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K H Wiedmann

Publications and source records attributed to K H Wiedmann.

At least 37 records · Page 2Linked to original sources
PubMed1990

Immunohistochemical demonstration of mitochondria in routinely processed tissue using a monoclonal antibody.

We report results obtained using the monoclonal antibody M-II 68, which recognizes inner mitochondrial membrane in routinely processed (formalin-fixed and paraffin-embedded) tissue by light microscopic immunohistochemistry. In ten normal brains, the range of immunoreactivity in various cell types and locations was defined. The most intense staining was observed in Purkinje cells, in neurons of cranial nerve nuclei, pons and substantia nigra, as well as in choroid plexus epithelial cells. By comparison with this control group, one case of primary mitochondrial encephalomyopathy exhibited increased staining of endothelial and vascular smooth muscle cells, choroid plexus epithelial cells, and neurons of various locations. Scattered ragged-red fibres were heavily labelled in one case of mitochondrial myopathy, while ten muscles without mitochondriopathy were left unstained. Our method is able to detect accumulations of mitochondria and increases in mitochondrial cristae density. It could prove useful for differential diagnosis of routine biopsy material and for clarification of cell types involved in mitochondrial cytopathies.

Adolescent↗
PubMed1990

Clonal analysis of infiltrating T lymphocytes in liver tissue in viral hepatitis A.

The pathogenic mechanism leading to liver tissue injury in hepatitis caused by hepatitis A virus is unclear. We have randomly established T-cell clones from liver biopsies from four patients with hepatitis A. A total of 578 clones was phenotypically analysed. During the acute phase of the disease CD8+ clones dominated over CD4+ clones, whereas in a biopsy taken late after onset of clinical syndromes more CD4+ than CD8+ clones were obtained. Interestingly, in a patient with a second exacerbation of the disease, more than 20% of all clones had the CD3+ WT31- CD4- CD8- 'NK-like' phenotype. All CD8+ clones had cytotoxic activity and approximately 50% of all CD8+ clones showed specific cytotoxicity against autologous fibroblasts infected with hepatitis A virus. The CD8+ cells also produced IFN-gamma in response to these target cells. Variable IFN-gamma production was observed with all types of T-cell clones. These results suggest that the liver injury in hepatitis A is not caused by a viral cytopathogenic effect but is due to an immunopathological reaction of sensitized cytotoxic T lymphocytes against infected hepatocytes. In addition, these studies show an enrichment of CD4-8-T-cell receptor alpha beta-chain-negative T lymphocytes at the site of an inflammation and suggest a role of these cells in an anti-viral reaction.

Acute Disease↗
PubMed1989

Ragged-red fibres detected in paraffin sections by a monoclonal antibody to inner mitochondrial membrane.

An immunohistochemical method is reported using the M-II68 monoclonal antibody, which detects mitochondrial accumulations ("ragged-red fibres") in routinely processed (formalin-fixed, paraffin-embedded) muscle tissue. Ten cases with electron-microscopically and histochemically proven mitochondrial myopathy featured 4% to 24% ragged-red fibres. In a series of 50 muscle biopsies without mitochondrial myopathy, scattered ragged-red fibres (less than 0.1%) were present in a few normal and pathological muscles. The immunohistochemical method is specific for mitochondria, does not require frozen tissue and permits rapid examination of large areas.

Antibodies, Monoclonal↗
PubMed1989

[Pathogenesis and clinical aspects of primary liver cell carcinomas].

The hepatocellular carcinoma is the most frequent primary liver cell carcinoma. On account of its geographical distribution with preferential occurrence in China, SE Asia and South Africa, exogenic causes are thought to be mainly responsible for its aetiopathogenesis. Besides mycotoxins, the hepatitis B virus infection (HBV) is particularly important. Integration of HBV-DNS into the hepatic cell DNS is considered to be an initiatory step in hepatocarcinogenesis. Clinically the tumour usually becomes manifest by upper abdominal complaints. Curative treatment can be promising only with very small tumours which can be detected most safely via ultrasound examination and alpha-1-fetoprotein determination.

Carcinoma, Hepatocellular↗
PubMed1989

Liver-derived cytotoxic T cells in hepatitis A virus infection.

An autologous in vitro model was developed to analyze the immunologic cause of liver tissue injury during hepatitis A virus (HAV) infection. Human T lymphocytes infiltrating the livers of two patients with acute HAV infection were isolated from liver biopsy cores, cloned, and expanded in vitro. Procedures using a cell culture system with HAV-infected autologous skin fibroblasts demonstrated that 42% and 53% of the liver-infiltrating CD8+ clones were HAV-specific and that they kill HAV-infected skin fibroblasts in a human leukocyte antigen-restricted manner. Data show virus-specific killing by liver-infiltrating T lymphocytes in man and support the hypothesis that liver cell injury in acute HAV infection is mediated by HAV-specific CD8+ T lymphocytes and is not caused by a cytopathic effect of the virus itself.

