Annales d'endocrinologie最新文献

{"title":"Nationwide implementation of exclusion non-invasive prenatal diagnosis for single-gene disorders: nine-year activity and performance analysis from the French public network.","authors":"Adrien Labarthe, Solène Doppler, Marie-Pierre Audrézet, Thierry Bienvenu, Nathalie Couque, Inès Defer, Victor Gravrand, France Leturcq, Luke Mansard, Emmanuelle Masson, Lucie Orhant Boimard, Nicolas Vaucouleur, Marie-Claire Vincent, Camille Verebi, Juliette Nectoux","doi":"10.1016/j.ando.2026.102519","DOIUrl":"https://doi.org/10.1016/j.ando.2026.102519","url":null,"abstract":"<p><strong>Introduction: </strong>Non-invasive prenatal diagnosis for single-gene disorders (SGD-NIPD) has progressively emerged as a reliable alternative to invasive prenatal procedures in selected high-risk situations. In France, an exclusion strategy targeting paternal or de novo pathogenic variants has been implemented through a coordinated nationwide public network. We report five-year activity data, key technical performance indicators, and future perspectives of this model.</p><p><strong>Methods: </strong>We conducted a retrospective multicenter study including all exclusion NIPD tests performed within the French public network between January 2017 and January 2026. Variant-specific assays were developed using droplet digital PCR (ddPCR). We analyzed activity trends, indication spectrum, assay availability, diagnostic reliability, and turnaround time.</p><p><strong>Results: </strong>A total of 2,038 exclusion NIPD tests were performed. Annual activity increased elevenfold between 2017 and 2025, reaching 611 tests in 2025. Indications comprised de novo variants (52%), autosomal recessive conditions (34%), and autosomal dominant disorders (13%). Across four centers, 1,133 validated variant-specific assays are currently available, covering 478 genes. Assay development success rate reached approximately 94%. No false-positive or false-negative results have been reported. The mean turnaround time was 6 days.</p><p><strong>Conclusion: </strong>Exclusion NIPD for single-gene disorders has achieved nationwide scalability within a public healthcare framework, combining analytical robustness, rapid result delivery, and broad disease coverage. Ongoing developments, including targeted haplotype-based approaches for maternally inherited variants within the national DANNIgene program, aim to extend the scope of non-invasive prenatal diagnosis. These advances may ultimately pave the way toward broader genomic inference strategies while maintaining structured clinical and ethical oversight.</p>","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":" ","pages":"102519"},"PeriodicalIF":2.9,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147494852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genome‑Wide Association Studies (GWAS) in 2026: from gene hunting to biological discovery in endocrine and cardiometabolic diseases.","authors":"Takiy-Eddine Berrandou","doi":"10.1016/j.ando.2026.102509","DOIUrl":"https://doi.org/10.1016/j.ando.2026.102509","url":null,"abstract":"<p><strong>Background: </strong>Genome-wide association studies (GWAS) emerged with expectations borrowed from Mendelian genetics, creating a gap between what the method can and cannot deliver. This gap has fuelled both unwarranted dismissal and unwarranted enthusiasm. For endocrine clinicians, the confusion is consequential because GWAS and clinical sequencing answer fundamentally different questions and serve different purposes.</p><p><strong>Purpose: </strong>This review defines what GWAS is designed to do, clarifies the state of the \"missing heritability\" debate in 2026, and evaluates the contribution of GWAS to endocrine and cardiometabolic disease biology, including thyroid function, reproductive timing, adrenal steroid traits, type 2 diabetes, and lipid disorders. It also addresses methodological advances in the modern GWAS toolkit, the current status of polygenic risk scores, and the lessons from applying GWAS to understudied vascular diseases with endocrinological relevance.