Les difficultés pratiques des communautés de pratique.

Nous analysons les difficultés liées à une tentative de "mise en œuvre" de communautés de pratique au sein d'une organisation hiérarchique. Nous nous intéressons plus particulièrement aux enjeux de pouvoir susceptibles de remettre en cause les communautés de pratique comme espaces d'apprentissage interstitiel. La recherche repose sur l'étude de quatre communautés de pratique au sein d'une même entreprise. L'étude est réalisée au moyen d'entretiens semi- directifs. Les résultats montrent les difficultés rencontrées, en particulier en raison du système de management de l'entreprise et de l'enjeu de pouvoir que représentent les communautés de pratique. Sur les quatre cas étudiés, un seul parvient à conserver la caractéristique fondamentale de l'auto-organisation. Dans deux autres cas, le fonctionnement devient hiérarchique et la communauté de pratique se transforme en groupe de travail. Le quatrième cas évolue vers une situation intermédiaire. De manière plus large, c'est la capacité d'une organisation hiérarchique à stimuler sans l'étouffer une forme originellement clandestine qui peut être mise en cause.Communauté de pratique; apprentissage; gestion de la connaissance; pouvoir;

Results of open reduction internal fixation versus percutaneous iliosacral screw fixation for unstable pelvic ring injuries: retrospective study of 36 patients.

Surgical stabilization of posterior pelvic ring fractures can be achieved by closed reduction and percutaneous fixation (CRPF) or by open reduction and internal fixation (ORIF). The aim of the present study is to compare the clinical results of both methods. Medical records of 36 patients consecutively operated for unstable pelvic ring injuries were retrospectively reviewed. We compared 22 patients treated with CRPF versus 14 patients stabilized by using ORIF between 2007 and 2017. The Majeed and Pohlemann scores were used to evaluate postoperative functional outcomes. Complications like blood loss, infection rate, Neurological injury, the operative time and the length of hospital stay were analyzed. The median Majeed pelvic score was 87 points for the CRPF technique compared with 69 points for the ORIF technique. The median Pohlemann score, operative time and length of hospitalization were similar between the two groups. The median blood loss for the CRPF technique was 300 ml compared to 500 ml for the ORIF technique. CRPF and ORIF procedure had each one neurological lesion. There was one case of infection in the ORIF group and none in the CRPF group. No measurements except for the blood loss have reached the significance threshold. The CRPF technique shows a clear decrease in blood loss. There was no statistically significant difference in the functional results, infection rate, neurological injury, operative time and hospital stay between both techniques

Human sarcopenia reveals an increase in SOCS-3 and myostatin and a reduced efficiency of Akt phosphorylation

Age-related skeletal muscle sarcopenia is linked with increases in falls, fractures, and death and therefore has important socioeconomic consequences. The molecular mechanisms controlling age-related muscle loss in humans are not well understood, but are likely to involve multiple signaling pathways. This study investigated the regulation of several genes and proteins involved in the activation of key signaling pathways promoting muscle hypertrophy, including GH/STAT5, IGF-1/Akt/GSK-3&beta;/4E-BP1, and muscle atrophy, including TNF&alpha;/SOCS-3 and Akt/FKHR/atrogene, in muscle biopsies from 13 young (20 &plusmn; 0.2 years) and 16 older (70 &plusmn; 0.3 years) males. In the older males compared to the young subjects, muscle fiber cross-sectional area was reduced by 40&ndash;45% in the type II muscle fibers. TNF&alpha; and SOCS-3 were increased by 2.8 and 1.5 fold, respectively. Growth hormone receptor protein (GHR) and IGF-1 mRNA were decreased by 45%. Total Akt, but not phosphorylated Akt, was increased by 2.5 fold, which corresponded to a 30% reduction in the efficiency of Akt phosphorylation in the older subjects. Phosphorylated and total GSK-3&beta; were increased by 1.5 and 1.8 fold, respectively, while 4E-BP1 levels were not changed. Nuclear FKHR and FKHRL1 were decreased by 73 and 50%, respectively, with no changes in their atrophy target genes, atrogin-1 and MuRF1. Myostatin mRNA and protein levels were significantly elevated by 2 and 1.4 fold. Human sarcopenia may be linked to a reduction in the activity or sensitivity of anabolic signaling proteins such as GHR, IGF-1, and Akt. TNF&alpha;, SOCS-3, and myostatin are potential candidates influencing this anabolic perturbation.<br /

CO Disrupts the Reduced H-Cluster of FeFe Hydrogenase. A Combined DFT and Protein Film Voltammetry Study

n/

MAPping out distribution routes for kinesin couriers

In the crowded environment of eukaryotic cells, diffusion is an inefficient distribution mechanism for cellular components. Long-distance active transport is required and is performed by molecular motors including kinesins. Furthermore, in highly polarized, compartmentalized and plastic cells such as neurons, regulatory mechanisms are required to ensure appropriate spatio-temporal delivery of neuronal components. The kinesin machinery has diversified into a large number of kinesin motor proteins as well as adaptor proteins that are associated with subsets of cargo. However, many mechanisms contribute to the correct delivery of these cargos to their target domains. One mechanism is through motor recognition of subdomain-specific microtubule (MT) tracks, sign-posted by different tubulin isoforms, tubulin post-translational modifications (PTMs), tubulin GTPase activity and MT associated proteins (MAPs). With neurons as a model system, a critical review of these regulatory mechanisms is presented here, with particular focus on the emerging contribution of compartmentalised MAPs. Overall, we conclude that – especially for axonal cargo – alterations to the MT track can influence transport, although in vivo, it is likely that multiple track-based effects act synergistically to ensure accurate cargo distribution

Role of cytoskeletal abnormalities in the neuropathology and pathophysiology of type I lissencephaly

Type I lissencephaly or agyria-pachygyria is a rare developmental disorder which results from a defect of neuronal migration. It is characterized by the absence of gyri and a thickening of the cerebral cortex and can be associated with other brain and visceral anomalies. Since the discovery of the first genetic cause (deletion of chromosome 17p13.3), six additional genes have been found to be responsible for agyria–pachygyria. In this review, we summarize the current knowledge concerning these genetic disorders including clinical, neuropathological and molecular results. Genetic alterations of LIS1, DCX, ARX, TUBA1A, VLDLR, RELN and more recently WDR62 genes cause migrational abnormalities along with more complex and subtle anomalies affecting cell proliferation and differentiation, i.e., neurite outgrowth, axonal pathfinding, axonal transport, connectivity and even myelination. The number and heterogeneity of clinical, neuropathological and radiological defects suggest that type I lissencephaly now includes several forms of cerebral malformations. In vitro experiments and mutant animal studies, along with neuropathological abnormalities in humans are of invaluable interest for the understanding of pathophysiological mechanisms, highlighting the central role of cytoskeletal dynamics required for a proper achievement of cell proliferation, neuronal migration and differentiation