Lung最新文献

{"title":"Stratifying GAP Stages by MUC5B rs35705950 T-Allele Carriage Refines Survival Prediction in IPF.","authors":"Joanne J van der Vis, Antje Prasse, Elisabetta A Renzoni, Carmel J W Stock, Toby M Maher, Francesco Bonella, Raphael Borie, Bruno Crestani, Wim A Wuyts, Philip L Molyneaux, Johannes C Kelder, Jan C Grutters, Coline H M van Moorsel","doi":"10.1007/s00408-025-00837-z","DOIUrl":"https://doi.org/10.1007/s00408-025-00837-z","url":null,"abstract":"<p><p>The genetic contribution to idiopathic pulmonary fibrosis (IPF) has become increasingly evident, enabling its translation into clinical practice. MUC5B rs35705950 has emerged as a promising prognostic biomarker. The gender-age-physiology (GAP)-model is regularly used for IPF survival prediction. In this retrospective real-world study, GAP-stages were stratified by MUC5B T-allele carriage. European patients with IPF were included in a discovery (n = 663), and replication (n = 738) cohort. The GAP+MUC5B-model was significantly more accurate compared to the GAP-model (all cohorts p < 0.001), with a modest improvement in discrimination (ΔC = 0.023; C = 0.685, 95%CI 0.665-0.704). Within each GAP-stage, T-allele carriers had significantly better median transplant-free survival outcomes than non-carriers (p < 0.001): In the combined cohort (n = 1401) survival for GAP-stage I T carriers was 70 months (m) vs 48m for T non-carriers; stage II T vs non-T: 41 vs 31m; stage III T vs non-T: 23 vs 12m. Addition of MUC5B rs35705950 T-carriership enhances GAP-based prognostication and aids clinical decision-making.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"85"},"PeriodicalIF":3.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742440","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":"Lung Tissue Compliance Interacts with Smooth Muscle and Drives Hyperresponsiveness in Mice with Experimental Asthma.","authors":"Sébastien Hecht, Andrés Rojas-Ruiz, Magali Boucher, Cyndi Henry, Jorge Soliz, Ynuk Bossé","doi":"10.1007/s00408-025-00840-4","DOIUrl":"10.1007/s00408-025-00840-4","url":null,"abstract":"<p><strong>Introduction: </strong>A recent study on BALB/c and C57BL/6 mice demonstrated a clear lack of association between the in vivo response to nebulized methacholine and the degree of airway narrowing ex vivo in a model of asthma induced by a daily exposure to house dust mite over 10 consecutive days. This finding raises the question of which factors determine the methacholine response in vivo.</p><p><strong>Methods: </strong>Herein, multiple linear regression analyses were used to determine which baseline physiological characteristics are associated with the methacholine response.</p><p><strong>Results: </strong>Among the 10 baseline characteristics studied, and depending on how the methacholine response was monitored during a concentration-response, lung tissue compliance was the most commonly and robustly associated with the methacholine response. Inspiratory capacity was the second most frequently associated.</p><p><strong>Conclusion: </strong>These results suggest that lung tissue compliance and inspiratory capacity may be two important determinants of the methacholine response in BALB/c and C57BL/6 mice with and without experimental asthma.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"84"},"PeriodicalIF":3.9,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12307465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144742439","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":"Evidence that Mast Cells Regulate the Cough Hypersensitivity Associated with Eosinophilic Bronchitis.","authors":"Li Yu, Qi Liu, Brendan J Canning","doi":"10.1007/s00408-025-00835-1","DOIUrl":"10.1007/s00408-025-00835-1","url":null,"abstract":"<p><strong>Purpose: </strong>Eosinophils have been implicated as key effectors in the emergence of chronic cough. But causality has not been firmly established, and many patients with cough secondary to eosinophilic bronchitis (EB) are likely misdiagnosed as asthmatics based on successful empiric trials using inhaled corticosteroids. Better diagnostics and more precise therapeutic strategies for EB and other diseases that lead to chronic cough remain important but unmet clinical needs.</p><p><strong>Methods: </strong>With the goal of better defining the mechanisms of cough in disease, we established a model of EB in guinea pigs using allergen challenges that induce a cough hypersensitivity responsive to steroid therapy.</p><p><strong>Results: </strong>The heightened cough responsiveness associated with the eosinophilic inflammation was mimicked by LTD₄ inhalation and prevented by cysLT₁ receptor blockade with pranlukast or montelukast. But cysLT₁ receptor antagonism failed to prevent the eosinophilic infiltration of the airways evoked by allergen challenge. Additionally, inhalation of the mast cell selective stimulant Compound 48/80 mimicked the effects of allergen challenge on cough but failed to significantly increase eosinophilic infiltration of the airways. We also observed that thromboxane A2, through TP receptor engagement, acts downstream from and simultaneously with the leukotrienes to promote cough hypersensitivity in EB.