Med最新文献

{"title":"Another complement inhibitor therapy for myasthenia gravis: Is it NIMBLE enough?","authors":"Linda L Kusner, Henry J Kaminski","doi":"10.1016/j.medj.2026.101186","DOIUrl":"https://doi.org/10.1016/j.medj.2026.101186","url":null,"abstract":"<p><p>The phase 3 NIMBLE trial demonstrated the efficacy of cemdisiran, an siRNA inhibitor of hepatic C5 synthesis, in patients with myasthenia gravis, making it the first complement inhibitor in the disease to employ this novel mechanism of action. These results expand the growing therapeutic landscape that already includes three FDA-approved complement inhibitors for myasthenia gravis.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 7","pages":"101186"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424874","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":"Atlas of human brain imaging-derived phenotypes and disease risk.","authors":"Qidong Liu, Junrong Guo, Jinfeng Yan, Siqi Yu, Yixin Hu, Yu Deng, Benhuang Yan, Ping Li, Jiajing Cai, Zhenghao Deng, Zixuan Wang, Jian Yu","doi":"10.1016/j.medj.2026.101185","DOIUrl":"10.1016/j.medj.2026.101185","url":null,"abstract":"<p><strong>Background: </strong>The brain plays a central role in coordinating physiological processes across organ systems, yet population-scale evidence linking brain structure and function alterations, as captured by neuroimaging, to multisystem disease risk remains limited.</p><p><strong>Methods: </strong>Leveraging multimodal magnetic resonance imaging (MRI) and linked health records from 64,836 participants, we performed a phenome-wide association study (PheWAS) to assess associations between 505 brain imaging-derived phenotypes (IDPs)-including T1-weighted, diffusion, and resting-state functional MRI measures-and 756 incident diseases spanning 15 organ systems, establishing the largest atlas of brain-disease risk to date.</p><p><strong>Findings: </strong>Across approximately 380,000 tests, 1,500 significant IDP-disease pairs were identified, revealing that brain alterations relate not only to neurological but also to peripheral conditions, such as circulatory, digestive, and metabolic disorders. Clustering and network analyses highlighted white matter-related IDPs as a central hub linking brain and multisystem health. Prediction models combining IDPs with clinical covariates improved disease discrimination, and Mendelian randomization suggested potential causal roles of white matter-related IDPs in cerebrovascular disorders.</p><p><strong>Conclusions: </strong>This PheWAS-based atlas advances population-level understanding of brain-body associations and provides a framework for exploring the potential of neuroimaging in cross-system disease risk assessment and therapeutic development. All associations are available through the open-access brain imaging-disease risk atlas (www.brainphewas.com).</p><p><strong>Funding: </strong>This research was supported by the National Natural Science Foundation of China (82271220).</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101185"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148273129","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":"A third way to breathe.","authors":"Takanori Takebe","doi":"10.1016/j.medj.2026.101147","DOIUrl":"https://doi.org/10.1016/j.medj.2026.101147","url":null,"abstract":"<p><p>In this Backstory, the authors recount how a question inspired by loach intestinal breathing grew into enteral ventilation with oxygenated perfluorodecalin: a translational effort shaped by multidisciplinary collaboration, large-animal validation, and the urgency of helping patients whose lungs can no longer cope.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 7","pages":"101147"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148424813","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":"Long-term remission of neuromyelitis optica with allogeneic hematopoietic stem cell transplant.","authors":"Giorgio Orofino, Angela Genchi, Maria Teresa Lupo Stanghellini, Matteo Doglio, Maddalena Noviello, Alessandra Mandelli, Paolo Vezzulli, Veronica Valtolina, Sara Mastaglio, Simona Piemontese, Elena Tassi, Francesca Ferrua, Maria Pia Cicalese, Roberto Furlan, Gianvito Martino, Andrea Assanelli, Massimo Bernardi, Consuelo Corti, Jacopo Peccatori, Francesca Tortorelli, Cristina Toffalori, Luca Vago, Chiara Bonini, Fabio Ciceri, Massimo Filippi, Lucia Moiola, Raffaella Greco","doi":"10.1016/j.medj.2026.101179","DOIUrl":"10.1016/j.medj.2026.101179","url":null,"abstract":"<p><strong>Background: </strong>Neuromyelitis optica (NMO) is a rare, aggressive, neurological autoimmune disorder. Despite several immunosuppressive drugs having been recently approved, some patients still experience frequent relapses, leading to disability accrual.</p><p><strong>Methods: </strong>We report the long-term follow-up of the two patients treated with allogeneic hematopoietic cell transplantation (alloHCT) for treatment-refractory anti-aquaporin-4 immunoglobulin G (AQP4-IgG)-positive NMO 16 and 15 years ago, respectively. Patients were followed with serial clinical, imaging, and immunological assessments.