Relations intersubjectives et marqueurs culturels dans les publicités anglaises et françaises

« Relations intersubjectives et marqueurs culturels dans les publicités anglaises et françaises » — Cette étude est basée sur un corpus comprenant d'une part des publicités nord-américaines de langue anglaise et leur traduction en français, d'autre part des publicités publiées en France. Elle se propose de montrer que les relations inter-énonciateurs sont aussi marquées dans les publicités françaises que dans les publicités anglaises. Elle se penchera également sur les rapports que l'émetteur établit avec le destinataire et la façon dont il lui présente son produit, ainsi que sur les différences culturelles que présentent un certain nombre de traductions."Intersubjective Relationships and Cultural Markers in English and French Advertisements" — This paper is based on a corpus consisting, on one hand, of English North American advertisements and their translations in French, and, on the other, of advertisements published in France. Its aim is to show that intersubjective relationships are as present in French advertisements as in English ones. This paper will also look into the relationship that the sender establishes with the receptor and the way in which he presents his product to him, as well as cultural differences presented by a certain number of translations

La question dans les « textes bilingues » : analyse contrastive

La question dans les « textes bilingues » : analyse contrastive – Cette analyse a pour but de montrer dans quels domaines particuliers l'usage de la question diffère en anglais et en français. Elle se propose d'attirer l'attention des traducteurs sur les parties du discours que les francophones abordent spontanément par une forme interrogative et les anglophones par une déclarative, afin que les textes bilingues puissent comporter une proportion de questions plus conforme à celle que l'on a relevée dans les textes bilingues.Using the Question in English and French: a Contrastive Analysis – This article shows the areas in which English and French depart in their usage of interrogation. It brings to the translator's attention the discursive contexts where francophones tend to use an interrogative and anglophones a declarative sentence. This will help maintain in translations a proportion of these forms more consistent with the patterns observed in original French or English texts

Notch2 Signaling Sensitizes Endothelial Cells to Apoptosis by Negatively Regulating the Key Protective Molecule Survivin

BACKGROUND: Notch signaling pathway controls key functions in vascular and endothelial cells (ECs) where Notch4 plays a major role. However, little is known about the contribution of other Notch receptors. This study investigated regulation of Notch2 and further examined its implication in EC dysfunction. METHODOLOGY/PRINCIPAL FINDINGS: Here, we provide evidence for a novel link between Notch and TNF signaling, where Notch2 is upregulated and activated in response to TNF. Forced expression of Notch2 intracellular domain in cultured ECs promotes apoptosis and allows the significant downregulation of several cell-death-related transcripts in a dose-dependent manner. In particular, activation of Notch2 led to a rapid decrease in survivin mRNA and protein expression, while survivin upregulation was obtained by the selective knockdown of Notch2 in ECs, indicating that survivin expression is controlled at the Notch level. Moreover, Notch2 silencing and ectopic expression of survivin, but not XIAP or Bcl2, rescued ECs from TNF and Notch2-mediated apoptosis, respectively. CONCLUSIONS/SIGNIFICANCE: In conclusion, TNF signaling activates Notch2 that sensitizes ECs to apoptosis via modulation of the key apoptosis regulator survivin. Overall, our findings also indicate that specific Notch receptors control distinct functions in vascular cells and inflammatory cytokines contribute to this specificity

Matrix Metalloproteinase-13 Predominates Over Matrix Metalloproteinase-8 as the Functional Interstitial Collagenase in Mouse Atheromata

Objective—Substantial evidence implicates interstitial collagenases of the matrix metalloproteinase (MMP) family in plaque rupture and fatal thrombosis. Understanding the compensatory mechanisms that may influence the expression of these enzymes and their functions, therefore, has important clinical implications. This study assessed in mice the relative effect of the 2 principal mouse collagenases on collagen content and other plaque characteristics. Approach and Results—Apolipoprotein E–deficient (apoE−/−) mice, MMP-13−/− apoE−/−, MMP-8−/− apoE−/− double knockout mice, and MMP-13−/− MMP-8−/− apoE−/− triple knockout mice consumed a high-cholesterol diet for 10 and 24 weeks. Both double knockout and triple knockout mice showed comparable atherosclerotic lesion formation compared with apoE−/− controls. Analysis of aortic root sections indicated that lesions of MMP-8/MMP-13–deficient and MMP-13–deficient mice accumulate more fibrillar collagen than apoE−/− controls and MMP-8−/− apoE−/− double knockout. We further tested the relative effect of MMPs on plaque collagenolysis using in situ zymography. MMP-13 deletion alone abrogated collagenolytic activity in lesions, indicating a predominant role for MMP-13 in this process. MMP-13 and MMP-13/MMP-8 deficiency did not alter macrophage content but associated with reduced accumulation of smooth muscle cells. Conclusions—These results show that among MMP interstitial collagenases in mice, MMP-13 prevails over MMP-8 in collagen degradation in atheromata. These findings provide a rationale for the identification and selective targeting a predominant collagenase for modulating key aspects of plaque structure considered critical in clinical complications, although they do not translate directly to human lesions, which also contain MMP-1

