Biomedical subjects

H Fusamoto

Publications and source records attributed to H Fusamoto.

At least 145 records · Page 8Linked to original sources

PubMed1992

Successful treatment of a hepatic cyst by one-shot instillation of minocycline chloride.

Hepatic cysts are not rare but usually are asymptomatic; however, large ones sometimes show clinical manifestations. Treatment of a solitary hepatic cyst by one-shot instillation of minocycline chloride is reported here; 500 mg of minocycline chloride was instilled into the hepatic cyst, 11 cm in diameter, through a percutaneous transhepatic cholangiography needle under ultrasound guidance. After 5 weeks, the cyst had decreased in size to 5 cm. Five months later, the cyst could not be detected by diagnostic imaging. Fifteen months after the treatment, no reaccumulated fluid was observed. Ultrasound-guided percutaneous one-shot instillation of minocycline chloride seems to be a safe, easy, and useful procedure for treating a hepatic cyst.

Cysts↗

PubMed1992

Enhanced expression of HLA class I by inhibited replication of hepatitis B virus.

HLA class I display on hepatitis B virus (HBV)-infected hepatocytes is important for limiting HBV infection. However, the effect of HBV replication on HLA class I expression on host cells has not been determined. Since acyclovir is known to inhibit HBV replication of the novel cell line HB611, which was transfected with HBV genome using human hepatoblastoma cells as the recipient and continuously replicates HBV DNA, we analyzed HLA class I expression on acyclovir-treated HB611 by quantitative flow cytometry. The results demonstrated that acyclovir treatment clearly increases the level of HLA class I on HB611, and suggested that HBV replication inhibits expression of HLA class I on infected hepatocytes. This effect of HBV replication on the host cell may be a means by which HBV evades immune surveillance to maintain chronic infection.

Acyclovir↗

PubMed1992

Dependence of ultrasonic attenuation of liver on pathologic fat and fibrosis: examination with experimental fatty liver and liver fibrosis models.

To clarify the effect of the pathological state of the liver on ultrasonic attenuation, we produced two experimental rabbit models. The influence of fat on ultrasonic attenuation was examined using a fatty liver model without liver fibrosis, and that of fibrosis on attenuation using a liver fibrosis model without fatty infiltration. Ultrasonic data were obtained in vivo directly from the liver, and an acoustic attenuation coefficient slope was obtained by the spectral difference method. Tissue components of the liver, namely the total lipid, hydroxyproline and water contents, were measured precisely by quantitative methods. We revealed that ultrasonic attenuation depends mainly on fatty infiltration of the liver and to a lesser extent on fibrosis, but not on the water content.

Adipose Tissue↗

PubMed1992

Portal vein aneurysm demonstrated by blood pool SPECT.

Portal vein aneurysms are rare and are occasionally suggested by ultrasound and usually confirmed by invasive angiography. Such a case was diagnosed by scintigraphic studies, most importantly blood pool SPECT, which clearly separates it from hepatic cysts.

Adult↗

PubMed1992

Ethanol stimulates immunoreactive endothelin-1 and -2 release from cultured human umbilical vein endothelial cells.

The present study employed enzyme-immunoassay to examine the effect of ethanol on endothelin-1 and/or -2(ET1 + 2) release from human umbilical vein endothelial cells. Thirty minutes of exposure to ethanol increased the release of immunoreactive ET1 + 2 from cultured endothelial cells in a dose-dependent manner. However, ethanol at concentrations of less than 400 mM did not induce any LDH release from the endothelial cells. Trypan blue exclusion test revealed that 400 mM solution of ethanol decreased the cell viability to 7.7%. Thus, ethanol was found to directly stimulate ET1 + 2 release from cultured human umbilical vein endothelial cells. This reaction of vascular endothelial cells against ethanol may be related to ethanol-induced cardiovascular diseases such as hypertension, myocardial infarction and stroke, as well as fatal alcohol syndrome.

Cells, Cultured↗

PubMed1992

Effect of intravascular ethanol on modulation of gastric mucosal integrity: possible role of endothelin-1.

