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S Matern

Publications and source records attributed to S Matern.

At least 37 records · Page 2Linked to original sources

[Solitary fibrous thoracic wall tumor. Progression with percutaneous radiotherapy].

HISTORY AND CLINICAL FINDINGS: A 81-year-old patient free of pain was referred to the university hospital for further evaluation and therapy of tumour masses in the right thorax. Clinical examination revealed dullness to percussion and reduced breathing in the right lower lung. INVESTIGATIONS: Computed tomography showed an enlarged solid tumour mass attached to the thoracic cavity and pleural effusion on the right side. Quantification of pulmonary perfusion presented significant defects in the right upper and middle lobe. DIAGNOSIS, TREATMENT AND COURSE: The pulmonary masses were biopsied under CT-guidance. Biopsy and immunohistochemical findings proved a malignant solitary fibrous tumour of the chest wall, a mesenchymal tumour of its own entity. Because of pain in the right arm and because of missing other reliable therapeutic options a palliative irradiation was performed. The tumour did increase in size due to radiotherapy and a severe right ventricular heart failure occurred. The patient died 5 months after diagnosis has been made. Autopsy revealed a transition of tumour cells to sarcomatic growth. CONCLUSION: In our case we conclude an accelerated progression of the solitary fibrous chest wall tumour in the course of irradiation. Whether the development of sarcomatic growth occurred as a result of radiotherapy remains speculative.

Aged↗

[Matrix metalloproteinases: Promoters of tumor invasion and metastasis - A review with focus on gastrointestinal tumors].

Degradation of basement membrane and extracellular matrix is crucial for invasion and metastasis of tumor cells. Proteolysis occurs via matrix metalloproteinases and is tightly controlled by specific endogenous proteinase inhibitors. This review will summarize the current view on the role of matrix metalloproteinases in tumor growth, invasion and metastasis and focus on the importance of matrix metalloproteinases in gastrointestinal cancer.

Animals↗

Cholesterol crystal binding of biliary immunoglobulin A: visualization by fluorescence light microscopy.

AIM: To assess potential contributions of biliary IgA for crystal agglomeration into gallstones, we visualized cholesterol crystal binding of biliary IgA. METHODS: Crystal binding biliary proteins were extracted from human gallbladder bile using lectin affinity chromatography.Biliary IgA was isolated from the bound protein fraction by immunoaffinity chromatography. Pure cholesterol monohydrate crystals were incubated with biliary IgA and fluoresceine isothiocyanate (FITC)conjugated anti IgA at 37 degree. Samples were examined under polarizing and fluorescence light microscopy with digital image processing. RESULTS: Binding of biliary IgA to cholesterol monohydrate crystals could be visualized with FITC conjugated anti IgA antibodies. Peak fluorescence occurred at crystal edges and dislocations. Controls without biliary IgA or with biliary IgG showed no significant fluorescence. CONCLUSION: Fluorescence light microscopy provided evidence for cholesterol crystal binding of biliary IgA. Cholesterol crystal binding proteins like IgA might be important mediators of crystal agglomeration and growth of cholesterol gallstones by modifying the evolving crystal structures in vivo.

Bile↗

Isoursodeoxycholic acid: metabolism and therapeutic effects in primary biliary cirrhosis.

