Thorax最新文献

{"title":"Journal club","authors":"Mohammed Azib Zahid","doi":"10.1136/thorax-2025-223733","DOIUrl":"https://doi.org/10.1136/thorax-2025-223733","url":null,"abstract":"Predicting response to omalizumab, an anti-IgE monoclonal, in severe allergic asthma is challenging. Djukanović et al (Am J Respir Crit Care Med. 2024;210(3):288–297. doi:10.1164/rccm.202310–1730OC) conducted the SoMOSA Study, to evaluate the clinical efficacy of omalizumab and to identify advanced omics biomarkers to guide therapy. The SoMOSA study was a 1 year, open-label, real-world study enrolling 216 patients with severe, uncontrolled atopic asthma, who were on high-dose inhaled corticosteroids (with or without maintenance oral corticosteroids) with at least two exacerbations in the previous year. Early response to omalizumab was assessed using the Global Evaluation of Treatment Effectiveness (GETE) score in the first 16 weeks. Early positive response was found in 63%, and 69% experienced a≥50% reduction in exacerbations over the full treatment period. Among those receiving maintenance oral corticosteroids, 57% were able to reduce their dose by at least half. Importantly, while conventional biomarkers (blood eosinophils, fractional exhaled nitric oxide, and total IgE) did not predict the response, analysis of exhaled breath via gas chromatography–mass spectrometry and plasma lipid profiling identified a distinct panel of volatile organic compounds and lipid markers that predicted clinical improvement with high accuracy (receiver …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"91 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144629683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Air pollution, genetic susceptibility and risk of progression from asthma to COPD","authors":"Guoxing Li, Ke Zhang, Teng Yang, Jianbo Jin, Xinbiao Guo, Yutong Samuel Cai, Jing Huang","doi":"10.1136/thorax-2024-222871","DOIUrl":"https://doi.org/10.1136/thorax-2024-222871","url":null,"abstract":"Background In the UK, an estimated 15% of asthma patients have concurrent chronic obstructive pulmonary disease (COPD), yet the underlying causes and mechanisms remain largely unexplored. This study aimed to investigate the roles of both ambient air pollution and genetic susceptibility in the progression from asthma to COPD. Methods 46 832 participants with asthma were recruited from the UK Biobank during the baseline period (2006–2010). Particulate matter with a diameter of 2.5 μm (PM2.5) and nitrogen dioxide (NO2) were estimated at baseline address using land-use regression models. Air pollution score reflected joint exposure to air pollution. Polygenic risk score was calculated using novel genetic signals identified for coexistence of asthma+COPD. Cox proportional hazards regression analysis was employed to quantify the risks of both ambient air pollution and genetic scores on incident COPD among asthmatics, adjusting for covariates. Results Over a median follow-up of 10.84 years, 3759 participants with asthma at baseline developed COPD. For an IQR increase in PM2.5 and NO2, the HR for developing COPD was 1.07 (95% CI: 1.02 to 1.11) and 1.10 (95% CI: 1.04 to 1.15), respectively. Adverse effects could be observed at concentrations as low as 8 µg/m3 for PM2.5 and 12 µg/m3 for NO2. A significant multiplicative interaction was identified between ambient air pollution and genetic susceptibility. Individuals with the highest genetic risk score exhibited the greatest risk, with an HR of 1.13 (95% CI: 1.05 to 1.22) per IQR increase in air pollution score (P interaction <0.05). Conclusions Ambient air pollution is strongly associated with progression from asthma to comorbidity COPD, particularly among individuals with high genetic risk. Data are available on reasonable request.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"143 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144678110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary mucormycosis masquerading as malignancy in a Non-Diabetic Patient","authors":"Honghui Jiang, Qian Yao, Lile Wang, Daiyan Fu","doi":"10.1136/thorax-2025-223335","DOIUrl":"https://doi.org/10.1136/thorax-2025-223335","url":null,"abstract":"A 75-year-old male with chronic obstructive pulmonary disease (COPD) (on inhaled fluticasone/umeclidinium/vilanterol and intermittent intravenous methylprednisolone) presented with a 4-week history of intermittently productive cough and mucoid sputum. He denied fever, weight loss or haemoptysis. The patient had a 40-pack-year smoking history but no diabetes, haematological malignancies or tuberculosis. Physical examination revealed bilaterally reduced breath sounds. Laboratory tests showed mild anaemia (haemoglobin 114 g/L) and elevated C-reactive protein (21.4 mg/L). Serum galactomannan and cryptococcal antigen tests were negative. Chest CT revealed a 15×11 mm solid nodule in the left lower lobe with short spiculation and lobulation (figure 1A). Given the suspicion of malignancy, a CT-guided percutaneous biopsy was performed. Periodic acid-Schiff (PAS) staining (figure 2A) revealed broad, non-septate hyphae (predominantly ranging from 5 to 20 µm in diameter) with right-angle branching. Polysaccharide immunofluorescence (figure 2B) highlighted