</p><p><strong>Key findings: </strong>GWAS maps polygenic architecture, prioritizes biological pathways and tissues, and supports therapeutic target validation using human genetic evidence. It does not provide molecular diagnoses in individual patients. Large meta-analyses have identified hundreds of robust loci for thyroid-stimulating hormone, age at menarche, age at natural menopause, cortisol binding, primary aldosteronism, and type 2 diabetes subtypes. Multi-ancestry designs improve discovery and fine-mapping resolution. In rare but well-phenotyped vascular conditions such as spontaneous coronary artery dissection and fibromuscular dysplasia, GWAS has identified biologically coherent loci and tested hormonal hypotheses, demonstrating that rigorous phenotyping can partly compensate for modest sample sizes. Polygenic risk scores can identify individuals at high genetic risk for common endocrine traits, but portability across ancestry groups and clinical implementation remain unresolved challenges.</p><p><strong>Conclusions: </strong>GWAS remains a relevant and productive tool in endocrine genetics in 2026, provided its outputs are interpreted correctly. Its role is interpretive and mechanistic rather than diagnostic. Integrated with sequencing, functional genomics, and Mendelian randomization, it offers a structured framework for moving from statistical association to biological understanding and, in selected contexts, to risk stratification research.</p>","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":" ","pages":"102509"},"PeriodicalIF":2.9,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147494811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imprinting disorders and multiple imprinting abnormalities (multilocus imprinting disturbances): new diagnoses, new perspectives.","authors":"Frédéric Brioude","doi":"10.1016/j.ando.2026.102515","DOIUrl":"https://doi.org/10.1016/j.ando.2026.102515","url":null,"abstract":"<p><p>Imprinting disorders result from (epi)genetic abnormalities affecting genomic regions whose expression depends on parental origin. Among these, multilocus imprinting disturbances (MLID) constitute a specific entity characterised by simultaneous alterations in several imprinted regions, often leading to complex phenotypes. In recent years, the identification of maternal genetic factors, particularly within the maternal subcortical complex (SCMC), has led to a better understanding of the origin of certain cases of MLID. At the same time, rapid advances in molecular analysis-methylation arrays, targeted NGS panels, and long-read sequencing approaches-have profoundly renewed diagnostic capabilities. Together, these advances now offer a more integrated view of the mechanisms, phenotypes, and genetic determinants of imprinting-related diseases.</p>","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":" ","pages":"102515"},"PeriodicalIF":2.9,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147494889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KDM1A pathogenic variants link epigenetic regulation to GIP-dependent Primary Bilateral Macronodular Adrenal Hyperplasia.","authors":"Fanny Chasseloup, Peter Kamenicky","doi":"10.1016/j.ando.2026.102516","DOIUrl":"https://doi.org/10.1016/j.ando.2026.102516","url":null,"abstract":"<p><p>Patients with primary bilateral macronodular adrenal hyperplasia, recently reclassified as bilateral macronodular adrenal disease (BMAD) have bilateral benign large adrenocortical nodules and variable cortisol excess. BMAD is considered a rare cause of overt Cushing's syndrome but a more frequent cause of bilateral adrenal incidentalomas. Initially considered a sporadic disease, the bilateral nature of the adrenal nodules and familial aggregation suggested a genetic origin. Indeed, genomic studies have improved our understanding of BMAD pathogenesis and identified several genetic events responsible for BMAD. As rare syndromic presentations were described, non-syndromic etiologies were also identified, suggesting distinct molecular backgrounds among BMAD cases. Firstly, germline heterozygous inactivating mutations of the