Contrast-enhanced intraductal ultrasonography for thickened bile duct wall.

PURPOSE: We carried out this study to evaluate the usefulness of contrast-enhanced intraductal ultrasonography (ceIDUS) in the differentiation of thickened bile duct wall at the hepatic bifurcation caused by malignant tumor from that caused by cholangitis. METHODS: Seven patients (two with primary sclerosing cholangitis [PSC], one with secondary sclerosing cholangitis [SSC], and four with bile duct carcinomas [BDC] at the hepatic bifurcation underwent endoscopic ceIDUS, in which we used Levovist. The recorded images of echo-brightness were analyzed histographically. RESULTS: The bile duct wall, in PSC and SSC, but not in BDC, was enhanced by Levovist. CONCLUSION: ceIDUS with histographic analysis may be useful for distinguishing thickened bile duct wall caused by malignant tumor from that caused by cholangitis.

[Spread of acute haemorrhagic conjunctivitis virus in virgin soil (Hokkaido, Japan): observation with serological surveys (author's transl)].

Acute haemorrhagic conjunctivitis (AHC), a novel disease caused with a new type of enterovirus, occurred for the first time in Sapporo City and other areas of Hokkaido in October of 1971. During first 4 months, 1,000 or more cases of AHC were reported in Sapporo and 2,300 cases in other areas. Thereafter, there are no epidemic of AHC in any areas, though there are sporadic cases up to date. To know the spread of exogenous agent, AHC virus, in Hokkaido, the neutralizing antibody was measured with sera of healthy adults resident in 12 separated districts of Hokkaido in 1973 and 1974. It was revealed that the positive reactors to AHC virus were found in 5 to 35% in all districts but one in 1974, and AHC virus was distributed in almost all the areas of Hokkaido within a period of two and half years after invasion. In addition, a sequential sero-survey to detect the spread of AHC virus has been carried out in Sapporo. A rate of neutralizing antibody positives in healthy adults did not show a clear increase on sera withdrawn one year after epidemic of AHC in comparison with those before epidemic, but show a remarkable increase on sera withdrawn later in spite of non-epidemic. An increase of antibody positive rate in non-epidemic period was also obtained from sera of healthy adults resident in districts other than Sapporo. These findings made doubt the changes in transmission on mode and/or in clinical pictures, and the viral mutation in biological character, such as temperature for propagation, may be supposed.

Preparation and characterization of a monoclonal antibody that inhibits myoblast fusion of avian skeletal myoblasts.

To investigate the mechanism of myoblast fusion using quail myoblasts transformed with a temperature-sensitive mutant of Rous sarcoma virus (QM-RSV cells), we prepared monoclonal antibodies against a cell surface antigen involved in myogenic differentiation. For this, a Balb/c mouse was immunized with the membrane fraction of QM-RSV cells, and hybridomas producing monoclonal antibodies were raised by fusion of spleen cells from the immunized mouse with myeloma cells. By analysis of the hybridoma supernatants, we obtained a monoclonal antibody, termed H-145, that strongly inhibited myoblast fusion. H-145 inhibited myoblast fusion dose-dependently, and its effect was readily reversed by its removal. H-145 promoted biochemical differentiation of the cells until 48 h. It did not affect a fusion-commitment step to differentiation, but inhibited a later step. Indirect immunofluorescence and immunoblot analyses showed that the antigen reacting with H-145 was a glycoprotein with a molecular weight of approximately 116 kDa. This antigen is present throughout differentiation, but as differentiation progresses, its expression increases and its distribution on the cell surface changes. The antigen purified by H-145 affinity chromatography failed to react with beta 1-integrin, alpha 5-integrin, NCAM, or N-cadherin on immunoblotting. Thus, H-145 antigen differs from these components that are known to be associated with myogenic differentiation. Consequently, the results suggest that H-145 antigen may be a new cell surface antigen associated with cell differentiation.

Hepatitis B core antigen stimulates interleukin-10 secretion by both T cells and monocytes from peripheral blood of patients with chronic hepatitis B virus infection.

In chronic hepatitis B virus (HBV) infection, immune responses to hepatitis B core antigen (HBcAg) are weak. Interleukin (IL)-10 is a potent immunosuppressive cytokine which we reported recently to be secreted in response to HBcAg by peripheral blood mononuclear cells (PBMCs) from patients with chronic HBV infection or healthy controls. Using an enzyme-linked immunospot assay, we compared the ability of HBcAg to stimulate IL-10 production by PBMC with that of lipopolysaccharide (LPS), phytohaemagglutinin-P and hepatitis C virus-derived antigens in 16 patients with chronic HBV infection and six healthy controls. Frequencies of IL-10 spot-forming cells (SFC) in response to HBcAg were comparable to those obtained with LPS in patients with chronic HBV infection. Frequencies of IL-10 SFC in response to HBcAg or to LPS were significantly higher in patients with chronic HBV infection than in healthy controls. IL-10 SFC in response to HBcAg consisted of 26-35% T cells, 62-70% monocytes and less than 1% B cells in patients with chronic HBV infection. Only monocytes contributed to IL-10 production in controls. Frequencies of HBcAg stimulated IL-10 SFC representing T cells and monocytes were significantly higher in patients with elevated serum alanine aminotransferase (ALT) and detectable HBV DNA than in patients with normal ALT and undetectable HBV DNA. The potent ability of HBcAg to stimulate IL-10 production by PBMC may contribute importantly to immune tolerance toward HBV.

Dynamic distribution of an antigen involved in differentiation of quail myoblasts transformed with Rous sarcoma virus: I. Requirement of its quantitative expression on the cell surface for myoblast fusion.

A monoclonal antibody, H-145, the antigen of which is a glycoprotein with a molecular weight of 116 kDa, inhibits the fusion of quail skeletal myoblasts transformed with the temperature-sensitive mutant of Rous sarcoma virus (ts-RSV) (QM-RSV cells). Its antigen shows a unique distribution pattern during myogenic differentiation, and is required continuously for the inhibition as reported previously. The H-145 antigen is expressed from as early as the presumptive myoblast stage, and its expression increases during differentiation. In presumptive myoblasts, H145 antigen is mainly accumulated in the Golgi apparatus. However, on transfer to conditions for differentiation, the antigen accumulated in the Golgi apparatus begins to become dispersed in the cytoplasm, and is gradually transported to the cell surface during differentiation, suggesting that transportation of H-145 antigen to the cell surface is required for myoblast fusion. To examine this possibility, we studied the effect of bafilomycin A1, which blocks transport of intracellular proteins between trans-Golgi cisternae and the cell surface. Treatment of QM-RSV cells with bafilomycin A1 inhibited myoblast fusion even at 41 degrees C, the temperature for myogenic differentiation. Under this condition, the antigen did not diffuse to the cell surface, but remained localized in the Golgi apparatus, as on culture at 35.5 degrees C, the non-differentiation condition. These results suggest that quantitative expression of H-145 antigen on the cell surface is a prerequisite for myoblast fusion upon differentiation of QM-RSV cells.