The influences of intravascular ethanol on gastric mucosal integrity and its relation to gastric circulation were investigated in rats. Ulcer formation of the gastric mucosa correlated with the blood ethanol concentration in the presence of 150 mM HCl in the rat stomach. Furthermore, the gastric mucosal hemoglobin concentration (IHb) and hemoglobin oxygen saturation (ISO2), estimated using organ reflectance spectrophotometry, decreased in a concentration-dependent manner with blood ethanol. In isolated, vascularly perfused rabbit stomach, various concentrations (10-400 mM) of ethanol infused into the celiac artery increased the perfusion pressure and released endothelin-1 (ET-1) from the gastric vasculature in a concentration-dependent manner. Moreover, a significant correlation existed between changes in the perfusion pressure and ET-1 concentration in effluents from the gastric vasculature. Furthermore, anti-ET-1 antibody reduced 100 mM ethanol-induced vasoconstriction in a concentration-dependent manner. The results indicate that intravascular ethanol increases the susceptibility of gastric mucosa to injury induced by intraluminal HCl by causing gastric vasoconstriction mediated by ET-1. Thus intravascular ethanol may play an important role in the mechanism of ethanol-induced gastric mucosal injury.

Animals↗

PubMed1992

Cetraxate improves ethanol-induced gastric mucosal congestion in anesthetized dogs.

Gastric mucosal microcirculatory disturbance in experimental animals is stressed as an important factor in the development of gastric ulceration induced by ethanol. In this study, we used a reflectance spectrophotometry system to investigate the effect of cetraxate on ethanol-induced gastric mucosal hemodynamics in anesthetized dogs. Forty percent ethanol caused a significant increase in the mucosal blood volume and a significant decrease in mucosal hemoglobin oxygenation. The changes in these parameters indicated mucosal congestion and tissue hypoxia. Topical administration of cetraxate (200 mg in 10 ml saline) prevented the increase in mucosal blood volume and decrease in mucosal hemoglobin oxygenation which had been induced by ethanol loading in the stomach. In conclusion, cetraxate showed a protective effect on mucosal microcirculation that resulted in the maintenance of the gastric mucosal integrity against ethanol loading in the gastric mucosa.

Administration, Topical↗

PubMed1992

Serum pre-S1 and pre-S2 antigens as prognostic markers in interferon therapy for chronic hepatitis B.

We investigated the changes of serum pre-S1 and pre-S2 antigens before and after interferon therapy in 35 carriers with HBeAg, to examine their clinical significance in the therapy. Both antigens were measured quantitatively by solid-phase enzyme immunoassays using monoclonal antibodies specific to each antigen. The titers of these antigens of responders before therapy were significantly lower (p less than 0.001) than those of non-responders (6.23 +/- 1.09 versus 8.65 +/- 2.09 and 4.46 +/- 1.27 versus 6.50 +/- 1.50, respectively). The titers decreased significantly 6 months after interferon therapy in the responders (p less than 0.05), whereas they did not change in the non-responders. Our findings indicate that pre-S1 and pre-S2 antigens have a close correlation with hepatitis B virus replication and are valuable markers for predicting the responsiveness to interferon therapy.

Adult↗

PubMed1992

Hepatitis B core antigen-specific interferon gamma production of peripheral blood mononuclear cells during acute exacerbation of chronic hepatitis B.

To examine the relationship between hepatitis B core antigen-specific interferon gamma production and the liver injury, we measured the sequential change in this production by peripheral blood mononuclear cells of seven patients with chronic hepatitis B. Four patients who experienced acute exacerbation showed increased interferon gamma production when the serum alanine aminotransferase level peaked or during the recovery phase. In the three patients who did not experience acute exacerbation, interferon gamma production gradually decreased in one who had a low peak of alanine aminotransferase but did not show significant change in the other two. Increased production of hepatitis B core antigen-specific interferon gamma at the time of acute exacerbation suggests that interferon gamma induced by hepatitis B core antigen plays a role in hepatocellular injury of patients with chronic hepatitis B.

Acute Disease↗

PubMed1992

[Protective effect of proton pump inhibitor on the gastric mucosa].

