Chinese medical journal pulmonary and critical care medicine最新文献

{"title":"Association of ratios of visceral fat area/subcutaneous fat area and muscle area/standard body weight at T12 CT level with the prognosis of acute respiratory distress syndrome","authors":"Hui Shen ,&nbsp;Ying He ,&nbsp;Fan Lu ,&nbsp;Xiaoting Lu ,&nbsp;Bining Yang ,&nbsp;Yi Liu ,&nbsp;Qiang Guo","doi":"10.1016/j.pccm.2024.05.004","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.05.004","url":null,"abstract":"<div><h3>Background</h3><p>It is well-known that body composition metrics can influence the prognosis of various diseases. This study investigated how body composition metrics predict acute respiratory distress syndrome (ARDS) prognosis, focusing on the ratio of visceral fat area (VFA) to subcutaneous fat area (SFA), SFA to standard body weight (SBW), VFA to SBW, and muscle area (MA) to SBW. These metrics were assessed at the level of the twelfth thoracic vertebra (T12 computed tomography [CT] level) to determine their correlation with the outcomes of ARDS. The goal was to utilize these findings to refine and personalize treatment strategies for ARDS.</p></div><div><h3>Methods</h3><p>Patients with ARDS admitted to the intensive care units (ICUs) of three hospitals from January 2016 to July 2023 were enrolled in this study. Within 24 hours of ARDS onset, we obtained chest CT scans to measure subcutaneous fat, visceral fat, and muscle area at the T12 level. We then compared these ratios between survivors and non-survivors. Logistic regression was employed to identify prognostic risk factors. Receiver operating characteristic (ROC) curve analysis was utilized to determine the optimal cutoff for predictors of in-hospital mortality. Based on this cutoff, patients with ARDS were stratified. To reduce confounding factors, 1:1 propensity score matching (PSM) was applied. We conducted analyses of clinical feature and prognostic differences pre- and post-PSM between the stratified groups. Additionally, Kaplan–Meier survival curves were generated to compare the survival outcomes of these groups.</p></div><div><h3>Results</h3><p>Of 258 patients with ARDS, 150 survived and 108 did not. Non-survivors had a higher VFA/SFA ratio (<em>P</em> &lt;0.001) and lower SFA/SBW and MA/SBW ratios (both <em>P</em> &lt;0.001). Key risk factors were high VFA/SFA ratio (OR=2.081; <em>P</em>=0.008), age, acute physiology and chronic health evaluation (APACHE) II score, and lactate levels, while MA/SBW and albumin were protective. Patients with a VFA/SFA ratio ≥0.73 were associated with increased mortality, while those with an MA/SBW ratio &gt;1.55 cm²/kg had lower mortality, both pre- and post-PSM (<em>P</em>=0.001 and <em>P</em> &lt;0.001, respectively). Among 170 patients with pulmonary-origin ARDS, 87 survived and 83 did not. The non-survivor group showed a higher VFA/SFA ratio (<em>P</em> &lt;0.001) and lower SFA/SBW and MA/SBW (<em>P</em>=0.003, <em>P</em> &lt;0.001, respectively). Similar risk and protective factors were observed in this cohort. For VFA/SFA, a value above the cutoff of 1.01 predicted higher mortality, while an MA/SBW value below the cutoff of 1.48 cm²/kg was associated with increased mortality (both <em>P</em> &lt;0.001 pre-/post-PSM).</p></div><div><h3>Conclusions</h3><p>Among all patients with ARDS, the VFA to SFA ratio, MA to SBW ratio at the T12 level, age, APACHE II score, and lactate levels emerged as independent risk factors for mortality.</p></di","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 106-118"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000331/pdfft?md5=e38d7a175826b55b02d8aa8234eef2e7&pid=1-s2.0-S2772558824000331-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141480123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding cachexia and its impact on lung cancer and beyond","authors":"Meiting Yue ,&nbsp;Zhen Qin ,&nbsp;Liang Hu ,&nbsp;Hongbin Ji","doi":"10.1016/j.pccm.2024.02.003","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.02.003","url":null,"abstract":"<div><p>Cancer cachexia is a multifactorial syndrome characterized by loss of body weight secondary to skeletal muscle atrophy and adipose tissue wasting. It not only has a significant impact on patients’ quality of life but also reduces the effectiveness and tolerability of anticancer therapy, leading to poor clinical outcomes. Lung cancer is a prominent global health concern, and the prevalence of cachexia is high among patients with lung cancer. In this review, we integrate findings from studies of lung cancer and other types of cancer to provide an overview of recent advances in cancer cachexia. Our focus includes topics such as the clinical criteria for diagnosis and staging, the function and mechanism of selected mediators, and potential therapeutic strategies for clinical application. A comprehensive summary of current studies will improve our understanding of the mechanisms underlying cachexia and contribute to the identification of high-risk patients, the development of effective treatment strategies, and the design of appropriate therapeutic regimens for patients at different disease stages.