Lung最新文献

{"title":"Lactate and Lactylation in Respiratory Diseases: from Molecular Mechanisms to Targeted Strategies.","authors":"Qi Jia, Quan Yuan, Xiangdong Chen, Zhiqiang Hu","doi":"10.1007/s00408-025-00848-w","DOIUrl":"https://doi.org/10.1007/s00408-025-00848-w","url":null,"abstract":"<p><strong>Introduction: </strong>Lactate has emerged as a multifunctional signaling molecule regulating various physiological and pathological processes. Furthermore, lactylation, a newly identified posttranslational modification triggered by lactate accumulation, plays significant roles in human health and diseases. This study aims to investigate the roles of lactate/lactylation in respiratory diseases.</p><p><strong>Methods: </strong>Comprehensive literature analysis was conducted using PubMed database, utilizing a range of keywords including \"lactate\", \"lactylation\", \"lung\", \"pulmonary\", and \"disease\".</p><p><strong>Results: </strong>Emerging evidence indicates that increased glycolytic flux, resultant lactate accumulation, and elevated lactylation levels play key roles in the pathogenesis of respiratory diseases, including lung cancer, idiopathic pulmonary fibrosis (IPF), acute lung injury/acute respiratory distress syndrome (ALI/ARDS), pulmonary hypertension (PH), and asthma. Under these conditions, the upregulation of glycolytic enzymes and increased lactate transport are observed. Elevated levels of lactate and lactylation profoundly influence multiple biological processes, such as inflammatory responses, immune cell activation, autophagy, ferroptosis, EMT, tumorigenesis, and fibrosis, and lactate/lactylation-targeted therapies have demonstrated therapeutic efficacy against diverse respiratory illnesses.</p><p><strong>Conclusions: </strong>Elevated levels of lactate and lactylation play key roles in the pathogenesis of various respiratory diseases, and lactate/lactylation-targeted therapies appear to be potential therapeutic strategies for these respiratory diseases.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"94"},"PeriodicalIF":3.9,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145030274","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":"Neuroinflammatory Consequences of Rhinovirus Infection in Human Epithelial and Neuronal Models.","authors":"Orla M Dunne, Nicola A M Roe, Aurélie Mousnier, S Lorraine Martin, Gerard P Sergeant, Imad About, Ikhlas El-Karim, Fionnuala T Lundy, Lorcan P McGarvey","doi":"10.1007/s00408-025-00846-y","DOIUrl":"10.1007/s00408-025-00846-y","url":null,"abstract":"<p><strong>Introduction: </strong>Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV's effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly via the release of mediators from infected epithelial cells.</p><p><strong>Methods: </strong>PNEs or primary bronchial epithelial cells (PBECs) were infected with the RV-A16 strain. Viral replication was confirmed by viral titration assays, immunofluorescence (IF) for the double-stranded RNA (dsRNA) replication intermediate and western blotting (WB). RNA sequencing was used to determine transcriptomic changes in PNEs, and inflammatory responses were assessed by inflammatory microarray. Calcium mobilisation assays were used to investigate the effect of interleukin-1β (IL-1β) on PNE transient receptor potential (TRP) A1 channel responses.</p><p><strong>Results: </strong>Viral titrations, WB and IF confirm RV-A16 entry and replication in PNEs and PBECs. Gene signatures associated with antiviral immune responses, sensory neuropathies and N-Methyl-D-aspartic acid (NMDA) receptor activity were upregulated in RV infected PNEs. Several cytokines were increased from PNEs and PBECs following RV infection, most notably IL-1β. Treatment of PNEs with IL-1β resulted in heightened TRPA1 channel sensitivity.</p><p><strong>Conclusion: </strong>We report the suitability of an airway neuronal model for the study of the direct effects of RV infection on nerves. RV-induced release of IL-1β from airway epithelium heightens neuronal TRPA1 responses suggesting a mechanism for virus-induced cough hypersensitivity.