Adult↗
PubMed1988

Human gamma interferon production by cytotoxic T lymphocytes sensitized during hepatitis A virus infection.

The production of interferon (IFN) during a chromium-51 release assay with hepatitis A virus (HAV)-infected fibroblasts and autologous peripheral blood lymphocytes from patients with acute HAV infection was studied to determine whether IFN plays a role in immunopathogenesis of hepatitis A infection in humans. Skin fibroblasts of eight patients after acute HAV infection and from two control persons without history of current or past HAV infection were infected with HAV. Peripheral blood lymphocytes were collected at different times after the onset of icterus and tested in a chromium-51 release assay against autologous HAV-infected skin fibroblasts for their cytolytic and IFN-producing activity. The IFN produced during the assay was characterized and found to have the properties of human gamma IFN. Cytotoxicity and gamma IFN release were virus specific. The cell types responsible for both functions were characterized and found to be in the HLA-dependent T8+ lymphocyte subset. Considering that gamma IFN has an antiviral effect on persistent HAV infection in vitro and that it probably accounts for stimulation of HLA class I antigen expression on hepatocytes, our experimental results presented here demonstrate that human gamma IFN produced by HAV-specific T cells may participate in pathogenesis of hepatitis A infection in humans.

Cells, Cultured↗
PubMed1985

Serum inhibitory factors (SIF) are of prognostic value in acute viral hepatitis.

Serum inhibitory factors (SIF) were analysed in relation to the natural course of acute viral hepatitis in 81 patients followed over a period of 1 year. 63 patients recovered completely (group 1), and 18 had a protracted course of hepatitis (group 2) as shown by persistent transaminase activity 6 months after onset. 11 patients in group 2 still had signs of liver disease after 1 year. A gradual fall of SIF activity (in 47 patients) heralded resolving hepatitis, whereas persistence of SIF (in 8 patients) correlated with inflammatory activity and failure of hepatitis B viral antigen elimination. Absence of SIF activity was associated with either an uncomplicated or a chronic course of hepatitis in 23 and 3 patients, respectively. Repeated determination of SIF may help to predict the final outcome of hepatitis. Both excessive and failure of SIF production may result in the development of chronic liver disease.

Acute Disease↗
PubMed1985

Basement membrane proteins and type III procollagen in murine schistosomiasis.

The livers of female CBA mice were examined 9 to 10 weeks after subcutaneous infection with Schistosoma mansoni. Cryostat liver sections and isolated liver cells were examined by indirect immunofluorescence using specific antibodies against basement membrane proteins (laminin, fibronectin and type IV collagen and type III collagen precursor. Liver cells were isolated by collagenase digestion, purification on Percoll density gradients and centrifugal elutriation to yield enriched fractions of hepatocytes, endothelial and Kupffer cells (Fractions I, II, III respectively). Infected animals yielded more than three times the control number of non-parenchymal cells; electron microscopy revealed that the increase in Fraction II was due mainly to eosinophilic leucocytes and in Fraction III due to Kupffer cells and macrophages from the schistosomal granulomata. Studies of cryostat liver sections showed that the schistosomal granulomata contained dense deposits of type III collagen precursor and fibronectin in the distribution of the reticulin fibres but laminin and type IV collagen were conspicuous only in new vessels in the periphery of the granuloma. Isolated liver cells showed fibronectin on their surface. Immunofluorescence studies could not be performed on Kupffer and endothelial cell fractions because of marked non-specific fluorescence. These experiments indicate that centrifugal elutriation is a useful method for isolating the constituent cells of murine schistosomal granulomata.

Animals↗
PubMed1985

Analysis of the antigenic composition of liver specific lipoprotein using murine monoclonal antibodies.

Eight monoclonal antibodies have been raised to antigenic determinants within the liver specific lipoprotein complex. Five of these determinants were species and the others non-species specific. No liver specific determinants were identified. Liver specific lipoprotein antigens recognised by the eight monoclonal antibodies were located either on the hepatocyte membrane and/or along the sinusoidal lining wall or in the cytoplasm of liver parenchymal cells. All antibodies but one reacted with the cell membrane of viable human hepatocytes. The molecular weights of four liver specific lipoprotein-determinants were determined by immunoprecipitation. These ranged from 22 000 to 164 000 daltons.