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 95-105"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000045/pdfft?md5=6b4623cf381c108a5969dd91be15c0e4&pid=1-s2.0-S2772558824000045-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141479693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell–cell interactions and communication dynamics in lung fibrosis","authors":"Ting Xie,&nbsp;Jiurong Liang,&nbsp;Barry Stripp,&nbsp;Paul W. Noble","doi":"10.1016/j.pccm.2024.04.001","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.04.001","url":null,"abstract":"<div><p>Cell–cell interactions are essential components of coordinated cell function in lung homeostasis. Lung diseases involve altered cell–cell interactions and communication between different cell types, as well as between subsets of cells of the same type. The identification and understanding of intercellular signaling in lung fibrosis offer insights into the molecular mechanisms underlying these interactions and their implications in the development and progression of lung fibrosis. A comprehensive cell atlas of the human lung, established with the facilitation of single-cell RNA transcriptomic analysis, has enabled the inference of intercellular communications using ligand–receptor databases. In this review, we provide a comprehensive overview of the modified cell–cell communications in lung fibrosis. We highlight the intricate interactions among the major cell types within the lung and their contributions to fibrogenesis. The insights presented in this review will contribute to a better understanding of the molecular mechanisms underlying lung fibrosis and may guide future research efforts in developing targeted therapies for this debilitating disease.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 63-71"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000252/pdfft?md5=02e0ead30d3d12cef2311866a3340fdc&pid=1-s2.0-S2772558824000252-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141479694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of nicotine dependence among smokers aged 40 years and older in China","authors":"Ying Ji ,&nbsp;Shu Cong ,&nbsp;Jing Fan ,&nbsp;Ning Wang ,&nbsp;Wenjing Wang ,&nbsp;Xuping Song ,&nbsp;Liwen Fang","doi":"10.1016/j.pccm.2024.05.003","DOIUrl":"https://doi.org/10.1016/j.pccm.2024.05.003","url":null,"abstract":"<div><h3>Background</h3><p>Nicotine dependence, also known as tobacco dependence, is a common chronic disease and a major risk factor for chronic respiratory diseases. The present study was designed to determine the prevalence of nicotine dependence and its changes among smokers aged 40 years and older in China, to analyze the characteristics of nicotine dependence among smokers, and to provide a reference for smoking cessation interventions.</p></div><div><h3>Methods</h3><p>The data were sourced from nationally representative large-sample surveys conducted during 2014–2015 and 2019–2020 in the Chinese population, covering 125 counties (districts) in 31 provinces, autonomous regions and municipalities. Variables related to smoking and nicotine dependence among residents ≥40 years old were collected in face-to-face interviews. A total of 20,062 and 18,975 daily smokers were included in the 2014–2015 and 2019–2020 surveys, respectively. The severity of nicotine dependence was evaluated according to the Fagerström Test for Nicotine Dependence and Heaviness of Smoking Index. The level and change in nicotine dependence among daily smokers aged ≥40 years were estimated using a complex weighted sampling design, and their influencing factors were analyzed.</p></div><div><h3>Results</h3><p>Levels of nicotine dependence among daily smokers aged ≥40 years in China could be divided into very low, low, medium, high, and very high, accounting for 31.1%, 27.9%, 13.4%, 20.5%, and 7.1% of the total, respectively. The average Fagerström Test for Nicotine Dependence score was 3.9 (95% confidence interval [CI]: 3.8–4.0), with the prevalence of medium–high nicotine dependence being 41.0% (95% CI: 39.0–42.9%) and that of high and very high nicotine dependence being 27.6% (95% CI: 26.0–29.3%), both of which were significantly higher in men than in women (both <em>P</em> &lt; 0.001). Among daily smokers, those with a low education level, age at smoking initiation &lt;18 years, and with smoking duration of ≥20 years had a higher degree of nicotine dependence. In terms of geographic region, the level of medium–high nicotine dependence in South China was higher than in other areas, and the decline in the prevalence of high nicotine dependence was the greatest in Northwest China (<em>P</em> &lt; 0.001). The prevalence of medium–high and high and very high nicotine dependence was significantly higher in men with chronic respiratory symptoms, chronic