fungal hyphae with intense fluorescence signals, revealing broad, non-septate hyphae with right-angle branching patterns. These histopathological findings are consistent with mucormycosis. Figure 1 (A) Axial chest CT on admission demonstrates a solid nodule with short spiculation and lobulation in the left lower lobe (arrow). (B) Follow-up chest CT after 5 months of therapy reveals a significant reduction in the …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"13 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144652227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of simvastatin on postoperative complications in patients undergoing one-lung ventilation during surgery: the Prevention HARP-2 randomised controlled trial","authors":"Adam Glass, Cecilia M O’Kane, Akesh Dhrampal, Eustace Fontaine, James Ryan, Mahmoud Loubani, Sridhar Rathinam, Babu Naidu, Ingeborg D Welters, Jon Silversides, Bilal Alkhaffar, Jeremy Hayden, Ewen Griffiths, David Chan, Annmarie Doran, Sorcha Toase, Christina Campbell, Ashley Agus, Gavin D Perkins, Daniel Francis McAuley, Murali Shyamsundar","doi":"10.1136/thorax-2025-223072","DOIUrl":"https://doi.org/10.1136/thorax-2025-223072","url":null,"abstract":"Rationale Surgeries that require one-lung ventilation have high rates of postoperative cardiopulmonary complications with associated morbidity and mortality. Statins may limit inflammation involved in the development of these complications. Objectives We tested the hypothesis that perioperative simvastatin use reduces postoperative cardiopulmonary complications, compared with placebo, in surgery requiring one-lung ventilation. Methods Randomised, double-blind, multicentre trial of simvastatin versus placebo in patients undergoing elective oesophagectomy, lobectomy or pneumonectomy at 15 sites throughout the UK. Planned sample size is 452 patients. Participants were randomised to either simvastatin 80 mg or placebo for 4 days preoperatively and up to 7 days postoperatively. Measurements The primary outcome measure was a composite endpoint of the incidence of acute respiratory distress syndrome, postoperative pulmonary complications, myocardial infarction and/or myocardial ischaemia during the first 7 days postoperatively or until hospital discharge. A modified intention-to-treat analysis excluded patients who did not receive the intervention preoperatively or proceed with the planned surgery. Main results 251 patients were randomised, 126 assigned to simvastatin and 125 to placebo, with 208 included in the modified intention-to-treat population. The trial was stopped early because of futility following recommendations from the data monitoring and ethics committee. The primary outcome occurred in 45/106 patients (42.5%) in the simvastatin group and 39/102 patients (38.2%) in the placebo group (OR 1.19 (95% CI 0.68 to 2.08); p=0.54). Secondary and safety outcomes were similar between the groups. Conclusion In patients undergoing one-lung ventilation, simvastatin did not reduce the incidence of postoperative cardiopulmonary complications. Trial registration number isrctn.org identifier, [ISRCTN48095567][1]. Data are available upon reasonable request. [1]: /external-ref?link_type=ISRCTN&access_num=ISRCTN48095567","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"697 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The changing face of inflammation following CFTR modulation: identifying new phenotypes of innate immunity","authors":"Katherine B Hisert, Milene T Saavedra","doi":"10.1136/thorax-2025-223460","DOIUrl":"https://doi.org/10.1136/thorax-2025-223460","url":null,"abstract":"Triple combination therapy for people with cystic fibrosis (pwCF) restores the activity of defective cystic fibrosis transmembrane conductance regulator (CFTR) proteins. For those fortunate to receive this therapy, it has fundamentally changed the nature of the disease.1 CFTR modulators markedly improve clinical outcomes and symptoms, reversing or alleviating pathologies such as mucous plugging and overly acidic small intestine pH. However, other manifestations of disease persist (established bronchiectasis, chronic airway infections with organisms such as Pseudomonas aeruginosa ). Optimal management of pwCF depends on continued accumulation of knowledge regarding how CFTR therapy changes CF disease. 2 When the first CFTR modulator (ivacaftor) was introduced, several studies characterised how CF pathology changed following enhancement of CFTR activity3–5; however, since only a small fraction of pwCF were eligible for ivacaftor, studies were limited. The approval of elexacaftor-tezacaftor-ivacaftor (ETI) for pwCF with at least one F508del mutation meant that >90% of pwCF would be eligible for modulator therapy. Many studies were organised around the globe to capture specimens and measurements from pwCF before and after initiation of ETI. Much attention has been paid to ETI’s effects on clinical parameters and pulmonary inflammation and infection, but fewer studies have focused on the effects of ETI on systemic inflammation. In this edition of Thorax , Maher and colleagues6 describe changes in systemic inflammatory cells and …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"21 