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"93"},"PeriodicalIF":3.9,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12414851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015770","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":"Emerging Therapeutics in COPD: Mapping Innovation to Treatable Traits.","authors":"Mario Cazzola, Vanessa M McDonald, Daiana Stolz, Paola Rogliani, Maria Gabriella Matera","doi":"10.1007/s00408-025-00844-0","DOIUrl":"10.1007/s00408-025-00844-0","url":null,"abstract":"<p><p>Chronic Obstructive Pulmonary Disease (COPD) is a complex, heterogeneous condition characterized by diverse clinical phenotypes and underlying pathobiological mechanisms. Traditional \"one-size-fits-all\" management strategies have limited effectiveness in addressing this heterogeneity. The Treatable Traits (TTs) approach represents a precision medicine paradigm that targets specific, identifiable, and modifiable traits in individual patients, regardless of diagnostic labels. This paper explores the alignment between the TTs framework and emerging pharmacological therapies, with a particular focus on anti-inflammatory agents and bronchodilators currently under investigation. Each drug category is mapped to relevant TTs, such as eosinophilic or neutrophilic inflammation, corticosteroid resistance, chronic bronchitis, and frequent exacerbations. This review highlights the importance of biomarker-driven phenotyping and real-world data in designing TT-based clinical trials. It emphasizes challenges such as trait instability over time, comorbidity clustering, and trial design heterogeneity. Moreover, we advocate for incorporating digital health tools, long-term follow-up, and cost-effectiveness analyses to ensure translational relevance. In conclusion, integrating emerging therapies with the TTs approach holds substantial promise for personalizing COPD management, improving outcomes, and facilitating targeted drug development.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"92"},"PeriodicalIF":3.9,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959585","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":"Age-Dependent Risk of Bronchial Asthma Exacerbation in Respiratory Syncytial Virus Co-infection.","authors":"Ken Arimura, Keiko Kan-O, Yasuto Sato, Ken Kikuchi, Hitomi Miura, Asako Sato, Mitsuko Kondo, Etsuko Tagaya","doi":"10.1007/s00408-025-00847-x","DOIUrl":"10.1007/s00408-025-00847-x","url":null,"abstract":"<p><strong>Introduction: </strong>Respiratory syncytial virus (RSV) and human metapneumovirus (hMPV) are common viral etiologies of respiratory infections. Although co-infection with other respiratory pathogens is frequently observed, its clinical significance remains unclear.</p><p><strong>Methods: </strong>We retrospectively analyzed 57,746 patients who underwent FILMARRAY®, a comprehensive multiplex polymerase chain reaction testing, between November 2020 and March 2023. Clinical features were compared between single infection and co-infection involving RSV or hMPV using χ² or Fisher's exact tests. Multiple logistic regression was performed to identify associations with bronchial asthma (BA) exacerbation, adjusting for age, sex, testing period, and RSV co-infection.</p><p><strong>Results: </strong>Among RSV-positive patients, co-infection was associated with higher prevalence of BA history, wheeze, BA exacerbation, combined BA history and exacerbation, systemic steroid use, and age under 6 years compared to that with single infection. RSV co-infection with coronavirus, parainfluenza virus, adenovirus, and rhinovirus/enterovirus was particularly associated with BA exacerbation. Age under 6 years and RSV co-infection were identified as independent risk factors for BA exacerbation using multiple logistic regression. In contrast, no associations were observed in the hMPV co-infection.</p><p><strong>Conclusion: </strong>RSV co-infection with other respiratory viruses increases the risk of BA exacerbation, especially in age under 6 years patients. Given the proven efficacy of RSV vaccine for adults and monoclonal antibody for high-risk children in preventing RSV-related lower respiratory tract disease, RSV-targeted prevention strategies for younger children appear effective in reducing respiratory disease burden.