Significant amounts of ursodeoxycholic acid (UDCA) used for the treatment of patients with primary biliary cirrhosis (PBC) become epimerized at C-3 to isoUDCA. We investigated the metabolism of isoUDCA and a possible pharmacologic effect in five patients (51.4 +/- 5.8 years old; 3 females, 2 males) with PBC and persistent elevations of gamma-glutamyl transpeptidase (gamma-GT) and alkaline phosphatase despite treatment with UDCA for more than one year. Serum samples were analyzed for bile acid metabolites and surrogate markers of cholestasis in 4-week intervals after 1 g/d UDCA, wash-out, 0.5 g/d isoUDCA, 0.75 g/d isoUDCA, 0.75 g/d UDCA, and two further periods with 1 g/d UDCA. Bile acids in urine were analyzed after wash-out, 0.5 and 0.75 g/d isoUDCA, and 0.75 and 1 g/d UDCA. During wash-out, AST, AP, and gamma-GT rose significantly (P < 0.05) but reversed to previous levels during the first isoUDCA period, with 0.5 g/d only. No further improvements were observed after increasing the dose of isoUDCA or switching back to UDCA. In serum, the relative amounts of isoUDCA and UDCA were 8.1 +/- 7.4% and 16.2 +/- 6.4% during 0.5 g/d isoUDCA, 6.2 +/- 2.5% and 45.0 +/- 4.1% during 0.75 g/d isoUDCA, and 0.5;-3% and 56.4;-60.0%, respectively, during UDCA. In urine, UDCA was the predominant bile acid both during isoUDCA and UDCA medications. The similar serum enrichment and urinary excretion of UDCA during administration of either isoUDCA or UDCA together with low concentrations of the intermediate of isomerization, 3-dehydro-UDCA, indicate a first-pass epimerization of isoUDCA to UDCA in the liver. Approximately 25% of serum isoUDCA and 10% of serum UDCA were conjugated with either glucuronic acid or N-acetylglucosamine, indicating hepatic formation and systemic secretion of glycosidic conjugates. In PBC patients, isoUDCA becomes isomerized to UDCA and has similar effects on surrogate markers of cholestasis. Thus, isoUDCA has pro-drug characteristics.

Bile Acids and Salts↗

[Clinical aspects and therapy of viral hepatitis].

Acute hepatitis can be caused by the enterically spread hepatitis A and E viruses and the parenterally spread hepatitis B, C or D viruses. The clinical features of acute viral hepatitis are similar among the five viruses and include non-specific symptoms and icterus. In general, a specific therapy is not necessary, but patients with fulminant hepatitis may require liver transplantation. For acute hepatitis C, the effect of interferon-alpha on the risk of chronicity is evaluated in clinical trials. Chronic hepatitis is defined as inflammatory reaction in the liver that continues without improvement for at least 6 months after infection with hepatitis B, C or D viruses. Hepatitis B resolves in more than 90% of the patients, but chronic infection can lead to liver cirrhosis and hepatocellular carcinoma. Chronic hepatitis C is an insidious disease, because early diagnosis is missed easily due to asymptomatic presentation and about 70% of infected patients develop chronic hepatitis. The benefits of interferon-alpha and/or nucleoside analogues have been proven in recent clinical trials that show sustained responses in more than a third of all patients with chronic viral hepatitis. The future treatment of chronic viral hepatitis will likely include immunomodulation and gene therapy.

Antiviral Agents↗

Increased TIMP-1 activity results in increased expression of gelatinases and altered cell motility.

Matrix metalloproteinases are proteolytic enzymes which play a major role in resorption of collagen and other components of the extracellular matrix. They are controlled by specific inhibitors, so-called tissue inhibitors of metalloproteinases (TIMPs). The balance between matrix metalloproteinases and TIMPs seems to play a major role in controlling extracellular matrix homeostasis and cell migration. The influence of TIMP-1 on migration behaviour was explored in human hepatoma cells transiently and stably transfected with mouse TIMP-1, and incubated with biologically active TIMP-1. Transfection and biosynthesis were verified by Northern blotting, Western blotting, metabolic labeling, and reverse zymography. Overexpression of and incubation with TIMP-1 resulted in suppressed migration and seemed to enhance cell-cell contact. Using gelatin zymography and Western blotting we measured a significant increase of matrix metalloproteinases-2 and matrix metalloproteinases-9 in cells transfected with TIMP-1. This new phenomenon may be of important physiological significance in modulating TIMP and MMP expression. Our results indicate a functional involvement of TIMP-1 in matrix homeostasis and some automatic control in matrix turnover.

Animals↗