Circulation: Genomic and Precision Medicine最新文献

{"title":"Family Screening in Patients With Dilated and Arrhythmogenic Cardiomyopathy: The Road Toward Gene-Specific Recommendations.","authors":"Sophie L V M Stroeks, Steven Muller, Nina J Beelen, Max F G H M Venner, Annette F Baas, Vanessa P M van Empel, Ingrid P C Krapels, Mark R Hazebroek, Anneline S J M Te Riele, Job A J Verdonschot","doi":"10.1161/CIRCGEN.124.004778","DOIUrl":"https://doi.org/10.1161/CIRCGEN.124.004778","url":null,"abstract":"","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004778"},"PeriodicalIF":6.0,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Yield of Genetic Testing for Long-QT Syndrome in Elderly Patients With Torsades de Pointes.","authors":"Daiki Tomidokoro, Toshihiro Nakamura, Satoshi Oka, Yuichiro Miyazaki, Akionori Wakamiya, Nobuhiko Ueda, Kenzaburo Nakajima, Tsukasa Kamakura, Mitsuru Wada, Kohei Ishibashi, Yuko Inoue, Koji Miyamoto, Satoshi Nagase, Shuichi Kitada, Yu Sakaue, Hirokazu Shiraishi, Tomoyuki Kabutoya, Kaoru Takami, Miwa Miyoshi, Naohiko Takahashi, Takeshi Soeki, Yukio Hiroi, Yoshihiro Asano, Seiko Ohno, Kengo Kusano, Takeshi Aiba","doi":"10.1161/CIRCGEN.124.004671","DOIUrl":"10.1161/CIRCGEN.124.004671","url":null,"abstract":"","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004671"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recreational and Occupational Physical Activity and Risk of Adverse Events in Truncating <i>MYBPC3</i> Founder Variant Carriers.","authors":"Fahima Hassanzada, Mark Jansen, Freyja H M van Lint, Laurens P Bosman, Amand F Schmidt, Dennis Dooijes, Danny van de Sande, Bristi Miah, Saskia N van der Crabben, Arthur A M Wilde, Ronald H Lekanne Deprez, Rudolf A de Boer, Imke Christiaans, Jan D H Jongbloed, Harald T Jorstad, Folkert W Asselbergs, J Peter van Tintelen, Annette F Baas, Anneline S J M Te Riele","doi":"10.1161/CIRCGEN.124.004561","DOIUrl":"10.1161/CIRCGEN.124.004561","url":null,"abstract":"<p><strong>Background: </strong><i>MYBPC3</i> founder variants cause hypertrophic cardiomyopathy leading to heart failure and malignant ventricular arrhythmias. Exercise is typically regarded as a risk factor for disease expression although evidence is conflicting. Stratifying by type of exercise may discriminate low- from high-risk activities in these patients. Here, we evaluate the effects of exercise, stratified by high-static and high-dynamic components, on the risk of major cardiomyopathy-related events (MCEs) and cardiomyopathy penetrance among <i>MYBPC3</i> founder variant carriers.</p><p><strong>Methods: </strong>We interviewed 188 carriers (57.4% male; aged 43.0±15.0 years) on exercise participation since the age of 10 years. The exercise was quantified as the metabolic equivalent of task-h/wk before the presentation. MCE was defined as a composite of malignant ventricular arrhythmia (sustained ventricular tachycardia/fibrillation), heart failure (heart failure hospitalizations or transplantation), and septal reduction therapy. Static and dynamic exercises were defined per the Bethesda classification. Associations of exercise with MCE and cardiomyopathy penetrance were adjusted for sex and assessed using Cox regression.</p><p><strong>Results: </strong>Overall, 43 (22.9%) subjects experienced MCE and 139 (73.9%) were diagnosed with cardiomyopathy. No association was found between overall physical activity and high-static activity with MCE (<i>P</i>=0.587 overall; <i>P</i>=0.322 high static) or cardiomyopathy penetrance (<i>P</i>=0.317 overall; <i>P</i>=0.623 high static). In contrast, high-dynamic activity was associated with malignant ventricular arrhythmia (dichotomized at the 75th percentile: adjusted hazard ratio, 3.26 [95% CI, 1.26-8.44]; <i>P</i>=0.015).</p><p><strong>Conclusions: </strong>Overall exercise participation does not generally increase the risk of adverse events among <i>MYBPC3</i> founder variant carriers. Nonetheless, an increased risk of malignant ventricular arrhythmia was observed among those engaged in the highest quartile of high-dynamic sports, suggesting that high-level high-intensity exercise activities should be entertained with caution.</p>","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":"17 6","pages":"e004561"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long Noncoding RNA TRIBAL Links the 8q24.13 Locus to Hepatic Lipid Metabolism and Coronary Artery Disease.","authors":"Sébastien Soubeyrand, Paulina Lau, Majid Nikpay, Lijiang Ma, Johan L M Bjorkegren, Ruth McPherson","doi":"10.1161/CIRCGEN.124.004674","DOIUrl":"10.1161/CIRCGEN.124.004674","url":null,"abstract":"<p><strong>Background: </strong>Genome-wide association studies identified a 20-Kb region of chromosome 8 (8q24.13) associated with plasma lipids, hepatic steatosis, and risk for coronary artery disease. The region is proximal to <i>TRIB1</i>, and given its well-established role in lipid regulation in animal models, TRIB1 has been proposed to mediate the contribution of the 8q24.13 locus to these traits. This region overlaps a gene encoding the primate-specific long noncoding RNA transcript <i>TRIBAL</i>/<i>TRIB1AL</i> (<i>TRIB1</i>-associated locus), but the contribution of TRIBAL to coronary artery disease risk remains untested.