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hereditary pulmonary veno-occlusive disease with a distinctive rare genetic pattern","authors":"Jia-Yong Qiu, Kai Zhang, Shen-Shen Huang, Xi-Qi Xu, Zhi-Cheng Jing","doi":"10.1136/thorax-2025-223444","DOIUrl":"https://doi.org/10.1136/thorax-2025-223444","url":null,"abstract":"A 26-year-old man presented with exertional dyspnoea and was diagnosed with pulmonary arterial hypertension (PAH) of uncertain aetiology at multiple hospitals. A high-resolution chest CT scan revealed two key findings: diffuse lobular-centred ground-glass nodules in both lungs and multiple lymph nodes in the hilar and mediastinal regions (figure 1A,B). Transthoracic echocardiography demonstrated moderate PAH (pulmonary artery systolic pressure 65 mmHg), right ventricular hypertrophy and left ventricular short-axis view with a ‘D’ shape (figure 1C). Right heart acoustic angiography revealed a patent foramen ovale (PFO; figure 1D). Pulmonary function tests showed severely reduced diffusion capacity. Right heart catheterisation confirmed precapillary PAH, with a pulmonary arterial wedge pressure of 13 mm Hg, pulmonary vascular resistance of 6.30 Wood units and cardiac output of 3.49 L/min. Figure 1 (A) High-resolution chest CT scan shows diffuse lobular-centred ground-glass nodules in both lungs and (B) lymph nodes in hilar and mediastinal regions. (C) Transthoracic echocardiography demonstrates left ventricular short-axis view with a ‘D’ shape. (D) Right heart acoustic angiography shows multiple microbubbles (arrows; 20/frame) …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"27 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144578036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antimicrobial resistance in chronic lung infection: the road to resistance","authors":"Wang Chun Kwok, Katharine Pates, Anand Shah, Louise Jackson, Freddy Frost","doi":"10.1136/thorax-2024-222396","DOIUrl":"https://doi.org/10.1136/thorax-2024-222396","url":null,"abstract":"Background Antimicrobial resistance (AMR) is a growing global health crisis and is particularly relevant to people living with chronic lung diseases such as bronchiectasis, cystic fibrosis and chronic obstructive pulmonary disease. These conditions frequently involve acute and chronic bacterial infections, requiring increased antibiotic usage and risk of AMR. Understanding the dynamics of AMR and emerging diagnostic and therapeutic strategies is crucial for optimising patient outcomes in this setting. Aims This review explores the interplay between AMR and chronic bacterial lung infections, examining current understanding of pathogen epidemiology, diagnostic strategies, clinical implications of resistance and the impact of treatments. Future directions in research and therapeutic innovation are also outlined. Narrative Key pathogens in chronic lung infections, such as Pseudomonas aeruginosa , Haemophilus influenzae , Staphylococcus aureus and Moraxella catarrhalis , exhibit diverse resistance mechanisms and AMR is linked to increased disease severity, exacerbation frequency and mortality, particularly with multidrug-resistant strains. Long-term antibiotic therapies, such as macrolides and inhaled agents, improve clinical outcomes but may drive resistance, necessitating ongoing efforts to understand how they can best be employed. Traditional diagnostic methods, such as culture-based antimicrobial susceptibility testing, often fail to capture the complexity of polymicrobial infections and resistomes. Although advanced techniques like next-generation sequencing and metagenomics are able to identify clinically relevant resistotypes, their development toward clinical utility is still in progress. Conclusions AMR in chronic lung infections represents a dynamic and multifaceted challenge. Novel antibiotics, precision medicine approaches and alternative therapies such as bacteriophages show promise but require further validation. Improved stewardship and individualised treatment strategies are critical for mitigating AMR and enhancing patient outcomes. Collaborative efforts among researchers, clinicians and policy-makers are vital to advancing care and combating this global threat.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"2 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying azithromycin responders with an individual treatment effect model in COPD.","authors":"Kenneth Verstraete, Iwein Gyselinck, Helene Huts, Remco Stuart Djamin, Michaël Staes, Sander Talman, Sarah Lindberg, Menno van der Eerden, Maarten De Vos, Wim Janssens","doi":"10.1136/thorax-2025-223095","DOIUrl":"https://doi.org/10.1136/thorax-2025-223095","url":null,"abstract":"<p><strong>Objective: </strong>Long-term azithromycin treatment effectively prevents acute exacerbations of chronic obstructive pulmonary disease (COPD). However, patients would benefit from better identification of responders and non-responders to minimise unnecessary exposure. We aimed to assess treatment effect heterogeneity and estimate individual treatment effects (ITEs) to distinguish patients most likely to benefit from prophylactic treatment.