Traduction comparée du français et de l'arabe

Cet article se propose de trouver des exemples en arabe et en français qui peuvent illustrer les procédés comparatifs de traduction élaborés par J. P. Vinay et J. Darbelnet dans leur ouvrage intitulé Stylistique comparée du français et de l'anglais, et complétés  plus tard par H. Chuquet et M. Paillard, dans leur ouvrage intitulé Approche linguistique des problèmes de traduction : anglais–français.  En fait, nous avons remarqué que ces procédés ne sont souvent abordés qu'occasionnellement dans les manuels de traduction français-arabe. Aussi, nous avons pensé qu'il serait nécessaire d'apporter notre pierre à cet édifice tout en jetant un regard critique. Nous montrerons à la fin de notre article les limites du modèle comparatif qui ne permet qu'une analyse descriptive et hors contexte, même s'il constitue un jalon important sur le chemin de la traduction et de la compréhension de deux systèmes langagiers différents.

De l'équivalence comparative à l'équivalence interprétative : critères d'équivalence dans deux versions arabes d'un roman de Kundera

Nous allons montrer dans cet article la différence entre la notion d'«équivalence» en traduction, telle qu'elle a été élaborée dans une perspective comparative, ainsi que dans une perspective interprétative. Nous allons ensuite nous appuyer sur les critères d'équivalence mis par le traductologue allemand Werner Koller  pour analyser  deux versions en arabe  du roman intitulé  «L'insoutenable légèreté de l'être» écrit par le romancier français (d'origine tchèque) Milan Kundera, à savoir la version de Afif Demashqia intitulée خفة الكائن التي لا تُحتمل»», et celle de Marie Toq intitulée « كائن لا تُحتمل خفته ». سنتناول بداية في هذا البحث مفهوم «التكافؤ» من منظوري الترجمة المقارِنة والترجمة التأويلية، وسنستند بعد ذلك إلى معايير التكافؤ  التي وضعها الألماني فيرنر كولر،  لنرصد آليات تطبيقها في  ترجمتين لرواية عنوانها  «L'insoutenable légèreté de l'être»  لـلروائي الفرنسي (من أصول تشيكية) «ميلان كونديرا»،  الترجمة الأولى لعفيف دمشقية موسومة بعنوان "خفة الكائن التي لا تُحتمل" والترجمة الثانية لماري طوق موسومة بعنوان "كائنٌ لا تُحتمل خفته"

Joint analysis of left ventricular expression and circulating plasma levels of Omentin after myocardial ischemia

BACKGROUND: Omentin-1, also known as Intelectin-1 (ITLN1), is an adipokine with plasma levels associated with diabetes, obesity, and coronary artery disease. Recent studies suggest that ITLN1 can mitigate myocardial ischemic injury but the expression of ITLN1 in the heart itself has not been well characterized. The purpose of this study is to discern the relationship between the expression pattern of ITLN1 RNA in the human heart and the level of circulating ITLN1 protein in plasma from the same patients following myocardial ischemia. METHODS: A large cohort of patients (n = 140) undergoing elective cardiac surgery for aortic valve replacement were enrolled in this study. Plasma and left ventricular biopsy samples were taken at the beginning of cardiopulmonary bypass and after an average of 82 min of ischemic cross clamp time. The localization of ITLN1 in epicardial adipose tissue (EAT) was also further characterized with immunoassays and cell fate transition studies. RESULTS: mRNA expression of ITLN1 decreases in left ventricular tissue after acute ischemia in human patients (mean difference 280.48, p = 0.001) whereas plasma protein levels of ITLN1 increase (mean difference 5.24, p \u3c 0.001). Immunohistochemistry localized ITLN1 to the mesothelium or visceral pericardium of EAT. Epithelial to mesenchymal transition in mesothelial cells leads to a downregulation of ITLN1 expression. CONCLUSIONS: Myocardial injury leads to a decrease in ITLN1 expression in the heart and a corresponding increase in plasma levels. These changes may in part be due to an epithelial to mesenchymal transition of the cells that express ITLN1 following ischemia. Trial Registration Clinicaltrials.gov ID: NCT00985049

The Long Noncoding RNA Landscape of the Ischemic Human Left Ventricle

Background—The discovery of functional classes of long noncoding RNAs (lncRNAs) has expanded our understanding of the variety of RNA species that exist in cells. In the heart, lncRNAs have been implicated in the regulation of development, ischemic and dilated cardiomyopathy, and myocardial infarction. Nevertheless, there is a limited description of expression profiles for these transcripts in human subjects. Methods and Results—We obtained left ventricular tissue from human patients undergoing cardiac surgery and used RNA sequencing to describe a lncRNA profile. We then identified a list of lncRNAs that were differentially expressed between pairs of samples before and after the ischemic insult of cardiopulmonary bypass. The expression of some of these lncRNAs correlates with ischemic time. Coding genes in close proximity to differentially expressed lncRNAs as well as coding genes that have coordinated expression with these lncRNAs are enriched in functional categories related to myocardial infarction including: heart function, metabolism, the stress response, and the immune system. Conclusions—We describe a list of lncRNAs that are differentially expressed after ischemia in the human heart. These genes are predicted to function in pathways consistent with myocardial injury. As a result, lncRNAs may serve as novel diagnostic and therapeutic targets for ischemic heart disease

G1 arrest and differentiation can occur independently of Rb family function

Repression of E2F target genes is required for cell cycle arrest in Rb family (Rb, p107, and p130)-deficient cells

Notch signaling inhibits hepatocellular carcinoma following inactivation of the RB pathway

Mice lacking all three Rb genes in the liver develop tumors resembling specific subgroups of human hepatocellular carcinomas, and Notch activity appears to suppress the growth and progression of these tumors

Functional Interactions between Retinoblastoma and c-MYC in a Mouse Model of Hepatocellular Carcinoma

Inactivation of the RB tumor suppressor and activation of the MYC family of oncogenes are frequent events in a large spectrum of human cancers. Loss of RB function and MYC activation are thought to control both overlapping and distinct cellular processes during cell cycle progression. However, how these two major cancer genes functionally interact during tumorigenesis is still unclear. Here, we sought to test whether loss of RB function would affect cancer development in a mouse model of c-MYC-induced hepatocellular carcinoma (HCC), a deadly cancer type in which RB is frequently inactivated and c-MYC often activated. We found that RB inactivation has minimal effects on the cell cycle, cell death, and differentiation features of liver tumors driven by increased levels of c-MYC. However, combined loss of RB and activation of c-MYC led to an increase in polyploidy in mature hepatocytes before the development of tumors. There was a trend for decreased survival in double mutant animals compared to mice developing c-MYC-induced tumors. Thus, loss of RB function does not provide a proliferative advantage to c-MYC-expressing HCC cells but the RB and c-MYC pathways may cooperate to control the polyploidy of mature hepatocytes