</p><p><strong>Methods: </strong>Using recently available expression quantitative trait loci data and hepatocyte models, we further investigated this locus by Mendelian randomization analysis. Following antisense oligonucleotide targeting of TRIBAL, transcription array, quantitative reverse transcription polymerase chain reaction, and enrichment analyses were performed and effects on apoB and triglyceride secretion were determined.</p><p><strong>Results: </strong>Mendelian randomization analysis supports a causal relationship between genetically determined hepatic <i>TRIBAL</i> expression and markers of hepatic steatosis and coronary artery disease risk. By contrast, expression data sets did not support expression quantitative trait loci relationships between coronary artery disease-associated variants and <i>TRIB1</i>. <i>TRIBAL</i> suppression reduced the expression of key regulators of triglyceride metabolism and bile acid synthesis. Enrichment analyses identified patterns consistent with impaired metabolic functions, including reduced triglyceride and cholesterol handling ability. Furthermore, <i>TRIBAL</i> suppression was associated with reduced hepatocyte secretion of triglycerides.</p><p><strong>Conclusions: </strong>This work identifies <i>TRIBAL</i> as a gene bridging the genotype-phenotype relationship at the 8q24.13 locus with effects on genes regulating hepatocyte lipid metabolism and triglyceride secretion.</p>","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004674"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11651355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular Disease Pathogenicity Predictor (CVD-PP): A Tissue-Specific In Silico Tool for Discriminating Pathogenicity of Variants of Unknown Significance in Cardiovascular Disease Genes.","authors":"Megan E Ramaker, Jawan W Abdulrahim, Kristin M Corey, Ryne C Ramaker, Lydia Coulter Kwee, William E Kraus, Svati H Shah","doi":"10.1161/CIRCGEN.123.004464","DOIUrl":"10.1161/CIRCGEN.123.004464","url":null,"abstract":"<p><strong>Background: </strong>Interpretation of variants of uncertain significance (VUSs) remains a challenge in the care of patients with inherited cardiovascular diseases (CVDs); 56% of variants within CVD risk genes are VUS, and machine learning algorithms trained upon large data resources can stratify VUS into higher versus lower probability of contributing to a CVD phenotype.</p><p><strong>Methods: </strong>We used ClinVar pathogenic/likely pathogenic and benign/likely benign variants from 47 CVD genes to build a predictive model of variant pathogenicity utilizing measures of evolutionary constraint, deleteriousness, splicogenicity, local pathogenicity, cardiac-specific expression, and population allele frequency. Performance was validated using variants for which the ClinVar pathogenicity assignment changed. Functional validation was assessed using prior studies in >900 identified VUS. The model utility was demonstrated using the Catheterization Genetics (CATHGEN) cohort.</p><p><strong>Results: </strong>We identified a top-ranked model that accurately prioritized variants for which ClinVar clinical significance had changed (n=663; precision-recall area under the curve, 0.97) and performed well compared with conventional in silico methods. This model (CVD pathogenicity predictor [CVD-PP]) also had high accuracy in prioritizing VUS with functional effects in vivo (precision-recall area under the curve, 0.58). In CATHGEN, there was a greater burden of higher CVD-PP scored VUS in individuals with dilated cardiomyopathy compared with controls (<i>P</i>=8.2×10^-¹⁵). Of individuals in CATHGEN who harbored highly ranked CVD pathogenicity predictor VUS meeting clinical pathogenicity criteria, 27.6% had clinical evidence of disease. Variant prioritization using this model increased genetic diagnosis in CATHGEN participants with a known clinical diagnosis of hypertrophic cardiomyopathy (7.8%-27.2%).</p><p><strong>Conclusions: </strong>We present a cardiac-specific model for prioritizing variants underlying CVD syndromes with high performance in discriminating the pathogenicity of VUS in CVD genes. Variant review and phenotyping of individuals carrying VUS of pathogenic interest support the clinical utility of this model. This model could also have utility in filtering variants as part of large-scale genomic sequencing studies.