</p><p><strong>Findings: </strong>Both patients showed sustained clinical and radiological remission without ongoing immunosuppressive therapy. AQP4-IgG antibodies became undetectable after transplantation and remained so throughout follow-up. No graft-versus-host disease occurred, and full donor chimerism was maintained. Longitudinal immune profiling revealed robust reconstitution of naive and memory T and B cell compartments, a resting phenotype in polyclonal T cells, and dynamic remodeling of regulatory T cells.</p><p><strong>Conclusions: </strong>AlloHCT induced durable, treatment-free remission over more than 15 years in two patients with highly refractory NMO spectrum disorder (NMOSD), accompanied by sustained clearance of pathogenic AQP4-IgG antibodies. This long-term disease control paralleled stable donor-derived immune reconstitution, notably with expansion and remodeling of regulatory T cells, providing a rationale for hypothesizing a mechanistic link to immune tolerance. These findings provide proof of concept that alloHCT can achieve deep, potentially curative disease modification in selected NMO cases, warranting further studies to better define patient selection, safety, and long-term benefit.</p><p><strong>Funding: </strong>No funding was received for this work.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101179"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148259790","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":"Loss of tumor suppressor NF2 mediates resistance to CAR T cell and anti-PD-1 therapy: Strategies to restore immunotherapy sensitivity.","authors":"Miguel A Lopez-Lago, Meriem Taleb, Mehek Ningoo, Tomoyo Okada, Xiaoyu Li, Hyun-Sung Lee, Bryan M Burt, Michael Offin, Navin K Chintala, Prasad S Adusumilli","doi":"10.1016/j.medj.2026.101149","DOIUrl":"10.1016/j.medj.2026.101149","url":null,"abstract":"<p><strong>Background: </strong>Investigating the biological mechanisms of acquired resistance to immunotherapy remains a necessity for effective treatment of solid tumors.</p><p><strong>Methods: </strong>Diffuse pleural mesothelioma (DPM) tumors, from immunocompetent and immunodeficient mouse models with acquired resistance to chimeric antigen receptor (CAR) T cell therapy were analyzed using flow cytometry, immunofluorescence, and ELISA. The interplay between genetic alterations in the cancer cell and site-specific tumor immune microenvironment (TIME) was characterized; therapies to reverse immunotherapy resistance were investigated.</p><p><strong>Findings: </strong>Analysis of tumors with acquired resistance to CAR T cell therapy demonstrated lower expression of tumor suppressor NF2. Enforced depletion of NF2 promoted resistance to CAR T cell and anti-PD-1 therapy in DPM but not in heterotopic subcutaneous tumors. Loss of NF2 was associated with accumulation of immunosuppressive complement receptor of immunoglobulin superfamily (CRIg)⁺ macrophages in pleural tumors, which was dependent on tumor-secreted chemokines and retinoic acid. Ablation of chemokines or pharmacologic inhibition of retinoic acid or the Hippo pathway by use of TEAD inhibitors restored sensitivity to CAR T cell therapy. Correspondingly, in two independent cohorts of patients, DPM tumors with NF2 copy-number loss, but not mutations, were associated with higher infiltration of M2 macrophages, lower infiltration and function of CD8 T cells, and an anti-PD-1-resistant gene signature.</p><p><strong>Conclusions: </strong>Our study uncovers a previously unknown mechanism of resistance to immunotherapy by identifying the dynamic interplay between cancer cell genetic alterations and the TIME.</p><p><strong>Funding: </strong>This research was funded in part through the NCI UG3CA290241, R01CA292664, R01CA235667, R01CA236615, and Department of War CA200437.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101149"},"PeriodicalIF":13.3,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13256109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinically actionable genomic and transcriptomic landscape of advanced neuroendocrine neoplasms.","authors":"Simon Kreutzfeldt, Leonidas Apostolidis, Małgorzata Oleś, Eva Krieghoff-Henning, Christoph E Heilig, Christoph Heining, Andreas Mock, Maria-Veronica Teleanu, Barbara Hutter, Laura Gieldon, Barbara Klink, Katja Beck, Daniela Richter, Annika Baude-Müller, Eva Reisinger, Nils Hammer, Leila Kamkar, Katrin Pfütze, Christina Geörg, Mario Lamping, Damian T Rieke, Sebastian Uhrig, Henning Jann, Ulrich-Frank Pape, Michael Allgäuer, Albrecht Stenzinger, Eva C Winkler, Bertram Wiedenmann, Dirk Jäger, Benedikt Brors, Daniel Hübschmann, Evelin Schröck, Ulrich Keilholz, Marianne Pavel, Peter Horak, Hanno Glimm, Stefan Fröhling","doi":"10.1016/j.medj.2026.101130","DOIUrl":"10.1016/j.medj.2026.101130","url":null,"abstract":"<p><strong>Background: </strong>Epithelial neuroendocrine neoplasms (NENs) are a rare and heterogeneous group of malignancies with limited treatment options. Comprehensive molecular characterization may reveal novel therapeutic opportunities for these clinically challenging tumors.