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Biomedical subjects

G Yamada

Publications and source records attributed to G Yamada.

At least 163 records · Page 9Linked to original sources
PubMed1982

Electron and immunoelectron microscopic study of Dane particle formation in chronic hepatitis B virus infection.

The site of Dane particle formation in hepatocytes was studied by routine electron and immunoelectron microscopy of liver biopsy specimens from 10 patients with hepatitis B e antigen-positive chronic active hepatitis. With routine electron microscopy, core particles were abundant in cytosol, often adjacent to the cell membrane, and occasionally in the microvilli. Figures suggestive of budding of endoplasmic reticulum with a core particle into the cisternae of endoplasmic reticulum were observed frequently. There were also figures suggestive of direct budding with a core particle from the surface of the cell. With the immunoelectron microscopy, the core particles were found to be positive for hepatitis B core antigen and the endoplasmic reticulum and the plasma membrane were positive for hepatitis B surface antigen. These findings suggest that the most plausible mode of formation of the Dane particle is by budding of hepatitis B surface antigen-positive endoplasmic reticulum membrane into the cisternae. In addition, formation of the Dane particle may also take place at the surface of the hepatocyte by a similar mechanism.

Cell Membrane↗
PubMed1981

Serodiagnosis of type A hepatitis by detection of immunoglobulin M-type antibody to hepatitis A virus.

Serum specimens from 12 patients with type A hepatitis were analyzed for immunoglobulin M-type antibody to hepatitis A virus (IgM anti-HA). A recently developed solid-phase radioimmunoassay kit for IgM anti-HA (HAVAB-M, Abbott Laboratories) and a competitive binding radioimmunoassay kit (HAVAB, Abbott Laboratories) with or without 2-mercaptoethanol treatment, as modified by Yano et al. (Acta Hepatol. Jpn. 21, 704-712, 1980) were used to obtain an M-index. All specimens obtained within 60 days of the onset of illness and specimens from 2 of 4 patients later than 60 days after the onset were positive with the HAVAB-M test. This test gave negative results to sera which were positive for anti-HA by a standard HAVAB test in the following: 3 patients with type B hepatitis; 5 with non-A, non-B hepatitis; 11 healthy adults; and 10 sera strongly positive for rheumatoid factor. The M-index for type A hepatitis in sera within 30 days of the onset (mean value of the M-index, m, = 1.52; standard deviation, SD, = 0.25) was significantly higher than that for non-A hepatitis (m = 1.05; SD = 0.15) and for healthy adults (m = 1.02; SD = 0.10). The simplicity and usefulness of the HAVAB-M test in diagnosis of acute type A hepatitis over those measuring the M-index by HAVAB tests were shown by direct comparison of the results.

Adult↗
PubMed1980

Determination of antibody to hepatitis B core antigen by radioimmunoassay in chronic liver disease.

Antibody to hepatitis B core antigen (anti-HBc) was measured by radioimmunoassay using CORAB (Abbott Laboratories) in 10 cases of chronic persistent hepatitis (CPH), 46 cases of chronic aggressive hepatitis (CAH), 33 cases of liver cirrhosis (LC) and 53 cases of hepatocellular carcinoma (HCC) in relation to hepatitis B surface antigen (HBsAg) and its antibody (anti-HBs). Ninety-eight point four percent of patients with HBsAg and 93.8% of patients with anti-HBs were positive for anti-HBc and the titers of anti-HBc in patients with HBsAg were significantly higher than those with anti-HBs. Thirty-five point five percent of patients negative for either HBsAg or anti-HBs were positive for anti-HBc. The titers of anti-HBc in patients with CPH, CAH and LC were relatively low, whereas 7 (46.8%) of the HCC patients negative for either HBsAg or anti-HBc had high titers of anti-HBc. The significance of the presence of anti-HBc alone is discussed.

Antibodies, Viral↗
PubMed1980

Electron microscopic observation of hepatitis B virus budding from hepatocytes into bile canaliculi.

