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Alfred Walz

Researcher at University of Bern

Publications -  77
Citations -  12871

Alfred Walz is an academic researcher from University of Bern. The author has contributed to research in topics: Chemokine & Peptide. The author has an hindex of 44, co-authored 77 publications receiving 12483 citations. Previous affiliations of Alfred Walz include Harvard University & University of Michigan.

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Neutrophil-activating peptide-1/interleukin 8, a novel cytokine that activates neutrophils.

TL;DR: It has been shown that CSa, formylmethionyl peptides, PAF, and LTB4 act via unrelated receptors, suggesting that neutrophil recruitment can result from the concerted action of multiple stimuli.
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The Functional Role of the ELR Motif in CXC Chemokine-mediated Angiogenesis

TL;DR: A functional role of the ELR motif is suggested in determining the angiogenic or angiostatic potential of CXC chemokines, supporting the hypothesis that the net biological balance between angiogenicity and angiOSTatic CXCs may play an important role in regulating overall angiogenesis.
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Chemokines: multiple levels of leukocyte migration control☆ ☆

TL;DR: New insights into the role of chemokines in leukocytes attraction and relocation will be discussed, with emphasis on the distinct levels of leukocyte migration control that ultimately determine the performance of the immune defense system.
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Interleukin-8 and development of adult respiratory distress syndrome in at-risk patient groups

TL;DR: Evidence is provided of a relation between the presence of interleukin-8 in early BAL samples and the development of ARDS, which reinforces the likely importance of neutrophils and the effects of their accumulation and activation in the pathogenesis of many cases of AR DS.
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A novel neutrophil-activating factor produced by human mononuclear phagocytes.

TL;DR: The biological properties of a neutrophil-activating factor (NAF), which was recently identified as a novel peptide of approximately 6,000 mol wt, are described and the NAF receptor can be distinguished from the receptors of C5a, FMLP, platelet-activated factor, and leukotriene B4 by the lack of cross-desensitization.