Le retour d'expérience

Dans l'avant propos de l'Archipel du danger, G.Y. Kervern et P. Rubise écrivent que "depuis le tremblement de terre de Lisbonne en 1755 et la polémique qui s'ensuit entre Voltaire et Rousseau sur la place de l'homme et de Dieu dans les catastrophes, l'homme s'est déclaré "Responsable du danger" passant donc d'un fatalisme résigné à un volontarisme moderne ouvrant la voie à la maîtrise du danger". Malgré des efforts croissants pour maîtriser le danger dont témoigne le développement de ces différentes sciences du danger -les cindyniques- dont nous avons eu des exemples variés pendant ces 3 jours, "l'être humain, conscient de ses limites, a rangé au placard le romantisme du zéro-risque et reconnaît même sportivement le besoin d'un certain danger pour se sentir exister". C'est au coeur de ce débat, entre la volonté de l'homme de maîtriser le danger et les limites de l'être humain , limites individuelles et collectives à le contrôler, qu'apparaît en toute évidence l'intérêt du "retour d'expérience" qu'on pourrait définir ainsi

Reverse Shock Emission Revealed in Early Photometry in the Candidate Short GRB 180418A

We present observations of the possible short GRB 180418A in $\gamma$-rays, X-rays, and in the optical. Early optical photometry with the TAROT and RATIR instruments show a bright peak ($\approx$ 14.2 AB mag) between $T+28$ and $T+90$ seconds that we interpret as the signature of a reversal shock. Later observations can be modeled by a standard forward shock model and show no evidence of jet break, allowing us to constrain the jet collimation to $\theta_j> 7^\circ$. Using deep late-time optical observations we place an upper limit of $r>24$ AB mag on any underlying host galaxy. The detection of the afterglow in the \textit{Swift} UV filters constrains the GRB redshift to $z<1.3$ and places an upper bound on the $\gamma$-ray isotropic equivalent energy $E_{\rm{\gamma,iso}} < 3 \times 10^{51}$ erg. The properties of this GRB (e.g. duration, hardness ratio, energetic, and environment) lie at the intersection between short and long bursts, and we can not conclusively identify its type. We estimate that the probability that it is drawn from the population of short GRBs is 10\%-30\%.Comment: Accepted por publication in Ap

Gestion des temps et régulations sociales : quelles incidences de la loi Aubry II sur l'organisation des entreprises et les conditions de travail des salariés ?

International audienc

A new application of smart walker for quantitative analysis of human walking

International audienceThis paper presents a new nonintrusive device for everyday gait analysis and health monitoring. The system is a standard rollator equipped with encoders and inertial sensors. The assisted walking of 25 healthy elderly and 23 young adults are compared to develop walking quality index. The subjects were asked to walk on a straight trajectory and an L-shaped trajectory respectively. The walking trajectory, which is missing in other gait analysis methods, is calculated based on the encoder data. The obtained trajectory and steps are compared with the results of a motion capture system. The gait analysis results show that new index obtained by using the walker measurements, and not available otherwise, are very discriminating, e.g., the elderly have larger lateral motion and maneuver area, smaller angular velocity during turning, their walking accuracy is lower and turning ability is weaker although they have almost the same walking velocity as the young people

