Search PubMed⌕ Search

Biomedical subjects

H E Schmidt

Publications and source records attributed to H E Schmidt.

32 records · Page 2Linked to original sources
PubMed1979

[Tumor localization in vivo on the basis of scintigraphic detection of clostridium rods by means of 131J-labeled antibodies and F(ab')2 antibody fragments].

The authors report about investigations for localization of tumours in vivo by scintigrafic iddntification of Clostridium butyricum Jena H8 by 131I-labelled antibodies and by 131I-labelled F(ab')2-fragment antibodies in mouse transplantation-tumour UVT 15264. The application of 131I-labelled anti-clostridial-rod-antibodies in tumour bearing mice demonstrates increase of radioactivity in tumours of animals, pretreated by spores, as well as in animals without pretreatment. These appearently unspecific increases of radioactivity could not be demonstrated by application of 131I-labelled F(ab')2-fragment antibodies directed against clostridial rods, but also the specific fixation of 131I-labelled F(ab')2-fragment antibodies in tumours of mice, pretreated by clostridial spores, could not be demonstrated. The results are discussed with regard to further investigations.

Animals↗
PubMedDate not supplied

Differences in the biological activity of TNF alpha and TNF beta correlate with their different abilities for binding to the target cells.

TNF alpha and TNF beta were compared regarding their binding to different types of target cells, cytotoxic/cytostatic activity against murine and human tumor cell lines as well as human capillary endothelial cells, their ability to induce differentiation in myeloid leukemia cell lines, and induction of hemorrhagic tumor necrosis and tumor regression as well as lethal toxicity in tumor-bearing mice. The results show considerable quantitative differences in the biological activity between TNF alpha and TNF beta depending on the type of target cell which has been used. TNF beta was 3 fold more cytotoxic than TNF alpha against murine L929 fibroblasts and 3-5 times more active concerning the induction of hemorrhagic tumor necrosis, complete tumor regression and more toxic in tumor-bearing mice. In contrast to this, TNF beta was markedly less cytotoxic against human capillary endothelial cells and the human mammary carcinoma cell line MCF7 and much less cytostatic against the human myeloid leukemia cell lines HL60 and U937. The lesser antiproliferative effect of TNF beta correlated with a lower ability for induction of differentiation in these cell lines. Competitive radioligand binding assays showed that TNF beta was about 4 fold more effective than TNF alpha in competing with 125I-labeled TNF alpha for the binding to murine L929 fibroblasts. But it was 15-20 times less effective in binding to the human MCF7 cells and the human myeloid leukemia cell lines HL60 and U937. This revealed that, at least for these targets, the differences in the biological activity between TNF alpha and TNF beta are due to different abilities for binding to the target cells. Possible mechanisms for these different binding abilities are discussed.

Animals↗