Clinical Respiratory Journal最新文献

{"title":"Therapeutic and Prognostic Potential of G Protein-Coupled Receptors in Lung Adenocarcinoma: Evidence From Transcriptome Data and In Vitro Experiments","authors":"Feiyan Yang,&nbsp;Jianye Yang,&nbsp;Guobiao Yang,&nbsp;Ya Zhang","doi":"10.1111/crj.70080","DOIUrl":"https://doi.org/10.1111/crj.70080","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>G protein-coupled receptors (GPCRs), the largest family of cell-surface molecules involve in various signal transduction, have recently been recognized as important drivers of cancer. However, few studies have reported on the potential of GPCRs as therapeutic targets or biomarkers in lung adenocarcinoma (LUAD).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The expression profiles and clinical data of LUAD in the GSE30219 and GSE18842 datasets of the Cancer Genome Atlas were analyzed. LUAD-associated module genes were screened utilizing weighted gene co-expression network analysis (WGCNA). Prognostic signature genes were identified by univariate Cox survival analysis, LASSO regression, and multivariate Cox regression analyses. The immune status was evaluated and drug sensitivity was determined, conducting in vitro experiments for validation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Patients with LUAD exhibited lower GPCR score than the controls, and 38 dysregulated GPCRs were identified by screening with differential analysis and WGCNA module genes. An optimal prognostic signature was identified, including OR51E1, LGR4, ADRB1, ADGRD1, and ADGRE3. The model established based on these five genes harbored moderate predictive performance for the survival of patients with LUAD. The risk score was negatively correlated with the infiltrating levels of multiple immune cells, including M2 macrophages, myeloid dendritic cells, and neutrophils, but positively correlated with fewer immune cells, such as Th1/Th2 CD4 + T cell. ADGRE3 and OR51E1 expression was positively correlated with drug sensitivity, including to cisplatin, ribociclib, and pevonedistat. Silencing OR51E1 inhibited the malignant cytological behaviors of LUAD cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>GPCRs demonstrated prognostic potential in LUAD, with five genes identified as potential therapeutic targets and prognostic biomarkers for LUAD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143944629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pressure Properties of a New Positive Expiratory Pressure Device—OpenUp Flow a Three-in-One Solution","authors":"Pär Wennberg,&nbsp;Bengt Sundberg,&nbsp;Elisabeth Westerdahl","doi":"10.1111/crj.70084","DOIUrl":"https://doi.org/10.1111/crj.70084","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>A new flow-regulated PEP device has been evaluated regarding functionality and pressure properties.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The three different resistance levels were assessed and evaluated at standardized flow rates of 10 and 18 L/min; Kruskal–Wallis test was used to analyse the differences in generated pressure between the different resistance levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A range of 3–31 cmH₂O was generated with airflows of 10 and 18 L/min. There was a significant difference in pressure among different resistance levels at both flow rates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Overall, there was a significant difference in pressure among different resistance levels at both flow rates, showing that the high resistance significantly increased pressure compared with low resistance. This new device is performing comparable with other resistors available in the market.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70084","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143939279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal Inference of Different Smoke Exposure Statuses and Influenza Risk: Insights From a Mendelian Randomization Study","authors":"Yanqi Guo,&nbsp;Haixia Chen,&nbsp;Shijie Wu,&nbsp;Jiesen Zhou,&nbsp;Zhihua Chen","doi":"10.1111/crj.70083","DOIUrl":"https://doi.org/10.1111/crj.70083","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Previous observational studies have suggested a potential association between smoking exposure and influenza infection risk. However, the impact of different smoke exposure statuses on susceptibility to influenza infection remains insufficiently explored. This study employs Mendelian randomization analysis to investigate the causal relationship between smoking exposure statuses, including current tobacco use, household smoking exposure, past smoking history, and the risk of influenza infection.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The summary-level data for this study were obtained from the FinnGen Consortium R11 and Neale Lab, both outcomes and exposures. To ensure robust results, we employed multiplicative random-effects inverse variance weighting, MR-Egger, and weighted median (WM) methods to analyze single-nucleotide polymorphisms (SNPs). We also conducted Cochran's <i>Q</i> test, MR-PRESSO, and the MR-Egger intercept test to assess heterogeneity and horizontal pleiotropy, ensuring accurate and reliable findings.