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935 results on '"François, Jérôme"'

1. Loss of phospholipase PLAAT3 causes a mixed lipodystrophic and neurological syndrome due to impaired PPARγ signaling

Author

Schuermans, Nika, El Chehadeh, Salima, Hemelsoet, Dimitri, Gautheron, Jérémie, Vantyghem, Marie-Christine, Nouioua, Sonia, Tazir, Meriem, Vigouroux, Corinne, Auclair, Martine, Bogaert, Elke, Dufour, Sara, Okawa, Fumiya, Hilbert, Pascale, Van Doninck, Nike, Taquet, Marie-Caroline, Rosseel, Toon, De Clercq, Griet, Debackere, Elke, Van Haverbeke, Carole, Cherif, Ferroudja Ramdane, Urtizberea, Jon Andoni, Chanson, Jean-Baptiste, Funalot, Benoit, Authier, François-Jérôme, Kaya, Sabine, Terryn, Wim, Callens, Steven, Depypere, Bernard, Van Dorpe, Jo, Poppe, Bruce, Impens, Francis, Mizushima, Noboru, Depienne, Christel, Jéru, Isabelle, and Dermaut, Bart

Published
2023
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2. Receptor interacting protein kinase‐3 mediates both myopathy and cardiomyopathy in preclinical animal models of Duchenne muscular dystrophy

Author

Maximilien Bencze, Baptiste Periou, Isabel Punzón, Inès Barthélémy, Valentina Taglietti, Cyrielle Hou, Louai Zaidan, Kaouthar Kefi, Stéphane Blot, Onnik Agbulut, Marianne Gervais, Geneviève Derumeaux, François‐Jérôme Authier, Laurent Tiret, and Fréderic Relaix

Subjects
Animal model, Cardiac failure, Duchenne muscular dystrophy, Fibrosis, Myogenesis, Myonecrosis, Diseases of the musculoskeletal system, RC925-935, Human anatomy, QM1-695
Abstract

Abstract Background Duchenne muscular dystrophy (DMD) is a progressive muscle degenerative disorder, culminating in a complete loss of ambulation, hypertrophic cardiomyopathy and a fatal cardiorespiratory failure. Necroptosis is the form of necrosis that is dependent upon the receptor‐interacting protein kinase (RIPK) 3; it is involved in several inflammatory and neurodegenerative conditions. We previously identified RIPK3 as a key player in the acute myonecrosis affecting the hindlimb muscles of the mdx dystrophic mouse model. Whether necroptosis also mediates respiratory and heart disorders in DMD is currently unknown. Methods Evidence of activation of the necroptotic axis was examined in dystrophic tissues from Golden retriever muscular dystrophy (GRMD) dogs and R‐DMDdel52 rats. A functional assessment of the involvement of necroptosis in dystrophic animals was performed on mdx mice that were genetically depleted for RIPK3. Dystrophic mice aged from 12 to 18 months were analysed by histology and molecular biology to compare the phenotype of muscles from mdxRipk3+/+and mdxRipk3−/− mice. Heart function was also examined by echocardiography in 40‐week‐old mice. Results RIPK3 expression in sartorius and biceps femoris muscles from GRMD dogs positively correlated to myonecrosis levels (r = 0.81; P = 0.0076). RIPK3 was also found elevated in the diaphragm (P ≤ 0.05). In the slow‐progressing heart phenotype of GRMD dogs, the phosphorylated form of RIPK1 at the Serine 161 site was dramatically increased in cardiomyocytes. A similar p‐RIPK1 upregulation characterized the cardiomyocytes of the severe DMDdel52 rat model, associated with a marked overexpression of Ripk1 (P = 0.007) and Ripk3 (P = 0.008), indicating primed activation of the necroptotic pathway in the dystrophic heart. MdxRipk3−/− mice displayed decreased compensatory hypertrophy of the heart (P = 0.014), and echocardiography showed a 19% increase in the relative wall thickness (P

Published
2023
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3. Clinical and functional characterization of a long survivor congenital titinopathy patient with a novel metatranscript-only titin variant

Author

Cardone, Nastasia, Moula, Melissa, Baelde, Rianne J., Biquand, Ariane, Villanova, Marcello, Metay, Corinne, Fiorillo, Chiara, Baratto, Serena, Merlini, Luciano, Sabatelli, Patrizia, Romero, Norma B., Relaix, Frederic, Authier, François Jérôme, Taglietti, Valentina, Savarese, Marco, de Winter, Josine, Ottenheijm, Coen, Richard, Isabelle, and Malfatti, Edoardo

Published
2023
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4. An up-to-date myopathologic characterisation of facioscapulohumeral muscular dystrophy type 1 muscle biopsies shows sarcolemmal complement membrane attack complex deposits and increased skeletal muscle regeneration

Author

Hubregtse, Lisanne, Bouman, Karlijn, Lama, Chéryane, Lassche, Saskia, de Graaf, Nicolas, Taglietti, Valentina, Küsters, Benno, Periou, Baptiste, Relaix, Frédéric, van Engelen, Baziel, Authier, François-Jerôme, Voermans, Nicol C., and Malfatti, Edoardo

Published
2024
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5. Widespread Myalgia and Chronic Fatigue: Phagocytes from Macrophagic Myofasciitis Patients Exposed to Aluminum Oxyhydroxide-Adjuvanted Vaccine Exhibit Specific Inflammatory, Autophagic, and Mitochondrial Responses

Author

Jean-Daniel Masson, Ghidaa Badran, Romain K. Gherardi, François-Jérôme Authier, and Guillemette Crépeaux

Subjects
myalgic encephalomyelitis/chronic fatigue syndrome, macrophagic myofasciitis, aluminum-based adjuvant, autophagy/LC3-associated phagocytosis, inflammation, mitochondrial metabolism, Chemical technology, TP1-1185
Abstract

(1) Background: Macrophagic myofasciitis (MMF) is an inflammatory histopathological lesion demonstrating long-term biopersistence of vaccine-derived aluminum adjuvants within muscular phagocytic cells. Affected patients suffer from widespread myalgia and severe fatigue consistent with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a poorly understood disorder suspected to result from chronic immune stimulation by infectious and inorganic particles. (2) Methods: In this study we determined the immuno-metabolic properties of MMF phagocytic cells compared to controls, at rest and upon exposure to aluminum oxyhydroxide adjuvant, with or without adsorbed antigens, using protein quantification and an oxygen consumption assay. (3) Results: MMF and control cells similarly internalized the adjuvant and vaccine but MMF cells specifically expressed Rubicon and Nox2, two molecules unique to the LC3-associated phagocytosis (LAP) machinery, a non-canonical autophagic pathway able to downregulate canonical autophagy. MMF cells exhibited an altered inflammatory secretome, producing more pain-inducing CXC chemokines and less TNF-α than controls, consistent with chronic myalgia and exhaustion of the immune system previously documented in ME/CFS. MMF cells exhibited mitochondrial metabolism dysfunction, with exacerbated reaction to adjuvanted vaccine, contrasting with limited spare respiratory capacity and marked proton leak weakening energy production. (4) Conclusions: MMF phagocytes seemingly use LAP to handle aluminum oxyhydroxide vaccine particles, secrete pain-inducing molecules, and exhibit exacerbated metabolic reaction to the vaccine with limited capacity to respond to ongoing energetic requests.

Published
2024
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6. Early Identification of Services in HTTPS Traffic

Author

Shbair, Wazen M., Cholez, Thibault, Francois, Jerome, and Chrisment, Isabelle

Subjects
Computer Science - Cryptography and Security
Abstract

Traffic monitoring is essential for network management tasks that ensure security and QoS. However, the continuous increase of HTTPS traffic undermines the effectiveness of current service-level monitoring that can only rely on unreliable parameters from the TLS handshake (X.509 certificate, SNI) or must decrypt the traffic. We propose a new machine learning-based method to identify HTTPS services without decryption. By extracting statistical features on TLS handshake packets and on a small number of application data packets, we can identify HTTPS services very early in the session. Extensive experiments performed over a significant and open dataset show that our method offers a good accuracy and a prototype implementation confirms that the early identification of HTTPS services is satisfied.

Published
2020

7. A Survey of HTTPS Traffic and Services Identification Approaches

Author

Shbair, Wazen M., Cholez, Thibault, Francois, Jerome, and Chrisment, Isabelle

Subjects
Computer Science - Cryptography and Security, Computer Science - Networking and Internet Architecture
Abstract

HTTPS is quickly rising alongside the need of Internet users to benefit from security and privacy when accessing the Web, and it becomes the predominant application protocol on the Internet. This migration towards a secure Web using HTTPS comes with important challenges related to the management of HTTPS traffic to guarantee basic network properties such as security, QoS, reliability, etc. But encryption undermines the effectiveness of standard monitoring techniques and makes it difficult for ISPs and network administrators to properly identify and manage the services behind HTTPS traffic. This survey details the techniques used to monitor HTTPS traffic, from the most basic level of protocol identification (TLS, HTTPS), to the finest identification of precise services. We show that protocol identification is well mastered while more precise levels keep being challenging despite recent advances. We also describe practical solutions that lead us to discuss the trade-off between security and privacy and the research directions to guarantee both of them.

