Effet de l’hydratation et du rapport E/C sur les paramètres de la rugosité de surface de pâtes cimentaires

Ce travail s'inscrit dans le cadre du projet national à Fond Unique Interministériel, nommé ERGOFORM (ERGOnomic FORMwork-Système de coffrage auto-stable diminuant la pénibilité de chantier), qui vise à mettre au point un procédé de coffrage innovant. Quatre pâtes de ciment ont été élaborées avec des rapports Eau sur Ciment (E/C) de respectivement 0,30, 0,35, 0,40 et 0,45. L'évolution des propriétés physiques et mécaniques des pâtes de ciment ont été mesurées : la porosité accessible à l'eau sous vide, les résistances à la compression et en flexion trois points. L'évolution des paramètres de rugosité en fonction du temps de cure a été analysée par microscopie interférométrique et microscopie électronique à balayage environnemental (MEB-E). Les résultats expérimentaux montrent que l'augmentation du dosage en ciment diminue la porosité accessible à l'eau et améliore les propriétés mécaniques à 24h (après décoffrage nommé T0). L'évolution de la porosité en fonction du temps de cure montre une augmentation se stabilisant après 4 jours d'immersion dans l'eau pour les pâtes cimentaires de rapports E/C de 0,40 et de 0,45 (Groupe 2). En revanche, cette augmentation se prolonge légèrement pour les pâtes de ciment 0,30 et 0,35 (Groupe 1). Par ailleurs, l'évolution des paramètres de rugosité est fonction du dosage en ciment. En effet, les analyses microscopiques et par diffraction des rayons X mettent en évidence une diminution de la quantité des pores en surface, mais aussi l'évolution des paramètres de rugosité par un changement de sa morphologie et la formation de portlandite même après 2 heures de cure normalisée. : The experimental study is part of the national project ERGOnomic FORMwork (Self-Stable Formwork System Reducing Site Difficulty) named ERGOFORM, which aims to develop an innovative formwork process for construction field. Four cement pastes were provided with different water-to-cement ratio (W/C), respectively, 0.30, 0.35, 0.40 and 0.45. The evolution of physical and mechanical properties of cement pastes was measured through water porosity under vacuum, compressive strength and flexural strength. The variation of the roughness parameters was performed by the interferometry microscope. The environmental scanning electron microscopy (E-SEM) was used to analyze the evolution of the surface morphology. The experimental results show that the increase of cement quantity decreases the water porosity and improves the mechanical properties of studied mix designs at 24 hours (after stripping, called T0). The evolution of porosity versus curing time shows that the variation stabilizes after 4 days of immersion in water for the ratio W/C 0.40 and 0.45, named G2 (Group 2). On the other hand, this variation slightly continued for cement pastes 0.30 and 0.35, named G1 (Group 1). Moreover, the evolution of roughness parameters is dependent on cement quantity in mix design. Indeed, the MEB coupling EDX and X-ray diffraction analyzes reveal a decrease in the amount of surface pores, but also the evolution of the roughness parameters by a change in its morphology and the formation of portlandite even after 2 hours of standardized cure

Diagnostic accuracy of procalcitonin in critically ill immunocompromised patients

<p>Abstract</p> <p>Background</p> <p>Recognizing infection is crucial in immunocompromised patients with organ dysfunction. Our objective was to assess the diagnostic accuracy of procalcitonin (PCT) in critically ill immunocompromised patients.</p> <p>Methods</p> <p>This prospective, observational study included patients with suspected sepsis. Patients were classified into one of three diagnostic groups: no infection, bacterial sepsis, and nonbacterial sepsis.</p> <p>Results</p> <p>We included 119 patients with a median age of 54 years (interquartile range [IQR], 42-68 years). The general severity (SAPSII) and organ dysfunction (LOD) scores on day 1 were 45 (35-62.7) and 4 (2-6), respectively, and overall hospital mortality was 32.8%. Causes of immunodepression were hematological disorders (64 patients, 53.8%), HIV infection (31 patients, 26%), and solid cancers (26 patients, 21.8%). Bacterial sepsis was diagnosed in 58 patients and nonbacterial infections in nine patients (7.6%); 52 patients (43.7%) had no infection. PCT concentrations on the first ICU day were higher in the group with bacterial sepsis (4.42 [1.60-22.14] vs. 0.26 [0.09-1.26] ng/ml in patients without bacterial infection, <it>P </it>< 0.0001). PCT concentrations on day 1 that were > 0.5 ng/ml had 100% sensitivity but only 63% specificity for diagnosing bacterial sepsis. The area under the receiver operating characteristic (ROC) curve was 0.851 (0.78-0.92). In multivariate analyses, PCT concentrations > 0.5 ng/ml on day 1 independently predicted bacterial sepsis (odds ratio, 8.6; 95% confidence interval, 2.53-29.3; <it>P </it>= 0.0006). PCT concentrations were not significantly correlated with hospital mortality.</p> <p>Conclusion</p> <p>Despite limited specificity in critically ill immunocompromised patients, PCT concentrations may help to rule out bacterial infection.</p