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our analysis demonstrated that elevated exposure to current tobacco smoking causally increased the risk of influenza infection, with (OR = 2.032, 95% CI 1.672–2.538, <i>p</i> &lt; 0.001) or without pneumonia (OR = 2.081, 95% CI 1.824–2.338, <i>p</i> = 0.015). No reverse causal relationship was found, and no bidirectional effects were observed for past smoking (OR = 1.108, 95% CI 0.543–2.258, <i>p</i> = 0.779) or household exposure (OR = 1.127, 95% CI −0.209–2.462, <i>p</i> = 0.939).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This analysis identified a significant causal association between current tobacco smoking and increased risk of influenza infection. However, no significant association was observed for other smoking exposures (e.g., former or household smoking). These findings emphasized the importance of considering different types of smoking exposure in clinical influenza prevention and treatment strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70083","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143944628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “The Relationship of Vitamin A and Neonatal Respiratory Diseases: A Meta-Analysis”","authors":"","doi":"10.1111/crj.70078","DOIUrl":"https://doi.org/10.1111/crj.70078","url":null,"abstract":"<p>\u0000 <span>Y. Li</span>, <span>R. Zhang</span>, <span>X. Li</span>, <span>Q. Zhai</span>, “ <span>The Relationship of Vitamin A and Neonatal Respiratory Diseases: A Meta-Analysis</span>,” <i>Clinical Respiratory Journal</i> <span>18</span>, no. <span>10</span> (<span>2024</span>), https://doi.org/10.1111/crj.70030.\u0000 </p><p>The Funding section is incomplete and should be revised to:</p><p>Funding: This work was financially supported by the Scientific Research Project of Weifang Health Committee of Shandong Province (wfwsjk2019-182), Weifang Youth Medical Talent Support Project, and Weifang Clinical Medical Research Center Cultivation Project (Clinical Medical Research Center for Neonatal Diseases).</p><p>The other elements of the paper remain the same.</p><p>We apologize for this error.</p>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70078","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP7-Mediated ICAM1 Facilitates Lipopolysaccharide-Induced Human Pulmonary Microvascular Endothelial Cell Injury to Accelerate Pediatric Acute Respiratory Distress Syndrome","authors":"Jing Li,&nbsp;Jing Wu,&nbsp;Lili Zhao,&nbsp;Lian Liu","doi":"10.1111/crj.70079","DOIUrl":"https://doi.org/10.1111/crj.70079","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Intercellular cell adhesion molecule 1 (ICAM1) has been confirmed to be abnormally expressed in acute respiratory distress syndrome (ARDS) patients. However, its role and mechanism in pediatric ARDS process need further revealed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Serum samples were selected from pediatric ARDS patients and age-matched healthy individuals. Lipopolysaccharide (LPS)-induced human pulmonary microvascular endothelial cells (HPMECs) were used to mimic ARDS cell models. Cell proliferation and apoptosis were tested by cell counting kit 8 assay, EdU assay, and flow cytometry. Oxidative stress and inflammation were assessed by corresponding kits. M1 macrophage polarization was evaluated via measuring CD86 positive cell rate. The expression levels of ICAM1, ubiquitin-specific peptidase 7 (USP7), and NF-κB pathway-related markers were detected by quantitative real-time PCR and western blot. The interaction between USP7 and ICAM1 was analyzed by Co-IP assay.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>LPS induced apoptosis, inflammation, oxidative stress, and M1 macrophage polarization, while suppressed proliferation in HPMECs. ICAM1 was upregulated in pediatric ARDS patients, and its knockdown alleviated HPMEC injury induced by LPS. USP7 positively regulated ICAM1 protein expression through deubiquitination. USP7 overexpression aggravated LPS-induced HPMEC apoptosis, inflammation, oxidative stress, and M1 macrophage polarization. Besides, ICAM1 upregulation could eliminate the inhibitory effect of USP7 knockdown on LPS-induced HPMEC injury. In addition, USP7 activated NF-κB pathway by promoting ICAM1 expression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>USP7-mediated ICAM1 upregulation could promote LPS-induced HPMEC injury by activating NF-κB pathway, which provided a new idea for the treatment of pediatric ARDS.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70079","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a Nomogram Model to Predict Mortality in ANCA-Associated Vasculitis Patients With Pulmonary Involvement","authors":"Qifang Guo,&nbsp;Yijia Shao,&nbsp;Le Yu,&nbsp;Xiuling Zhang,&nbsp;Jingjing Shang,&nbsp;Xueqin Feng,&nbsp;Wei Zhou,&nbsp;Xinwang Duan","doi":"10.1111/crj.70067","DOIUrl":"https://doi.org/10.1111/crj.70067","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Risk assessment and prognosis prediction are crucial for patients with pulmonary involvement in antineutrophil cytoplasimc antibody associated vasculitis (AAV). This study was conducted to create and internally validate a prognostic model for mortality of pulmonary involvement in patients with AAV that provides individualized risk assessments.