Med最新文献

{"title":"A bimodal large language model reduces misalignment in patient education: A double-blinded randomized trial.","authors":"Peixing Wan, Zigeng Huang, Haoquan Huang, Guihan Liang, Mingyan Guo, Sulin Xu, Xinti Sun, Wenjun Tang, Dajun Pei, Jing Chen, Yulan Nie, Shaofen Deng, Yizhi Zhou, Hongru Duan, Rong Zhang, Xiaoying Xu, Erfu Hai, Minghui Cao, Erping Long","doi":"10.1016/j.medj.2026.101263","DOIUrl":"10.1016/j.medj.2026.101263","url":null,"abstract":"<p><strong>Background: </strong>Effective patient education requires accurate communication aligned with patients' emotional and semantical needs. Text-based large language models (LLMs) lack access to non-verbal cues, which may contribute to misaligned responses.</p><p><strong>Methods: </strong>We evaluated emotional and semantic misalignment in a text-based LLM using 64,200 utterances from 16,583 patient education cases across six departments and three centers. Dolphin was developed integrating text and audio cues and evaluated through emotion recognition, semantic consistency assessment, branch-level ablations, and a double-blinded randomized trial against a matched text-based LLM comparator (Chinese Clinical Trial Registry: (ChiCTR2500095933).</p><p><strong>Findings: </strong>The text-based LLM showed emotional misalignment in 36.7% of responses and semantic misalignment in 28.3% of cases, with higher misalignment under greater burden. Dolphin outperformed the text-based LLM in emotion recognition accuracy (0.886 vs. 0.713) and semantic consistency (84.9% vs. 82.1%; both adjusted p < 0.001). Ablations supported contribution of audio branches. Dolphin received higher expert ratings than the text-based LLM and human educators (all p < 0.001). In 555 patients, Dolphin was associated with greater patient satisfaction (98.6% vs. 93.8%), suggestion acceptance (76.1% vs. 58.9%; p < 0.001), proactive disclosure (44.6% vs. 26.5%; p < 0.001), and fewer 7-day unplanned recontact (12.9% vs. 22.9%; p = 0.002). No unsafe recommendations or safety events were identified.</p><p><strong>Conclusions: </strong>Compared with text-based LLM, Dolphin improved emotional-semantic alignment and patient-education outcomes, supporting bimodal alignment as a strategy for reducing misalignment-driven communication failures.</p><p><strong>Funding: </strong>National Natural Science Foundation of China, State Key Laboratory Special Fund, and Chinese Academy of Medical Sciences Innovation Fund.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101263"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798789","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":"Melanoma to rhabdomyosarcoma plasticity in the setting of immunotherapy.","authors":"Andrew D Knight, Emily J Robitschek, Jia-Ren Lin, Tyler Aprati, Giuseppe Tarantino, Jaijia Chen, Dennie T Frederick, Alvin Shi, Ana B Larque, Benchun Miao, Rumya S Raghavan, Tatyana Sharova, John H Shin, Peter Sorger, Manolis Kellis, Keith T Flaherty, Nir Hacohen, Genevieve M Boland, Ivan Chebib, David Liu, Ryan J Sullivan, Arnav Mehta","doi":"10.1016/j.medj.2026.101266","DOIUrl":"10.1016/j.medj.2026.101266","url":null,"abstract":"<p><strong>Background: </strong>Acquired resistance to immune checkpoint inhibitors (ICIs) remains a significant challenge in the treatment of metastatic melanoma. Phenotypic plasticity, such as dedifferentiation and transdifferentiation, is an increasingly recognized mechanism of treatment resistance.</p><p><strong>Methods: </strong>We present a case of a 70-year-old man with metastatic melanoma who experienced progression through sequential treatments including pembrolizumab in combination with the HDAC inhibitor entinostat and ipilimumab. During treatment, a histologically distinct pleomorphic rhabdomyosarcoma (RMS) emerged at metastatic sites. Longitudinally acquired tumor samples representing both phenotypes were analyzed using whole-exome sequencing (WES), RNA sequencing (RNA-seq), and high-plex tissue imaging (spatial proteomics).</p><p><strong>Findings: </strong>WES revealed driver mutations (e.g., NRAS and NF1) and loss of heterozygosity (LOH) shared between phenotypes indicating a common ancestral clone. Phylogenetic analysis demonstrated an early divergence of the phenotypes, with each later acquiring unique mutations. RNA-seq showed mutually exclusive expression of lineage-specific markers as well as epithelial-mesenchymal transition and myogenic gene set enrichment in the RMS samples. High-plex imaging identified distinct tumor microenvironments, with RMS lesions enriched in CD163⁺ macrophages.</p><p><strong>Conclusions: </strong>This case provides molecular evidence of phenotypic plasticity occurring under the selective pressure of immune checkpoint inhibitor therapy.</p><p><strong>Funding: </strong>This study was supported by the National Institutes of Health (K12CA087723 and K08CA234458), the Doris Duke Charitable Foundation, and Adelson Medical Research Foundation.