Published
2020

8. Clinical and functional characterization of a long survivor congenital titinopathy patient with a novel metatranscript-only titin variant

Author

Nastasia Cardone, Melissa Moula, Rianne J. Baelde, Ariane Biquand, Marcello Villanova, Corinne Metay, Chiara Fiorillo, Serena Baratto, Luciano Merlini, Patrizia Sabatelli, Norma B. Romero, Frederic Relaix, François Jérôme Authier, Valentina Taglietti, Marco Savarese, Josine de Winter, Coen Ottenheijm, Isabelle Richard, and Edoardo Malfatti

Subjects
Congenital myopathy, Titin, Titinopathy, Rigid spine, Metatranscript, N2A titin isoform, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Congenital titinopathies are an emerging group of a potentially severe form of congenital myopathies caused by biallelic mutations in titin, encoding the largest existing human protein involved in the formation and stability of sarcomeres. In this study we describe a patient with a congenital myopathy characterized by multiple contractures, a rigid spine, non progressive muscular weakness, and a novel homozygous TTN pathogenic variant in a metatranscript-only exon: the c.36400A > T, p.Lys12134*. Muscle biopsies showed increased internalized nuclei, variability in fiber size, mild fibrosis, type 1 fiber predominance, and a slight increase in the number of satellite cells. RNA studies revealed the retention of intron 170 and 171 in the open reading frame, and immunoflourescence and western blot studies, a normal titin content. Single fiber functional studies showed a slight decrease in absolute maximal force and a cross-sectional area with no decreases in tension, suggesting that weakness is not sarcomere-based but due to hypotrophy. Passive properties of single fibers were not affected, but the observed increased calcium sensitivity of force generation might contribute to the contractural phenotype and rigid spine of the patient. Our findings provide evidence for a pathogenic, causative role of a metatranscript-only titin variant in a long survivor congenital titinopathy patient with distal arthrogryposis and rigid spine.

Published
2023
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10. Exploratory Data Analysis of a Network Telescope Traffic and Prediction of Port Probing Rates

Author

Zakroum, Mehdi, Houmz, Abdellah, Ghogho, Mounir, Mezzour, Ghita, Lahmadi, Abdelkader, François, Jérôme, and Koutbi, Mohammed El

Subjects
Computer Science - Cryptography and Security, Computer Science - Artificial Intelligence, Computer Science - Machine Learning
Abstract

Understanding the properties exhibited by large scale network probing traffic would improve cyber threat intelligence. In addition, the prediction of probing rates is a key feature for security practitioners in their endeavors for making better operational decisions and for enhancing their defense strategy skills. In this work, we study different aspects of the traffic captured by a /20 network telescope. First, we perform an exploratory data analysis of the collected probing activities. The investigation includes probing rates at the port level, services interesting top network probers and the distribution of probing rates by geolocation. Second, we extract the network probers exploration patterns. We model these behaviors using transition graphs decorated with probabilities of switching from a port to another. Finally, we assess the capacity of Non-stationary Autoregressive and Vector Autoregressive models in predicting port probing rates as a first step towards using more robust models for better forecasting performance., Comment: IEEE Intelligence and Security Informatics

Published
2018
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11. Changes in amyloidosis phenotype over 11 years in a cardiac amyloidosis referral centre cohort in France

Author

Damy, Thibaud, Zaroui, Amira, de Tournemire, Marie, Kharoubi, Mounira, Gounot, Romain, Galat, Arnault, Guendouz, Soulef, Funalot, Benoit, Itti, Emmanuel, Roulin, Louise, Audard, Vincent, Fanen, Pascale, Leroy, Vincent, Poulot, Elsa, Belhadj, Karim, Mallet, Sophie, Deep Singh Chadah, Gagan, Planté-Bordeneuve, Violaine, Gendre, Thierry, Chevalier, Xavier, Guignard, Sandra, Bequignon, Emilie, Bartier, Sophie, Folliguet, Thierry, Lemonier, François, Audureau, Etienne, Tixier, Denis, Canoui-Poitrine, Florence, Lefaucheur, Jean-Pascal, Souvannanorath, Sarah, Authier, Francois-Jerome, Maupou, Steven, Hittinger, Luc, Molinier-Frenkel, Valérie, David, Jean-Philippe, Broussier, Amaury, Oghina, Silvia, and Teiger, Emmanuel

Published
2023
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14. Duchenne muscular dystrophy trajectory in R-DMDdel52 preclinical rat model identifies COMP as biomarker of fibrosis

Author

Valentina Taglietti, Kaouthar Kefi, Iwona Bronisz-Budzyńska, Busra Mirciloglu, Mathilde Rodrigues, Nastasia Cardone, Fanny Coulpier, Baptiste Periou, Christel Gentil, Melissa Goddard, François-Jérôme Authier, France Pietri-Rouxel, Edoardo Malfatti, Peggy Lafuste, Laurent Tiret, and Frederic Relaix

Subjects
Duchenne muscular dystrophy, Skeletal muscle, Preclinical modelling, Translational medicine, Long QT, scRNAseq, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Duchenne muscular dystrophy (DMD) is a fatal muscle-wasting disorder caused by mutations in the Dystrophin gene and for which there is currently no cure. To bridge the gap between preclinical and therapeutic evaluation studies, we have generated a rat model for DMD that carries an exon 52 deletion (R-DMDdel52) causing a complete lack of dystrophin protein. Here we show that R-DMDdel52 animals recapitulated human DMD pathophysiological trajectory more faithfully than the mdx mouse model. We report that R-DMDdel52 rats displayed progressive and severe skeletal muscle loss associated with fibrotic deposition, fat infiltration and fibre type switch. Early fibrosis was also apparent in the cardiac muscle. These histological modifications led to severe muscle, respiratory and cardiac functional impairments leading to premature death around 1 year. Moreover, DMD muscle exhibited systemic inflammation with a mixed M1/M2 phenotype. A comparative single cell RNAseq analysis of the diaphragm muscle was performed, revealing cellular populations alteration and molecular modifications in all muscle cell types. We show that DMD fibroadipogenic progenitors produced elevated levels of cartilage oligomeric matrix protein, a glycoprotein responsible for modulating homeostasis of extracellular matrix, and whose increased concentration correlated with muscle fibrosis both in R-DMDdel52 rats and human patients. Fibrosis is a component of tissue remodelling impacting the whole musculature of DMD patients, at the tissue level but most importantly at the functional level. We therefore propose that this specific biomarker can optimize the prognostic monitoring of functional improvement of patients included in clinical trials.

Published
2022
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16. Systematic review and meta-analysis of cognitive impairment in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

Author

Mehdi Aoun Sebaiti, Mathieu Hainselin, Yannick Gounden, Carmen Adella Sirbu, Slobodan Sekulic, Lorenzo Lorusso, Luis Nacul, and François Jérôme Authier

Subjects
Medicine, Science
Abstract

Abstract Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is commonly associated with cognitive complaints. To bring out the neuropsychological symptomatology inherent to ME/CFS, we conducted a systematic review according to PRISMA and MOOSE guidelines of the literature through the analysis of 764 studies published between 1988 and 2019 by using PubMed Central website and Clarivate analytics platform. We performed a meta-analysis to delineate an idea of the neuropsychological profile inherent in ME/CFS. The clinical picture typically affects visuo-spatial immediate memory (g = − 0.55, p = 0.007), reading speed (g = − 0.82, p = 0.0001) and graphics gesture (g = − 0.59, p = 0.0001). Analysis also revealed difficulties in several processes inherent in episodic verbal memory (storage, retrieval, recognition) and visual memory (recovery) and a low efficiency in attentional abilities. Executive functions seemed to be little or not affected and instrumental functions appeared constantly preserved. With regard to the complexity and heterogeneity of the cognitive phenotype, it turns out that determining a sound clinical picture of ME/CFS cognitive profile must go through a neuropsychological examination allowing a complete evaluation integrating the notion of agreement between the choice and the number of tests and the complexity intrinsic to the pathology.

Published
2022
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18. Characterizing Acute-Onset Small Fiber Neuropathy

Author

Gendre, Thierry, primary, Lefaucheur, Jean-Pascal, additional, Nordine, Tarik, additional, Baba-Amer, Yasmine, additional, Authier, François-Jérôme, additional, Devaux, Jérôme, additional, and Créange, Alain, additional

Published
2024
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20. A recurrent RYR1 mutation associated with early-onset hypotonia and benign disease course

Author

Valérie Biancalana, John Rendu, Annabelle Chaussenot, Helen Mecili, Eric Bieth, Mélanie Fradin, Sandra Mercier, Maud Michaud, Marie-Christine Nougues, Laurent Pasquier, Sabrina Sacconi, Norma B. Romero, Pascale Marcorelles, François Jérôme Authier, Antoinette Gelot Bernabe, Emmanuelle Uro-Coste, Claude Cances, Bertrand Isidor, Armelle Magot, Marie-Christine Minot-Myhie, Yann Péréon, Julie Perrier-Boeswillwald, Gilles Bretaudeau, Nicolas Dondaine, Alison Bouzenard, Mégane Pizzimenti, Bruno Eymard, Ana Ferreiro, Jocelyn Laporte, Julien Fauré, and Johann Böhm

Subjects
Neuromuscular disorder, Congenital myopathy, Calcium, Muscle weakness, Excitation–contraction coupling, Triad, Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract The ryanodine receptor RyR1 is the main sarcoplasmic reticulum Ca2+ channel in skeletal muscle and acts as a connecting link between electrical stimulation and Ca2+-dependent muscle contraction. Abnormal RyR1 activity compromises normal muscle function and results in various human disorders including malignant hyperthermia, central core disease, and centronuclear myopathy. However, RYR1 is one of the largest genes of the human genome and accumulates numerous missense variants of uncertain significance (VUS), precluding an efficient molecular diagnosis for many patients and families. Here we describe a recurrent RYR1 mutation previously classified as VUS, and we provide clinical, histological, and genetic data supporting its pathogenicity. The heterozygous c.12083C>T (p.Ser4028Leu) mutation was found in thirteen patients from nine unrelated congenital myopathy families with consistent clinical presentation, and either segregated with the disease in the dominant families or occurred de novo. The affected individuals essentially manifested neonatal or infancy-onset hypotonia, delayed motor milestones, and a benign disease course differing from classical RYR1-related muscle disorders. Muscle biopsies showed unspecific histological and ultrastructural findings, while RYR1-typical cores and internal nuclei were seen only in single patients. In conclusion, our data evidence the causality of the RYR1 c.12083C>T (p.Ser4028Leu) mutation in the development of an atypical congenital myopathy with gradually improving motor function over the first decades of life, and may direct molecular diagnosis for patients with comparable clinical presentation and unspecific histopathological features on the muscle biopsy.