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A cohort of 150 patients diagnosed with AAV at the Second Affiliated Hospital of Nanchang University Hospital between January 2013 and July 2022 was included, using data obtained from the Chinese Rheumatism Data Center (CRDC). The model was developed using Cox proportional hazards regression and the least absolute shrinkage and selection operator. To validate the model, assessments were conducted for discrimination, calibration, and through decision curve analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The mean survival time of lung involvement AAV patients was 57.0 ± 4.1 months. In the final predictive model for death, four clinical variables were included: age at baseline, history of tumors, baseline hemoglobin level, and the level of the percentage of forced vital capacity to the normal predicted value. One-, two-, and three-year AAV patients with pulmonary involvement mortality probability-predictive nomogram were established. Internal validation of the model was conducted, yielding Harrell's concordance index (0.884), a Brier score of 0.088, and a calibration curve indicating satisfactory performance.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We constructed a risk model utilizing easily accessible clinical risk factors, which could accurately forecast the future mortality risk associated with pulmonary involvement in AAV patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Case of Lung Squamous Cell Carcinoma Harboring TP53 Mutation and PLPP5-FGFR1 Fusion Gene","authors":"Meng Xiao-ru,&nbsp;Shi Xiao-Xiong,&nbsp;Gao Qian,&nbsp;Qu Ya-jing,&nbsp;Huo Li-li,&nbsp;Gao Yan-Yan,&nbsp;Xu Peng-peng,&nbsp;Ma Guan-nan,&nbsp;Ren Gui-bing","doi":"10.1111/crj.70074","DOIUrl":"https://doi.org/10.1111/crj.70074","url":null,"abstract":"<p>Lung squamous cell carcinoma (LUSC) is one of the most common subtype of lung cancer and is associated with the poor prognoses. The fibroblast growth factor receptor (FGFR) family is known to be activated through fusions with various partners across multiple cancer types, including nonsmall cell lung cancer (NSCLC). FGFR inhibitors are currently undergoing clinical evaluation for the treatment of tumors harboring these fusions. While FGFR1 amplification has been well-documented in numerous NSCLC datasets, the characterization of specific FGFR fusion variants remains limited. In this study, we identified a novel PLPP5-FGFR1 fusion in a 65-year-old male patient with lung squamous cell carcinoma through targeted RNA sequencing. The fusion junction was located between exon 1 of PLPP5 and exon 5 of FGFR1, and the result was validated by Sanger sequencing. To our knowledge, this is the first reported case of a PLPP5-FGFR1 fusion coexisting with a TP53 mutation in LUSC. These findings broaden the spectrum of potential translocation partners in FGFR1 fusions, and the clinical implications of this novel fusion on treatment outcomes and prognosis warrant further investigation and long-term follow-up.</p>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143840602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Physical Exercises in Asthma: An Umbrella Review of Systematic Review and Meta-Analysis","authors":"Fuchun Huang,&nbsp;Shuang Yang,&nbsp;Mingxuan Ma,&nbsp;Jialin Zhang,&nbsp;Hua Liu","doi":"10.1111/crj.70075","DOIUrl":"https://doi.org/10.1111/crj.70075","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>As a disease-modifying strategy, physical exercise has been demonstrated to significantly improve quality of life, exercise capacity, and lung function in individuals with asthma. However, the quality and robustness of this evidence has not been thoroughly examined in many large-scale investigations. In order to assess the evidence addressing the effects of physical exercise in patients with asthma, we therefore carried out an umbrella review.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive search of the PubMed, Web of Science, and Cochrane databases for systematic reviews and meta-analyses of the effects of physical activity on asthma was conducted up to December 31, 2022. The study was registered in Prospero (CRD42023382921). For every qualified systematic review and meta-analysis, we extracted information on the main characteristics and general findings. The GRADE tool was utilized to quantify the strength of the evidence, and the AMSTAR2 score was employed to evaluate the methodological quality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 1254 articles were searched, and 42 independent results were identified as eligible in the 11 articles that were included. Of the 42 unique outcomes, two were rated as high, two as medium, and the rest as low or very low. Physical exercise is beneficial for improving QoL, exercise capacity, and lung function in patients with asthma.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>According to our research, physical activity benefits QoL of patients with asthma, exercise tolerance, and lung function. In the future, further evidence from superior prospective studies will be required because the quality of the available evidence is now insufficient.