Adult↗
PubMed1983

Anti-actin antibodies of IgM and IgG class in chronic liver diseases detected by fluorometric immunoassay.

Using a sensitive fluoroimmunoassay, anti-actin antibodies (AA) of the IgM and IgG classes were measured in 240 patients with various chronic liver diseases and in 211 patients with non-hepatic autoimmune muscle, heart, malignant and inflammatory bowel diseases. Thirty-two out of 40 patients (80%) with autoimmune chronic active hepatitis (CAH) had AA only of the IgG class (geom. mean X = 1.78, SEM +/- 0.07) and only three patients (8%) had both IgG and IgM AA, the latter in lower titres. In patients with primary biliary cirrhosis (PBC) and AMA-positive cholestatic CAH, AA of both IgM and IgG classes were equally represented (60% IgG and 64% IgM AA in PBC, 73% IgG and 51% IgM AA in cholestatic CAH) but the titres were very low (geom. mean IgG AA in PBC 1.035, SEM +/- 0.03, in cholestatic CAH 1.18, SEM +/- 0.02). In contrast to autoimmune (lupoid) CAH, AA were rare in HBsAg positive CAH (9/43, 21%) and only present in low titres. However, in six out of 21 patients with anti-HBs and anti-HBc-positive chronic active hepatitis, high AA of IgG class were found, suggesting the autoimmune type of liver disease. In NANB virus-induced chronic liver disease after blood transfusion, AA were only occasionally found (IgG antibodies 1/19, IgM antibodies 3/19) and none were found in the eight patients with sporadic NANB hepatitis. They were also rare in 30 patients with alcoholic liver disease (3/30, 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1982

Diagnostic significance of quantitative determination of hepatitis B surface antigen in acute and chronic hepatitis B infection.

HBsAg was determined quantitatively by radioimmunoassay and by Laurell electrophoresis in sera of 90 patients with acute hepatitis B, 57 patients with chronic hepatitis B, and 154 HBsAg positive blood donors. Of 55 patients with clearance of HBsAg from the circulation within six months, 54 (98%) showed an at least 50% reduction in concentration within 16 days. All 55 patients had such a decrease within 20 days. No such decrease was found in seven patients with acute hepatitis B who became HBsAg carriers. Therefore, quantitative HBsAg concentration in paired sera seems to be a reliable and early prognostic marker in acute hepatitis B. In patients with clearance of HBsAg most of the antigen is already present in the circulation at hospitalization and is eliminated with a mean half-life of 8.8 days. Patients with chronic hepatitis exhibit on average nearly the same HBsAg concentration (about 40,000 ng/ml) as patients with acute hepatitis B at hospitalization (about 39,000 ng/ml) and HBsAg positive blood donors on average a lower HBsAg concentration (about 8,000 ng/ml).

Blood Donors↗
PubMed1981

[Irritable colon].

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Colonic Diseases, Functional↗
PubMed1979

[Severe megaloblastic anaemia by triamterene in a patient with alcoholic liver cirrhosis (author's transl)].

Mucosal ulceration and severe bone-marrow insufficiency with marked megaloblastic transformation occurred during treatment with triamterene in a patient with decompensated alcoholic liver cirrhosis and malnutrition. When the triamterene-containing preparation was stopped and folinic acid administered the haematological picture improved, but the patient died, with signs of hepatocellular insufficiency, of gastro-intestinal bleeding. The serum folic-acid level was markedly reduced due to the chronic malnutrition, while the vitamin B12 level was within normal limits. This observation indicates that when the pool of folic-acid coenzymes is reduced, triamterene can cause megaloblastic anaemia due to its folic-acid antagonism. Triamterene should, therefore, be given to patients with borderline folic-acid reservoirs, chronic alcoholism or during pregnancy, only under careful serial control of the blood picture.

Anemia, Macrocytic↗
PubMedDate not supplied

Hepatitis B virus and HLA antigen display in the liver during chronic hepatitis B virus infection.

an analysis of the expression of the histocompatibility antigens in the livers of patients with chronic hepatitis B virus infection and normal subjects has demonstrated an increased expression of HLA-A, B, C antigens on the hepatocytes of patients with a low level of viral replication (HBe antibody positive) as compared with patients who exhibit a high level of viral replication (HBe antigen positive) and controls. This increase in the expression of histocompatibility antigens on the hepatocytes was associated with a decrease in the membrane expression of viral antigens by the same cells. These differences in the density of HLA and viral antigen display may influence the efficiency of T-cell cytolysis of hepatitis B virus-infected hepatocytes.

Biopsy↗