ARMC5 gene, discovered in 2013, are now known to account for around 20-25% of sporadic cases and most familial cases. A second molecular group was later identified, characterized by germline heterozygous pathogenic variants and loss of heterozygosity of the lysine demethylase 1A gene (KDM1A, or LSD1) in familial and sporadic GIP-dependent BMAD, representing less than 5% of BMAD cases. Similarly to ARMC5, the stepwise inactivation of KDM1A, an epigenetic regulator gene, supports a tumor suppressor model of tumorigenesis. The latter, more heterogeneous, molecular group remains globally unelucidated, with the exception of reports of pathogenic variants in genes involved in the PKA and cAMP signaling pathways. In all cases, genetic counseling should be offered to identify affected members and to screen for BMAD.</p>","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":" ","pages":"102516"},"PeriodicalIF":2.9,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147494803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"THE KEY DATA FROM THE 2025 ESE/ESPE CONGRESS: Chronic hypoparathyroidism in adults.","authors":"Geneviève Crouzeix, Philippe Caron","doi":"10.1016/j.ando.2026.102504","DOIUrl":"https://doi.org/10.1016/j.ando.2026.102504","url":null,"abstract":"","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":" ","pages":"102504"},"PeriodicalIF":2.9,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147379950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proceedings of the annual meeting of the European Consortium of Lipodystrophies (ECLip) Paris, France, 20-21 May 2025.","authors":"Camille Vatier, David Araújo-Vilar, Baris Akinci, Thierry Arnould, Carine Beaupère, Elise Bismuth, Rebecca J Brown, Giovanni Ceccarini, Philippe Collas, Alessandra Gambineri, Donatella Gilio, Sharon Halperin, Sonja Janmaat, Sophie Lamothe, Giovanna Lattanzi, Margherita Maffei, Ormond A MacDougald, Héléna Mosbah, Estelle Nobecourt, Elif A Oral, Justin Rochford, Ferruccio Santini, Eric C Schirmer, Julia von Schnurbein, Robert Semple, Daniel Tews, Martin Wabitsch, Marie-Christine Vantyghem, Corinne Vigouroux","doi":"10.1016/j.ando.2025.102432","DOIUrl":"10.1016/j.ando.2025.102432","url":null,"abstract":"<p><p>Lipodystrophy syndromes are rare diseases characterized by anatomical and functional defects of adipose tissue, frequently leading to severe insulin resistance-associated metabolic complications. Subtypes of lipodystrophy syndromes differ in: their clinical presentation, with generalized or partial loss of adipose tissue; in their origin, either genetic or acquired; and in their comorbidities, forming a heterogeneous group of disorders of different severity. The European Consortium of Lipodystrophies (ECLip) was founded in 2014 as a non-profit network of health professionals, scientists and patient associations. ECLip aims to promote international collaborations to increase pathophysiological and clinical knowledge, and improve the management of lipodystrophy syndromes. ECLip now comprises 59 groups from 30 countries from Europe and beyond. The consortium developed in parallel to the increased awareness of clinical diagnosis, the growing scientific interest for these diseases at the crossroads between adipose tissue biology, whole body metabolism, genetics and immunity, and to the emergence of new pharmacological approaches. The ECLip congress, held every 18 months, aims to discuss the recent achievements and projects in the field of lipodystrophies, to consolidate ECLip activities and to promote future collaborations, highlighting clinical and fundamental aspects as well as patients' perspectives. Oral communications presented during the meeting in Paris, France, in 2025 are summarized in these minutes.</p>","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":" ","pages":"102432"},"PeriodicalIF":2.