</p>","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004464"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142521172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Complex Genetics of Spontaneous Coronary Artery Dissection: A Guide for Clinicians.","authors":"Lucy McGrath-Cadell, Stephanie Hesselson, David W M Muller, Jason C Kovacic, Eleni Giannoulatou, Robert M Graham","doi":"10.1161/CIRCGEN.124.004800","DOIUrl":"10.1161/CIRCGEN.124.004800","url":null,"abstract":"","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004800"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-Specific Association Between Genetic Risk of Psychiatric Disorders and Cardiovascular Diseases.","authors":"Jiayue-Clara Jiang, Kritika Singh, Rachana Nitin, Lea K Davis, Naomi R Wray, Sonia Shah","doi":"10.1161/CIRCGEN.124.004685","DOIUrl":"10.1161/CIRCGEN.124.004685","url":null,"abstract":"<p><strong>Background: </strong>Though epidemiological studies show increased cardiovascular disease (CVD) risks among individuals with psychiatric disorders, findings on sex differences in comorbidity have been inconsistent.</p><p><strong>Methods: </strong>This genetic epidemiology study examined the sex-specific association between the genetic risk of 3 psychiatric disorders (major depression [MD], schizophrenia, and bipolar disorder), estimated using polygenic scores (PGSs), and risks of 3 CVDs (atrial fibrillation [AF], coronary artery disease [CAD], and heart failure [HF]) in 345 169 European-ancestry individuals (UK Biobank), with analyses replicated in an independent BioVU cohort (n=49 057). Mediation analysis was conducted to determine whether traditional CVD risk factors could explain any observed sex difference.</p><p><strong>Results: </strong>In the UK Biobank, a 1-SD increase in PGS_MD was significantly associated with the incident risks of all 3 CVDs in females after multiple testing corrections (hazard ratio [HR]_AF-female=1.04 [95% CI, 1.02-1.06]; <i>P</i>=1.5×10^-⁴; HR_CAD-female=1.07 [95% CI, 1.04-1.11]; <i>P</i>=2.6×10^-⁶; and HR_HF-female=1.09 [95% CI, 1.06-1.13]; <i>P</i>=9.7×10^-¹⁰), but not in males. These female-specific associations remained even in the absence of any psychiatric disorder diagnosis or psychiatric medication use. Although mediation analysis demonstrated that the association between PGS_MD and CVDs in females was partly mediated by baseline body mass index, hypercholesterolemia, hypertension, and smoking, these risk factors did not explain the higher risk compared with males. The association between PGS_MD and CAD was consistent between females who were premenopausal and postmenopausal at baseline, while the association with AF and HF was only observed in the baseline postmenopausal cohort. No significant association with CVD risks was observed for the PGS of schizophrenia or bipolar disorder. The female-specific positive association of PGS_MD with CAD risk was replicated in BioVU.</p><p><strong>Conclusions: </strong>Genetic predisposition to MD confers a greater risk of CVDs in females versus males, even in the absence of any depression diagnosis. This study warrants further investigation into whether genetic predisposition to depression could be useful for improving cardiovascular risk prediction, especially in women.</p>","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004685"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11651350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Patient Perceptions of Emerging Gene Therapies for Arrhythmogenic Right Ventricular Cardiomyopathy.","authors":"Emma M Schopp, Leonore Okwara, Crystal Tichnell, Amy Turriff, Brittney Murray, Andreas S Barth, Hugh Calkins, Leila Jamal, Cynthia A James","doi":"10.1161/CIRCGEN.124.004759","DOIUrl":"10.1161/CIRCGEN.124.004759","url":null,"abstract":"<p><strong>Background: </strong>No disease-specific therapy currently exists for arrhythmogenic right ventricular cardiomyopathy (ARVC), a progressive cardiogenetic condition conferring elevated risk for ventricular arrhythmias, heart failure, and sudden cardiac death. Emerging gene therapies have the potential to fill this gap. However, little is known about how adults with ARVC, or any other inherited cardiomyopathy or arrhythmia syndrome, appraise the risks and benefits of gene therapy research and which considerations may influence their decisions about clinical trial participation.