Annual Update in Intensive Care and Emergency Medicine 2011 by M. A. D. van Zoelen, A. Achouiti, T. van der Poll (auth.),

By M. A. D. van Zoelen, A. Achouiti, T. van der Poll (auth.), Prof. Jean-Louis Vincent (eds.)

The Annual replace compiles the latest advancements in experimental and medical examine and perform in a single accomplished reference booklet. The chapters are written via good well-known specialists within the box of in depth care and emergency drugs. it really is addressed to every person fascinated with inner medication, anesthesia, surgical procedure, pediatrics, in depth care and emergency medicine.

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Liu Y, Chen GY, Zheng P (2009) CD24-Siglec G/10 discriminates danger- from pathogenassociated molecular patterns. Trends Immunol 30: 557 – 561 6. Liu R, Mori S, Wake H, et al (2009) Establishment of in vitro binding assay of high mobility group box-1 and S100A12 to receptor for advanced glycation endproducts: heparin’s effect on binding. Acta Med Okayama 63: 203 – 211 7. Bierhaus A, Stern DM, Nawroth PP (2006) RAGE in inflammation: a new therapeutic Target? Curr Opin Investig Drugs 7: 985 – 991 8.

Van der Poll I in the regulation of cell migration in several ways. First of all, RAGE is a counterreceptor for integrins on leukocytes; in particular, RAGE has been identified as a binding partner for the β2 integrins, Mac-1 and p150, 95 [8]. Second, by the interaction of RAGE with β2 integrin-mediated leukocyte recruitment in vivo: RAGE-/mice displayed a diminished number of adherent inflammatory cells on the peritoneum after CLP [9] and a reduction in neutrophil influx in the peritoneal cavity after thioglycollate peritonitis [8].

These paradoxical effects do not seem to be mediated by cannabinoid receptors. Rimonabant reduced indomethacin-induced intestinal ulcers to a similar extent in wild-type, and in CB1R knock-out mice [42]. These effects appear to be mediated by down-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 [43]. It is important to highlight that the effect of rimonabant seems to be specific to that compound, and is not shared by other CB1R antagonists, such as AM215 [44]. Of note, rimonabant, which was being marketed for weight loss but being tested for improving cardiovascular outcomes, induced a level of serious neuropsychiatric effects that was deemed unacceptable by regulatory authorities, and both the drug and the trial were abruptly terminated [45].

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