Published
2021
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21. Widespread Myalgia and Chronic Fatigue: Phagocytes from Macrophagic Myofasciitis Patients Exposed to Aluminum Oxyhydroxide-Adjuvanted Vaccine Exhibit Specific Inflammatory, Autophagic, and Mitochondrial Responses.

Author

Masson, Jean-Daniel, Badran, Ghidaa, Gherardi, Romain K., Authier, François-Jérôme, and Crépeaux, Guillemette

Subjects
CHRONIC fatigue syndrome, FATIGUE (Physiology), IMMUNE system, MYALGIA, PHAGOCYTES
Abstract

(1) Background: Macrophagic myofasciitis (MMF) is an inflammatory histopathological lesion demonstrating long-term biopersistence of vaccine-derived aluminum adjuvants within muscular phagocytic cells. Affected patients suffer from widespread myalgia and severe fatigue consistent with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a poorly understood disorder suspected to result from chronic immune stimulation by infectious and inorganic particles. (2) Methods: In this study we determined the immuno-metabolic properties of MMF phagocytic cells compared to controls, at rest and upon exposure to aluminum oxyhydroxide adjuvant, with or without adsorbed antigens, using protein quantification and an oxygen consumption assay. (3) Results: MMF and control cells similarly internalized the adjuvant and vaccine but MMF cells specifically expressed Rubicon and Nox2, two molecules unique to the LC3-associated phagocytosis (LAP) machinery, a non-canonical autophagic pathway able to downregulate canonical autophagy. MMF cells exhibited an altered inflammatory secretome, producing more pain-inducing CXC chemokines and less TNF-α than controls, consistent with chronic myalgia and exhaustion of the immune system previously documented in ME/CFS. MMF cells exhibited mitochondrial metabolism dysfunction, with exacerbated reaction to adjuvanted vaccine, contrasting with limited spare respiratory capacity and marked proton leak weakening energy production. (4) Conclusions: MMF phagocytes seemingly use LAP to handle aluminum oxyhydroxide vaccine particles, secrete pain-inducing molecules, and exhibit exacerbated metabolic reaction to the vaccine with limited capacity to respond to ongoing energetic requests. [ABSTRACT FROM AUTHOR]

Published
2024
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22. A recurrent RYR1 mutation associated with early-onset hypotonia and benign disease course

Author

Biancalana, Valérie, Rendu, John, Chaussenot, Annabelle, Mecili, Helen, Bieth, Eric, Fradin, Mélanie, Mercier, Sandra, Michaud, Maud, Nougues, Marie-Christine, Pasquier, Laurent, Sacconi, Sabrina, Romero, Norma B., Marcorelles, Pascale, Authier, François Jérôme, Gelot Bernabe, Antoinette, Uro-Coste, Emmanuelle, Cances, Claude, Isidor, Bertrand, Magot, Armelle, Minot-Myhie, Marie-Christine, Péréon, Yann, Perrier-Boeswillwald, Julie, Bretaudeau, Gilles, Dondaine, Nicolas, Bouzenard, Alison, Pizzimenti, Mégane, Eymard, Bruno, Ferreiro, Ana, Laporte, Jocelyn, Fauré, Julien, and Böhm, Johann

Published
2021
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25. HuMa: A Multi-layer Framework for Threat Analysis in a Heterogeneous Log Environment

Author

Navarro, Julio, Legrand, Véronique, Lagraa, Sofiane, François, Jérôme, Lahmadi, Abdelkader, De Santis, Giulia, Festor, Olivier, Lammari, Nadira, Hamdi, Fayçal, Deruyver, Aline, Goux, Quentin, Allard, Morgan, Parrend, Pierre, Hutchison, David, Series editor, Kanade, Takeo, Series editor, Kittler, Josef, Series editor, Kleinberg, Jon M., Series editor, Mattern, Friedemann, Series editor, Mitchell, John C., Series editor, Naor, Moni, Series editor, Pandu Rangan, C., Series editor, Steffen, Bernhard, Series editor, Terzopoulos, Demetri, Series editor, Tygar, Doug, Series editor, Weikum, Gerhard, Series editor, Imine, Abdessamad, editor, Fernandez, José M., editor, Marion, Jean-Yves, editor, Logrippo, Luigi, editor, and Garcia-Alfaro, Joaquin, editor

Published
2018
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26. Receptor interacting protein kinase‐3 mediates both myopathy and cardiomyopathy in preclinical animal models of Duchenne muscular dystrophy

Author

Bencze, Maximilien, primary, Periou, Baptiste, additional, Punzón, Isabel, additional, Barthélémy, Inès, additional, Taglietti, Valentina, additional, Hou, Cyrielle, additional, Zaidan, Louai, additional, Kefi, Kaouthar, additional, Blot, Stéphane, additional, Agbulut, Onnik, additional, Gervais, Marianne, additional, Derumeaux, Geneviève, additional, Authier, François‐Jérôme, additional, Tiret, Laurent, additional, and Relaix, Fréderic, additional

Published
2023
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29. Hemifacial myohyperplasia is due to somatic muscular PIK3CA gain-of-function mutations and responds to pharmacological inhibition

Author

Bayard, Charles, primary, Segna, Eleonora, additional, Taverne, Maxime, additional, Fraissenon, Antoine, additional, Hennocq, Quentin, additional, Periou, Baptiste, additional, Zerbib, Lola, additional, Ladraa, Sophia, additional, Chapelle, Célia, additional, Hoguin, Clément, additional, Kaltenbach, Sophie, additional, Villarese, Patrick, additional, Asnafi, Vahid, additional, Broissand, Christine, additional, Nemazanyy, Ivan, additional, Autret, Gwennhael, additional, Goudin, Nicolas, additional, Legendre, Christophe, additional, Authier, François-Jérôme, additional, Viel, Thomas, additional, Tavitian, Bertrand, additional, Gitiaux, Cyril, additional, Fraitag, Sylvie, additional, Duong, Jean-Paul, additional, Delcros, Clarisse, additional, Sergent, Bernard, additional, Picard, Arnaud, additional, Dussiot, Michael, additional, Guibaud, Laurent, additional, Khonsari, Roman, additional, and Canaud, Guillaume, additional

Published
2023
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30. Automated image-analysis method for the quantification of fiber morphometry and fiber type population in human skeletal muscle

Author

Perla C. Reyes-Fernandez, Baptiste Periou, Xavier Decrouy, Fréderic Relaix, and François Jérôme Authier

Subjects
Automated image analysis, Muscle fiber quantification, Human muscle cross-sections, Fiber type populations, Biomedical imaging, Clinical diagnosis, Diseases of the musculoskeletal system, RC925-935
Abstract

Abstract Background The quantitative analysis of muscle histomorphometry has been growing in importance in both research and clinical settings. Accurate and stringent assessment of myofibers’ changes in size and number, and alterations in the proportion of oxidative (type I) and glycolytic (type II) fibers is essential for the appropriate study of aging and pathological muscle, as well as for diagnosis and follow-up of muscle diseases. Manual and semi-automated methods to assess muscle morphometry in sections are time-consuming, limited to a small field of analysis, and susceptible to bias, while most automated methods have been only tested in rodent muscle. Methods We developed a new macro script for Fiji-ImageJ to automatically assess human fiber morphometry in digital images of the entire muscle. We tested the functionality of our method in deltoid muscle biopsies from a heterogeneous population of subjects with histologically normal muscle (male, female, old, young, lean, obese) and patients with dermatomyositis, necrotizing autoimmune myopathy, and anti-synthetase syndrome myopathy. Results Our macro is fully automated, requires no user intervention, and demonstrated improved fiber segmentation by running a series of image pre-processing steps before the analysis. Likewise, our tool showed high accuracy, as compared with manual methods, for identifying the total number of fibers (r = 0.97, p

Published
2019
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31. Hydrogenation of Xylose to Xylitol in the Presence of Bimetallic Nanoparticles Ni3Fe Catalyst in the Presence of Choline Chloride

Author

Naseeb Ullah, François Jérôme, and Karine De Oliveira Vigier

Subjects
hydrogenation, sugars, deep eutectic solvents, Chemical technology, TP1-1185, Chemistry, QD1-999
Abstract

Hydrogenation of sugars to sugars alcohols is of prime interest for food applications for instance. Xylose obtained from the hemicellulose fraction of lignocellulosic biomass can be hydrogenated to xylitol. Herein, we conducted catalytic hydrogenation reactions in a non-conventional media approach by using choline chloride, a non-toxic naturally occurring organic compound that can form a deep eutectic solvent with xylose. Acknowledging the benefits of cost-effective transition metal-based alloys, Ni3Fe1 bimetallic nanoparticles were utilized as a hetero-catalyst. Under optimized reaction conditions (110 °C, 3 h and 30 bar H2), a highly concentrated feed of xylose (76 wt.%) was converted to 80% of xylitol, showing the benefit of using choline chloride. Overall, the catalytic conversion activity and the product selectivity in the substrate-assisted DES media are relatively high but, the recyclability of the catalyst should be improved in the presence of such media.