</p><p><strong>Methods: </strong>We used data from 1025 patients of the MACRO trial to assess the ITE of azithromycin on annual exacerbation rate. A Causal Forest was used as a causal machine learning model. We independently validated our findings using data from 83 patients of the COLUMBUS trial.</p><p><strong>Results: </strong>The tertile of patients with the best predicted ITE within MACRO and within the COLUMBUS independent validation cohort showed significant and substantially greater reductions in annual exacerbation rates (in MACRO -0.50, rate ratio 0.70, p=0.01, in COLUMBUS: -2.28, rate ratio 0.43, p<0.001) compared with the average treatment effect across the entire cohort (MACRO -0.35, rate ratio 0.83, p=0.01 and COLUMBUS -1.28, rate ratio 0.58, p=0.001). Conversely, no significant treatment effect was observed in the remaining two-thirds of patients. Primary determinants of ITE included respiratory symptoms, white blood cell count, haemoglobin, C-reactive protein and forced vital capacity. Smoking status did not emerge as a significant predictor.</p><p><strong>Conclusion: </strong>Based on five easily obtainable parameters to predict ITE, we identified treatment effect heterogeneity in COPD subjects treated with azithromycin maintenance therapy and found a small subgroup of responders driving the average reduction in exacerbations reported in previous trials.</p>","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":""},"PeriodicalIF":9.0,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144561284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biological drivers of the host response in sepsis","authors":"W Joost Wiersinga, Tom van der Poll","doi":"10.1136/thorax-2024-222012","DOIUrl":"https://doi.org/10.1136/thorax-2024-222012","url":null,"abstract":"Sepsis is a life-threatening syndrome driven by a dysregulated host response to infection. Immune dysregulation arises from responses that initially were activated to protect against pathogens and preserve tissue integrity. Disturbed resistance mechanisms can result in excessive inflammation alongside immunosuppression, each of which is considered important biological drivers of the immunopathology of sepsis. Key inflammatory drivers are excessive proinflammatory cytokine activity, complement and coagulation system activation and endothelial dysfunction. Conversely, sepsis-induced immunosuppression is marked by lymphocyte exhaustion, reduced monocyte human leucocyte antigen-DR expression, and the emergence of myeloid-derived suppressor cells. Within this complex immunological environment, the gut microbiome influences host immunity through the release of short-chain fatty acids and bacterial metabolites. Thus far, immunomodulatory trials in patients with sepsis paid little attention to the identification of dominant biological drivers, which might enrich the population for those who are more likely to respond to a certain intervention. Recently, retrospective analyses of such trials, as well as small prospective trials, have provided proof of concept that subgroups of sepsis patients can be identified with specific immunological profiles, either based on a single biomarker or on high-dimensional data, that respond differently to immunomodulation. This review explores the biological drivers of sepsis immunopathology, highlighting the challenges in translating preclinical insights into effective therapies and the potential of personalised medicine approaches to improve sepsis outcomes.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"15 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144547232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Journal club","authors":"George Doumat","doi":"10.1136/thorax-2025-223657","DOIUrl":"https://doi.org/10.1136/thorax-2025-223657","url":null,"abstract":"Neutrophilic inflammation is a key driver of bronchiectasis progression and exacerbations. Brensocatib, an oral inhibitor of dipeptidyl peptidase 1 (DPP1), prevents activation of neutrophil serine proteases. The phase III randomised double-blind ASPEN trial (N Engl J Med 2025;392:1569–1581) evaluated the efficacy and safety of once-daily brensocatib at 10 mg or 25 mg compared with placebo over 52 weeks in 1721 patients with non-cystic fibrosis bronchiectasis across 35 countries. The annualised rate of adjudicated pulmonary exacerbations was significantly reduced with brensocatib. Patients receiving 10 mg and 25 mg experienced 1.02 and 1.04 exacerbations per year respectively, compared with 1.29 in the placebo group. This corresponded to rate ratios of 0.79 (95% CI, 0.68 to 0.92; p=0.004) and 0.81 (95%CI, 0.69 to 0.94; p=0.005). Time to first exacerbation was delayed with both doses, and nearly half of brensocatib-treated patients remained exacerbation-free at 1 year compared with 40.3% in the placebo group. Lung function decline was smallest in the 25 mg group, with an average decline of 24 milliliters compared with 62 milliliters with placebo (p=0.04). Quality of life, as measured by the Respiratory Symptoms domain of the Quality of Life–Bronchiectasis questionnaire, improved more with brensocatib, especially at the higher dose. The incidence of adverse events was …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"22 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144296122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}