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Werner Falk

Researcher at University of Regensburg

Publications -  179
Citations -  16095

Werner Falk is an academic researcher from University of Regensburg. The author has contributed to research in topics: Cytokine & Tumor necrosis factor alpha. The author has an hindex of 59, co-authored 179 publications receiving 15458 citations. Previous affiliations of Werner Falk include German Cancer Research Center & Heidelberg University.

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Monoclonal antibody-mediated tumor regression by induction of apoptosis

TL;DR: Histological thin sections of the regressing tumor showed that anti-APO-1 was able to induce apoptosis in vivo, suggesting induction of apoptosis as a consequence of a signal mediated through cell surface molecules like APO- 1 may be a useful therapeutic approach in treatment of malignancy.
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Treatment of murine colitis by Lactococcus lactis secreting interleukin-10.

TL;DR: Using two mouse models, it is shown that the therapeutic dose of IL-10 can be reduced by localized delivery of a bacterium genetically engineered to secrete the cytokine.
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A 48-well micro chemotaxis assembly for rapid and accurate measurement of leukocyte migration

TL;DR: A 48-well chemotaxis chamber to minimize manipulation time and amount of material required by the larger blindwell or Boyden chemot axis chamber is designed, suitable for clinical research on the functional state of monocytes in large groups of patients.
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Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Sequence identity with the Fas antigen.

TL;DR: The APO-1 antigen was expressed upon transfection of APo-1 cDNA into BL60-P7 Burkitt's lymphoma cells and conferred sensitivity towards anti-APO- 1-induced apoptosis to the transfectants.
Journal Article

Requirement of endogenous tumor necrosis factor/cachectin for recovery from experimental peritonitis.

TL;DR: During the early phase of peritonitis endogenous TNF may stimulate nonlymphoid cells such as granulocytes, macrophages, platelets, and fibroblasts to ingest bacteria and to localize inflammation, respectively, which may determine survival.