Approche globale de l'adolescent en consultation de médecine générale (difficultés, représentation)

INTRODUCTION: La médecine de l'adolescent est une discipline médico-psycho-social en différente de la pédiatrie et de la médecine adulte. L'objectif principal de notre étude est d'appréhender les différentes représentations, difficultés et mécanismes d'adaptation du médecin généraliste face à l'adolescent en consultation. METHODES: En basant notre étude sur la théorisation ancrée, nous avons réalisé des entretiens individuels de 10 médecins généralistes. Les entretiens ont été retranscrits manuellement, puis analysés selon 3 étapes (la codification des éléments, leur catégorisation la modélisation du phénomène) avant la phase de théorisation. RESULTATS: L'analyse de ces entretiens montre que l'accueil de l'adolescent est un schéma complexe, mêlant la contextualisation de la consultation, le raisonnement clinique, la qualité du rapport entre le médecin et l'adolescent et le choix des actions à mettre en œuvre. Dans ce cadre, le médecin cherche consciemment ou inconsciemment la meilleure conduite à tenir face à l'adolescent, que ce soit par la prise en charrge de la demande, par l'évaluation de la santé physique de l'adolescent, par la gestion du parent, ou par l'établissement d'un lien avec l'adolescent. CONCLUSION: Ce travail a permis de décrire la complexité de l'accueil de l'adolescent en médecine générale, ainsi que les facteurs influençant son déroulement. Comme dans les autres enquêtes réalisées sur ce sujet, il montre que les difficultés ressenties par les médecins généralistes face à l'adolescent sont situées à différents niveaux de la consultation, ce qui nous a permis de proposer des solutions afin de faciliter l'accueil de ce dernierAIX-MARSEILLE2-BU Méd/Odontol. (130552103) / SudocSudocFranceF

Hsp70, l’ange gardien de GATA-1 lors de la différenciation des globules rouges

National audienc

No impact of cancer and plague-relevant FPR1 polymorphisms on COVID-19

International audienceFormyl peptide receptor 1 (FPR1) is a pattern-recognition receptor that detects bacterial as well as endogenous danger-associated molecular patterns to trigger innate immune responses by myeloid cells. A single nucleotide polymorphism, rs867228 (allelic frequency 19-20%), in the gene coding for FPR1 accelerates the manifestation of multiple carcinomas, likely due to reduced anticancer immunosurveillance secondary to a defect in antigen presentation by dendritic cells. Another polymorphism in FPR1, rs5030880 (allelic frequency 12-13%), has been involved in the resistance to plague, correlating with the fact that FPR1 is the receptor for Yersinia pestis. Driven by the reported preclinical effects of FPR1 on lung inflammation and fibrosis, we investigated whether rs867228 or rs5030880 would affect the severity of coronavirus disease-19 (COVID-19). Data obtained on patients from two different hospitals in Paris refute the hypothesis that rs867228 or rs5030880 would affect the severity of COVID-19

Multilayer intraclonal heterogeneity in chronic myelomonocytic leukemia

International audienceThe functional diversity of cells that compose myeloid malignancies, i.e., the respective roles of genetic and epigenetic heterogeneity in this diversity, remains poorly understood. This question is addressed in chronic myelomonocytic leukemia, a myeloid neoplasm in which clinical diversity contrasts with limited genetic heterogeneity. To generate induced pluripotent stem cell clones, we reprogrammed CD34+ cells collected from a patient with a chronic myelomonocytic leukemia in which whole exome sequencing of peripheral blood monocyte DNA had identified 12 gene mutations, including a mutation in KDM6A and two heterozygous mutations in TET2 in the founding clone and a secondary KRAS(G12D) mutation. CD34+ cells from an age-matched healthy donor were also reprogrammed. We captured a part of the genetic heterogeneity observed in the patient, i.e. we analyzed five clones with two genetic backgrounds, without and with the KRAS(G12D) mutation. Hematopoietic differentiation of these clones recapitulated the main features of the patient's disease, including overproduction of granulomonocytes and dysmegakaryopoiesis. These analyses also disclosed significant discrepancies in the behavior of hematopoietic cells derived from induced pluripotent stem cell clones with similar genetic background, correlating with limited epigenetic changes. These analyses suggest that, beyond the coding mutations, several levels of intraclonal heterogeneity may participate in the yet unexplained clinical heterogeneity of the disease

Caspase Inhibition Modulates Monocyte-Derived Macrophage Polarization in Damaged Tissues

Circulating monocytes are recruited in damaged tissues to generate macrophages that modulate disease progression. Colony-stimulating factor-1 (CSF-1) promotes the generation of monocyte-derived macrophages, which involves caspase activation. Here, we demonstrate that activated caspase-3 and caspase-7 are located to the vicinity of the mitochondria in CSF1-treated human monocytes. Active caspase-7 cleaves p47PHOX at aspartate 34, which promotes the formation of the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase complex NOX2 and the production of cytosolic superoxide anions. Monocyte response to CSF-1 is altered in patients with a chronic granulomatous disease, which are constitutively defective in NOX2. Both caspase-7 down-regulation and radical oxygen species scavenging decrease the migration of CSF-1-induced macrophages. Inhibition or deletion of caspases prevents the development of lung fibrosis in mice exposed to bleomycin. Altogether, a non-conventional pathway that involves caspases and activates NOX2 is involved in CSF1-driven monocyte differentiation and could be therapeutically targeted to modulate macrophage polarization in damaged tissues

Membrane-associated Hsp72 from tumor-derived exosomes mediates STAT3-dependent immunosuppressive function of mouse and human myeloid-derived suppressor cells

International audienc