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101266"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798752","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":"Emerging therapeutic directions for inotropic therapy in heart failure.","authors":"Gianluigi Pironti, Christoph Maack, Daniel C Andersson, Lars H Lund","doi":"10.1016/j.medj.2026.101073","DOIUrl":"10.1016/j.medj.2026.101073","url":null,"abstract":"<p><p>Heart failure (HF) remains a major global health burden despite advances in pharmacological and device-based therapies. Current guideline-directed medical therapy (GDMT) slows disease progression through neurohormonal modulation but does not address the fundamental deficit in contractile function, particularly in patients with advanced HF with reduced ejection fraction (HFrEF). Conventional inotropes improve contractility but worsen outcomes. Recent advances have identified novel therapeutic approaches that enhance cardiac contractility without the deleterious effects of conventional inotropes. This review examines pathophysiologic mechanisms compromising contractility in HFrEF and therapeutic strategies that enhance contractility, spanning both traditional calcium-dependent inotropes and emerging classes of small molecules. Their mechanisms of action, along with supporting preclinical and clinical data, are discussed to highlight their future therapeutic potential. These novel strategies reflect a paradigm shift from indirect neurohormonal modulation toward direct myocardial modulation, potentially reshaping the therapeutic landscape for both acute and chronic HF with targeted, efficacious, and safer interventions.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101073"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147595337","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":"Beyond treatment intensification: The next questions after CAPITAL.","authors":"Rei Ogawa, Junki Mizusawa","doi":"10.1016/j.medj.2026.101271","DOIUrl":"https://doi.org/10.1016/j.medj.2026.101271","url":null,"abstract":"<p><p>The CAPITAL trial shows that SOX improves survival over S-1 after D2 gastrectomy for stage II-III gastric cancer.¹ Its broader implication is that further progress will depend on how patients are selected and how systemic therapy is integrated with surgery, not only on the choice of regimen.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 9","pages":"101271"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945621","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":"Generalized myasthenia gravis: Clinical trials to watch.","authors":"Sarah Hoffmann, Paolo Doksani, James F Howard","doi":"10.1016/j.medj.2026.101270","DOIUrl":"https://doi.org/10.1016/j.medj.2026.101270","url":null,"abstract":"<p><p>Generalized myasthenia gravis is undergoing a highly dynamic phase of therapeutic development, with ongoing trials increasingly targeting upstream immune mechanisms. This Trial Watch highlights six studies evaluating B cell survival modulation, lymphocyte-directed immune reconstitution, BCMA- and CD19-directed CAR-T cell therapy, T cell engagement, and response-guided combination therapy, and considers their implications for future treatment strategies.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 9","pages":"101270"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945709","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":"Engineered mesenchymal stem cells regulate integrated stress response for fibrosis therapy.","authors":"Jie Yu, Shuhua Yin, Jiong Li, Yilin Zhang, Xiuli Zhong, Nuo Zhou, Wei Li, Yixin Wang, Renke Li, Minjie Sun, Zhaoting Li","doi":"10.1016/j.medj.2026.101261","DOIUrl":"10.1016/j.medj.2026.101261","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary fibrosis is a fatal disease with limited therapeutic options. Aberrant activation of the integrated stress response (ISR) disrupts proteostasis and promotes fibrogenesis, yet effective strategies for targeted ISR regulation in fibrotic diseases remain insufficiently explored.</p><p><strong>Methods: </strong>Here, we engineered mesenchymal stem cells (MSCs) as living carriers for targeted co-delivery of ISRIB and nicotinamide mononucleotide (NMN). ISRIB- and NMN-loaded liposomes were conjugated onto MSCs through cleavable linkers (M-Lip@IN), enabling MSC-mediated homing and microenvironment-responsive cargo release in fibrotic lesions.</p><p><strong>Findings: </strong>M-Lip@IN effectively accumulated in fibrotic lungs and promoted local liposome release. ISRIB directly regulated pathological ISR activation, whereas NMN supported NAD(H)-SIRT1-related metabolic homeostasis, collectively enabling coordinated regulation of epithelial stress responses. Augmented by MSC-mediated biological support, M-Lip@IN reduced collagen deposition, inhibited profibrotic signaling, improved epithelial cell composition, promoted lung repair, and ameliorated bleomycin-induced pulmonary fibrosis, with additional antifibrotic effects observed in carbon-tetrachloride-induced liver fibrosis.