</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143840601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Comment on ‘Screening for Obstructive Sleep Apnea Before Coronary Angiography’","authors":"Baris Demirkol,&nbsp;Celal Satici","doi":"10.1111/crj.70077","DOIUrl":"https://doi.org/10.1111/crj.70077","url":null,"abstract":"<p>Obstructive sleep apnea (OSA) is closely associated with cardiovascular diseases, and its impact on coronary heart disease (CHD) has been increasingly investigated [<span>1, 2</span>]. The pathophysiological mechanisms of OSA, such as recurrent nocturnal hypoxemia and increased sympathetic nervous system activation, can lead to endothelial dysfunction and early atherosclerotic changes, thereby heightening the risk of CHD [<span>2-4</span>]. Additionally, OSA shares common characteristics with other major cardiovascular risk factors, including hypertension, obesity, and metabolic syndrome, further underscoring the strong relationship between these conditions [<span>5, 6</span>]. Therefore, effective screening and management of OSA may play a significant role in the prevention and treatment of CHD.</p><p>We have reviewed with great interest the study by Guo Pei et al., titled “Screening for Obstructive Sleep Apnea Before Coronary Angiography,” which highlights the importance of OSA screening prior to coronary angiography [<span>7</span>]. While this valuable study contributes to the literature, we believe it could yield more impactful results with some refinements.</p><p>First, since the primary focus of the study is the importance of OSA screening, selecting OSA rather than CHD as the primary endpoint might be more appropriate. This adjustment could better align the study with its focus on assessing the clinical implications of OSA and provide a more coherent framework for its objectives. Presenting and comparing the characteristics of OSA (+) and OSA (−) groups, along with conducting a multivariable analysis of these data, could also enhance the clarity and interpretability of the findings. Logistic regression analyses based on these groups could more effectively evaluate the independent predictors of OSA detection.</p><p>The current multivariable analysis model includes parameters with high collinearity (e.g., total cholesterol, LDL, HDL), which may adversely affect the model's accuracy and result in multicollinearity issues. Evaluating the model's fit using measures such as the Hosmer–Lemeshow test and considering alternative models could help better elucidate the independent effects of each parameter.</p><p>Lastly, performing a receiver operating characteristic (ROC) analysis to clarify the relationship between OSA screening and Gensini scores could provide a more precise determination of a cut-off value with high sensitivity for OSA. This additional analysis would facilitate a more practical interpretation of the results and enhance the study's clinical applicability.</p><p>Baris Demirkol and Celal Satici contributed to the study's design and implementation, the evaluation and analysis of the results, and the drafting of the manuscript.</p><p>The authors declare no conflicts of interest.</p>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70077","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143827019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ruxolitinib for Emergency Treatment of COVID-19–Associated Cytokine Storm: Findings From an Expanded Access Study","authors":"Jeffrey Weinstein,&nbsp;Nikhil Jagan,&nbsp;Shawnta Lorthridge-Jackson,&nbsp;J. E. Hamer-Maansson,&nbsp;Peg Squier","doi":"10.1111/crj.70050","DOIUrl":"https://doi.org/10.1111/crj.70050","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>This expanded access program (EAP) provided ruxolitinib (oral, selective Janus kinase [JAK]1/JAK2 inhibitor) for emergency treatment of COVID-19–associated cytokine storm in patients eligible for hospitalization (NCT04355793).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Patients received ruxolitinib 5 mg twice daily (preferred regimen when tolerated) or once daily for ≤ 14 days, or until determination of no clinical benefit was made. Outcomes were clinical status, physician-assessed clinical benefit, and serious adverse event (SAE) incidence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Of 312 patients, 45.5% achieved ≥ 1-point clinical status improvement. Physician-assessed clinical benefit was reported in 42.6% of evaluable patients. SAEs occurred in 42.9%, with 2.6% experiencing an SAE suspected to be ruxolitinib related.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Overall, some hospitalized patients with COVID-19–associated cytokine storm who received ruxolitinib experienced clinical status improvement; ruxolitinib was well tolerated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Trial Registration</h3>\u0000 \u0000 <p>ClinicalTrials.gov identifier: NCT04355793</p>\u0000 </section>\u0000 </div>","PeriodicalId":55247,"journal":{"name":"Clinical Respiratory Journal","volume":"19 4","pages":""},"PeriodicalIF":1.9,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/crj.70050","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143793521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}