Published
2022
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34. Role of Lung Ultrasound in the Assessment of Hydration Status of Chronic Haemodialysis Patients

Author

Sylviane Fomekong Dongmo, Jean-Roger Tapouh Moulion, Denis Georges Teuwafeu, Samory Guedje Chuangueu, François Jérôme Kaze Folefack, and Boniface Moifo

Subjects
General Medicine
Abstract

Background Fluid overload is frequent in haemodialysis (HD) and is one of the major factors of cardiovascular morbidity and mortality for chronic haemodialysis patients. The main challenge with chronic haemodialysis patients is indeed the maintenance of a normal extracellular volume through dry weight determination. Our study aimed at assessing the role of lung ultrasound in the detection of B-lines for the determination of hydration status in chronic haemodialysed patients. Methods We conducted a cross sectional study including 31 patients undergoing chronic HD treatment for at least 3 months, in Yaounde University Teaching Hospital dialysis unit. Lung ultrasonography and clinical examinations were performed immediately before dialysis, and 30 minutes after dialysis. Differences between variables before and after dialysis were measured to assess dialysis’s effect. Association between categorical variables was assessed with Chi-squared test or Fischer test, and Rho’s Spearman coefficient for quantitative variables. Results There were reduction in median of B-lines score after dialysis [12(7–26) versus 8(5–13)], clinical score [2(1–3) versus 0((-1)-2)], mean of systolic blood pressure (164.74 ± 26.50 versus 158.48 ± 27.89), frequency of dyspnoea in patients (32.3% versus 6.5%); and raising frequency of cramps in patients (0% versus 19.4%), all statistically significant (p ≤ 0.031). B-lines score before and after dialysis was associated with dyspnoea and raised jugular venous pressure (p

Published
2023

36. Bio-Based Solvents

Author

François Jérôme, Rafael Luque, François Jérôme, Rafael Luque

Published
2017

39. Systemic light chain amyloidosis myopathy responsive to daratumumab monotherapy

Author

Diana Maria Chitimus, Edouard Berling, Laurent Garderet, Nadia Venturelli, Edoardo Malfatti, François Jérôme Authier, Guillaume Nicolas, Pascal Laforêt, and Claire Lefeuvre

Subjects
Neurology, Neurology (clinical)
Abstract

Amyloid myopathy is a rare and severe manifestation of systemic light chain (AL) amyloidosis. Early diagnosis and staging are mandatory for optimal therapy, given the rapid progression of muscle weakness. Despite the efficacy of bortezomib-based treatment regimens, there is a lack of therapeutic alternatives in non-responsive patients.The case report of a patient with systemic AL amyloidosis myopathy treated with daratumumab is presented.A 70-year-old man displayed severe proximal muscle weakness which had developed over a 10-month period. Blood tests revealed an immunoglobulin A lambda monoclonal gammopathy, whilst muscle biopsy showed amyloid deposits within the arteriolar walls, confirming the diagnosis of amyloid myopathy associated with AL amyloidosis. Initial treatment with a bortezomib-based regimen showed no clinical or hematological improvement. After switching to daratumumab monotherapy, our patient achieved a favorable evolution with respect to functional muscle scoring and a complete hematological response.To our knowledge, this is the first case report of an amyloid myopathy showing a remarkable clinical improvement in response to daratumumab monotherapy. It thereby highlights the potential of daratumumab as a monotherapeutical approach to the treatment of amyloid myopathy complicating AL amyloidosis.

Published
2022

41. RAMSES: Revealing Android Malware Through String Extraction and Selection

Author

Dolberg, Lautaro, Jérôme, Quentin, François, Jérôme, State, Radu, Engel, Thomas, Akan, Ozgur, Series editor, Bellavista, Paolo, Series editor, Cao, Jiannong, Series editor, Coulson, Geoffrey, Series editor, Dressler, Falko, Series editor, Ferrari, Domenico, Series editor, Gerla, Mario, Series editor, Kobayashi, Hisashi, Series editor, Palazzo, Sergio, Series editor, Sahni, Sartaj, Series editor, Shen, Xuemin Sherman, Series editor, Stan, Mircea, Series editor, Xiaohua, Jia, Series editor, Zomaya, Albert Y., Series editor, Tian, Jing, editor, Jing, Jiwu, editor, and Srivatsa, Mudhakar, editor

Published
2015
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42. Proceedings of the 23rd Paediatric Rheumatology European Society Congress: part one

