundle branch block. Both two patients made good recovery regarding clinical data and symptoms.

Aorta↗
PubMed1992

[Choleretic effects of taurine on experimentally-induced intrahepatic cholestasis].

When a lymphokine, the cholestatic factor, is intravenously injected into rats through a mesenteric vein, remarkable reductions in bile flow and bile acid excretion are observed. However when taurine was injected with the cholestatic factor, the reduction in bile flow and bile acid excretion were significantly suppressed. Moreover, injection of taurine with cholestatic factor resulted in the decreases of both bile acid-dependent bile flow and vesicular transport but not bile acid-independent bile flow. Not significant choleretic effects were noted when taurine alone was administered to normal rats.

Animals↗