</p><p><strong>Methods: </strong>Within a nationwide precision oncology program, we performed whole-genome/exome and transcriptome sequencing in 168 patients with a diagnosis of advanced NEN from diverse anatomic origins, followed by evaluation of real-world outcomes associated with molecularly guided interventions.</p><p><strong>Findings: </strong>Our analysis revealed substantial molecular heterogeneity across advanced NENs, including distinct genetic profiles between low-grade and high-grade tumors, as well as alterations specific to particular tissues of origin. Candidate therapeutic targets included elevated tumor mutational burden induced by temozolomide exposure, rare actionable kinase mutations, overexpression of targetable antigens, and signatures of homologous recombination deficiency, providing a rationale for immune checkpoint blockade, kinase inhibitors, antibody-drug conjugates, poly(ADP-ribose) polymerase (PARP) inhibitors, and platinum-based therapies, respectively. Overall, 144 patients (85.7%) received molecularly guided treatment recommendations, of which 85 were implemented in 57 patients (39.6%). Among 68 evaluable therapy outcomes, 47 (69.1%) demonstrated clinical benefit (objective response, n = 25; disease stabilization, n = 22). At the patient level, 34 of the 57 treated (59.6%) experienced clinical benefit from at least one therapy (objective response, n = 18; disease stabilization, n = 16).</p><p><strong>Conclusions: </strong>Comprehensive genomic and transcriptomic profiling identified distinct molecular alteration patterns and therapeutic vulnerabilities among different classes of epithelial NENs from various tissues, warranting further investigation in anatomic-site-specific studies. Our outcome data underscore the clinical utility of broad molecular profiling in patients with advanced NENs lacking further standard treatment options.</p><p><strong>Funding: </strong>Funding for the study was institutional.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101130"},"PeriodicalIF":11.8,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147821613","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":"A window to breathe again.","authors":"Andrés París-Muñoz, Rosa M Alcobendas-Rueda, Cristina Verdú-Sánchez, Antonio Pérez-Martínez","doi":"10.1016/j.medj.2026.101072","DOIUrl":"10.1016/j.medj.2026.101072","url":null,"abstract":"<p><p>In this Backstory, the authors recount how a 10-year-old girl with rapidly progressive MDA5-positive dermatomyositis survived fulminant lung failure on ECMO and received compassionate-use CD19 chimeric antigen receptor (CAR)-T therapy. The interdisciplinary team then followed her immune reconstitution and clinical recovery, ultimately supporting discharge and offering a potential blueprint for personalized cellular therapy in similarly critical cases.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 6","pages":"101072"},"PeriodicalIF":13.3,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148240411","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 thyroid-liver axis in MASLD: From metabolic control to clinical translation.","authors":"Yasmina Chouik, Cyrielle Caussy, Frank Tacke","doi":"10.1016/j.medj.2026.101173","DOIUrl":"10.1016/j.medj.2026.101173","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver diseases worldwide, with growing incidence paralleling the rise in clinical and economic burden. Recently, resmetirom has emerged as the first approved pharmacotherapy for metabolic dysfunction-associated liver steatohepatitis (MASH) with fibrosis, partially mimicking thyroid hormone (TH) actions in the liver with good safety and promising therapeutic potential. The thorough understanding of hepatic TH availability and signaling, exerting pleiotropic actions in several key biological processes including lipid homeostasis, enabled this breakthrough in hepatology. Here, we summarize current knowledge on the thyroid signaling axis and, in particular, its role in regulating lipid metabolism in the liver in both healthy and pathological conditions. We discuss the development of thyromimetics, initially as lipid-lowering drugs and further as hepatic lipid-clearing therapies against MASH, permitted by achieving TH receptor β selectivity and liver specificity, and analyze results from clinical trials while awaiting long-term outcome data.