</p><p><strong>Conclusions: </strong>These results suggest that mast cells and not eosinophils may be essential to the emergence of cough hypersensitivity in EB. We speculate that therapeutic strategies targeting mast cells, cysLT₁ receptors, and TP receptors may represent endotype-specific treatments for chronic cough.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"82"},"PeriodicalIF":3.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12287148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144698960","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":"Airway Mucus Plugs in Patients with Chronic Cough: A Single-Center Observational Study.","authors":"Kyongmin Sarah Beck, Dae Hee Han, Hyun-Seob Jeon, Juyoung Shin, Sook Young Lee, Woo-Jung Song, Hwa Young Lee","doi":"10.1007/s00408-025-00839-x","DOIUrl":"10.1007/s00408-025-00839-x","url":null,"abstract":"<p><strong>Background: </strong>This study investigated the prevalence of mucus plugs and their clinical associations in patients with chronic cough.</p><p><strong>Methods: </strong>Chest computed tomography (CT) scans were evaluated in patients with chronic cough and healthy controls.</p><p><strong>Results: </strong>Among 82 patients with chronic cough and 71 controls, mucus plugs were identified in 31.7% and 5.6%, respectively. Higher mucus plug scores were associated with older age, elevated fractional exhaled nitric oxide (FeNO), and lower total Cough Hypersensitivity Questionnaire (CHQ) scores (all P < 0.05). Regression analysis revealed associations with higher FeNO and lower total CHQ scores (Model 1: R² = 0.396, P < 0.001), and with higher immunoglobulin (Ig) E levels (Model 2: R² = 0.388, P < 0.001). Mucus plug scores did not differ by 1-month treatment response.</p><p><strong>Conclusions: </strong>Mucus plugs were prevalent in chronic cough and associated with type 2 airway inflammation. Their clinical significance warrants further investigation.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"83"},"PeriodicalIF":4.6,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144698959","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":"ICD-10 Diagnostic Coding Patterns and Clinical Correlates in Refractory Chronic Cough: Analysis from the Korean Chronic Cough Registry.","authors":"Min-Hye Shin, Young-Jae Lee, Kyung Eun Park, Yeonhee Kim, Ha-Kyeong Won, Kyung-Min Ahn, Ji-Su Shim, Min-Hye Kim, Jin An, Jiung Jeong, Young-Chan Kim, Hwa Young Lee, Sung-Yoon Kang, Han-Ki Park, Eun-Jung Jo, Seung-Eun Lee, So Ri Kim, Yoon-Seok Chang, Byung-Jae Lee, Alyn H Morice, Woo-Jung Song","doi":"10.1007/s00408-025-00836-0","DOIUrl":"https://doi.org/10.1007/s00408-025-00836-0","url":null,"abstract":"<p><p>The International Classification of Diseases (ICD) system plays a key role in health data classification but currently lacks a specific code for refractory chronic cough (RCC). This study analyzed ICD-10 coding patterns among 331 RCC patients enrolled in the Korean Chronic Cough Registry. Each patient had a median of 3 [IQR: 2-4] ICD-10 codes at their most recent outpatient visit. The most frequently assigned primary code was R05 (Cough), recorded in 80.4% of cases. Patients with R05 as their primary code tended to have fewer identifiable etiologies but reported more cough hypersensitivity symptoms. Additionally, the number of ICD-10 codes correlated with both cough severity and cough-specific quality-of-life impairment. In a pooled analysis including RCC and non-RCC cases, the R05 code showed high specificity (80.5%) but low sensitivity (25.8%) for RCC. These findings support the need for a dedicated ICD code to accurately capture RCC in clinical and epidemiological contexts.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"81"},"PeriodicalIF":4.6,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667927","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":"From Glucotoxicity to Lung Injury: Emerging Perspectives on Diabetes-Associated Respiratory Complications.","authors":"Hongmei Yu, Jie Liu, Xiaojuan He","doi":"10.1007/s00408-025-00834-2","DOIUrl":"https://doi.org/10.1007/s00408-025-00834-2","url":null,"abstract":"<p><p>Emerging evidence highlights glucose toxicity as a pivotal driver of diabetic respiratory complications, characterized by hyperglycemia-induced metabolic dysregulation and multi-organ damage. The lung, a metabolically active organ, exhibits unique susceptibility to glucose toxicity due to its exposure to oxidative stress, inflammatory cascades, and disrupted metabolic reprogramming, particularly in glycolysis and mitochondrial dysfunction. Diabetes-associated respiratory complications encompass increased susceptibility to respiratory infections, acute respiratory distress syndrome (ARDS) with macrophage-driven glycolytic shifts, and gestational diabetes mellitus (GDM)-associated fetal lung dysplasia via impaired epithelial differentiation. Future research should prioritize metabolic dysregulation-targeted therapies, gut-lung axis modulation, and personalized approaches to address the interplay between hyperglycemia, oxidative stress, and immune dysregulation. Elucidating genetic and epigenetic modifiers of glucotoxicity will further advance therapeutic strategies for diabetes-associated pneumopathy. This review provides an overview of epidemiological burden, lung structural and functional changes, pathophysiological mechanisms, clinical outcomes and complications, therapeutic and preventive strategies, unanswered questions, and future directions of diabetes-associated respiratory complications.