Author

F. De Benedetti, J. Anton, M. Gattorno, H. Lachmann, I. Kone-Paut, S. Ozen, J. Frenkel, A. Simon, A. Zeft, E. Ben-Chetrit, H. M. Hoffman, Y. Joubert, K. Lheritier, A. Speziale, J. Guido, Roberta Caorsi, Federica Penco, Alice Grossi, Antonella Insalaco, Maria Alessio, Giovanni Conti, Federico Marchetti, Alberto Tommasini, Silvana Martino, Romina Gallizzi, Annalisa Salis, Francesca Schena, Francesco Caroli, Alberto Martini, Gianluca Damonte, Isabella Ceccherini, Marco Gattorno, Marie-Louise Frémond, Carolina Uggenti, Lien Van Eyck, Isabelle Melki, Darragh Duffy, Vincent Bondet, Yoann Rose, Bénédicte Neven, Yanick Crow, Mathieu P. Rodero, Yvonne Kusche, Johannes Roth, Katarzyna Barczyk-Kahlert, Giovanna Ferrara, Annalisa Chiocchetti, Silvio Polizzi, Josef Vuch, Diego Vozzi, Anna Mondino, Erica Valencic, Serena Pastore, Andrea Taddio, Flavio Faletra, Umberto Dianzani, Ugo Ramenghi, Qing Zhou, Xiaomin Yu, Erkan Demirkaya, Natalie Deuitch, Deborah Stone, Wanxia Tsai, Amanda Ombrello, Tina Romeo, Elaine F. Remmers, JaeJin Chae, Massimo Gadina, Steven Welch, Seza Ozen, Rezan Topaloglu, Mario Abinun, Daniel L. Kastner, Ivona Aksentijevich, Donatella Vairo, Rosalba Monica Ferraro, Giulia Zani, Jessica Galli, Micaela De Simone, Marco Cattalini, Elisa Fazzi, Silvia Giliani, Ebun Omoyinmi, Ariane Standing, Dorota Rowczenio, Annette Keylock, Sonia Melo Gomes, Fiona Price-Kuehne, Sira Nanthapisal, Claire Murphy, Thomas Cullup, Lucy Jenkins, Kimberly Gilmour, Despina Eleftheriou, Helen Lachmann, Philip Hawkins, Nigel Klein, Paul Brogan, Anita Dhanrajani, Mercedes Chan, Stephanie Pau, Janet Ellsworth, Jaime Guzman, Florence A. Aeschlimann, Marinka Twilt, Simon W. Eng, Shehla Sheikh, Ronald M. Laxer, Diane Hebert, Damien Noone, Christian Pagnoux, Susanne M. Benseler, Rae S. Yeung, Christoph Kessel, Katrin Lippitz, Toni Weinhage, Claas Hinze, Helmut Wittkowski, Dirk Holzinger, Niklas Grün, Dirk Föll, Pieter Van Dijkhuizen, Federica Del Chierico, Clara Malattia, Alessandra Russo, Denise Pires Marafon, Nienke M. ter Haar, Silvia Magni-Manzoni, Sebastiaan J. Vastert, Bruno Dallapiccola, Berent Prakken, Fabrizio De Benedetti, Lorenza Putignani, Berna Eren Fidanci, Kenan Barut, Serap Arıcı, Dogan Simsek, Mustafa Cakan, Ezgi D. Batu, Sezgin Şahin, Ayşenur Kısaarslan, Ebru Yilmaz, Özge Basaran, Ferhat Demir, Kubra Ozturk, Zübeyde Gunduz, Betül Sozeri, Balahan Makay, Nuray Ayaz, Onder Yavascan, Ozlem Aydog, Yelda Bilginer, Zelal Ekinci, Dilek Yıldız, Faysal Gök, Muferret Erguven, Erbil Unsal, Ozgur Kasapcopur, For the FMF Arthritis Vasculitis and Orphan Disease Research in Paediatric Rheumatology (FAVOR), Hafize E. Sönmez, Betül Sözeri, Yonatan Butbul, Seza Özen, Claudia Bracaglia, Giusi Prencipe, Manuela Pardeo, Geneviève Lapeyre, Emiliano Marasco, Walter Ferlin, Robert Nelson, Cristina de Min, N. Ruperto, H. I. Brunner, P. Quartier, T. Constantin, E. Alexeeva, K. Marzan, N. Wulffraat, R. Schneider, S. Padeh, V. Chasnyk, C. Wouters, J. B. Kuemmerle-Deschner, T. Kallinich, B. Lauwerys, E. Haddad, E. Nasonov, M. Trachana, O. Vougiouka, K. Leon, E. Vritzali, A. Martini, D. Lovell, PRINTO/PRCSG, Stefano Volpi, Claudia Pastorino, Francesca Kalli, Alessia Omenetti, Sabrina Chiesa, Arinna Bertoni, Paolo Picco, Gilberto Filaci, Elisabetta Traggiai, Marie-Louise Fremond, Naoki Kitabayashi, Olivero Sacco, Isabelle Meyts, Marie-Anne Morren, Carine Wouters, Eric Legius, Isabelle Callebaut, Christine Bodemer, Frederic Rieux-Laucat, Mathieu Rodero, Nadia Jeremiah, Alexandre Belot, Eric Jeziorski, Didier Bessis, Guilhem Cros, Gillian I. Rice, Bruno Charbit, Anne Hulin, Nihel Khoudour, Consuelo Modesto Caballero, Monique Fabre, Laureline Berteloot, Muriel Le Bourgeois, Philippe Reix, Thierry Walzer, Despina Moshous, Stéphane Blanche, Alain Fischer, Brigitte Bader-Meunier, Frédéric Rieux-Laucat, K. Annink, N. ter Haar, S. Al-Mayouf, G. Amaryan, K. Barron, S. Benseler, P. Brogan, L. Cantarini, M. Cattalini, A. Cochino, F. Dedeoglu, A. De Jesus, O. Dellacasa, E. Demirkaya, P. Dolezalova, K. Durrant, G. Fabio, R. Gallizzi, R. Goldbach-Mansky, E. Hachulla, V. Hentgen, T. Herlin, M. Hofer, H. Hoffman, A. Insalaco, A. Jansson, I. Koné-Paut, A. Kozlova, J. Kuemmerle-Deschner, R. Laxer, S. Nielsen, I. Nikishina, A. Ombrello, E. Papadopoulou-Alataki, A. Ravelli, D. Rigante, R. Russo, Y. Uziel, Nienke ter Haar, Jerold Jeyaratnam, Anna Simon, Matteo Doglio, Jordi Anton, Consuelo Modesto, Pierre Quartier, Esther Hoppenreijs, Luca Cantarini, Loredana Lepore, Inmaculada Calvo Penades, Christina Boros, Rita Consolini, Donato Rigante, Ricardo Russo, Jana Pachlopnik Schmid, Thirusha Lane, Nicolino Ruperto, Joost Frenkel, Chiara Passarelli, Elisa Pisaneschi, Virginia Messia, Antonio Novelli, Fabrizio Debenedetti, P. A. Brogan, X. Wei, Martina Finetti, Francesca Orlando, Elisabetta Cortis, Angela Miniaci, Nicola Ruperto, Charlotte Eijkelboom, Pavla Dolezalova, Isabelle Koné-Paut, Marija Jelusic-Drazic, Liliana Bezrodnik, Mari Carmen Pinedo, Valda Stanevicha, Marielle van Gijn, Silvia Federici, Hermann Girschick, Gerd Ganser, Susan Nielsen, Troels Herlin, Sulaiman Mohammed Al-Mayouf, Michael Hofer, Jasmin Kuemmerle-Deschner, Susanne Schalm, Annette Jansson, on behalf of PRINTO and Eurofever registry, Marta Marchi, Chiara Marini, Angelo Ravelli, Alberto Garaventa, Sonia Carta, Enrica Balza, Patrizia Castellani, Caterina Pellecchia, Silvia Borghini, Maria Libera Trotta, Anna Rubartelli, Andrew Henrey, Thomas Loughin, Roberta Berard, Natalie Shiff, Roman Jurencak, Susanne Benseler, Lori Tucker, on behalf of ReACCh-Out Investigators, Charalampia Papadopoulou, Ying Hong, Petra Krol, Yiannis Ioannou, Clarissa Pilkington, Hema Chaplin, Stephania Simou, Marietta Charakida, Lucy Wedderburn, Lynn R. Spiegel, Sara Ahola Kohut, Jennifer Stinson, Paula Forgeron, Miriam Kaufman, Nadia Luca, Khush Amaria, Mary Bell, J Swart, F. Boris, E. Castagnola, A. Groll, G. Giancane, G. Horneff, H. I. Huppertz, T. Wolfs, E. Alekseeva, V. Panaviene, F. Uettwiller, V. Stanevicha, L. M. Ailioaie, E. Tsitami, S. Kamphuis, G. Susic, F. Sztajnbok, B. Flato, A. Pistorio, Stephanie J. W. Shoop, Suzanne M. M. Verstappen, Janet E. McDonagh, Wendy Thomson, Kimme L. Hyrich, CAPS, Maarit Tarkiainen, Pirjo Tynjala, Pekka Lahdenne, Janne Martikainen, Acute-JIA Study Group, Meredyth Wilkinson, Christopher Piper, Georg Otto, Claire T. Deakin, Stefanie Dowle, Stefania Simou, Daniel Kelberman, Claudia Mauri, Elizabeth Jury, David Isenberg, Lucy R. Wedderburn, Kiran Nistala, I. Foeldvari, D. J. Lovell, G. Simonini, M. Bereswill, J. Kalabic, Kiem Oen, Brian M. Feldman, Brenden Dufault, Jennifer Lee, Karen Watanabe Duffy, Ciaran Duffy, ReACCh-Out Investigators, N. Tzaribachev, G. Vega-Cornejo, I. Louw, A. Berman, I. Calvo, R. Cuttica, F. Avila-Zapata, R. Cimaz, E. Solau-Gervais, R. Joos, G. Espada, X. Li, M. Nys, R. Wong, S. Banerjee, For Pediatric Rheumatology International Trials Organization (PRINTO)/Pediatric Rheumatology Collaborative Study Group (PRCSG), Rebecca Nicolai, Margherita Verardo, Adele D’Amico, Luisa Bracci-Laudiero, Gian Marco Moneta, Gillian Rice, Anne-Laure Mathieu, Sulliman O. Omarjee, Tracy A. Briggs, James O’Sullivan, Simon Williams, Rolando Cimaz, Eve Smith, Michael W. Beresford, Yanick J. Crow, GENIAL Investigators, UK JSLE Study Group, Madeleine Rooney, Nick Bishop, joyce davidson, Clarissa pilkington, Michael Beresford, Jacqui Clinch, Rangaraj Satyapal, Helen Foster, Janet Gardner Medwin, Janet McDonagh, Sue Wyatt, On Behalf of the British Society for Paediatric and Adolescent Rheumatology, Valentina Litta Modignani, Francesco Baldo, Stefano Lanni, Alessandro Consolaro, Giovanni Filocamo, Helen J. Lachmann, on behalf of Eurofever Registry, Gianmarco Moneta, Camilla