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144765811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"20-Hydroxyecdysone induces brown adipose tissue glycogen accumulation in obese gerbil model: Histochemical study","authors":"Z. Bellahreche, O. Sihali-Beloui, N. Semiane, A. Mallek, Y. Dahmani","doi":"10.1016/j.ando.2023.07.469","DOIUrl":"https://doi.org/10.1016/j.ando.2023.07.469","url":null,"abstract":"Obesity is a major public health problem. It is defined as an abnormal or excessive accumulation of fat harmful to health. Although the majority of obesity studies focus on changes in white adipose tissue, investigations into brown adipose tissue and its activation are becoming an increasingly popular area of interest. In this study, we attempted to examine the effects of 20-hydroxyecdysone (20E) on the glycogen amount stored in interscapular brown adipose tissue (IBAT). 15 gerbils were divided into: control group submitted to natural diet, two experimental groups submitted to high-calorie-diet supplemented or not with 20E. At the end of the experimental period, the animals were sacrificed and the IBAT was fixed in 10% formalin. Sections of 5 micrometers were made and stained with periodic acid-Schiff (PAS), to highlight the polysaccharides. Glycogen quantification in IBAT was performed using ImageJ software (NIH, Bethesda, MD, USA). PAS staining demonstrated that in the control gerbils, IBAT had strong cytoplasmic presence of glycogen. However, in the high-calorie diet group, the microscopy images had weaker PAS staining with lipid droplets infiltration compared to control group. We observed an important IBAT cytoplasm staining with PAS in group treated with 20E, indicating cells glycogen overload with reduction of lipid droplets accumulation. The quantification of glycogen had confirmed the qualitative study. Although the relationship between brown adipose tissue and glycogen storage remains underestimated and misunderstood, these preliminary results show that 20E could activate obese gerbil's brown adipocytes to store more glycogen.","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":"65 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135274371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L’hémiballisme secondaire à l’hyperglycémie non cétosique : une situation rare","authors":"Z. Habbadi, I. Gam","doi":"10.1016/j.ando.2023.07.455","DOIUrl":"https://doi.org/10.1016/j.ando.2023.07.455","url":null,"abstract":"Le diabète déséquilibré peut entraîner des complications neurologiques comme des crises épileptiques et des troubles de conscience. L’hémiballisme est une manifestation plus rare. Le mécanisme expliquant la survenue de ces mouvements anormaux lors d’une hyperglycémie sans cétose reste mal élucidé. Patiente de 67 ans, hypertendue sous traitement, diabétique de type 2 depuis 4 ans sous association metformine et insuline. Admise aux urgences neurologiques pour des mouvements anormaux de l’hémicorps droit d’apparition brutale. Ces mouvements prédominent au niveau proximal, d’abord au niveau du membre supérieur droit, puis au membre inférieur homolatéral à type de flexion extension et de rotation. Ils sont brusques et irréguliers altérant sa qualité de vie. Le bilan étiologique révèle une hyperglycémie à 5 g/L sans hyperosmolarité ni cétonurie ni syndrome infectieux associé. La TDM cérébrale montre une atteinte du striatum gauche. L’évolution était marquée par la disparition de l’hémiballisme deux semaines après l’équilibre glycémique et la mise sous neuroleptique à faible dose. L’hémiballisme est un mouvement unilatéral rapide, brutal, non rythmique, non suppressible, dû à une atteinte du striatum controlatéral. Bien que rare, l’hyperglycémie non cétosique est l’une de ses causes. Dans ce cadre, plusieurs hypothèses sont avancées. En effet, l’épuisement de l’acide gamma-aminobutyrique et de l’acétate au cours de l’hyperglycémie sans cétose, avec le manque d’énergie et l’acidose métabolique, serait à l’origine de l’apparition des mouvements anormaux. Le diagnostic est radiologique et le traitement repose sur l’équilibre glycémique.","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":"28 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135274381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiothyréose : à propos de neuf cas","authors":"W. Ben Hilel, I. Rojbi, S. Mekni, S. Essayeh, K. Khiari, I. Ben