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"91"},"PeriodicalIF":3.9,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959606","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":"Changes in Lung Function and Patient-Reported Outcomes in Patients with Idiopathic Pulmonary Fibrosis.","authors":"Jamie L Todd, Megan L Neely, Anne S Hellkamp, Daniel A Culver, Justin M Oldham, Peide Li, Divya C Patel, Scott M Palmer","doi":"10.1007/s00408-025-00845-z","DOIUrl":"https://doi.org/10.1007/s00408-025-00845-z","url":null,"abstract":"<p><p>We evaluated relationships between changes in lung function and changes in patient-reported outcomes (PROs) in 736 patients with idiopathic pulmonary fibrosis (IPF) enrolled in the IPF-PRO Registry. Weak correlations were observed between changes in percent predicted values for forced vital capacity or diffusing capacity of the lungs (DLco) and changes in St George's Respiratory Questionnaire (SGRQ) total and activity scores and the 12-item Short Form Survey (SF-12) physical component summary score over 12-month periods. Patients who had a deterioration in SGRQ activity score or SF-12 PCS score of ≥ 5 units had numerically larger declines in lung function than other patients, but the differences were small. The weak relationships observed between changes in lung function and changes in PROs underscore the importance of evaluating both changes in lung function and changes in HRQL in clinical practice and clinical trials.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"90"},"PeriodicalIF":3.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959637","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":"Sputum Transcriptomic Analysis and Clustering Reveals Insight Into Asthma Heterogeneity.","authors":"Janne Goossens, Anne-Charlotte Jonckheere, Sien De Boodt, Ellen Dilissen, Nora Marain, Tatjana Decaesteker, Alvaro Cortes, Jeroen A Vanoirbeek, Sven F Seys, Lieven Dupont, Dominique M A Bullens","doi":"10.1007/s00408-025-00843-1","DOIUrl":"10.1007/s00408-025-00843-1","url":null,"abstract":"<p><strong>Introduction: </strong>Asthma is a heterogenous disease shaped by different inflammatory pathways. The aim is to investigate transcriptomic profiles in asthmatic patients and associate these with inflammation, airway damage and lung function.</p><p><strong>Methods: </strong>Adult asthma patients attending the outpatient pneumology clinic in our tertiary center, underwent diagnostic sputum induction and upon consent remaining sputum RNA was used for bulk RNA-sequencing (n = 56) coupled with unsupervised clustering. A retrospective analysis of comorbidities was performed. Sputum cytokine mRNA levels were determined via qPCR. Airway damage markers were determined in sputum supernatant RESULTS: Unsupervised clustering subdivided all asthmatic patients in one of three clusters. Cluster 1 contained most of the pauci-granulocytic asthma patients in whom oxidative stress was upregulated and TLR-signalling and several cytokine pathways down-regulated. Cluster 2 had upregulated S100 family signalling pathway genes, was mostly associated to type 2 inflammation with elevated sputum eosinophils, epithelial damage, IL-4 mRNA levels and allergy. Asthma patients in cluster 3 had worse lung function, upregulated inflammatory genes, increased sputum neutrophils and calprotectin levels.</p><p><strong>Conclusion: </strong>Three different asthma clusters could be identified bridging over the classical type 2/non-type 2 classification.</p><p><strong>Clinical trial: </strong>ClinicalTrials.gov Identifier: NCT01224938 registered on 19 October 2010.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"89"},"PeriodicalIF":3.9,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883144","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":"Modified Tracheobronchoplasty for Chronic Cough Due to Excessive Dynamic Airway Collapse: A Case Series.","authors":"Alessandro Gonfiotti, Alessandra Sorano, Massimo O Jaus, Giulia Fabietti, Luca Voltolini, Giovanni A Fontana, Federico Lavorini","doi":"10.1007/s00408-025-00842-2","DOIUrl":"10.1007/s00408-025-00842-2","url":null,"abstract":"","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"88"},"PeriodicalIF":3.9,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855723","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":"Serum Cytokeratin 18 and Fragment as Biomarkers for Severity and Prognosis in Acute Exacerbation of Chronic Obstructive Pulmonary Disease.","authors":"Ming-Yan Liu, Kai-Xin Qu, Kai-Shu Ma, Zhen-Yu Cheng, Xiang Cai, Hai-Long Miu, Meng-Xue Liu, Yi-Qun Wang, Hui Zhao, Ling Zheng, Lin Fu, Jin Yang","doi":"10.1007/s00408-025-00841-3","DOIUrl":"10.1007/s00408-025-00841-3","url":null,"abstract":"<p><strong>Background: </strong>Cytokeratin (CK)18 is present in the bronchi and alveolar epithelium of the lung, and its cleavage product, CK-18M30, serves as a biological marker of apoptosis. However, the specific roles of CK-18 and CK-18M30 in acute exacerbation of chronic obstructive pulmonary disease (AECOPD) remain unclear.