19/12/19, MM. Pannetier, Pericaud, Aubignac faisant partie de la délégation des comités de défense des intérêts des étudiants français qui sont reçus aujourd'hui par le ministre [Léon] Bérard de l'Instruction publique : [photographie de presse] / [Agence Rol]

Référence bibliographique : Rol, 57267

The long form of FLIP is an activator of caspase-8 at the Fas death-inducing signaling complex.

Death receptors, such as Fas and tumor necrosis factor-related apoptosis-inducing ligand receptors, recruit Fas-associated death domain and pro-caspase-8 homodimers, which are then autoproteolytically activated. Active caspase-8 is released into the cytoplasm, where it cleaves various proteins including pro-caspase-3, resulting in apoptosis. The cellular Fas-associated death domain-like interleukin-1-beta-converting enzyme-inhibitory protein long form (FLIP(L)), a structural homologue of caspase-8 lacking caspase activity because of several mutations in the active site, is a potent inhibitor of death receptor-induced apoptosis. FLIP(L) is proposed to block caspase-8 activity by forming a proteolytically inactive heterodimer with caspase-8. In contrast, we propose that FLIP(L)-bound caspase-8 is an active protease. Upon heterocomplex formation, a limited caspase-8 autoprocessing occurs resulting in the generation of the p43/41 and the p12 subunits. This partially processed form but also the non-cleaved FLIP(L)-caspase-8 heterocomplex are proteolytically active because they both bind synthetic substrates efficiently. Moreover, FLIP(L) expression favors receptor-interacting kinase (RIP) processing within the Fas-signaling complex. We propose that FLIP(L) inhibits caspase-8 release-dependent pro-apoptotic signals, whereas the single, membrane-restricted active site of the FLIP(L)-caspase-8 heterocomplex is proteolytically active and acts on local substrates such as RIP.

Instruction sur l'exercice de la cavalerie... Du 29 juin 1753

[Acte. 1753-06-29]

Instruction sur l'exercice de l'infanterie...

[Acte. 1753-06-29]

Instruction sur l'exercice de l'infanterie...

[Acte. 1753-06-29]

Special Investigation of Certain Grants Administered by The Department of Curriculum and Instruction, College of Education, Iowa State University of Science and Technology, For the Period September 1, 1999 through November 30, 2003

State University Audit Report - Special Investigation

Special Investigation of Certain Grants Administered by The Department of Curriculum and Instruction, College of Education, Iowa State University of Science and Technology, For the Period September 1, 1999 through November 30, 2003

State University Audit Report - Special Investigation

Temporal diffeomorphic free-form deformation: application to motion and strain estimation from 3D echocardiography

This paper presents a new registration algorithm, called Temporal Di eomorphic Free Form Deformation (TDFFD), and its application to motion and strain quanti cation from a sequence of 3D ultrasound (US) images. The originality of our approach resides in enforcing time consistency by representing the 4D velocity eld as the sum of continuous spatiotemporal B-Spline kernels. The spatiotemporal displacement eld is then recovered through forward Eulerian integration of the non-stationary velocity eld. The strain tensor iscomputed locally using the spatial derivatives of the reconstructed displacement eld. The energy functional considered in this paper weighs two terms: the image similarity and a regularization term. The image similarity metric is the sum of squared di erences between the intensities of each frame and a reference one. Any frame in the sequence can be chosen as reference. The regularization term is based on theincompressibility of myocardial tissue. TDFFD was compared to pairwise 3D FFD and 3D+t FFD, bothon displacement and velocity elds, on a set of synthetic 3D US images with di erent noise levels. TDFFDshowed increased robustness to noise compared to these two state-of-the-art algorithms. TDFFD also proved to be more resistant to a reduced temporal resolution when decimating this synthetic sequence. Finally, this synthetic dataset was used to determine optimal settings of the TDFFD algorithm. Subsequently, TDFFDwas applied to a database of cardiac 3D US images of the left ventricle acquired from 9 healthy volunteers and 13 patients treated by Cardiac Resynchronization Therapy (CRT). On healthy cases, uniform strain patterns were observed over all myocardial segments, as physiologically expected. On all CRT patients, theimprovement in synchrony of regional longitudinal strain correlated with CRT clinical outcome as quanti ed by the reduction of end-systolic left ventricular volume at follow-up (6 and 12 months), showing the potential of the proposed algorithm for the assessment of CRT.

