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Biomedical subjects

G Hess

Publications and source records attributed to G Hess.

At least 235 records · Page 13Linked to original sources
PubMed1977

[Methodical problems for evidence of the hepatitis-B-surface and hepatitis-B-core antigens in tissue (author's transl)].

Liver biopsy material of 22 in the serum HBsAg positive patients was tested with the fluorescent antibody technique for the localization of HBcAg and HBsAg in the liver tissue. Comparative studies were done with the following tissue preparation techniques: Cryostat technique, freeze drying, freeze substitution, cold ethanol paraffin embedding technique (SAINTE MARIE) and isolated liver cells. The investigations revealed the following results: 1. No HB-components could be detected with the cold ethanol paraffin embedding technique and freeze substitution. 2. Using the cryostat technique HBsAg could be demonstrated in 16/22 (cytoplasmatic localization) and HBcAg in 8/22 (nuclear localization). 3. With freeze drying HBsAg and HBcAg could be found in the same cases. The excellent tissue preparation allowed a correct localization of the HB-components to the cell structure. 4. In comparison to cryostat sections in isolated liver cells HBcAg could be demonstrated in 11/16 and HBcAg in 8/8 cases.

Fluorescent Antibody Technique↗
PubMed1977

e System and intrahepatocelullar HBcAG and HBsAG in HBsAG positive patients with liver diseases and healthy carriers.

Patients with hepatitis-B surface antigen positive liver diseases and healthy carriers were studied for the presence of e-antigen and anti-e as well as for intrahepatocellular HBsAG and hepatitis-B core antigen. The e-antigen was demonstrated in 9 out of 12 patients with chronic perisitent hepatitis, in 15 out of 39 patients with chronic active hepatitis, in 3 out of 40 patients with acute type B hepatitis, and in 2 out of 9 patients with a protracted course of type B hepatitis. No e-antigen was found in healthy HBsAG carriers nor in patients with complete recovery from type B hepatitis one year after onset of the disease. Anti-e was detected in 24 out of 61 healthy HBsAG carriers with a normal liver histology and in one patient with a mild form of a chronic persistent hepatitis. The presence of e-antigen in serum was highly associated with the presence of HBcAG in the nuclei of the liver cells. Twenty-seven out of 29 e-positive patients had HBcAG in the liver cell nuclei. In contrast, none of 20 patients with anti-e in serum had HBcAG in the liver cells.

Acute Disease↗
PubMed1977

Simultaneous presence of HBsAg and anti-HBs in the serum of different subtypes (serological and immunofluorescent studies).

Serological and immunofluorescent studies were performed in 3 patients with the simultaneous presence of HBsAg and anti-HBs in the serum. Our investigations revealed the following results: HBsAg and anti-HBs in the serum were of different subtypes. HBsAg in the serum and in the liver had the same subtype. HBsAg in the liver did not react with the circulating anti-HBs in the patient's own serum. HBsAg-anti-HBs immune complexes could not be detected in the serum or in the liver tissue. These phenomena can most readily be explained by at least 2 contacts with hepatitis-B-viruses of different subtypes, one leading to immune tolerance and the other to an immune response. In a follow-up study there was no evidence for a short-term change in HBsAg subtype. Unexplained remains the cause why one contact with HBV did lead to immune tolerance and a second to an immune response.

Adult↗
PubMed1977

The demonstration of subtype (D or Y)-specific determinants on the surface of the presumed hepatitis B virus.

Dane particles isolated from the sera of HBsAg/ad and HBsAg/ay carriers were reacted with monospecific antibodies to the d and y subtype-specific determinants of HBsAg/. Dane particles from HBsAg/ad expressed the d determinant on their surfaces and those from HBsAg/ay sera contained the y specificity. Both complete (DNA-P and HBcAg) and defective (HBcAg alone) Dane particles expressed the subtype-specific determinants.

Epitopes↗
PubMed1976

[The characterization of clinically healthy hepatitis-b-surface-antigen (HBsAg)-carriers. Clinical, biochemical, histiological and immunological investigations in 129 case of a prospective study (author's transl)].

