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W Horn

Publications and source records attributed to W Horn.

52 records · Page 3Linked to original sources

[Juvenile melanoma; a clinical and histological study].

Investigations were carried out in 52 female and 18 male patients, aged between 2 and 49 years, with juvenile melanoma. The tumor occured as a solitary tumor in all cases except one. It was mainly localized on the head (54%), and the extremities, on the trunk in three cases only. In 35% the tumor could be diagnosed clinically. Light microscopy revealed in 37.1% spindle cells, in 17.1% epitheloid cells, and in 45.7% the juvenile melanoma was of the mixed type. A proliferation of the vascular endothelial cells (37.1%) as well as immature looking mast cells in the tumor region were prominent findings. A transepidermal elimination of tumor cell nests was noted in one case. The other results are in agreement with earlier descriptions of this tumor.

Adolescent↗

[Spasmolytics. 5].

Explore the source record for details and available documents.

Aniline Compounds↗

Effects of the protease inhibitor antipain on cell malignant transformation.

BACKGROUND: Several natural products have been found to exhibit a chemopreventive activity both in in vivo and in vitro experimental systems. Among them, protease inhibitors seem to play a key role in the regulation of growth and phenotypic expression of transformed cells as well as in the regulation of the late events of carcinogenesis. We evaluated the effect of antipain (AP), a natural protease inhibitor, on chemically induced BALB/c 3T3 cell transformation, on invasion and chemotactic motility of transformed cells and on their gelatinase expression. METHODS: BALB/c 3T3 cells were plated and exposed to 2.5 micrograms/ml 3-MCA or 50 micrograms/ml, 1,2-DBE. The effect of a non-cytotoxic dosage of AP (10 microM) was studied by: a) pretreating cells with AP for 48 hours before the carcinogen exposure; b) adding AP simultaneously to the carcinogen treatment; c) chronic addition of AP at each medium change throughout the experimental duration. The effectiveness of the treatment was analysed as the ability to reduce or inhibit the occurrence of transformed foci. Modulation of the invasive phenotype by anti-transforming dosages of AP was evaluated by in vitro Matrigel invasion assay. Gelatin zymography was performed in order to assess AP regulation of proteolytic enzymes, such as metalloproteases, involved in invasion and metastasis. RESULTS: AP treatment can reduce the transformation rate both in 3-MCA- and 1,2-DBE-initiated cells. Its effectiveness depends on the administration schedule, and chronic addition seems to be the most effective treatment. The concentration of AP, which is effective in the antitransformation assay, is not able to significantly affect the migration and invasion of chemically transformed cells or their gelatinase activity. CONCLUSIONS: AP can suppress chemically induced BALB/c 3T3 cell transformation through mechanisms which do not involve modulation of the invasive phenotype.

3T3 Cells↗

In vitro effects of fenretinide on cell-matrix interactions.

BACKGROUND: Understanding the molecular basis of the metastatic spread of cancer and the underlying mechanisms is crucial for the development and appropriate clinical use of novel therapeutic agents directed at prevention of metastasis. Retinoids have been reported to inhibit cell proliferation, modulate cell differentiation, enhance apoptosis and to prevent the conversion of in situ cancer to locally invasive malignancy by suppressing the invasive process as well as by inhibiting angiogenesis. Fenretinide (4-HPR), a synthetic derivative of retinoic acid, is less toxic than natural retinoids and is active in the prevention and treatment of a variety of tumours in animal models. Its efficacy in cancer chemoprevention and therapy has been investigated in clinical trials. MATERIALS AND METHODS: In order to evaluate the effects of 4-HPR on the late stages of tumour progression, chemically transformed BALB/c 3T3 cells, showing a fully malignant phenotype, were exposed to 4-HPR (0.25-10 microM; 72 hours pre-treatment) and then analysed for in vitro invasive ability. The possible mechanisms of action responsible for the anti-invasive activity of 4-HPR were investigated, analysing cellular adhesion, motility, and proteolytic capability. RESULTS: Data showed that 4-HPR significantly inhibited the invasive phenotype of chemically transformed cells; the reduction in Matrigel invasion was dose-dependent and seemed not to be related to cytotoxic effects or reduction in cell proliferation rates induced by 4-HPR assayed doses. The 4-HPR-induced decrease in chemotactic motility of transformed cells correlated well with the invasion inhibition. 4-HPR, at active concentrations, differently affected cell adhesion to the extracellular matrix, depending on the coating substrate used (laminin, collagen IV, fibronectin and vitronectin). 4-HPR treatment significantly enhanced cell adhesion to laminin, while reducing cell-vitronectin attachment. It did not modify the attachment of the cells to fibronectin and collagen IV. Zymographic analysis failed to demonstrate 4-HPR involvement in the modulation of the activity and expression of gelatine degrading enzymes. CONCLUSION: These data suggest that 4-HPR inhibits tumour cell invasion through a basement-like matrix, by suppressing chemotactic motility and by altering cell-matrix interactions.

3T3 Cells↗

[Reconstruction of a suicide by a homemade firearm].

A 34 years old man shot himself by a selfmade muzzle-loader. He pluged one end of a waterpipe, used a cylindrical lead shot (Cal. 1.2 cm, length 2.15 cm, mass 22.7 g), special black powder (about 4 g, from fire-crackers; powder with an admixture of aluminium) and kindled the weapon in front of his chest by a slowmatch. He died immediately by retained missile of chest. The weapon flew away like a rocket. Unused projectils and powder (found in the flat) and the uninjured pipe allowed to copy the event. Velocity and energy of shot and weapon were determined, also the recoil of the pipe and the highest force of a hand to hold it fast. Experimental investigations and calculations correspondet well to the findings af the case.

Adult↗

Serum laminin P1 levels do not reflect critically elevated portal pressure in patients with liver cirrhosis.

BACKGROUND/AIMS: Laminin P1 serum levels run parallel to the accumulation of hepatic extracellular matrix in patients with liver cirrhosis. Recent studies reported a correlation between laminin P1 and portal pressure, leading to the proposal that laminin P1 may be used to identify patients with critically elevated portal pressure in liver cirrhosis. So far, most of the data has been obtained from patients with alcoholic liver disease. METHODOLOGY: We studied the relationship between laminin P1 serum levels and portal hypertension in 34 patients with liver cirrhosis, mostly of non-alcoholic etiology. Using hepatic venous catheterisation the hepatic venous pressure gradient (HVPG), an estimate of portal hypertension, was measured. Laminin P1 was compared to the HVPG and the size of esophageal varices. RESULTS: Serum laminin P1 was elevated in all samples. However, laminin P1 did not significantly correlate with either portal hypertension or the size of esophageal varices. Furthermore, laminin P1 measurement did not identify patients with critically elevated portal pressure using a HVPG of either 12 mmHg or 16 mmHg as cut-off points. CONCLUSION: The use of laminin P1 serum levels to diagnose critically elevated portal pressure in liver cirrhosis cannot be supported for etiologies other than alcoholic liver disease.

Adult↗