Measuring Pavement Profile at the Slip-Form Paver, May 2005

Pavement profile or smoothness has been identified nationally as a good measure of highway user satisfaction. This has led highway engineers to measure profiles of both operating and new highways. Operational highway profiles are often measured with high-speed inertial profilers. New highway profiles are usually measured with profilographs in order to establish incentives or disincentives for pavement construction. In most cases, these two processes do not measure the same value from the “cradle to grave” life of pavements. In an attempt to correct the inconsistency between measuring techniques, lightweight profilers intended to produce values to be used for construction acceptance are being made that measure the same profile as high-speed inertial profilers. Currently, two profiler systems have been identified that can measure pavement profile during construction. This research has produced a field evaluation of the two systems. The profilers evaluated in this study are able to detect roughness in the final profile, including localized roughness and roughness at joints. Dowel basket ripple is a significant source of pavement surface roughness. The profilers evaluated in this study are able to detect dowel basket ripple with enough clarity to warn the paving crew. String-line disturbances degrade smoothness. The profilers evaluated in this study are able to detect some string-line disturbances during paving operations. The profilers evaluated in this study are not currently able to produce the same absolute International Roughness Index (IRI) values on the plastic concrete that can be measured by inertial profilers on the hardened concrete. Construction application guidelines are provided.

Contrasting the form and use of reformulation markers

This paper deals with the form and use of reformulation markers in research papers written in English, Spanish and Catalan. Considering the form and frequency of themarkers, English papers tends to prefer simple fixed markers and includes less reformulators than Spanish and Catalan. On the contrary, formal Catalan and Spanish papers include more markers, some of which are complex and allow for some structural variability. As for use, reformulation markers establish dynamic relationships between portions of discourse which can be identified in our corpus with expansion, reduction, and permutation. The analysis of the corpus shows that English authors usually reformulate to add more information to the concept (expansion), whereas Catalan and Spanish authors reduce the contents or the implicatures of the previous formulation more frequently than English.

Autosis is a Na+,K+-ATPase-regulated form of cell death triggered by autophagy-inducing peptides, starvation, and hypoxia-ischemia.

A long-standing controversy is whether autophagy is a bona fide cause of mammalian cell death. We used a cell-penetrating autophagy-inducing peptide, Tat-Beclin 1, derived from the autophagy protein Beclin 1, to investigate whether high levels of autophagy result in cell death by autophagy. Here we show that Tat-Beclin 1 induces dose-dependent death that is blocked by pharmacological or genetic inhibition of autophagy, but not of apoptosis or necroptosis. This death, termed "autosis," has unique morphological features, including increased autophagosomes/autolysosomes and nuclear convolution at early stages, and focal swelling of the perinuclear space at late stages. We also observed autotic death in cells during stress conditions, including in a subpopulation of nutrient-starved cells in vitro and in hippocampal neurons of neonatal rats subjected to cerebral hypoxia-ischemia in vivo. A chemical screen of ~5,000 known bioactive compounds revealed that cardiac glycosides, antagonists of Na(+),K(+)-ATPase, inhibit autotic cell death in vitro and in vivo. Furthermore, genetic knockdown of the Na(+),K(+)-ATPase α1 subunit blocks peptide and starvation-induced autosis in vitro. Thus, we have identified a unique form of autophagy-dependent cell death, a Food and Drug Administration-approved class of compounds that inhibit such death, and a crucial role for Na(+),K(+)-ATPase in its regulation. These findings have implications for understanding how cells die during certain stress conditions and how such cell death might be prevented.