Celani, Bilade Cherqaoui, Linda Rossi-Semerano, Perrine Dusser, Véronique Hentgen, Claire Grimwood, Linda Rossi, Isabelle Kone Paut, Veronique Hentgen, Denise Lasigliè, Denise Ferrera, Giulia Amico, Marco Di Duca, Laura Obici, Roberto Ravazzolo, Ryuta Nishikomori, Juan Arostegui, Andrea Petretto, Chiara Lavarello, Elvira Inglese, Federica Vanoni, Michaël Hofer, on behalf of EUROFEVER PROJECT, P. N. Hawkins, T. van der Poll, U. A. Walker, H. H. Tilson, Pascal N. Tyrrell, Raphaela Goldbach-Mansky, Norbert Blank, Hal M. Hoffman, Elisabeth Weissbarth-Riedel, Boris Huegle, Tilmann Kallinich, Ahmet Gul, Marlen Oswald, Fatma Dedeoglu, Aki Hanaya, Takako Miyamae, Manabu Kawamoto, Yumi Tani, Takuma Hara, Yasushi Kawaguchi, Satoru Nagata, Hisashi Yamanaka, Almira Ćosićkić, Fahrija Skokić, Belkisa Čolić, Sanimir Suljendić, Anna Kozlova, Irina Mersiyanova, Mariya Panina, Lily Hachtryan, Vasiliy Burlakov, Elena Raikina, Alexey Maschan, Anna Shcherbina, Banu Acar, Meryem Albayrak, Betul Sozeri, Sezgin Sahin, Amra Adrovic, Nese Inan, Serhan Sevgi, Caroline M. Andreasen, Anne Grethe Jurik, Mia B. Glerup, Christian Høst, Birgitte T. Mahler, Ellen-Margrethe Hauge, Cecilia Lazea, Laura Damian, Calin Lazar, Rodica Manasia, Chloe M. Stephenson, Vimal Prajapati, Paivi M. Miettunen, Dilek Yılmaz, Yavuz Tokgöz, Yasin Bulut, Harun Çakmak, Ferah Sönmez, Elif Comak, Gülşah Kaya Aksoy, Mustafa Koyun, Sema Akman, Yunus Arıkan, Ender Terzioğlu, Osman Nidai Özdeş, İbrahim Keser, Hüseyin Koçak, Ayşen Bingöl, Aygen Yılmaz, Reha Artan, X. Xu, Fatemeh F. Mehregan, Vahid Ziaee, Mohammad H. Moradinejad, Francesco La Torre, Clotilde Alizzi, Pio D’Adamo, G. Junge, J. Gregson, Hasmik Sargsyan, Hulya Zengin, Berna E. Fidanci, Cagla Kaymakamgil, Dilek Konukbay, Dilek Yildiz, Faysal Gok, Iris Stoler, Judith Freytag, Banu Orak, Christine Seib, Lars Esmann, Eva Seipelt, Faekah Gohar, Dirk Foell, Ismail Dursun, Sebahat Tulpar, Sibel Yel, Demet Kartal, Murat Borlu, Funda Bastug, Hakan Poyrazoglu, Zubeyde Gunduz, Kader Kose, Mehmet E. Yuksel, Abdullah Calıskan, Ahmet B. Cekgeloglu, Ruhan Dusunsel, Katerina Bouchalova, Jana Franova, Marcel Schuller, Marie Macku, Katerina Theodoropoulou, Raffaella Carlomagno, Annette von Scheven-Gête, Claudia Poloni, Laura O. Damian, Dan Cosma, Amanda Radulescu, Dan Vasilescu, Liliana Rogojan, Simona Rednic, Mihaela Lupse, Lien De Somer, Pierre Moens, Rocio Galindo Zavala, Laura Martín Pedraz, Esmeralda Núñez Cuadros, Gisela Díaz-Cordovés Rego, Antonio L. Urda Cardona, Ilaria Dal Forno, Sara Pieropan, Ombretta Viapiana, Davide Gatti, Gloria Dallagiacoma, Paola Caramaschi, Domenico Biasi, Daniel Windschall, Ralf Trauzeddel, Hartwig Lehmann, Rainer Berendes, Maria Haller, Manuela Krumrey-Langkammerer, Antje Nimtz-Talaska, Philipp Schoof, Ralf Felix Trauzeddel, Christine Nirschl, Estefania Quesada-Masachs, Carla Aguilar Blancafort, Sara Marsal Barril, Francisca Aguiar, Rita Fonseca, Duarte Alves, Ana Vieira, Alberto Vieira, Jorge A. Dias, Iva Brito, Gordana Susic, Vera Milic, Goran Radunovic, Ivan Boricic, Pauline Marteau, Catherine Adamsbaum, Michel De Bandt, Irène Lemelle, Chantal Deslandre, Tu Anh Tran, Anne Lohse, Elisabeth Solau-Gervais, Pascal Pillet, Julien Wipff, Cécile Gaujoux-Viala, Sylvain Breton, Valérie Devauchelle-Pensec, Sandra Gran, Olesja Fehler, Stefanie Zenker, Michael Schäfers, Thomas Vogl, Severine Guillaume Czitrom, EH Pieter Van Dijkhuizen, Silvia Magni Manzoni, Francesca Magnaguagno, Laura Tanturri de Horatio, Nienke M. Ter Haar, Annemieke S. Littooij, Vitor A. Teixeira, Raquel Campanilho-Marques, Ana F. Mourão, Filipa O. Ramos, Manuela Costa, Wafa A. Madan, Orla G. Killeen, Adriana Rodriguez Vidal, Diana Sueiro Delgado, Maria Isabel Gonzalez Fernandez, Berta Lopez Montesinos, Aleksey Kozhevnikov, Nina Pozdeeva, Mikhail Konev, Evgeniy Melchenko, Vladimir Kenis, Gennadiy Novik, Aysenur Pac Kısaarslan, Butsabong Lerkvaleekul, Suphaneewan Jaovisidha, Witaya Sungkarat, Niyata Chitrapazt, Praman Fuangfa, Thumanoon Ruangchaijatuporn, Soamarat Vilaiyuk, Dan Ø. Pradsgaard, Arne Hørlyck, Anne H. Spannow, Carsten W. Heuck, Talia Diaz, Fernando Garcia, Lorenia De La Cruz, Nadina Rubio, Joanna Świdrowska-Jaros, Elzbieta Smolewska, Mirta Lamot, Lovro Lamot, Mandica Vidovic, Edi Paleka Bosak, Ivana Rados, Miroslav Harjacek, Nikolay Tzaribachev, Polymnia Louka, Romiesa Hagoug, Chiara Trentin, Olga Kubassova, Mark Hinton, Mikael Boesen, Olena A. Oshlianska, Illya A. Chaikovsky, G. Mjasnikov, A. Kazmirchyk, Umberto Garagiola, Irene Borzani, Paolo Cressoni, Fabrizia Corona, Eszter Dzsida, Giampietro Farronato, Antonella Petaccia, Alenka Gagro, Agneza Marija Pasini, Goran Roic, Ozren Vrdoljak, Lucija Lujic, Matija Zutelija-Fattorini, Monika M. Esser, Deepthi R. Abraham, Craig Kinnear, Glenda Durrheim, Mike Urban, Eileen Hoal, Victoria B. Nikolayenko, Kubilay Şahin, Yasar Karaaslan, Adele Civino, Giovanni Alighieri, Sergio Davì, Roberto Rondelli, Andrea Magnolato, Francesca Ricci, Alma Olivieri, Valeria Gerloni, Bianca Lattanzi, Francesca Soscia, Alessandro De Fanti, Stefania Citiso, Lorenzo Quartulli, Maria Cristina Maggio, Manuela Marsili, Maria Antonietta Pelagatti, Valentino Conter, Franca Fagioli, Andrea Pession, Marco Garrone, Mariangela Rinaldi, Jaime De Inocencio, Stella Garay, Daniel J. Lovell, Berit Flato, EPOCA Study Group, Angela Aquilani, Simona Cascioli, Ivan Caiello, Denise Pires-Marafón, Rita Carsetti, Emily Robinson, Salvatore Albani, Wilco de Jager, Sytze de Roock, Trang Duong, Justine Ellis, Kimme Hyrich, Laetitia Jervis, Daniel Lovell, Lucy Marshall, Elizabeth D. Mellins, Kirsten Minden, Jane Munro, Peter A. Nigrovic, Jason Palman, Sunil Sampath, Laura E. Schanberg, Susan D. Thompson, Richard Vesely, Chris Wallace, Chris Williams, Qiong Wu, Nico Wulffraat, Rae S. M. Yeung, M. B. Seyger, D. Arikan, J. K. Anderson, A. Lazar, D. A. Williams, C. Wang, R. Tarzynski-Potempa, J. S. Hymans, Gabriele Simonini, Erika Scoccimarro, Irene Pontikaki, Teresa Giani, Alessandro Ventura, Pier Luigi Meroni, Gaetana Minnone, Marzia Soligo, Luigi Manni, Luisa Bracci Laudiero, Noortje Groot, I. Grein, N. M. Wulffraat, R. Schepp, G. Berbers, C. C. Barbosa Sandoval de Souza, V. Paes Leme Ferriani, G. Pileggi, S. de Roock, Ingrid H. R. Grein, Silvia Scala, Elisa Patrone, Casper Schoemaker, on behalf of Dutch JIA patient organization, Wendy Costello, on behalf of ENCA, Suzanne Parsons, Jean-David Cohen, Damien Bentayou, Marc-Antoine Bernard Brunel, Sonia Trope, Jens Klotsche, Miriam Listing, Martina Niewerth, Gerd Horneff, Angelika Thon, Hans-Iko Huppertz, Kirsten Mönkemöller, Ivan Foeldvari, ICON study group, Achille Marino, Stefano Stagi, Niccolò Carli, Federico Bertini, Adriana S. Díaz-Maldonado, Sally Pino, Pilar Guarnizo, Alfonso Ragnar Torres-Jimenez, Berenice Sanchez-Jara, Eunice Solis-Vallejo, Adriana Ivonne Cespedes-Cruz, Maritza Zeferino-Cruz, Julia Veronica Ramirez-Miramontes, Ankur Kumar, Anju Gupta, Deepti Suri, Amit Rawat, Nandita Kakkar, Surjit Singh, Özge A. Gücenmez, Erbil Ünsal, Bo Magnusson, Karina Mördrup, Anna Vermé, Christina Peterson, Board of the Swedish Pediatric Rheumatology Registry, Caroline Freychet, Jean Louis Stephan, Cathryn E. Harkness, Leanne Foster, Emma Henry, Pauline Taggart, Coskun F. Ozkececi, Esra Kurt, Gokalp Basbozkurt, Daiva Gorczyca, Jacek Postępski, Aleksandra Czajkowska, Bogumiła Szponar, Mariola Paściak, Anna Gruenpeter, Iwona Lachór-Motyka, Daria Augustyniak, Edyta Olesińska, Emediong S. Asuka, Tatyana Golovko, Samuel U. Aliejim, Emilio Inarejos Clemente, Estibaliz Iglesias Jimenez, Joan Calzada Hernandez, Sergi Borlan Fernandez, Clara Gimenez Roca, David Moreno Romo, Natalia Rodriguez Nieva, Juan Manuel Mosquera Angarita, Jordi Anton Lopez, Esmeralda Nuñez-Cuadros, Gisela