Birgit Ledermann

TL;DR: Perforin-deficient mice have been generated by homologous recombination to determine whether the effects of CDS+ cytolytic T cells and natural killer cells are mediated by pore formation involving perform, and perforin is therefore a key effector molecule for T-cell- and natural Killer- cell-mediated cy tolysis.

TL;DR: The perforin- and Fas-based mechanisms may account for all T cell-mediated cytotoxicity in short-term in vitro assays, and no third mechanism was detected.

TL;DR: These mice resemble major features of AD pathology and suggest a central role of A beta in the pathogenesis of the disease.

TL;DR: Evidence for a role of Fas-dependent cytotoxicity as a T cell effector mechanism in vivo is lacking, and current data suggest that the main function of Fas may be in regulation of the immune response and apparently less at the level of an effector mechanisms in host defense.

TL;DR: It is demonstrated that a single molecular target, and indeed a specific residue (N265) located within the GABAA receptor β3 subunit, is a major determinant of behavioral responses evoked by the intravenous anesthetics etomidate and propofol, whereas volatile anesthetic appear to act via a broader spectrum of molecular targets.