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Biomedical subjects

W Arnold

Publications and source records attributed to W Arnold.

At least 469 records · Page 26Linked to original sources
PubMed1976

[Mesothelioma in syrian hamster. V. Macroscopic and histologic investigation of transplanted mesothelioma in solid and ascitic form (author's transl)].

Transplantable mesothelioma lines are described, which have been inoculated successively either s.c. or i.p. in solid and ascitic form. Increases of the degree of malignancy could be demonstrated for macroscopically biological parameters. The latent periods became shorter with increasing in vivo passages. In the histological picture, progressive dedifferentiation of the tumour cells with rising tendency towards infiltrative growth was observed.

Abdominal Neoplasms↗
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

Organ-specificity and diagnostic value of cell-mediated immunity against a liver-specific membrane protein: studies in hepatic and non-hepatic diseases.

In chronic active hepatitis (CAH, n=58) 70% of the HBsAg negative and 48% of the HBsAg positive cases showed a CMI against human liver specific proteins (HLPI). Using HBsAg as antigen only 12% of the HBsAg negative and 24% of the HBsAg positive cases gave a CMI response. On the basis of HBsAg and autoantibodies in the serum CAH patients could be divided into 4 subgroups. A close correlation between CMI against HLPI, sex, ANA and HL-A-8 could be detected. In a follow-up study of patients with acute virus B hepatitis (n=62) CMI against HBsAg was detected in 60% of the cases in the acute phase of the disease but in 15% only 3-6 months after the onset of the illness (n=40). In patients who developed a chronic HBsAg carrier status 3 of 5 cases remained persistently positive with HLPI as antigen in the migration inhibition test. - In non-hepatic diseases in which immunological abnormalities may be present (malignant diseases n=46, diabetes mellitus n=27, active tuberculosis, n=18 and untreated systemic lupus erythematodes, n=5) only 26% of patients with malignant diseases showed a migration inhibition with HLPI. - Using different antigens such as human liver specific proteins (HLP), rabbit liver specific proteins (RLP), brucella suis antigen and tuberculin it was possible to demonstrate the validity of the two-step migration inhibition test to detect CMI. The results with different antigens in hepatic and non-hepatic diseases demonstrated that cell-mediated immunity of HLPI is an organ specific immune reaction which is associated with acute and chronic active liver diseases as a time limited or long-lasting phenomenon. Positive reactions in some tumor patients suggest that different mechanisms may elicit an autoimmune reaction against liver antigens.

Antibodies↗
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↗
PubMed1975

[Investigations concerning the fixation of hepatitis B-antigen (HBAg) on peripheral lymphocytes and isolated hepatocytes in patients with inflammatory liver diseases. (author's transl)].

The fixation of HBAg on lymphocytes was investigated in 127 patients with various inflammatory liver diseases. The fixation of HBAg on lymphocytes and isolated hepatocytes as well as the fixation of IgG on isolated hepatocytes were studied in 60 cases. Membrane-fixed HBAg could in no case be demonstrated on isolated hepatocytes whether these cells were derived from patients with or without HBAg in the serum. HBAg on hymphocytes was detectable in most cases of acute hepatitis during the phase when HBAg disappeared from the serum. HBAg on lymphocytes was detectable in most cases of acute hepatitis during the phase when HBAg disappeared from the serum (time of immunoelimination). Membrane-fixed IgG could be mainly demonstrated in HBAg positive acute hepatitis with a protracted course or in HBAg-positive active chronic hepatitis and signs of inflammatory activity. The results obtained for HBAg-carriers indicate (a) an immunological tolerance against HBAg, (b) a persistance of the virus infection in liver cells, and (c) an antibody-mediated cyto- and histotoxicity as a pathogenetic principle for the course of certain chronic liver diseases. The antigenic determinant of the membrane-fixed antibody is not known until now.

Binding Sites, Antibody↗
PubMed1975

The fate of injected human IgG in the mouse liver: Uptake, immunological inactivation, and lysosomal reactions.

1. Human IgG is stored in the form of remarkable droplets in the cytoplasm of mouse hepatocytes following intravenous injection. 2. The earliest protein uptake occurs within 1 minute after injection and droplets can be found up to 32 hours thereafter; 64 hours p.i. the foreign protein is no longer visible in hepatocytes. 3. Electron microscopy reveals that the uptake occurs by a process of "macropinocytosis". The resulting protein droplets fuse with primary lysosomes and are transformed into phagolysosomes. 4. At the same time as the phagolysosomes are formed the IgG-droplets loose their immunological activity--as early as 2 hours after injection.

Acid Phosphatase↗
PubMed1975

[Vascular degeneration in otosclerosis and its influence on the mesenchymal reaction of the mucoperiost].

38 samples of middle ear mucosa were taken from different patients during stapes surgery in otosclerosis. The samples were studied light-and electronmicroscopically without decalcification. Considerable pathologic changes in the organisation of the capillaries (endothelial hydrops, proliferation of the intima and of the adventitia, total obliteration o the vessels) cause pathologic reactions on the mesenchymal elements of the submucosa. Next to fibrolysis or hyalinosis of the collagen fibers the fibrocyts show features of undergoing lysis. Free and cellular bound calcium deposits are located in these lytic areas. The epithelial lining also shows unusual inclusions as glycogen and acid mucopolysaccharides and an alterated basement membrane. We belive that the changes of the connective tissue and of the epithelium are secundary to the capillary obstruction.

Apatites↗
PubMed1975

[Reaction of the middle ear mucous membrane in tubal obstruction].

1. Tubal obstruction causes a rapid rise in transepithelial cytopempsis. The squamous epithelial cells show numerous vesicles carrying subepithelial fluid (extracellular fluid) to the middle ear cavity. 24 hours following tubal obstruction a widespread rupture of the epithelial junctions can be observed. Subepithelial fluid, consisting of lymphfluid, transsudate and later exsudate, enters the middle ear cavity without passing a cellular barrier. 2. Long lasting negative pressure provoces a cellular differentiation (metaplasia!) of the formerly squamous epithelium to a high, cylindric cell layer with new functions: ciliary movement and secretory activity. 3. Ablation of the tympanic membrane to expose the middle ear to air after 2-4 days, causes a stop in the epithelial differentiation but no regeneration to the normal histological flat formation. 4. Studies of samples of human middle ear mucosa in serous otitis or sero-mucous otitis show exactly the same results as during the different stages of our animal experiments.

Animals↗