Diaz-Cordovés, Rocío Galindo-Zavala, Antonio Urda-Cardona, Antonio Fernández-Nebro, Daniel Álvarez de la Sierra, Marina Garcia Prat, Mónica Martínez Gallo, Ricardo Pujol Borrell, Ana M. Marín Sánchez, Etienne Merlin, Sylvie Fraitag, Jean-Louis Stephan, Federico Annoni, Giancarla Di Landro, Sofia Torreggiani, Marta Torcoletti, Georgina Tiller, Jo Buckle, Angela Cox, Peter Gowdie, Roger C. Allen, Jonathan D. Akikusa, Hayde G. Hernández-Huirache, Edel R. Rodea-Montero, William Fahy, Christelle Sordet, Karin B. Berggren, Johanna T. Kembe, Joyce Bos, Wineke Armbrust, Marco van Brussel, Jeanette Cappon, Pieter Dijkstra, Jan Geertzen, Elizabeth Legger, Marion van Rossum, Pieter Sauer, Otto Lelieveld, Levent Buluc, Gur Akansel, Bahar Muezzinoglu, Ljubov Rychkova, Tatyana Knyazeva, Anna Pogodina, Tatyana Belova, Tamara Mandzyak, Ekaterina Kulesh, Alessandro Cafarotti, Cosimo Giannini, Roberta Salvatore, Giuseppe Lapergola, Caterina Di Battista, Maria Loredana Marcovecchio, Raffaella Basilico, Piernicola Pelliccia, Francesco Chiarelli, Luciana Breda, Beverley Almeida, Sarah Tansley, Harsha Gunawardena, Neil McHugh, Juvenile Dermatomyositis Research Group (JDRG), Jessie Aouizerate, Marie De Antonio, Christine Barnerias, Guillaume Bassez, Isabelle Desguerre, Romain Gherardi, Jean-Luc Charuel, François-Jérôme Authier, Cyril Gitiaux, C. H. Spencer, Rabheh Abdul Aziz, Chack-Yung Yu, Brent Adler, Sharon Bout-Tabaku, Katherine Lintner, Melissa Moore-Clingenpeel, Liza McCann, Nicola Ambrose, Mario Cortina-Borja, Juvenile Dermatomyositis Cohort and Biomarker Study (JCDBS), Prasad T. Oommen, Fabian Speth, Johannes-Peter Haas, Working Group “Juvenile Dermatomyositis” of the German Society for Paediatric and Adolescent Rheumatology (GKJR), Claudio Lavarello, Gabriella Giancane, Angela Pistorio, Lisa Rider, Rohit Aggarwal, Sheila K. Oliveira, Ruben Cuttica, Michel Fischbach, Gary Sterba, Karine Brochard, Frank Dressler, Patrizia Barone, Ruben Burgos-Vargas, Elizabeth Candell Chalom, Marine Desjonqueres, Graciela Espada, Anders Fasth, Stella Maris Garay, Rose-Marie Herbigneaux, Claire Hoyoux, Chantal Job Deslandre, Frederick W. Miller, Jiri Vencovsky, Erdal Sag, Gulsev Kale, Haluk Topaloglu, Beril Talim, Francesco Zulian, Tadej Avcin, Roberto Marini, Anne Pagnier, Michel Rodiere, Christine Soler, Rebecca Ten Cate, Yosef Uziel, Jelena Vojinovic, Ana V. Villarreal, Nydia Acevedo, Yuridiana Ramirez, Enrique Faugier, Rocio Maldonado, Bita Arabshahi, John H. Lee, Ian Leibowitz, Lawrence O. Okong’o, Jo Wilmshurst, Monika Esser, Christiaan Scott, Ezgi Deniz Batu, Nagehan Emiroglu, Hafize Emine Sonmez, Gokcen Dilsa Tugcu, Zehra Serap Arici, Ebru Yalcin, Deniz Dogru, Ugur Ozcelik, Mithat Haliloglu, Nural Kiper, Masato Yashiro, Mutsuko Yamada, Toshihiko Yabuuchi, Tomonobu Kikkawa, Nobuyuki Nosaka, Yosuke Fujii, Yukie Saito, Hirokazu Tsukahara, Sulaiman M. Al-Mayouf, Nora AlMutiari, Mohammed Muzaffer, Rawiah shehata, Adel Al-Wahadneh, Reem Abdwani, Safia Al-Abrawi, Mohammed Abu-shukair, Zeyad El-Habahbeh, Abdullah Alsonbul, Aleksandra Szabat, Monika Chęć, Violetta Opoka-Winiarska, Biman Saikia, Ranjana W. Minz, Christine Arango, Clara Malagon, Maria D. P. Gomez, Angela C. Mosquera, Ricardo Yepez, Tatiana Gonzalez, Camilo Vargas, GRIP study group, Marta Balzarin, Biagio Castaldi, Elena Reffo, Francesca Sperotto, Giorgia Martini, Alessandra Meneghel, Ornella Milanesi, Ozgur Kasapçopur, Maria Teresa Terreri, Ekaterina Alexeeva, Maria Katsicas, Mikhail Kostik, Thomas Lehman, W.-Alberto Sifuentes-Giraldo, Vanessa Smith, Flavio Sztajnbok, Tadey Avcin, Maria Jose Santos, Dana Nemcova, Cristina Battagliotti, Liora Harel, Mahesh Janarthanan, Kathryn Torok, Nicola Helmus, Eileen Baildem, Michael Blakley, Kim Fligelstone, Antonia Kienast, Clare Pain, Amanda Saracino, Gabriele Simoni, Lisa Weibel, Maria K. Osminina, Nathalia A. Geppe, Olga V. Niconorova, Olesya V. Karashtina, Oksana V. Abbyasova, Olga V. Shpitonkova, Sinem Durmus, Hafize Uzun, Angela Mauro, Eleonora Fanti, Fabio Voller, Franca Rusconi, Fernando Garcia-Rodriguez, Ana V. Villarreal-Treviño, Angel J. Flores-Pineda, Paola B. Lara-Herrea, Diego R. Salinas-Encinas, Talia Diaz-Prieto, Maria R. Maldonado-Velazquez, Sarbelio Moreno-Espinosa, Enrique Faugier-Fuentes, Mirella Crapanzano, Ilaria Parissenti, Man S. Parihar, Pandiarajan Vignesh, ManojKumar Rohit, Kavitha Gopalan, Savita V. Attri, Alan Salama, David Jayne, Mark Little, Yulia Kostina, Galina Lyskina, Olga Shpitonkova, Alena Torbyak, Olga Shirinsky, Maria Francesca Gicchino, Maria Cristina Smaldone, Mario Diplomatico, Alma Nunzia Olivieri, C H. Spencer, Richard McClead, Hiren Patel, Chung-Yung Yu, Dita Cebecauerová, Tomáš Dallos, Edita Kabíčková, Martin Kynčl, Daniela Chroustová, Jozef Hoza, Dana Němcová, Vladimír Tesař, Pavla Doležalová, Tuncay Hazirolan, Fatih Ozaltin, Fabiola Almeida, Isabela H. Faria de Paula, Maíra M. Sampaio, Fernando N. Arita, Andressa G. Alves, Maria Carolina Santos, Eunice M. Okuda, Silvana B. Sacchetti, Fernanda Falcini, Marini Francesca, Gemma Lepri, Marco Matucci-Cerinic, Maria Luisa Brandi, Hakan Kisaoglu, Sema Misir, Selim Demir, Yuksel Aliyazicioglu, Mukaddes Kalyoncu, Carlos Eduardo Ramalho, Fabiola D. Almeida, Joan Calzada-Hernández, Rosa Bou, Estíbaliz Iglesias, Judith Sánchez-Manubens, Fredy Hermógenes Prada Martínez, Clara Giménez Roca, Sergi Borlan Fernández, Marek Bohm, Kamran Mahmood, Valentina Leone, Mark Wood, Ken-Ichi Yamaguchi, Satoshi Fujikawa, Working Group of Behçet’s Disease, Pediatric Rheumatology Association of Japan (PRAJ), Kyu Yeun Kim, Do Young Kim, Dong Soo Kim, Maka Ioseliani, Ivane Chkhaidze, Maia Lekishvili, Nana Tskhakaia, Shorena Tvalabeishvili, Aleksandre Kajrishvili, Maiko Takakura, Masaki Shimizu, Natsumi Inoue, Mao Mizuta, Akihiro Yachie, Giovanni Corsello, Maryam Piram, Carla Maldini, Sandra Biscardi, Nathalie Desuremain, Catherine Orzechowski, Emilie Georget, Delphine Regnard, Isabelle Kone-Paut, Alfred Mahr, Mihaela Sparchez, Zeno Sparchez, Nydia Acevedo Silva, Ana V. Villarreal Treviño, Yuridiana Ramirez Loyola, Talia Diaz Prieto, Enrique Faugier Fuentes, Maria D. R. Maldonado Velazquez, Pilar Perez, Sagar Bhattad, Ranjana Minz, Jitendra Shandilya, Pediatric Allergy and Immunology Unit, PGIMER, Chandigarh, Ana Villarreal, Yuridiana Ramírez, Zeynep Birsin Özçakar, Suat Fitoz, Fatos Yalcinkaya, Annacarin Horne, Francesca Minoia, Francesca Bovis, Sergio Davi, Priyankar Pal, Kimo Stein, Sandra Enciso, Michael Jeng, Despoina Maritsi, Randy C. Cron, Anne Thorwarth, Sae Lim von Stuckrad, Angela Rösen-Wolff, Hella Luksch, Patrick Hundsdoerfer, Peter Krawitz, Nuray Aktay Ayaz, Doğan Simsek, Şebnem Sara Kılıc, Emine Sonmez, Aysenur Pac Kisaarslan, Ozge Altug Gucenmez, Z. Serap Arıcı, Fatih Kelesoglu, Zelal Ekinci Ekinci, Maria Miranda-Garcia, Carolin Pretzer, Michael Frosch, F. Gohar, Angela McArdle, Niamh Callan, Belinda Hernandez, Miha Lavric, Oliver FitzGerald, Stephen R. Pennington, Joachim Peitz, Joern Kekow, Ariane Klein, Anna C. Schulz, Frank Weller-Heinemann, Anton Hospach, J-Peter Haas, BIKER collaborative group, Karen Put, Jessica Vandenhaute, Anneleen Avau, Annemarie van Nieuwenhuijze, Ellen Brisse, Tim Dierckx, Omer Rutgeerts, Josselyn E. Garcia-Perez, Jaan Toelen, Mark Waer, Georges Leclercq, An Goris, Johan Van Weyenbergh, Adrian Liston, Patrick Matthys, Carine H. Wouters, Yasuo Nakagishi, Michael J. Ombrello, Victoria Arthur, Anne Hinks, Patricia Woo, International Childhood Arthritis Genetics (INCHARGE) Consortium, Barbara Stanimirovic, Biljana Djurdjevic-Banjac, Olivera Ljuboja, Boris Hugle, MArgarita Onoufriou, Olga Vougiouka, Kenza Bouayed, Sanae El Hani, Imane Hafid, Nabiha Mikou, Nunu Shelia, Mari Laan, Jaanika Ilisson, and Chris Pruunsild