A refined molecular taxonomy of breast cancer

The current histoclinical breast cancer classification is simple but imprecise. Several molecular classifications of breast cancers based on expression profiling have been proposed as alternatives. However, their reliability and clinical utility have been repeatedly questioned, notably because most of them were derived from relatively small initial patient populations. We analyzed the transcriptomes of 537 breast tumors using three unsupervised classification methods. A core subset of 355 tumors was assigned to six clusters by all three methods. These six subgroups overlapped with previously defined molecular classes of breast cancer, but also showed important differences, notably the absence of an ERBB2 subgroup and the division of the large luminal ER+ group into four subgroups, two of them being highly proliferative. Of the six subgroups, four were ER+/PR+/AR+, one was ER−/PR−/AR+ and one was triple negative (AR−/ER−/PR−). ERBB2-amplified tumors were split between the ER−/PR−/AR+ subgroup and the highly proliferative ER+ LumC subgroup. Importantly, each of these six molecular subgroups showed specific copy-number alterations. Gene expression changes were correlated to specific signaling pathways. Each of these six subgroups showed very significant differences in tumor grade, metastatic sites, relapse-free survival or response to chemotherapy. All these findings were validated on large external datasets including more than 3000 tumors. Our data thus indicate that these six molecular subgroups represent well-defined clinico-biological entities of breast cancer. Their identification should facilitate the detection of novel prognostic factors or therapeutical targets in breast cancer

Combined Inactivation of pRB and Hippo Pathways Induces Dedifferentiation in the Drosophila Retina

Functional inactivation of the Retinoblastoma (pRB) pathway is an early and obligatory event in tumorigenesis. The importance of pRB is usually explained by its ability to promote cell cycle exit. Here, we demonstrate that, independently of cell cycle exit control, in cooperation with the Hippo tumor suppressor pathway, pRB functions to maintain the terminally differentiated state. We show that mutations in the Hippo signaling pathway, wts or hpo, trigger widespread dedifferentiation of rbf mutant cells in the Drosophila eye. Initially, rbf wts or rbf hpo double mutant cells are morphologically indistinguishable from their wild-type counterparts as they properly differentiate into photoreceptors, form axonal projections, and express late neuronal markers. However, the double mutant cells cannot maintain their neuronal identity, dedifferentiate, and thus become uncommitted eye specific cells. Surprisingly, this dedifferentiation is fully independent of cell cycle exit defects and occurs even when inappropriate proliferation is fully blocked by a de2f1 mutation. Thus, our results reveal the novel involvement of the pRB pathway during the maintenance of a differentiated state and suggest that terminally differentiated Rb mutant cells are intrinsically prone to dedifferentiation, can be converted to progenitor cells, and thus contribute to cancer advancement

Lysophosphatidic Acid Acyltransferase β (LPAATβ) Promotes the Tumor Growth of Human Osteosarcoma

Osteosarcoma is the most common primary malignancy of bone with poorly characterized molecular pathways important in its pathogenesis. Increasing evidence indicates that elevated lipid biosynthesis is a characteristic feature of cancer. We sought to investigate the role of lysophosphatidic acid acyltransferase β (LPAATβ, aka, AGPAT2) in regulating the proliferation and growth of human osteosarcoma cells. LPAATβ can generate phosphatidic acid, which plays a key role in lipid biosynthesis as well as in cell proliferation and survival. Although elevated expression of LPAATβ has been reported in several types of human tumors, the role of LPAATβ in osteosarcoma progression has yet to be elucidated.Endogenous expression of LPAATβ in osteosarcoma cell lines is analyzed by using semi-quantitative PCR and immunohistochemical staining. Adenovirus-mediated overexpression of LPAATβ and silencing LPAATβ expression is employed to determine the effect of LPAATβ on osteosarcoma cell proliferation and migration in vitro and osteosarcoma tumor growth in vivo. We have found that expression of LPAATβ is readily detected in 8 of the 10 analyzed human osteosarcoma lines. Exogenous expression of LPAATβ promotes osteosarcoma cell proliferation and migration, while silencing LPAATβ expression inhibits these cellular characteristics. We further demonstrate that exogenous expression of LPAATβ effectively promotes tumor growth, while knockdown of LPAATβ expression inhibits tumor growth in an orthotopic xenograft model of human osteosarcoma.Our results strongly suggest that LPAATβ expression may be associated with the aggressive phenotypes of human osteosarcoma and that LPAATβ may play an important role in regulating osteosarcoma cell proliferation and tumor growth. Thus, targeting LPAATβ may be exploited as a novel therapeutic strategy for the clinical management of osteosarcoma. This is especially attractive given the availability of selective pharmacological inhibitors