129 blood donors found to be HBsAg-positive on routine testing were studied for evidence of hepatic disease. Twelve had already lost the antigen from the serum when histologically examined. None of these has had clinical or histological evidence of inflammatory liver disease. Two of the 129 patients showed mild icteric hepatitis, cleared the antigen during the follow up and became anti-HBs positive. The remaining 115 patients who appeared clinically healthy and who had no history of previous icteric liver disease remained HBsAg positive during a mean follow up period of 17.3 +/- 3.0 months. Forty patients from these had a normal liver histology and 37 mild to distinct steatosis but no signs of inflammatory liver disease. 11 patients a mild nonspecific mesenchymal activity but no focal necrosis, 16 patients had mild infiltration in portal tracts and a few necrotic parenchymal cells with mesenchymal reaction, 6 patients had chronic persistent hepatitis, 4 chronic aggressive hepatitis, and 1 definite posthepatic cirrhosis.

Adolescent↗
PubMed1976

[Immune response to HBsAg, HBcAg and e-antigen in patients with acute hepatitis and HBsAg carriers with and without liver diseases].

Humoral and/or cell-mediated (CMI) immune responses to HBAg components, human and rabbit liver specific proteins (HLP and RLP) and tuberculin were tested in patients with acute virus B and non-B-hepatitis, asymptomatic HBsAg carriers and HBsAg positive chronic active hepatitis (CAH). Furthermore, the presence of HBsAg, HBcAg and/or "e"-antigen has been studied in patients with sera and/or liver tissue. Asymptomatic HBsAg carriers are characterized by a status of immunological tolerance against HBsAg. HBcAg in liver nuclei could not be detected. All sera were positive for anti-HBc, some had anti "e". - Patients with uneventful acute virus-B-hepatitis developed CMI against HBsAg 4-6 weeks and anti-HBs 4-6 months after onset of the disease. Acute virus hepatitis without detectable HBsAg are defined as non-B-hepatitis by negative humoral and cell-mediated immune reaction against HBsAg 1-12 months after onset of the disease. - Patients with type B chronic active hepatitis are characterized by inadequate CMI against HBsAg without immune elimination of virus and virusantigens. Acute and chronic type-B-hepatitis showed temporary or constant CMI against HLP. These findings suggest an alteration or a carrier function of membrane antigens of virus infected hepatocytes or an induction of new membrane antigens by a virus. The results indicate that recovery from type B-hepatitis is associated with the ability to elicit a specific immune response to HBsAg. Furthermore immune responses to virus, virus antigens and virusinfected hepatocytes seemed to be the pathogenic principle of virus induced acute and chronic liver diseases.

Antibody Formation↗
PubMed1975

The diagnostic significance of intrahepatocellular hepatitis-B-surface-antigen (HBsAg), hepatitis-B-core-antigen (HBcAg) and IgG for the classification of inflammatory liver diseases. (Studies on HBsAg-positive and -negative patients).

Liver biopsies of patients with inflammatory liver diseases and clinically healthy HBsAg-carriers were examined for presence of intracellular HBsAg, HBcAg and IgG by direct immunofluorescence. The studies revealed the following results: 1. In most cases healthy HBsAg-carriers had HBsAg in the cytoplasm, but they did never show HBcAg in the nuclei of hepatocytes. 2. In the early phase some patients with HBsAg-positive acute hepatitis had HBcAg and/or HBsAg in their hepatocytes. In a normal course with complete recovery the immunoelimination may clear either phenomenon at variable stages of the disease. 3. Cases one year after complete recovery of acute virus B-hepatitis had no HB-components in their liver tissue. 2 cases without immunoelimination of HBsAg developed chronic active hepatitis within one year and had HBcAg in their liver cell nuclei. 4. Patients with HBsAg-positive CAH and highly inflammatory activity had HBcAg in the nuclei and a low percentage of cells with HBsAg in the cytoplasm of hepatocytes. HBsAg-negative cases with CAH never had HB-components in their tissue. 5. Patients with HBsAg-positive and -negative CAH in complete remission never had HBcAg and HBsAg in their hepatocytes. 6. Most cases with HBsAg-positive acute hepatitis and chronic active hepatitis positive for HBcAg had also IgG in the same liver cell nuclei. The coincidence of this finding gives strong evidence for the presence of anti-HBc in these liver cell nuclei. The importance of this finding for the course of the disease is unknown.

Acute Disease↗
PubMed1971

Between two worlds.

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Adaptation, Psychological↗