Subjects
Pediatrics, RJ1-570, Diseases of the musculoskeletal system, RC925-935
Published
2017
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43. Les myosites à éosinophiles idiopathiques

Author

Cécile Fermon, François-Jérôme Authier, and Laure Gallay

Abstract

Les myosites à éosinophiles appartiennent au groupe des myopathies inflammatoires idiopathiques et sont définies par un infiltrat inflammatoire musculaire composé de polynucléaires éosinophiles. Il n’existe pas à ce jour de consensus concernant le diagnostic et le traitement de ces patients. Grâce à une revue exhaustive de la littérature, les principales caractéristiques cliniques et histologiques, ainsi que le traitement et l’évolution des patients, ont été résumés dans cette synthèse. Cette revue a permis de distinguer trois sous-groupes de myosites à éosinophiles : la forme focale, la forme diffuse et les périmyosites à éosinophiles. Un algorithme de traitement et de prise en charge est proposé, et les principaux diagnostics différentiels sont discutés.

Published
2022

44. Thyroid-stimulating hormone receptor signaling restores skeletal muscle stem cell regeneration in rats with muscular dystrophy

Author

Taglietti, Valentina, primary, Kefi, Kaouthar, additional, Rivera, Lea, additional, Bergiers, Oriane, additional, Cardone, Nastasia, additional, Coulpier, Fanny, additional, Gioftsidi, Stamatia, additional, Drayton-Libotte, Bernadette, additional, Hou, Cyrielle, additional, Authier, François-Jérôme, additional, Pietri-Rouxel, France, additional, Robert, Matthieu, additional, Bremond-Gignac, Dominique, additional, Bruno, Claudio, additional, Fiorillo, Chiara, additional, Malfatti, Edoardo, additional, Lafuste, Peggy, additional, Tiret, Laurent, additional, and Relaix, Frédéric, additional

Published
2023
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46. Distinct interferon signatures stratify inflammatory and dysimmune myopathies

Author

Muriel Rigolet, Cyrielle Hou, Yasmine Baba Amer, Jessie Aouizerate, Baptiste Periou, Romain K Gherardi, Peggy Lafuste, and François Jérôme Authier

Subjects
Medicine
Abstract

Objective The role of interferons (IFN) in the pathophysiology of primary inflammatory and dysimmune myopathies (IDM) is increasingly investigated, notably because specific neutralisation approaches may constitute promising therapeutic tracks. In present work we analysed the muscular expression of specific IFNα/β and IFNγ-stimulated genes in patients with various types of IDM.Methods 39 patients with IDM with inclusion body myositis (IBM, n=9), dermatomyositis (DM, n=10), necrotising autoimmune myopathies (NAM, n=10) and antisynthetase myositis (ASM, n=10), and 10 controls were included. Quantification of expression levels of IFNγ, ISG15, an IFNα/β-inducible gene and of six IFNγ-inducible genes (GBP2, HLA-DOB, HLA-DPB, CIITA, HLA-DRB and HLA-DMB) was performed on muscle biopsy samples.Results DM usually associated with strong type I IFNα/β signature, IBM and ASM with prominent type II IFNγ signature and NAM with neither type I nor type II IFN signature. Immunofluorescence study in ASM and IBM showed myofibre expression of major histocompatibility class 2 (MHC-2) and CIITA, confirming the induction of the IFNγ pathway. Furthermore, MHC-2-positive myofibres were observed in close proximity to CD8+ T cells which produce high levels of IFNγ.Conclusion Distinct IFN signatures allow a more distinct segregation of IDMs and myofibre MHC-2 expression is a reliable biomarker of type II IFN signature.

Published
2019
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48. Anti-SAE autoantibody in dermatomyositis: original comparative study and review of the literature

Author

Juliette Demortier, Mathieu Vautier, Olivier Chosidow, Laure Gallay, Didier Bessis, Alice Berezne, Nadège Cordel, Jean Schmidt, Amar Smail, Pierre Duffau, Marie Jachiet, Edouard Begon, Jeremy Gottlieb, François Chasset, Julie Graveleau, Myriam Marque, Elise Cesbron, Amandine Forestier, Séverine Josse, Nicolas Kluger, Caroline Beauchêne, Yannick Le Corre, Valentine Pagis, Aude Rigolet, Perrine Guillaume-Jugnot, François-Jérôme Authier, Nelly Guilain, Nathalie Streichenberger, Sarah Leonard-Louis, Samia Boussouar, Océane Landon-Cardinal, Olivier Benveniste, and Yves Allenbach

Subjects
Rheumatology, Pharmacology (medical)
Abstract

Objective Among specific autoantibodies in DM, the anti–small ubiquitin-like modifier activating enzyme (SAE) antibody is rare. We aim to describe the clinical characteristics, cancer prevalence, and muscle pathology of anti-SAE–positive DM. Methods Patients with a diagnosis of DM and sera positive for the anti-SAE antibody were recruited from 19 centres in this retrospective observational study. The available muscular biopsies were reviewed. We conducted a comparison with anti-SAE–negative DM and a review of the literature. Results Of the patients in the study (n = 49), 84% were women. Skin involvement was typical in 96% of patients, with 10% having calcinosis, 18% ulceration and 12% necrosis; 35% presented with a widespread skin rash. Muscular disease affected 84% of patients, with mild weakness [Medical Research Council (MRC) scale 4 (3, 5)], although 39% of patients had dysphagia. Muscular biopsies showed typical DM lesions. Interstitial lung disease was found in 21% of patients, mainly with organizing pneumonia pattern, and 26% of patients showed dyspnoea. Cancer-associated myositis was diagnosed in 16% of patients and was responsible for the majority of deaths, its prevalence being five times that of the general population. IVIG therapy was administered to 51% of the patients during the course of the disease. Comparison with anti-SAE–negative DM (n = 85) showed less and milder muscle weakness (P = 0.02 and P = 0.006, respectively), lower creatinine kinase levels (P Conclusion Anti-SAE positive DM is a rare subgroup associated with typical skin features but a potentially diffuse rash, a mild myopathy. Interstitial lung disease defines an organizing pneumonia pattern. Cancer associated DM prevalence is five times that of the general population. Trial registration ClinicalTrials.gov, http://clinicaltrials.gov, NCT04637672.

Published
2023

49. Thyroid-stimulating hormone receptor signaling restores skeletal muscle stem cell regeneration in rats with muscular dystrophy

Author

Valentina Taglietti, Kaouthar Kefi, Lea Rivera, Oriane Bergiers, Nastasia Cardone, Fanny Coulpier, Stamatia Gioftsidi, Bernadette Drayton-Libotte, Cyrielle Hou, François-Jérôme Authier, France Pietri-Rouxel, Matthieu Robert, Dominique Bremond-Gignac, Claudio Bruno, Chiara Fiorillo, Edoardo Malfatti, Peggy Lafuste, Laurent Tiret, and Frédéric Relaix

Subjects
General Medicine
Abstract

Duchenne muscular dystrophy (DMD) is a severe and progressive myopathy leading to motor and cardiorespiratory impairment. We analyzed samples from patients with DMD and a preclinical rat model of severe DMD and determined that compromised repair capacity of muscle stem cells in DMD is associated with early and progressive muscle stem cell senescence. We also found that extraocular muscles (EOMs), which are spared by the disease in patients, contain muscle stem cells with long-lasting regenerative potential. Using single-cell transcriptomics analysis of muscles from a rat model of DMD, we identified the gene encoding thyroid-stimulating hormone receptor ( Tshr ) as highly expressed in EOM stem cells. Further, TSHR activity was involved in preventing senescence. Forskolin, which activates signaling downstream of TSHR, was found to reduce senescence of skeletal muscle stem cells, increase stem cell regenerative potential, and promote myogenesis, thereby improving muscle function in DMD rats. These findings indicate that stimulation of adenylyl cyclase leads to muscle repair in DMD, potentially providing a therapeutic approach for patients with the disease.

Published
2023

50. European Network on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (EUROMENE): Expert Consensus on the Diagnosis, Service Provision, and Care of People with ME/CFS in Europe

Author

Luis Nacul, François Jérôme Authier, Carmen Scheibenbogen, Lorenzo Lorusso, Ingrid Bergliot Helland, Jose Alegre Martin, Carmen Adella Sirbu, Anne Marit Mengshoel, Olli Polo, Uta Behrends, Henrik Nielsen, Patricia Grabowski, Slobodan Sekulic, Nuno Sepulveda, Fernando Estévez-López, Pawel Zalewski, Derek F. H. Pheby, Jesus Castro-Marrero, Giorgos K. Sakkas, Enrica Capelli, Ivan Brundsdlund, John Cullinan, Angelika Krumina, Jonas Bergquist, Modra Murovska, Ruud C. W. Vermuelen, and Eliana M. Lacerda

Subjects
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, diagnosis, health services, care, Medicine (General), R5-920
Abstract

Designed by a group of ME/CFS researchers and health professionals, the European Network on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (EUROMENE) has received funding from the European Cooperation in Science and Technology (COST)—COST action 15111—from 2016 to 2020. The main goal of the Cost Action was to assess the existing knowledge and experience on health care delivery for people with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) in European countries, and to enhance coordinated research and health care provision in this field. We report our findings and make recommendations for clinical diagnosis, health services and care for people with ME/CFS in Europe, as prepared by the group of clinicians and researchers from 22 countries and 55 European health professionals and researchers, who have been informed by people with ME/CFS.

Published
2021
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