</p><p><strong>Conclusions: </strong>Our study presents an engineered MSC-based platform that integrates lesion targeting, responsive drug release, and coordinated regulation of epithelial stress responses. By combining ISR modulation with metabolic resilience, M-Lip@IN restores stress homeostasis, improves epithelial cell composition, and promotes lung repair. These findings support targeted ISR regulation as a potential therapeutic strategy for pulmonary fibrosis and other fibrotic diseases.</p><p><strong>Funding: </strong>This work was supported by the Shenzhen Science and Technology Program, the Guangdong Basic and Applied Basic Research Foundation, the National Natural Science Foundation of China, the University Development Research Start-up Fund, and the Pengcheng Peacock Project Special Fund.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101261"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148725138","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":"Multiomics profiling of plasma reveals lipid-immune dysregulation and exosome remodeling in mpox and mpox-HIV co-infection.","authors":"Siqi Yong, Jiaying Zhang, He Tian, Zehua Wang, Shaohua Zhang, Robin Barry Chan, Yingjuan Zhou, Guibin Wang, Lianchun Liang, Zhifeng Song, Jingwen Han, Gaofeng Ma, Sin Man Lam, Yingmei Feng, Guanghou Shui","doi":"10.1016/j.medj.2026.101264","DOIUrl":"10.1016/j.medj.2026.101264","url":null,"abstract":"<p><strong>Background: </strong>Monkeypox virus (MPXV) infects diverse human cell types, and human immunodeficiency virus (HIV) co-infection is common. The immunometabolic consequences of MPXV infection, and how it may be altered by HIV, remain poorly defined.</p><p><strong>Methods: </strong>We performed quantitative plasma lipidomics and precise metabolomics in a discovery cohort (n = 81) comprising MPXV-monoinfected (MPLWOH), MPXV-HIV-coinfected (MPLWH), and HIV-monoinfected (PLWH) patients and healthy controls, integrating exosome proteomics, cytokine profiling, and transcriptomics of exosome-treated HepG2 and A549 cells for functional interpretation. An independent validation cohort (n = 65) was used to assess cross-cohort reproducibility.</p><p><strong>Findings: </strong>MPXV infection induced broad lipid remodeling, with elevations in phosphatidylserine (PS) and phosphatidylethanolamine (PE) and reductions in phosphatidylcholine (PC), lysophospholipids, cholesteryl ester (CE), and exosomal lecithin-cholesterol acyltransferase (LCAT) and lipoprotein lipase (LPL). These lipid alterations were correlated with tissue injury markers and inflammatory cytokines. The MPLWH group exhibited more severe metabolic disruption, including marked sulfatide (SL) depletion, lower cholesterol and high-density lipoprotein cholesterol (HDL-c), and extensive rewiring of lipid-cytokine associations. SL depletion in MPLWH correlated with abundances of COPI-mediated retrograde trafficking proteins in exosomes. Transcriptomic profiling of exosome-treated cells provided functional validation: MPLWOH exosomes induced lipid metabolism and repair-associated epithelial programs, while MPLWH exosomes drove phospholipid remodeling and acute inflammatory and mucosal barrier-stress responses.</p><p><strong>Conclusions: </strong>MPXV infection reprograms host lipid metabolism and exosome composition, with HIV co-infection amplifying inflammatory, metabolic, and trafficking disruptions. These convergent multi-omics signatures link systemic lipid dysregulation to exosome-mediated immunomodulation and identify potential targets for host-directed interventions.</p><p><strong>Funding: </strong>This study was funded by the Major Project of Guangzhou National Laboratory.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101264"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798799","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 fear in the waiting room.","authors":"Felipe Pereira, Joseph Magagnoli, Meenakshi Ambati, Talita Fernandes de Oliveira, Juliana Angélica Estevão de Oliveira, Vinicius Oliveira Pesquero, Lucas Zago Ribeiro, Dante Akira Kondo Kuroiwa, Fernando Korn Malerbi, Sergio Atala Dib, Nilva Bueno Moraes, Michel Eid Farah, Eduardo Buchele Rodrigues, Jayakrishna Ambati","doi":"10.1016/j.medj.2026.101292","DOIUrl":"10.1016/j.medj.2026.101292","url":null,"abstract":"<p><p>In this Backstory, the authors describe the journey from a basic science laboratory to the first randomized clinical trial of an anti-inflammasome drug for an eye disease, told through the lives of the patients whose situation made the question impossible to ignore.