Nacef","doi":"10.1016/j.ando.2023.07.254","DOIUrl":"https://doi.org/10.1016/j.ando.2023.07.254","url":null,"abstract":"La cardiothyréose, complication majeure de l’hyperthyroïdie peut révéler ou survenir après le diagnostic la maladie. L’objectif de ce travail est de décrire le profil clinique, paraclinique et évolutif de la cardiothyréose. Il s’agissait d’une étude rétrospective descriptive réalisée à partir des patients hyperthyroïdiens hospitalisés dans notre service entre 2008 et 2022. Le diagnostic de cardiothyréose était retenu devant un trouble de rythme, une insuffisance cardiaque ou coronaire. Au total, 4 % des patients hyperthyroïdiens avaient une cardiothyréose (9/227). L’âge moyen était 55 ± 12 ans avec un sexe ratio = 2. La fréquence cardiaque moyenne était à 166 ± 32. L’amaigrissement et les palpitations étaient les signes prédominants retrouvés chez huit patients. L’hyperthyroïdie était fruste chez un patient. Le taux moyen de TSH était à 0,032 ± 0,02 U/ml et de FT4 à 3,5 ± 1,96 ng/dl [VN : 0,7–1,48]. Huit patients avaient une maladie de Basedow. L’arythmie cardiaque par fibrillation atriale (ACFA) était objectivée chez tous les patients et révélatrice de l’hyperthyroïdie dans trois cas. L’association ACFA et insuffisance cardiaque étaient présente chez deux patients. L’ETT montrait Une FEVG inférieure à 50 % et une HTAP dans deux cas. Le bisoprolol a été prescrit chez cinq patients. Parmi les six patients suivis après normalisation de la FT4, on obtenait la conversion de l’ACFA chez trois. La cardiothyréose est une complication sérieuse de l’hyperthyroïdie pouvant menacer le pronostic vital. L’ACFA est la forme clinique la plus fréquente et le retour au rythme sinusal n’est pas constant après contrôle de l’hyperthyroïdie, d’où l’intérêt du diagnostic et de prise en charge précoce de l’hyperthyroïdie.","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135274386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hospitalisations pour maladies hypophysaires : profil épidémiologique et évolutif sur 13 ans","authors":"M. Baklouti, H. Ben Ayed, N. Hentati, O. Laajili, M. Trigui, F. Hadj Kacem, G. Nasri, R. Karray, J. Jdidi, S. Yaich, J. Dammak","doi":"10.1016/j.ando.2023.07.178","DOIUrl":"https://doi.org/10.1016/j.ando.2023.07.178","url":null,"abstract":"Les maladies hypophysaires (MH) constituent un des motifs les plus répondus en endocrinologie, dont la prise en charge pourrait parfois nécessiter l’hospitalisation. L’objectif de cette étude était de dresser le profil épidémiologique et évolutif des hospitalisations pour MH sur une période de 13 ans. Il s’agissait d’une étude rétrospective ayant inclus les patients hospitalisés pour MH dans le CHU Hedi Chaker Sfax, Tunisie, durant la période 2006–2018. Sur un total de 148 596 admissions, 240 patients (0,16 %) étaient hospitalisés pour MH. Le sexe ratio était de 0,55. L’âge médian était de 43 ans (Intervalle interquartile (IIQ) = [30,7–53] ans). Ils y avaient 39 patients (16,3 %) âgés de plus de 60 ans. 158 patients (65,8 %) étaient hospitalisés pour une insuffisance hypophysaire et 82 cas (34,2 %) étaient admis pour un hyperaldostéronisme. La durée médiane du séjour était de 7 jours (IIQ = [5–10]). Une durée > 7 jours était notée chez 119 patients (49,6 %). Au total, 14 patients (5,8 %) présentaient des comorbidités associés, dont 5 (2 %) étaient endocriniennes. Le taux de létalité était de 0,4 %. L’étude des tendances chronologiques a montré une allure globale significativement à la baisse (Rho = (–0,83) ; p < 0,001)), de même que pour insuffisance hypophysaire (Rho = (–0,8) ; p = 0,001) et pour hyperaldostéronisme (Rho = (–0,73) ; p = 0,003). Malgré leurs tendances chronologiques à la baisse, les MH continuent à être une source de morbidité en milieu de soins, notamment chez les adultes jeunes. Une prise en charge adéquate et continue de ces maladies est primordiale pour prévenir les formes graves.","PeriodicalId":93871,"journal":{"name":"Annales d'endocrinologie","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135274403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}