In electron microscopic observation of a liver biopsy obtained from a hepatitis B surface antigen-positive patient, noncoated core particles were occasionally seen budding into the hepatocytic cisterni and many Dane particles were found in the pericanalicular vesicles of hepatocytes. Noncoated core particles were also localized in clusters within the bleb of microvilli. There were some core particles being protruded from microvilli into the lumen of bile canaliculi by budding. These findings suggest hepatitis B virus being released from the hepatocyte to the bile canaliculi by two different modes; through vesicle by reversed phagocytosis and from the microvilli by budding.

Bile Canaliculi↗
PubMed1980

Immunoelectron microscopic observation of hepatitis B surface antigen on the surface of liver cells from patients with hepatitis B virus infection.

A recently modified method using peroxidase labeled antibodies for light and electron microscopic demonstration of hepatitis B virus (HBV) was applied to the evaluation of hepatitis B surface antigen (HBsAg) on the surface of liver cells in biopsy specimens from 24HBsAg chronic carriers. Membranous distribution of HBsAg was demonstrated in diffuse or scattered hepatocytes in all 4 asymptomatic carriers and in 3 of the 20 patients with HBsAg-positive chronic active hepatitis or liver cirrhosis. In these patients with membranous expression of HBsAg, hepatitis B e antigen, Dane particles and DNA polymerase were often detected in sera, and large amounts of hepatitis B core antigen appeared in the liver. These results suggest that membrane-bound HBsAg may be expressed by the HBV genome. The ultrastructural study of liver cells showing membranous expression disclosed dense deposits of reaction product indicative of HBsAg on the cell membrane and/or on assembled particles within the extracellular space. In some hepatocytes showing both diffuse cytoplasmic and membranous expression of HBsAg, HBsAg-positive membrane of cisternae open to the intercellular space was connected with the liver cell membrane. These findings supported the conjecture that HBV associated antigens are integrated into the liver cell membrane.

Hepatitis B↗
PubMed1978

Hepatitis B. Cytologic localization of virus antigens and the role of the immune response.

Antigens of the hepatitis B virus have been localized within liver tissue by various immunologic, histochemical, and electron microscopic methods. The abundance and distribution of these virus antigens are in part determined by the host immune response. This interaction of immune mechanisms with the hepatitis B virus may be related to the pathogenesis and natural history of human hepatitis B virus infection.

Animals↗
PubMed1977

Hepatitis B core and surface antigens in liver tissue. Light and electron microscopic localization by the peroxidase-labeled antibody method.

Hepatitis B core antigen (HBcAg) and hepatitis B surface antigen (HBsAg) were localized in human liver tissues by the peroxidase-labeled antibody method at the light and electron microscopic levels. Several methods of fixation, staining, and inhibition of endogenous peroxidase activity were studied. The periodate-lysine-paraformaldehyde fixative effectively preserved the tissue structure and the antigenicity of both antigens, and the peroxidase-labeled Fab' fraction of IgG penetrated well into hepatocytes. HBcAg was present in nuclei, or cytoplasm of hepatic cells, or both. In nuclei, the antigen was found both in virus-like particles of approximately 20 nm. diameter and in nuclear ground substance. In the cytoplasm, the antigen was found on membrane-bound ribosomes and free polysomes, and also in the ground substance of the cytosol near ribosomes and around nuclear membranes, especially near nuclear pores. HBcAg-positive virus-like particles were also demonstrated sparsely or in clusters in the cytoplasm. HBsAg was not present in nuclei but was found in the perinuclear space and in cisternae of endoplasmic reticulum, and on nuclear, endoplasmic reticulum, and cell membranes of hepatic cells. HBsAg-positive 25- to 30-nm. wide tubular forms, round particles (probably cross-sections of tubular forms), and a few large particles of 40 to 50 nm. diameter were seen in cisternae. Such HBsAg-positive particles were also present in the intercellular space and in Disse's space. These findings suggest that HBcAg produced on the cytoplasmic ribosomes migrates through nuclear pores to the nucleus and is assembled into core particles there. These particles may then move through nuclear pores to the cytoplasm where they are invested with HBsAg-positive membrane in cisternae of endoplasmic reticulum or as they enter the endoplasmic reticulum. These virus particles are then released together with other HBsAg-positive forms into the intercellular space by reversed phagocytosis.

Animals↗