</p><p><strong>Methods: </strong>Twenty adults with clinically diagnosed and gene-positive ARVC participated in semi-structured interviews that explored perceptions of gene therapy and hypothetical decision-making for gene therapy clinical trial participation. Interview transcripts were qualitatively coded and analyzed.</p><p><strong>Results: </strong>Participants expressed enthusiasm for gene therapy with varied levels of personal interest in trial participation. Although clinical severity appeared to be associated with an elevated interest in early trial participation, participants anticipated weighing both personal and trial-specific factors including life stage, trial stage, risks, benefits, participation burden, study leadership, and anticipated cost of future gene therapy. Adaptation to living with ARVC and involvement in the ARVC patient community were also relevant to decision-making about trial participation. Potential ethical concerns included unquestioning trust in clinical teams collaborating on industry-led trials and vulnerability of those recently diagnosed or with high perceived severity of ARVC symptoms.</p><p><strong>Conclusions: </strong>Several characteristics of the individual and trial warrant consideration during the informed consent process. Insights from this study may affect trial planning and communication with participants who have inherited cardiac conditions.</p>","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004759"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11651351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygenic Prediction of Recurrent Events After Early-Onset Myocardial Infarction.","authors":"Maddalena Ardissino, Elvezia Maria Paraboschi, Samuel A Lambert, Lois G Kim, Martin Kelemen, Giuseppe Maglietta, Antonio Crocamo, Giulia Magnani, Serena Bricoli, Luigi Vignali, Giampaolo Niccoli, Marco Tubaro, Libor Pastika, Arunashis Sau, Fu Siong Ng, Antonio de Marvao, Michael C Honigberg, Pradeep Natarajan, Adam J Nelson, Michael Inouye, Emanuele Di Angelantonio, Rosanna Asselta, Diego Ardissino, Adam S Butterworth","doi":"10.1161/CIRCGEN.124.004687","DOIUrl":"10.1161/CIRCGEN.124.004687","url":null,"abstract":"<p><strong>Background: </strong>Myocardial infarction (MI) is a complex disease caused by both lifestyle and genetic factors. This study aims to investigate the predictive value of genetic risk, in addition to traditional cardiovascular risk factors, for recurrent events following early-onset MI.</p><p><strong>Methods: </strong>The Italian Genetic Study of Early-Onset Myocardial Infarction is a cohort study enrolling patients with MI before 45 years. Monogenic variants causing familial hypercholesterolemia were identified, and a coronary artery disease polygenic score (PGS) was calculated. Ten-fold cross-validated Cox proportional hazards models were fitted sequentially including all clinical variables, the PGS, and monogenic variants on the composite outcome of cardiovascular death, recurrent MI, stroke, or revascularization.</p><p><strong>Results: </strong>During a 19.9-year follow-up, 847 (50.7%) patients experienced recurrent events. Each 1-SD higher PGS was associated with a 21% higher hazard of recurrent events (hazard ratio, 1.21 [95% CI, 1.13-1.31]; <i>P</i>=4.04×10^-6). Except for secondary prevention, PGS was the strongest determinant of recurrent event risk (C index, 0.56 [95% CI, 0.54-0.58]) compared with clinical risk factors. Overall, predictive performance of clinical risk factors (C index, 0.69 [95% CI, 0.67-0.71]) improved after adding the PGS (C index, 0.69 [95% CI, 0.68-0.71]; <i>P</i>=0.006). When dividing the population by PGS quintiles, the highest fifth had a 57% higher hazard of recurrent events than the lowest fifth (hazard ratio, 1.57 [95% CI, 1.26-1.96]; <i>P</i>=5.57×10^-5).</p><p><strong>Conclusions: </strong>When compared with other clinical risk factors, PGS was the strongest predictor of event recurrence among patients with an early-onset MI. Though the discriminative power of recurrent event prediction in this cohort was modest, the addition of PGS significantly improved discrimination.</p>","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004687"},"PeriodicalIF":6.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11651354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polygenic Risk in Families With Dilated Cardiomyopathy.","authors":"Jamie-Lee M Thompson, Renee Johnson, Michael Troup, Emma M Rath, Paul E Young, Magdalena J Soka, Monique Ohanian, Ingrid S Tarr, Eleni Giannoulatou, Diane Fatkin","doi":"10.1161/CIRCGEN.124.004558","DOIUrl":"10.1161/CIRCGEN.124.004558","url":null,"abstract":"","PeriodicalId":10326,"journal":{"name":"Circulation: Genomic and Precision Medicine","volume":" ","pages":"e004558"},"PeriodicalIF":6.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}