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"80"},"PeriodicalIF":4.6,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642915","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":"Soluble Transferrin Receptor-1 in Pulmonary Hypertension Associated with COPD.","authors":"Oleh Myronenko, Pero Curcic, Philipp Douschan, Katarina Zeder, Teresa John, Susanne Suessner, Konrad Hoetzenecker, Gabor Kovacs, Andrea Olschewski, Horst Olschewski, Vasile Foris","doi":"10.1007/s00408-025-00833-3","DOIUrl":"10.1007/s00408-025-00833-3","url":null,"abstract":"<p><strong>Purpose: </strong>The pulmonary vascular involvement of COPD ranges from severe airway obstruction without pulmonary hypertension (PH) to mild airway obstruction with severe PH. Iron-dependent molecular regulators like hypoxia-inducible factor-2 (HIF-2) may contribute to these phenotypic variations. We explored the role of soluble transferrin receptor-1 (sTfR1) for diagnosis and prognosis of PH associated with COPD.</p><p><strong>Methods: </strong>We analyzed COPD outpatients who underwent right heart catheterization and performed unsupervised clustering analysis based on sTfR1 levels and non-invasive clinical parameters to identify specific COPD phenotypes. Additionally, we examined explanted end-stage COPD lungs for TfR1 expression and iron deposition.</p><p><strong>Results: </strong>sTfR1 was associated with mean pulmonary artery pressure (mPAP) (r = 0.45, p < 0.001), pulmonary vascular resistance (PVR) (r = 0.395, p < 0.001) and poor survival. sTfR1 predicted severe PH (AUROC [95% CI], 0.72 [0.61-0.83]), and AUROC was further improved based on a combination of sTfR1 and low hemoglobin (0.82 [0.73-0.92]). sTfR1-based cluster analysis distinguished three COPD phenotypes with significantly different survival. One of the two clusters with poor survival was characterized by moderate airway obstruction and moderate PH but elevated sTfR1, anemia and inflammation. In explanted COPD lungs, TfR1-positive and iron-laden cells, most likely, consisted of macrophages, and iron-loaded cell density was negatively correlated with mPAP in patients with moderate/severe PH (r = - 0.681, p = 0.015).</p><p><strong>Conclusions: </strong>Elevated sTfR1 predicts poor prognosis in patients with COPD and, particularly in combination with low hemoglobin, may serve as a biomarker for severe PH in COPD, identifying a distinct phenotype with systemic inflammation, anemia and iron deficiency.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"79"},"PeriodicalIF":4.6,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637394","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":"Use of Telomere Length as a Biomarker in Idiopathic Pulmonary Fibrosis.","authors":"Caroline Dahlqvist, Thomas Planté-Bordeneuve, Trejsi Muca, Anne de Leener, Benoît Ghaye, Emmanuel Coche, Anabelle Decottignies, Marie-Astrid van Dievoet, Antoine Froidure","doi":"10.1007/s00408-025-00830-6","DOIUrl":"10.1007/s00408-025-00830-6","url":null,"abstract":"<p><strong>Background: </strong>Telomere shortening, a hallmark of cellular aging, is associated with poor outcomes in idiopathic pulmonary fibrosis (IPF). This study aimed to explore the relationships between telomere length (TL), pulmonary function tests, and telomere-related gene (TRG) mutations in a real-world IPF population.</p><p><strong>Methods: </strong>We included IPF patients from two Belgian academic hospitals, collecting demographic and clinical data. TL was measured using Flow-FISH and expressed as a percentile. Short TL was defined as below the 10th percentile (P10), and very short TL as below the 1st percentile (P1).</p><p><strong>Results: </strong>We analysed 143 patients (106 men, 74%), with a median age of 70 years. Thirty patients (21%) met the European Respiratory Society (ERS) criteria for familial pulmonary fibrosis (FPF). Short TL was found in 74 patients (50%), predominantly in men (p < 0.05). Patients with short TL experienced a greater decline in lung function over 24 months compared to those with normal TL (- 4% vs + 3% FVC, p < 0.05; - 7% vs - 3% DLCO, p < 0.05). Patients with very short TL were younger at diagnosis and tended to have a more pronounced FVC decline (- 5% vs - 1%, p = 0.06). TRG variants were identified in 16 individuals, occurring more frequently in those with short (14/27, 52%) or very short TL (10/20, 50%).