Publications by authors named "JOSKE R"

The Directions program provides an administratively efficient method to screen for psychological disorders in a primary-care setting (FOCUS), confirm the need for treatment, and monitor progress (COMPASS-PC). The instruments are psychometrically sound and grounded in an established theory of mental-health treatment. The present study reports the relationships between FOCUS, COMPASS-PC, and the Hamilton Depression scale for a sample of patients who have been diagnosed as major depressive disorder, dysthymia, or depressive syndrome by standardized criteria (i.

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The fine specificity of autoantibodies to human hepatocyte plasma membranes in autoimmune chronic active hepatitis was determined by one-dimensional immunoblotting. Sera from 12 patients with "classical" autoimmune chronic active hepatitis contained autoantibodies recognizing many human hepatocyte plasma membrane polypeptides in the 15 to 220 kD range. Many of these autoantibodies titrated beyond 1:80,000 and some may be potentially "pathological.

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Circulating autoantibodies reacting with human hepatocyte plasma membranes (HHPM) were quantitated in acute and chronic liver disease using an enzyme-linked immunosorbent assay (ELISA). Anti-HHPM were found most frequently in patients with chronic active hepatitis (CAH), a disease postulated to result from autoimmune processes directed at organ-specific antigens on the surface of hepatocytes. The high incidence of anti-HHPM in CAH (75%) contrasted significantly with all other groups assayed, including primary biliary cirrhosis (44%), alcoholic liver disease (21%), acute viral hepatitis (17%), and chronic persistent hepatitis (8%).

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Five years after completing adjuvant chemotherapy for osteosarcoma of the fibula, a 20-year-old woman developed an esophageal carcinoma. The association between prior chemotherapy and radiation exposure, and the significance of genetic factors and family history are discussed. This case exemplifies the importance of continued follow-up of the long-term survivors of tumor management.

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An open-lung biopsy performed in a 15-year-old girl because of left sided pulmonary nodules revealed striking angiocentric necrotising granulomas. No acid fast bacilli (AFB) were cultured or demonstrated in tissue sections, however, the diagnosis of tuberculosis was suggested. Anti-tuberculous therapy resulted in both clinical and radiological cure within 12 months.

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An enzyme-linked immunosorbent assay (ELISA) using plates coated with hepatocyte plasma membranes (HPM) was developed for the measurement of antibodies directed at hepatocyte surface antigens. Precoating ELISA plates with poly-L-lysine (PLL) provided firm attachment for the adsorption of HPM. The use of HPM, in preference to whole hepatocytes, excludes pathologically irrelevant cytoplasmic antigens.

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Indirect and direct evidence is presented that normal, non-immune mice have cells which suppress antibody production to murine liver specific lipoprotein (LSP) autoantigens with little or no effect on the response to a closely related foreign antigen complex, rabbit LSP. Suppressor control mechanisms were suggested in low responder BALB/c mice which produced LSP autoantibody only after exposure to low dose X-irradiation or treatment with cyclophosphamide. Adoptive transfer experiments in X-irradiated BALB/c mice and untreated C57BL/6 mice showed that cells from normal mouse spleen prevented LSP autoantibody production when put into the circulation of mice prior to immunization with foreign rabbit LSP.

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Autoantibodies to liver specific lipoprotein (LSP) are produced following acute non-fatal hepatitis in murine cytomegalovirus (MCMV) infected mice. Both C57B1 and BALB/c mice produced a transient LSP autoantibody response demonstrated by passive haemagglutination and enzyme linked immunosorbent assay. C57Bl mice produced both IgM and IgG LSP autoantibody and BALB/c mice produced only IgM autoantibody.

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Autoantibody to the hepatocyte membrane antigen, liver-specific lipoprotein (LSP) was induced in mice by immunization with LSP-containing protein preparations from human, rat, rabbit and mouse liver and also with purified allogeneic LSP. Each of the strains of mice used (C57B1, BALB/c, C3H) showed the capacity to produce high titre autoantibody to LSP. Autoantibody to LSP demonstrated by passive haemagglutination was absorbed by normal mouse hepatocytes but not by kidney or spleen cells and reacted with the cell membrane of normal mouse hepatocytes by immunofluorescence.

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A survey was made on 50 patients with active chronic hepatitis (ACH) seen in Perth, Western Australia. The aetiology varied: three cases followed metabolic disease, 8 drugs or alcohol, 12 were due to hepatitis B and no cause in 27. There was a male preponderance in the first three groups and a female preponderance in the idiopathic group.

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The incidence of PLC in the Pacific Basin varies from 0.9/100,000 (age-standardized) in women in New South Wales, Australia, to 34.2/100,000 in Singapore Chinese men.

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Two cases are reported of large pre-splenic aneurysms of the splenic artery in patients with chronic liver disease, and three others cited from the literature. Four of the five died from rupture of the aneurysm. All patients were parous females with chronic liver disease, and in four of the five this was known to be present before pregnancy.

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IgE (reaginic antibody) levels have been estimated on 160 occasions in 120 patients with liver disease. IgE levels were significantly raised in patients with untreated active chronic hepatitis, and returned towards normal with steroid or immunosuppressive therapy. They were also increased in patients with liver disease associated with alcoholism.

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A female aged 60 years with heterozygous alpha-1-antitrypsin deficiency developed a progressive and ultimately fatal liver disease with the clinical, biochemical, immunological and histological characteristics of active chronic hepatitis. It is suggested that the hepatic disease of A-AT deficiency be included among the types of liver disease which may initiate a progressive immunopathic response.

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A man aged 38 years developed chronic liver disease with characteristics of both haemochromatosis and active chronic hepatitis. Two of his relatives were found to have selective IgA deficiency. It is suggested that this case provides evidence that haemochromatosis may initiate active chronic hepatitis in a genetically susceptible subject.

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