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101173"},"PeriodicalIF":11.8,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148158466","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":"Sintilimab and lenvatinib plus hepatic arterial infusion chemotherapy and embolization as conversion therapy for uHCC: A phase 2 trial.","authors":"Jiliang Qiu, Zhenkun Huang, Wei He, Chenwei Wang, Chuanmiao Xie, Jingxian Shen, Muyan Cai, Yichuan Yuan, Ruhai Zou, Binkui Li, Yunfei Yuan","doi":"10.1016/j.medj.2026.101132","DOIUrl":"10.1016/j.medj.2026.101132","url":null,"abstract":"<p><strong>Background: </strong>Transarterial chemoembolization (TACE) or systemic treatments are recommended for unresectable hepatocellular carcinoma (uHCC) but have low conversion-to-resection rates. This single-arm phase II trial (PLATIC) aims to investigate the conversion efficacy of PD-1 inhibitor sintilimab, lenvatinib plus TACE and hepatic arterial infusion chemotherapy (TACE-HAIC) in uHCC.</p><p><strong>Methods: </strong>57 uHCC patients received 200 mg of sintilimab and lenvatinib (8/12 mg for body weight <60 kg or ≥60 kg) and TACE-HAIC every 3-4 weeks. The primary endpoint was conversion-to-resection rate. A historical-based cohort treated with TACE-HAIC was included as control.</p><p><strong>Findings: </strong>After a median of three treatment cycles, 44 (77.2%; 95% confidence interval [CI], 0.64-0.87]) patients underwent conversion resection. The objective response rates were 80.7% (95% CI, 0.68-0.90) according to modified Response Evaluation Criteria in Solid Tumors (mRECIST) and 43.8% (95% CI, 0.31-0.58) according to RECIST 1.1. Grade ≥ 3 treatment-related adverse events (TRAEs) occurred in 37 (64.9%) patients; no treatment-related deaths were reported. Among the 44 patients receiving resection, the median progression-free survival (PFS) was 17.3 months, and the median overall survival (OS) was unavailable. After inverse probability of treatment weighting analysis, the PLATIC cohort exhibited longer PFS (hazard ratio [HR] = 0.55, 95% CI, 0.33-0.94; p = 0.020) and OS (HR, 0.50, 95% CI, 0.28-0.92; p = 0.029) than the historical cohort.</p><p><strong>Conclusions: </strong>Sintilimab, lenvatinib, and TACE-HAIC demonstrated favorable conversion-to-resection rates and acceptable TRAEs in uHCC.</p><p><strong>Funding: </strong>Supported by grants from the National Natural Science Foundation of China (no. 82172815 and 82272887) and Cancer Innovative Research Program of Sun Yat-sen University Cancer Center (no. PT22040201).</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101132"},"PeriodicalIF":13.3,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843563","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":"Capturing multi-disease states on a spectrum with machine learning and routine clinical data.","authors":"Iain S Forrest, Ben O Petrazzini, Robert Chen, Ashira D Blazer, Sascha N Goonewardena, Kuan-Lin Huang, Judy Cho, Girish N Nadkarni, Alexander D Charney, Robert S Rosenson, Ghislain Rocheleau, Daniel M Jordan, Ron Do","doi":"10.1016/j.medj.2026.101150","DOIUrl":"10.1016/j.medj.2026.101150","url":null,"abstract":"<p><strong>Background: </strong>Diseases exist on spectra of risk factors, cellular perturbations, organ dysfunction, and clinical manifestations. It is unknown whether the analysis of routine laboratory tests and vitals using artificial intelligence presents a scalable and portable system for capturing the spectral nature of common diseases.</p><p><strong>Methods: </strong>We constructed and validated machine learning models targeting seven common diseases-atrial fibrillation, breast cancer, coronary artery disease, migraine, rheumatoid arthritis, schizophrenia, and type 2 diabetes-using routine clinical measurements from 394,957 electronic health records (EHRs) in the BioMe Biobank and UK Biobank. The Resulting model outputs, termed spectral health index from machine measurements of electronic records (SHIMMER), were assessed for association with disease diagnosis, risk factors, biomarkers, onset, survival, complications, and medications in two cohorts.</p><p><strong>Findings: </strong>SHIMMER was associated with disease diagnosis, known risk factors, and biomarkers in expected directions in both cohorts. With greater SHIMMER, the prevalence of risk factors, complications, and medications continuously increased; for instance, age and hypertension, stroke risk and cardiac arrest, and beta blockers increased, respectively, with atrial fibrillation SHIMMER. Biomarker levels for type 2 diabetes, such as glucose, hemoglobin A1c, C-reactive protein, and triglycerides, changed stepwise as SHIMMER increased. Rising SHIMMER also revealed gradations of earlier disease onset and decreased survival, particularly for coronary artery disease and schizophrenia.</p><p><strong>Conclusions: </strong>A holistic, non-invasive marker derived from machine learning trained on routine clinical measurements snapshots multiple common diseases on a spectrum, quantifying disease risk, severity, onset, survival, sequela, and treatment.</p><p><strong>Funding: </strong>This study was supported in part by the National Institutes of Health.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101150"},"PeriodicalIF":13.3,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13225617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}