Une lecture de la relation maître-apprenti à Kaboul : transmission et acquisition des savoirs liés aux arts de la calligraphie et de la peinture miniature

Tableau d'honneur de la Faculté des études supérieures et postdorales, 2015-2016Cette recherche entend mettre en lumière les modalités de transmission et d'acquisition des savoirs liés aux arts islamiques de la calligraphie et de la peinture miniature. Cette monographie se veut une immersion dans le monde de l'artiste afghan, une rencontre avec son altérité. Elle se focalise plus particulièrement sur la relation maître-apprenti qui se déroule dans les ateliers de l'Institut pour les arts et l'architecture afghans de la Turquoise Mountain, à Kaboul. La relation maître-apprenti, une relation institutionnalisée ancienne et sacrée en Asie, est le point central de cette recherche, à partir duquel s'articuleront toutes nos observations et interprétations. Savoir-être, connu sous le vocable adab, et savoir-faire s'entremêlent durant la formation de l'artiste ; une formation qui vise à former la personne dans sa totalité. La visée de cette recherche ethnographique est donc celle de saisir la nature de la relation maître-apprenti et des processus par lesquels ces savoir-faire et savoir-être se transmettent, s'approprient et s'acquièrent.This research aims to spotlight the means of knowledge transmission and acquisition related to the Islamic arts of calligraphy and miniature painting. This monograph represents an immersion in the reality of the Afghan artist, an encounter with his/her alterity. It especially focuses on the master-apprentice relationship inside the art workshops of the Turquoise Mountain’s Institute for Afghan Arts and Architecture, in Kabul. The master-apprentice relationship, an ancient and sacred relationship in the East, is the focal point of this research, from which our observations and explanations are drawn. Personal qualities and attributes of good behavior, known as adab, and practical know-how are jointly developed in the training of the apprentice; a training that educates the person in a holistic manner. The intention of this ethnographic research is then to understand the nature of the master-apprentice relationship and the nature of processes through which these different knowledges are transmitted, appropriated and acquired

The neural correlates of referential communication : taking advantage of sparse-sampling fMRI to study verbal communication with a real interaction partner

This paper introduces an innovative functional magnetic resonance imaging (fMRI) protocol to study real verbal interactions while limiting the impact of speech-related movement artefacts. This protocol is based on a sparse sampling acquisition technique and allowed participants to complete a referential communication task with a real interaction partner. During verbal interactions, speakers adjust their verbal productions depending on their interlocutors' knowledge of the referents being mentioned. These adjustments have been linked to theory of mind (ToM), the ability to infer other's mental states. We thus sought to determine if the brain regions supporting ToM would also be activated during a referential communication task in which participants have to present movie characters that vary in their likelihood of being known by their interlocutor. This pilot study establishes that the sparse sampling strategy is a viable option to study the neural correlates of referential communication while minimizing movement artefacts. In addition, the brain regions supporting ToM were recruited during the task, though specifically for the conditions where participants could adjust their verbal productions to the interlocutor's likely knowledge of the referent. This study therefore demonstrates the feasibility and relevance of a sparse-sampling approach to study verbal interactions with fMRI, including referential communication

Cardiotrophin 1 is involved in cardiac, vascular, and renal fibrosis and dysfunction

Cardiotrophin 1 (CT-1), a cytokine belonging to the interleukin 6 family, is increased in hypertension and in heart failure. We aimed to study the precise role of CT-1 on cardiac, vascular, and renal function; morphology; and remodeling in early stages without hypertension. CT-1 (20 g/kg per day) or vehicle was administrated to Wistar rats for 6 weeks. Cardiac and vascular functions were analyzed in vivo using M-mode echocardiography, Doppler, and echo tracking device and ex vivo using a scanning acoustic microscopy method. Cardiovascular and renal histomorphology were measured by immunohistochemistry, RT-PCR, and Western blot. Kidney functional properties were assessed by serum creatinine and neutrophile gelatinase-associated lipocalin and microalbuminuria/creatininuria ratio. Without alterations in blood pressure levels, CT-1 treatment increased left ventricular volumes, reduced fractional shortening and ejection fraction, and induced myocardial dilatation and myocardial fibrosis. In the carotid artery of CT-1–treated rats, the circumferential wall stress-incremental elastic modulus curve was shifted leftward, and the acoustic speed of sound in the aorta was augmented, indicating increased arterial stiffness. Vascular media thickness, collagen, and fibronectin content were increased by CT-1 treatment. CT-1–treated rats presented unaltered serum creatinine concentrations but increased urinary and serum neutrophile gelatinase-associated lipocalin and microalbuminuria/creatininuria ratio. This paralleled a glomerular and tubulointerstitial fibrosis accompanied by renal epithelial-mesenchymal transition. CT-1 is a new potent fibrotic agent in heart, vessels, and kidney able to induce cardiovascular-renal dysfunction independent from blood pressure. Thus, CT-1 could be a new target simultaneously integrating alterations of heart, vessels, and kidney in early stages of heart failure