Recommandations préanalytiques pour les analyses de protéomique clinique des fluides biologiques

International audienc

ESR, raman and conductivity studies on fractionated poly(2-methoxyaniline-5-sulfonic acid)

Synthesis methods used to produce poly(2-methoxyaniline-5-sulfonic acid) (PMAS), a water soluble, self-doped conducting polymer, have been shown to form two distinctly different polymer fractions with molecular weights of approximately 2 kDa and 8 -10 kDa. The low molecular weight (LMWT) PMAS fraction is redox inactive and non-conducting while the high molecular weight (HMWT) PMAS is electro-active with electrical conductivities of 0.94 0.05 S cm-1. Previous investigations have illustrated the different photochemical and electrochemical properties of these fractions, but have not correlated these properties with the structural and electronic interactions that drive them. Incomplete purification of the PMAS mixture, typically via bag dialysis, has been shown to result in a mixture of approximately 50:50 HMWT:LMWT PMAS with electrical conductivity significantly lower at approximately 0.10 to 0.26 S cm-1. The difference between the electrical conductivities of these fractions has been investigated by the controlled addition of the non-conducting LMWT PMAS fraction into the HMWT PMAS composite film with the subsequent electronic properties investigated by solid-state ESR and Raman spectroscopies. These studies illustrate strong electronic intereactions of the insulating LMWT PMAS with the emeraldine salt HMWT PMAS to substantially alter the population of the electronic charge carriers in the conducting polymer. ESR studies on these mixtures, when compared to HMWT PMAS, exhibited a lower level of electron spin in the presence of LMWT PMAS indicative of the the formation of low spin bipolarons without a change the oxidation state of the conducting HMWT fraction

ΔNp63α silences a microRNA program to aberrantly initiate a wound healing program that promotes TGFβ-induced metastasis.

Primary cancer cell dissemination is a key event during the metastatic cascade, but context-specific determinants of this process remain largely undefined. Multiple reports have suggested that the p53 (TP53) family member p63 (TP63) plays an anti-metastatic role through its minor epithelial isoform containing the N-terminal transactivation domain (TAp63). However, the role and contribution of the major p63 isoform lacking this domain, ΔNp63α, remain largely undefined. Here, we report a distinct and TAp63-independent mechanism by which ΔNp63α-expressing cells within a TGFβ-rich microenvironment become positively selected for metastatic dissemination. Orthotopic transplantation of ΔNp63α-expressing human osteosarcoma cells into athymic mice resulted in larger and more frequent lung metastases than transplantation of control cells. Mechanistic investigations revealed that ΔNp63α repressed miR-527 and miR-665, leading to the upregulation of two TGFβ effectors, SMAD4 and TβRII (TGFBR2). Furthermore, we provide evidence that this mechanism reflects a fundamental role for ΔNp63α in the normal wound healing response. We show that ΔNp63α-mediated repression of miR-527/665 controls a TGFβ-dependent signaling node that switches off anti-migratory miR-198 by suppressing the expression of the regulatory factor, KSRP (KHSRP). Collectively, these findings reveal that a novel microRNA network involved in the regulation of physiological wound healing responses is hijacked and suppressed by tumor cells to promote metastatic dissemination

Thin-Capped Atheromata With Reduced Collagen Content in Pigs Develop in Coronary Arterial Regions Exposed to Persistently Low Endothelial Shear Stress

Objective—The mechanisms promoting the focal formation of rupture-prone coronary plaques in vivo remain incompletely understood. This study tested the hypothesis that coronary regions exposed to low endothelial shear stress (ESS) favor subsequent development of collagen-poor, thin-capped plaques. Approach and Results—Coronary angiography and 3-vessel intravascular ultrasound were serially performed at 5 consecutive time points in vivo in 5 diabetic, hypercholesterolemic pigs. ESS was calculated along the course of each artery with computational fluid dynamics at all 5 time points. At follow-up, 184 arterial segments with previously identified in vivo ESS underwent histopathologic analysis. Compared with other plaque types, eccentric thin-capped atheromata developed more in segments that experienced lower ESS during their evolution. Compared with lesions with higher preceding ESS, segments persistently exposed to low ESS (<1.2 Pa) exhibited reduced intimal smooth muscle cell content; marked intimal smooth muscle cell phenotypic modulation; attenuated procollagen-I gene expression; increased gene and protein expression of the interstitial collagenases matrix-metalloproteinase-1, -8, -13, and -14; increased collagenolytic activity; reduced collagen content; and marked thinning of the fibrous cap. Conclusions—Eccentric thin-capped atheromata, lesions particularly prone to rupture, form more frequently in coronary regions exposed to low ESS throughout their evolution. By promoting an imbalance of attenuated synthesis and augmented collagen breakdown, low ESS favors the focal evolution of early lesions toward plaques with reduced collagen content and thin fibrous caps—2 critical determinants of coronary plaque vulnerability.Novartis (Firm)Boston Scientific CorporationBehrakis Foundation (Research Fellowship)Hellenic Heart FoundationHellenic Atherosclerosis SocietyNational Institutes of Health (U.S.) (Grant RO1 GM49039