</p><p><strong>Methods: </strong>This study enrolled 289 patients with AECOPD who met the inclusion criteria. Demographic information and clinical characteristics of the patients were documented. A 3-year follow-up period was implemented to evaluate acute exacerbations and mortality. Serum CK-18 and CK-18M30 concentrations were measured using enzyme-linked immunosorbent assays.</p><p><strong>Results: </strong>Serum concentrations of CK-18/CK-18M30 at admission in patients with AECOPD were higher than those in the control group. As severity increased, serum CK-18/CK-18M30 levels increased progressively in AECOPD patients. Pearson's correlation analysis revealed that serum CK-18/CK-18M30 concentrations were positively correlated with several clinical parameters. Linear and logistic regression models demonstrated positive correlations between serum CK-18 and CK-18M30 levels at admission and severity scores. Furthermore, higher serum CK-18/CK-18M30 levels at admission were associated with increased frequency of death and acute exacerbation in patients with AECOPD within 3 years.</p><p><strong>Conclusion: </strong>Serum CK-18/CK-18M30 levels at admission were positively correlated with severity and poor prognosis in patients with AECOPD within 3 years. Therefore, serum CK-18 and CK-18M30 concentrations may serve as novel diagnostic and prognostic biomarkers for patients with AECOPD.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"87"},"PeriodicalIF":3.9,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144821941","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":"Unnerving Cough in CANVAS: Cough Hypersensitivity Despite Airway Nerve Depletion.","authors":"Barnaby Hirons, Katherine Rhatigan, William McNulty, Richard D Turner, James H Hull, Caroline J Jolley, Robert D Hadden, Ana Ribeiro, Andrea Cortese, Peter S P Cho, Safa Al-Sarraj, Jordi Serra, Peter Bannister, Chadwick B Smith, Matthew G Drake, Surinder S Birring","doi":"10.1007/s00408-025-00838-y","DOIUrl":"10.1007/s00408-025-00838-y","url":null,"abstract":"<p><strong>Introduction: </strong>Cerebellar ataxia with neuropathy and vestibular areflexia syndrome (CANVAS) is a genetic neurodegenerative condition associated with chronic cough and cough hypersensitivity. The neuropathic mechanisms underlying cough in CANVAS are unknown. In a father and son with CANVAS-associated cough, we investigated clinical and neuropathophysiological features including bronchial and skin biopsies.</p><p><strong>Methods: </strong>Patients completed assessments for cough severity (visual analogue scale, VAS), impact (Leicester Cough Questionnaire, LCQ), triggers (Cough Hypersensitivity Questionnaire), objective frequency with Leicester Cough Monitor, and reflex sensitivity with capsaicin cough challenge. Bronchoscopic airway biopsies were analysed for nerve morphology and compared to a healthy control. Neurological assessments included skin biopsies, nerve conduction studies, and microneurography.</p><p><strong>Results: </strong>The father (age 62) and son (age 37) had advanced and early CANVAS, with a refractory chronic cough of 37 and 9 years duration, respectively. The cough in the father and son was of moderate severity (VAS 58 and 54 mm) and impact (LCQ score 15.9 and 13.1), with raised objective cough frequencies of 6 and 16 coughs hr^-1, and heightened cough reflex sensitivity to capsaicin with concentrations to evoke five coughs (C5) of 14.9 and 3.3 μmol L^-1, respectively. Bronchoscopic airway biopsies demonstrated severely depleted sensory small nerve fibres in the father and son compared to a healthy control: median (IQR) total nerve length 0 (0-0) and 0 (0-125) μm vs 944 (461-1323) μm, respectively. Skin biopsies showed absent intraepidermal nerve fibres, with densities of 0.0 fibres.mm^-1 in both patients. Functional microneurography revealed nociceptor fibre paucity and dysfunction.</p><p><strong>Conclusion: </strong>In CANVAS, despite the loss of bronchial and cutaneous nerve fibres, there was heightened cough reflex sensitivity. Further studies are needed to elucidate underlying neural mechanisms.</p>","PeriodicalId":18163,"journal":{"name":"Lung","volume":"203 1","pages":"86"},"PeriodicalIF":3.9,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12334521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144799545","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":"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}