Although many authors reported that proton pump inhibitor showed mucosal protective activity, the precise mechanism is still unclear. In this study, we investigated the effect of proton pump inhibit on gastric mucosal hemodynamics, using a reflectance spectrophotometry system. The proton pump inhibitors had no effect on the gastric mucosal hemodynamics prior to the state of hemorrhagic shock state. However, during the hemorrhagic shock, proton pump inhibitors significantly inhibited the decrease in tissue oxygenation and significantly reduced ulcer formation. In conclusion, proton pump inhibitors maintained tissue oxygenation resulting in reduction of ulcer formation.

Adenosine Triphosphatases↗

PubMed1992

Changes in serum human hepatocyte growth factor levels after transcatheter arterial embolization and partial hepatectomy.

We examined the changes in serum human hepatocyte growth factor (hHGF), also called "scatter factor," levels after transcatheter arterial embolization (TAE) and partial hepatectomy (PH) in patients with hepatocellular carcinoma and metastatic liver tumor. In most cases, the serum hHGF levels increased transiently 1-3 days after TAE or PH, and then decreased nearly to the basal levels in 1 wk, suggesting that hHGF may play an important role in liver regeneration in humans. The mean amount of increase in serum hHGF levels after PH was 0.38 ng/ml, which was greater than that after TAE (0.16 ng/ml). In three cases of TAE followed by PH, two showed a greater increase in serum hHGF levels with PH than with TAE, but the third showed the reverse result. Because the rate of increase in serum ALT levels did not affect that of serum hHGF levels, the degree of liver injury induced by TAE or PH does not seem to be a determinant in serum hHGF elevation.

Carcinoma, Hepatocellular↗

PubMed1992

Jejunal varices as a cause of massive gastrointestinal bleeding.

Jejunal varices are not a common manifestation of portal hypertension. This report describes a 46-yr-old man with recurrent massive gastrointestinal bleeding from jejunal varices arising in an area of adhesions between the intestine and the omentum. The bleeding site was identified by exploratory laparotomy. Medical therapy, including vasopressin infusion via the superior mesenteric artery, was of limited success for controlling acute variceal bleeding. However, jejunal resection and anastomosis resulted in complete resolution of the bleeding, and the patient has experienced no recurrent bleeding over a 3-yr follow-up period. A review of the literature shows that this syndrome is characterized by portal hypertension, generally due to liver cirrhosis; frequently, there is a history of abdominal surgery, and the syndrome presents with hematochezia but without hematemesis. Accurate preoperative diagnosis is often difficult. We propose that bleeding from jejunal varices, though uncommon, should be considered under such clinical conditions.

Gastrointestinal Hemorrhage↗

PubMed1991

Signal transduction pathways in the induction of HLA class I antigen expression on Huh 6 cells by interferon-gamma.

This study investigated the intracellular signal transduction regulating the appearance of HLA class I antigens on Huh 6 cells induced by interferon-gamma. The expression was blocked by a protein kinase C inhibitor, H-7, but not by a calmodulin antagonist, W-7, nor by a protein kinase A inhibitor, H-8, at low dose. The antigen expression was induced by a direct activator of protein kinase C, phorbol myristate acetate, but not by calcium ionophore A23187 nor an analog of cAMP, dbcAMP. Therefore, we concluded that protein kinase C is involved in the expression of HLA class I antigens on Huh 6 cells induced by interferon-gamma but Ca(2+)-calmodulin and cAMP are not.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1991

Chronic effect of intragastric ammonia on gastric mucosal structures in rats.

The prevalence of Helicobacter pylori (HP) in the gastric mucosa of patients with chronic atrophic gastritis has been reported to be significantly higher than in normal mucosa. To clarify the role of HP in the etiology of chronic atrophic gastritis, we assessed the effect of ammonia on the gastric mucosal structure in rats, since HP has a strong urease activity and produces abundant amounts of ammonia. Ammonia administered orally at 0.01% and 0.1% as drinking water for two to four weeks decreased the mucosal thickness and the parietal cell number and oxyntic gland number in a dose- and time-dependent manner. The decrease of mucosal thickness was significantly greater in the antral mucosa than in the body mucosa. The border between the antral and body mucosa shifted toward the cardia, reflecting the decrease in oxyntic gland numbers. Furthermore, intracellular mucin was also decreased in a dose- and time-dependent manner, especially in the antral mucosa. Thus, ammonia chronically administered orally in rats led to changes in gastric mucosal structures and functions. The results suggest that the ammonia produced by HP partly plays an etiologic role in chronic atrophic gastritis.