</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":"7 9","pages":"101292"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945754","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":"Concomitant lipid-lowering and anticoagulation therapy for recurrent venous thromboembolism prevention: A Bayesian meta-analysis.","authors":"Harsini Raaja Sulochana, Yufan Yang, Laura Bindila, Ioannis T Farmakis, Stavros V Konstantinides, Luca Valerio, Philipp S Wild, Vincent Ten Cate","doi":"10.1016/j.medj.2026.101262","DOIUrl":"10.1016/j.medj.2026.101262","url":null,"abstract":"<p><strong>Background: </strong>It is unclear whether combined anticoagulation (AC) plus lipid-lowering therapies (LLTs) enhance AC efficacy for venous thromboprophylaxis while maintaining an acceptable safety profile.</p><p><strong>Methods: </strong>A systematic literature search was conducted in PubMed, Cochrane CENTRAL library, and Web of Science, including randomized controlled trials (RCTs) and observational studies published until May 2026. The associations of LLT+AC vs. AC monotherapy with efficacy outcomes (i.e., recurrent venous thromboembolism [rVTE] and post-thrombotic syndrome [PTS] risk), safety outcomes (i.e., major bleeding), and other outcomes were analyzed. A Bayesian random-effects meta-analysis was used to aggregate study estimates (95% credible interval [CrI]) and calculate the posterior probability of benefit (relative risk [RR] < 1).</p><p><strong>Findings: </strong>The search yielded 28 (17 observational studies and 11 RCTs) studies eligible for meta-analysis. The pooled effect size of LLT+AC vs. AC alone for rVTE was RR = 0.73 [95% CrI: 0.58; 1.05, P(RR < 1) = 0.97]. In addition, there was a 17% lower risk observed for PTS [RR = 0.83, 95% CrI: 0.40; 1.59, P(RR < 1) = 0.74]. Major bleeding risk was 15% lower [RR = 0.85, 95% CrI: 0.76; 0.96, P(RR < 1) = 0.99]. Combined LLT+AC reduced D-dimer [log SMD = -0.15; 95% CrI: -0.43; 0.13, P(SMD < 0) = 0.88] and C-reactive protein levels [log SMD = -0.86; 95% CrI: -1.48; -0.08; P(SMD < 0) = 0.98] relative to AC monotherapy.</p><p><strong>Conclusions: </strong>The available evidence suggests potential benefit of LLT+AC combination therapy over AC monotherapy, with respect to both safety and efficacy, though further evidence from RCTs is necessary to generate conclusive evidence.</p><p><strong>Funding: </strong>DIASyM research core (BMBF 031L0219).</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101262"},"PeriodicalIF":13.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798802","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":"AI-driven therapeutic antisense oligonucleotide for processing-deficient progeroid laminopathies.","authors":"Lin Lv, Chang Liu, Lidan Hu, Lefan Cai, Jinzhao Liang, Hanying Jia, Ningyuan You, Haoluo Xi, Yanhong Feng, Jingjing Wang, Zhekai Li, Qiuyang Yu, Gang Wang, Jin Zhang, Hongguang Xia, Xudong Fu, Leslie B Gordon, Jianhua Mao, Zhihong Liu, Ning Shen","doi":"10.1016/j.medj.2026.101193","DOIUrl":"10.1016/j.medj.2026.101193","url":null,"abstract":"<p><strong>Background: </strong>Progeroid laminopathies (PLs), including Hutchinson-Gilford progeria syndrome (HGPS), are rare premature aging disorders in which cardiovascular complications drive early mortality. Antisense oligonucleotides (ASOs) represent a promising therapeutic strategy, yet optimal design principles and their impact on cardiovascular pathology remain insufficiently defined.</p><p><strong>Methods: </strong>We developed an AI-driven pipeline to design ASOs targeting the 3'UTR of LMNA transcripts to suppress processing-deficient pathogenic lamin A isoforms. Lead candidates were evaluated in patient-derived induced pluripotent stem cell-derived cardiomyocytes (PL-iCMs), 3D cardiac organoids, and LMNA transgenic mouse models. Efficacy, toxicity, and systemic transcriptional responses were assessed using molecular, histological, and serum biochemical analyses.</p><p><strong>Findings: </strong>The optimized ASO, LM2556, selectively reduced progerin and farnesylated pre-lamin A expression while preserving lamin C. LM2556 mitigated cellular senescence and improved structural and functional phenotypes in PL-iCMs and cardiac organoids. In vivo, LM2556 decreased pathogenic lamin A isoforms across multiple tissues without evidence of hepatotoxicity or nephrotoxicity. Long-term administration ameliorated progeroid features, improved cardiovascular pathology, extended median lifespan by 82.86%, and enhanced overall healthspan in LMNA transgenic mice.</p><p><strong>Conclusions: </strong>These findings establish an AI-based framework for therapeutic ASO design and provide proof-of-concept evidence that targeting the 3'UTR of LMNA transcripts can effectively suppress pathogenic lamin A isoforms and ameliorate systemic progeroid phenotypes.</p><p><strong>Funding: </strong>This work was funded by the National Natural Science Foundation of China (82450116 and 82502251).</p>","PeriodicalId":29964,"journal":{"name":"Med","volume":" ","pages":"101193"},"PeriodicalIF":13.3,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148369987","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}