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✨ Génération du profil synthétique IA en cours…
Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.
Influence scientifique
16
16 articles ont été cités au moins 16fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.
h-index
Total citations reçues
636
Nombre de fois où d'autres équipes ont mentionné ses publications dans leurs propres travaux.
Publications totales
58
Articles, revues et chapitres référencés dans les bases académiques internationales.
Articles influents
25
Publications ayant marqué leur domaine — chacune citée au moins 10 fois par d'autres chercheurs.
i10-index
Thématiques principales
Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).
Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
Clinical rheumatology · 2020
Rheumatology (Oxford, England) · 2025
Abstract Objectives This study investigates the molecular and functional implications of reduced Suv3-like RNA helicase (SUV3) expression in the interferon (IFN)-enriched subset of monocytes from childhood Sjögren’s disease (cSjD). SUV3 is known to unwind double-stranded RNAs (dsRNAs) for homeostatic RNA decay within mitochondria. Methods Using single-cell RNA sequencing, we analysed highly inflammatory IFN-enriched CD14+ monocytes from cSjD patients. To model SUV3 deficiency, we performed SUV3 knockdown in monocytic cells and studied the origin, localization and accumulation of dsRNAs in the cytosol. Formaldehyde crosslinking immunoprecipitation (fCLIP)-qPCR identified an intracellular sensor of dsRNAs. We further examined patient monocytes using J2 anti-dsRNA antibodies and transmission electron microscopy (TEM) for subcellular localization. In vitro assays assessed the impact of SUV3 knockdown on oxidative stress, ATP production, migration and phagocytosis. Results SUV3 knockdown led to the accumulation of mitochondrial-dsRNAs (mt-dsRNAs) outside of the mitochondria, where they interacted with protein kinase R (PKR). This activated PKR, triggering a type I IFN signature and upregulating proinflammatory cytokines linked to fatigue. TEM revealed mt-dsRNAs in mitochondrial-derived vesicles and multi-vesicular bodies. Notably, cSjD monocytes had a significantly higher frequency of dsRNA-positive cells compared with controls (39% vs 0.08%, P < 0.002). SUV3 depletion also increased superoxide and ROS production, while impairing ATP synthesis, migration and phagocytosis, which are key innate immune functions. These defects were partially or fully reversed by co-knockdown of PKR. Conclusion SUV3 is the key driver for defective innate immune functions through mt-dsRNA-mediated PKR activation, which enhances cellular stress, mitochondrial dysfunction and inflammatory signatures, uncovering a novel mechanism in cSjD pathogenesis.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Lupus · 2023 · Observational Study
Alvarado RN, Alle G, Tobar-Jaramillo MA, Palomino LC, et al.
Clinical rheumatology · 2020 · Journal Article
Masson W, Rossi E, Mora-Crespo LM, Cornejo-Peña G, et al.
Datawork and the Future of Digital Humanities
A discussion of the relationship between digital humanities and the sciences, with a special focus on computational literary criticism.
Datawork and the Future of Digital Humanities
A discussion of the relationship between digital humanities and the sciences, with a special focus on computational literary criticism.
Source : DataCite — DOIs pour datasets, logiciels, protocoles, registres patient. Hors articles (déjà couverts).
Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.
Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.
Lupus · 2023
Objective The aim is to analyze health care resource utilization (HCRU) of patients with lupus (SLE) from a health management organization (HMO) in Buenos Aires, Argentina, compared with matched controls and comparing periods of flare, low disease activity, and remission. Methods This is a retrospective observational study including all SLE incident cases (ACR 1997/SLICC 2012 criteria) between 2000 and 2020 and 5 matched controls. Clinical data and HCRU (medical and nonmedical consultations, lab and imaging tests performed, emergency room visits, hospitalizations, and drugs prescribed) were obtained from administrative databases and electronic medical records. For each patient with SLE, an activity state was determined in every month of follow-up: flare (BILAG A or 2 BILAG B); low disease activity (LLDAS); remission (DORIS definition); or intermediate activity (not fulfilling any of previous). Incidence rates for each HCRU item and incidence rate ratios between SLE and control patients were and between remission and flare periods were calculated. Multivariate negative binomial logistic regression analyses were performed for identification of variables associated with major resource use. Results A total of 62 SLE and 310 control patients were included, 88.7% were women, the median age at diagnosis was 46 years, and were followed for more than 8 years. Patients with SLE contributed with 537.2 patient-years (CI 95% 461.1–613.3) and controls with 2761.9 patient-years (CI 95% 2600.9–2922.8). HCRU in patients with SLE was significantly higher than in controls in all items, even in remission periods. Patients with SLE remained 74.4% of the time in remission, 12.1% in LLDAS, 12.2% in intermediate activity, and 1.3% in flare (there were 64 flares in 36 patients). HCRU was significantly higher during flare periods compared with remission periods. Number of flares was independently associated with emergency department consultations, lab tests and X-ray performed, number of drugs prescribed, and hospitalizations. Conclusion Significantly more HCRU was observed in patients with SLE in flare compared to remission periods.
Clinical rheumatology · 2020 · Journal Article
Masson W, Rossi E, Mora-Crespo LM, Cornejo-Peña G, et al.
Rheumatology (Oxford, England) · 2025 · Journal Article
Yoon J, Jang D, Kim MC, Paek J, et al.