Measurement invariance of the short version of the problematic mobile phone use questionnaire (PMPUQ-SV) across eight languages

The prevalence of mobile phone use across the world has increased greatly over the past two decades. Problematic Mobile Phone Use (PMPU) has been studied in relation to public health and comprises various behaviours, including dangerous, prohibited, and dependent use. These types of problematic mobile phone behaviours are typically assessed with the short version of the Problematic Mobile Phone Use Questionnaire (PMPUQ-SV). However, to date, no study has ever examined the degree to which the PMPU scale assesses the same construct across different languages. The aims of the present study were to (i) determine an optimal factor structure for the PMPUQ-SV among university populations using eight versions of the scale (i.e., French, German, Hungarian, English, Finnish, Italian, Polish, and Spanish); and (ii) simultaneously examine the measurement invariance (MI) of the PMPUQ-SV across all languages. The whole study sample comprised 3038 participants. Descriptive statistics, correlations, and Cronbach's alpha coefficients were extracted from the demographic and PMPUQ-SV items. Individual and multigroup confirmatory factor analyses alongside MI analyses were conducted. Results showed a similar pattern of PMPU across the translated scales. A three-factor model of the PMPUQ-SV fitted the data well and presented with good psychometric properties. Six languages were validated independently, and five were compared via measurement invariance for future cross-cultural comparisons. The present paper contributes to the assessment of problematic mobile phone use because it is the first study to provide a cross-cultural psychometric analysis of the PMPUQ-SV

Identification of natural killer markers associated with fatal outcome in COVID-19 patients

IntroductionIncreasing evidence has shown that coronavirus disease 19 (COVID-19) severity is driven by a dysregulated immunological response. Previous studies have demonstrated that natural killer (NK) cell dysfunction underpins severe illness in COVID-19 patients, but have lacked an in-depth analysis of NK cell markers as a driver of death in the most critically ill patients.MethodsWe enrolled 50 non-vaccinated hospitalized patients infected with the initial virus or the alpha variant of SARS-CoV-2 with moderate or severe illness, to evaluate phenotypic and functional features of NK cells.ResultsHere, we show that, consistent with previous studies, evolution NK cells from COVID-19 patients are more activated, with the decreased activation of natural cytotoxicity receptors and impaired cytotoxicity and IFN-γ production, in association with disease regardless of the SARS-CoV-2 strain. Fatality was observed in 6 of 17 patients with severe disease; NK cells from all of these patients displayed a peculiar phenotype of an activated memory-like phenotype associated with massive TNF-α production.DiscussionThese data suggest that fatal COVID-19 infection is driven by an uncoordinated inflammatory response in part mediated by a specific subset of activated NK cells

STAT5-and hypoxia-dependent upregulation of AXL

Internal tandem duplication in Fms-like tyrosine kinase 3 (FLT3-ITD) is the most frequent mutation observed in acute myeloid leukemia (AML) and correlates with poor prognosis. FLT3 tyrosine kinase inhibitors are promising for targeted therapy. Here, we investigated mechanisms dampening the response to the FLT3 inhibitor quizartinib, which is specific to the hematopoietic niche. Using AML primary samples and cell lines, we demonstrate that convergent signals from the hematopoietic microenvironment drive FLT3-ITD cell resistance to quizartinib through the expression and activation of the tyrosine kinase receptor AXL. Indeed, cytokines sustained phosphorylation of the transcription factor STAT5 in quizartinib-treated cells, which enhanced AXL expression by direct binding of a conserved motif in its genomic sequence. Likewise, hypoxia, another well-known hematopoietic niche hallmark, also enhanced AXL expression. Finally, in a xenograft mouse model, inhibition of AXL significantly increased the response of FLT3-ITD cells to quizartinib exclusively within a bone marrow environment. These data highlight a new bypass mechanism specific to the hematopoietic niche that hampers the response to quizartinib through combined upregulation of AXL activity. Targeting this signaling offers the prospect of a new therapy to eradicate resistant FLT3-ITD leukemic cells hidden within their specific microenvironment, thereby preventing relapses from FLT3-ITD clones