</p><p><strong>Conclusion: </strong>Short TL is common in both sporadic and familial IPF and serves as a predictive biomarker for accelerated lung function decline. Additionally, the presence of short TL is indicative of an underlying TRG mutation.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"78"},"PeriodicalIF":4.6,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591613","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":"Electronic-Nose Technology for Lung Cancer Detection: A Non-Invasive Diagnostic Revolution.","authors":"A M Dhanush Gowda, Akanksha D Dessai, Usha Y Nayak","doi":"10.1007/s00408-025-00828-0","DOIUrl":"10.1007/s00408-025-00828-0","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer (LC) remains a leading cause of cancer-related mortality worldwide, primarily due to late-stage diagnosis and the absence of effective early detection methods.</p><p><strong>Objective: </strong>This review aims to explore the principles, technological advancements, current limitations, and future prospects of electronic nose (E-nose) systems in the early detection of lung cancer.</p><p><strong>Methods: </strong>The review analyzes recent literature on E-nose devices that detect volatile organic compounds (VOCs) in exhaled breath, focusing on their integration with artificial intelligence (AI) and machine learning for pattern recognition and diagnostic classification.</p><p><strong>Results: </strong>E-noses have demonstrated high sensitivity and specificity in differentiating cancerous from non-cancerous breath samples. However, challenges such as sensor stability, lack of standardization in breath collection, demographic variability, and the need for large training datasets for AI models limit their clinical adoption.</p><p><strong>Conclusion: </strong>Despite current limitations, E-nose technology shows strong potential as a rapid, non-invasive, and cost-effective tool for early LC screening. Enhancing sensor durability, improving data processing, and conducting large-scale validation studies are critical next steps. Integration with imaging and molecular biomarkers may further improve diagnostic accuracy and clinical utility.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"76"},"PeriodicalIF":4.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238155/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584296","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":"Effectiveness of Nintedanib in Progressive Pulmonary Fibrosis Assessed by Progression Criteria: An Italian, Observational, Multicenter Study.","authors":"Michele Mondoni, Francesco Varone, Fabrizio Luppi, Paolo Cameli, Stefania Cerri, Mariangela Valentina Puci, Jacopo Cefalo, Simone Contino, Alessia Martini, Bruno Iovene, Giacomo Sgalla, Giovanni Franco, Umberto Zanini, Tommaso Pianigiani, Akter Dilroba, Daniele Puggioni, Athina Patsoura, Benedetta Mosole, Olga Torre, Elena Bargagli, Luca Richeldi, Giovanni Sotgiu","doi":"10.1007/s00408-025-00832-4","DOIUrl":"10.1007/s00408-025-00832-4","url":null,"abstract":"<p><strong>Purpose: </strong>Pulmonary fibrosis is defined as progressive based on the combination of radiological, clinical, and functional criteria. Nintedanib can reduce the rate of lung function decline, but no data are available on its effectiveness to hamper disease progression evaluated by these criteria. The primary aim of the study was to assess the number of patients with progressive pulmonary fibrosis (PPF) who no longer meet progression criteria after one year of treatment with nintedanib.</p><p><strong>Methods: </strong>A retrospective, observational, multicenter study was carried out in Italy.</p><p><strong>Results: </strong>172 patients (91 (52.9%) males) with PPF were recruited, and 135 (78.5%) completed one year of treatment. After one year, 87 (64.4%) patients no longer met INBUILD progression criteria, while 107 (79.3%) did not meet 2022 ATS/ERS/JRS/ALAT guidelines criteria. Nintedanib hampered progression regardless of inclusion criteria, radiological pattern, and etiological diagnosis. Forced vital capacity (FVC) decline was significantly higher in the 12 months before than in those of treatment (mean, SD): 2512.3 (863.2) ml vs. 2313.6 (821.9) ml; p < 0.0001; 2313.6 (821.9) vs. 2335.7 (865.1); p = 0.82). FVC decline was significantly higher in the year before than in the year of treatment regardless of radiological pattern, etiological subtypes, and respiratory function. Diarrhea (mostly mild) was the most frequent adverse event (51.7%). A permanent discontinuation of the drug was recorded in 15 (9%) patients.</p><p><strong>Conclusion: </strong>Nintedanib is effective and safe in patients with PPF. Besides slowing lung function decline, it hampers progression regardless of etiological diagnosis, radiological pattern, respiratory function, and baseline inclusion criteria.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"77"},"PeriodicalIF":4.6,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584295","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}