NF-kappa B genes have a major role in Inflammatory Breast Cancer

<p>Abstract</p> <p>Background</p> <p>IBC (Inflammatory Breast cancer) is a rare form of breast cancer with a particular phenotype. New molecular targets are needed to improve the treatment of this rapidly fatal disease. Given the role of NF-κB-related genes in cell proliferation, invasiveness, angiogenesis and inflammation, we postulated that they might be deregulated in IBC.</p> <p>Methods</p> <p>We measured the mRNA expression levels of 60 NF-κB-related genes by using real-time quantitative RT-PCR in a well-defined series of 35 IBCs, by comparison with 22 stage IIB and III non inflammatory breast cancers. Twenty-four distant metastases of breast cancer served as "poor prognosis" breast tumor controls.</p> <p>Results</p> <p>Thirty-five (58%) of the 60 NF-κB-related genes were significantly upregulated in IBC compared with non IBC. The upregulated genes were NF-κB genes (<it>NFKB1</it>, <it>RELA</it>, <it>IKBKG</it>, <it>NFKBIB</it>, <it>NFKB2</it>, <it>REL</it>, <it>CHUK</it>), apoptosis genes (<it>MCL1L</it>, <it>TNFAIP3/A20</it>, <it>GADD45B</it>, <it>FASLG</it>, <it>MCL1S</it>, <it>IER3L</it>, <it>TNFRSF10B/TRAILR2</it>), immune response genes (<it>CD40</it>, <it>CD48</it>, <it>TNFSF11/RANKL</it>, <it>TNFRSF11A/RANK</it>, <it>CCL2/MCP-1</it>, <it>CD40LG</it>, <it>IL15</it>, <it>GBP1</it>), proliferation genes (<it>CCND2</it>, <it>CCND3</it>, <it>CSF1R</it>, <it>CSF1</it>, <it>SOD2</it>), tumor-promoting genes (<it>CXCL12</it>, <it>SELE</it>, <it>TNC</it>, <it>VCAM1</it>, <it>ICAM1</it>, <it>PLAU/UPA</it>) or angiogenesis genes (<it>PTGS2/COX2</it>, <it>CXCL1/GRO1</it>). Only two of these 35 genes (<it>PTGS2/COX2 </it>and <it>CXCL1/GRO1</it>)were also upregulated in breast cancer metastases. We identified a five-gene molecular signature that matched patient outcomes, consisting of <it>IL8 </it>and <it>VEGF </it>plus three NF-κB-unrelated genes that we had previously identified as prognostic markers in the same series of IBC.</p> <p>Conclusion</p> <p>The NF-κB pathway appears to play a major role in IBC, possibly contributing to the unusual phenotype and aggressiveness of this form of breast cancer. Some upregulated NF-κB-related genes might serve as novel therapeutic targets in IBC.</p

Exquisite Sensitivity of TP53 Mutant and Basal Breast Cancers to a Dose-Dense Epirubicin−Cyclophosphamide Regimen

BACKGROUND: In breast cancers, only a minority of patients fully benefit from the different chemotherapy regimens currently in use. Identification of markers that could predict the response to a particular regimen would thus be critically important for patient care. In cell lines or animal models, tumor protein p53 (TP53) plays a critical role in modulating the response to genotoxic drugs. TP53 is activated in response to DNA damage and triggers either apoptosis or cell-cycle arrest, which have opposite effects on cell fate. Yet, studies linking TP53 status and chemotherapy response have so far failed to unambiguously establish this paradigm in patients. Breast cancers with a TP53 mutation were repeatedly shown to have a poor outcome, but whether this reflects poor response to treatment or greater intrinsic aggressiveness of the tumor is unknown. METHODS AND FINDINGS: In this study we analyzed 80 noninflammatory breast cancers treated by frontline (neoadjuvant) chemotherapy. Tumor diagnoses were performed on pretreatment biopsies, and the patients then received six cycles of a dose-dense regimen of 75 mg/m(2) epirubicin and 1,200 mg/m(2) cyclophosphamide, given every 14 days. After completion of chemotherapy, all patients underwent mastectomies, thus allowing for a reliable assessment of chemotherapy response. The pretreatment biopsy samples were used to determine the TP53 status through a highly efficient yeast functional assay and to perform RNA profiling. All 15 complete responses occurred among the 28 TP53-mutant tumors. Furthermore, among the TP53-mutant tumors, nine out of ten of the highly aggressive basal subtypes (defined by basal cytokeratin [KRT] immunohistochemical staining) experienced complete pathological responses, and only TP53 status and basal subtype were independent predictors of a complete response. Expression analysis identified many mutant TP53-associated genes, including CDC20, TTK, CDKN2A, and the stem cell gene PROM1, but failed to identify a transcriptional profile associated with complete responses among TP53 mutant tumors. In patients with unresponsive tumors, mutant TP53 status predicted significantly shorter overall survival. The 15 patients with responsive TP53-mutant tumors, however, had a favorable outcome, suggesting that this chemotherapy regimen can overcome the poor prognosis generally associated with mutant TP53 status. CONCLUSIONS: This study demonstrates that, in noninflammatory breast cancers, TP53 status is a key predictive factor for response to this dose-dense epirubicin–cyclophosphamide regimen and further suggests that the basal subtype is exquisitely sensitive to this association. Given the well-established predictive value of complete responses for long-term survival and the poor prognosis of basal and TP53-mutant tumors treated with other regimens, this chemotherapy could be particularly suited for breast cancer patients with a mutant TP53, particularly those with basal features