Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

To improve the adhesive properties of artificial fibrillar contact structures, the attachment systems of beetles from the family Chrysomelidae were chosen to serve as a model. Biomimetic mushroom-shaped fibrillar adhesive microstructure inspired by these systems was characterized using a variety of measurement techniques and compared with a control flat surface made of the same material. Results revealed that pull-off force and peel strength of the structured specimens are more than twice those of the flat specimens. In contrast to the control system, the structured one is found to be very tolerant to contamination and able to recover its adhesive properties after being washed in a soap solution. Based on the combination of several geometrical principles found in biological attachment devices, the presented microstructure exhibits a considerable step towards the development of an industrial dry adhesive.

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Acetylcholinesterase (AChE) rapidly hydrolyzes acetylcholine. At the neuromuscular junction, AChE is mainly anchored in the extracellular matrix by the collagen Q, whereas in the brain, AChE is tethered by the proline-rich membrane anchor (PRiMA).The AChE-deficient mice, in which AChE has been deleted from all tissues, have severe handicaps. Surprisingly, PRiMA KO mice in which AChE is mostly eliminated from the brain show very few deficits. We now report that most of the changes observed in the brain of AChE-deficient mice, and in particular the high levels of ambient extracellular acetylcholine and the massive decrease of muscarinic receptors, are also observed in the brain of PRiMA KO. However, the two groups of mutants differ in their responses to AChE inhibitors. Since PRiMA-KO mice and AChE-deficient mice have similar low AChE concentrations in the brain but differ in the AChE content of the peripheral nervous system, these results suggest that peripheral nervous system AChE is a major target of AChE inhibitors, and that its absence in AChE-deficient mice is the main cause of the slow development and vulnerability of these mice. At the level of the brain, the adaptation to the absence of AChE is nearly complete.

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