Administration, Oral↗

PubMed1991

Two-dimensional flow cytometric analysis of intrahepatic lymphocyte subsets from patients with chronic hepatitis.

Peripheral and intrahepatic lymphocyte subsets were analyzed in 22 patients with chronic hepatitis by two-dimensional flow cytometry. Activated T cells in the liver significantly increased compared with those in the peripheral blood. Helper T cells increased, but the CD4+ cells decreased due to a marked decrease of suppressor inducer T cells. CD8+ cells increased due to a increase of both cytotoxic T and suppressor T cells. Fc-receptor-positive cells, which increased significantly, were not NK cells but Fc-receptor-bearing T cells. In comparison with immunohistochemical methods, flow cytometric analysis enables more objective quantitation and simpler two-color staining of intrahepatic lymphocytes. Our findings using this method suggest that activated T cells and helper T cells have important roles in hepatitis and that hepatocellular injury may be generated not only by cytotoxic T cells but also by Fc-receptor-bearing T cells.

Adult↗

PubMed1991

Effect of ethanol on endothelin-1 release from gastric vasculature.

The effects of ethanol on gastric vasculature in isolated vascularly perfused rabbit stomach was investigated. The isolated stomach was perfused with Krebs-Henseleit solution containing 3% dextran bubbled with 95% O2 and 5% CO2 at a rate of 12 ml/min. After mixture and perfusion of 10 mM to 400 mM of ethanol, perfusion pressure and endothelin-1 concentration in effluent from gastric vasculature were measured. Perfusion pressure and endothelin-1 concentration in effluent increased in a dose-dependent manner with increasing ethanol concentrations. In conclusion, the data suggest that ethanol may stimulate the release of endothelin from gastric vasculature and may cause gastric ischemia due to vasoconstriction resulting in acute gastric mucosal injury.

Animals↗

PubMed1991

Extrahepatic portal vein aneurysm associated with a tortuous portal vein.

Portal vein aneurysm is rare and its etiology is controversial. A case of extrahepatic portal vein aneurysm associated with an unusually tortuous portal vein is described. Real-time ultrasonography showed anechoic masslike lesions at the porta hepatis communicating with the superior mesenteric vein and intrahepatic portal branches. This suggested the presence of two saccular portal vein aneurysms, 27 x 21 mm and 21 x 13 mm in size. Magnetic resonance imaging and portal venography confirmed the portal vein aneurysms and an unusually tortuous portal vein curving caudally between them. The liver was histologically normal and there was no evidence of portal hypertension. It is speculated that these portal vein aneurysms may have been congenital and that the associated tortuous portal vein might have been secondary to hemodynamic changes in the portal venous system.

Adult↗

PubMed1991

Ultrasonic tissue characterization of chronic liver disease using cepstral analysis.

To evaluate the morphological changes in chronic liver disease by means of ultrasonography, cepstral analysis was applied to the ultrasonic waveforms obtained with a 10-MHz transducer during peritoneoscopy. Assuming that liver tissue was a collection of semiregularly arrayed small scatters of ultrasound, the spaces between scatterers of the liver could be measured by means of cepstral analysis. From the distribution of the spaces between scatterers, two statistical parameters, mode and kurtosis, were determined for each patient. The mode of spaces between scatterers for liver cirrhosis was significantly larger than that for chronic hepatitis and nonspecific change. The mode of spaces between scatterers was correlated with the size of hepatic lobules or nodules. The kurtosis of spaces between scatterers for chronic hepatitis and liver cirrhosis was significantly smaller than that for nonspecific change. As a preliminary study for noninvasive application of this technique, cepstral analysis was also applied to the ultrasonogram obtained through the abdominal wall with a 3.5-MHz transducer. The results obtained with a 3.5-MHz transducer were correlated well with those obtained with a 10-MHz transducer. These results suggest the possibility of noninvasive evaluation of the structural changes in chronic liver disease.

Chronic Disease↗