obstructive pulmonary disease (COPD), and/or chronic respiratory diseases than in men without these conditions (all <em>P</em> &lt; 0.05). The prevalence of high and very high nicotine dependence in women with chronic respiratory symptoms and chronic respiratory diseases was significantly higher than that in women without these conditions (both <em>P</em> &lt; 0.05). Compared with that during 2014–2015, the prevalence of high nicotine dependence among daily smokers decreased during 2019–2020 by 4.5 percentage points in the total ","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 119-131"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S277255882400032X/pdfft?md5=e325d93d5c1aef7ba786643c409d2ec5&pid=1-s2.0-S277255882400032X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141479691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers in idiopathic pulmonary fibrosis: Current insight and future direction","authors":"Zhen Zheng,&nbsp;Fei Peng,&nbsp;Yong Zhou","doi":"10.1016/j.pccm.2024.04.003","DOIUrl":"10.1016/j.pccm.2024.04.003","url":null,"abstract":"<div><p>Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive interstitial lung disease with a dismal prognosis. Early diagnosis, accurate prognosis, and personalized therapeutic interventions are essential for improving patient outcomes. Biomarkers, as measurable indicators of biological processes or disease states, hold significant promise in IPF management. In recent years, there has been a growing interest in identifying and validating biomarkers for IPF, encompassing various molecular, imaging, and clinical approaches. This review provides an in-depth examination of the current landscape of IPF biomarker research, highlighting their potential applications in disease diagnosis, prognosis, and treatment response. Additionally, the challenges and future perspectives of biomarker integration into clinical practice for precision medicine in IPF are discussed.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 72-79"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000240/pdfft?md5=381b53fe7d1a86f6287eea01a6e1c1aa&pid=1-s2.0-S2772558824000240-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141409116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single nucleotide variants in lung cancer","authors":"Xiaoling Tian,&nbsp;Zhe Liu","doi":"10.1016/j.pccm.2024.04.004","DOIUrl":"10.1016/j.pccm.2024.04.004","url":null,"abstract":"<div><p>Germline genetic variants, including single-nucleotide variants (SNVs) and copy number variants (CNVs), account for interpatient heterogeneity. In the past several decades, genome-wide association studies (GWAS) have identified multiple lung cancer-associated SNVs in Caucasian and Chinese populations. These variants either reside within coding regions and change the structure and function of cancer-related proteins or reside within non-coding regions and alter the expression level of cancer-related proteins. The variants can be used not only for cancer risk assessment and prevention but also for the development of new therapies. In this review, we discuss the lung cancer-associated SNVs identified to date, their contributions to lung tumorigenesis and prognosis, and their potential use in predicting prognosis and implementing therapeutic strategies.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 2","pages":"Pages 88-94"},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000264/pdfft?md5=bb52d1cb9ef04c234bd98f2910d8ef23&pid=1-s2.0-S2772558824000264-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141414989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A crucial role of neutrophil extracellular traps in pulmonary infectious diseases","authors":"Ting Pan ,&nbsp;Jae Woo Lee","doi":"10.1016/j.pccm.2023.10.004","DOIUrl":"10.1016/j.pccm.2023.10.004","url":null,"abstract":"<div><p>Neutrophil extracellular traps (NETs), extrusions of intracellular DNA with attached granular material that exert an antibacterial effect through entangling, isolating, and immobilizing microorganisms, have been extensively studied in recent decades. The primary role of NETs is to entrap and facilitate the killing of bacteria, fungi, viruses, and parasites, preventing bacterial and fungal dissemination. NET formation has been described in many pulmonary diseases, including both infectious and non-infectious. NETs are considered a double-edged sword. As innate immune cells, neutrophils release NETs to kill pathogens and remove cellular debris. However, the deleterious effects of excessive NET release in lung disease are particularly important because NETs and by-products of NETosis can directly induce epithelial and endothelial cell death while simultaneously inducing inflammatory cytokine secretion and immune-mediated thrombosis. Thus, NET formation must be tightly regulated to preserve the anti-microbial capability of NETs while minimizing damage to the host. In this review, we summarized the recent updates on the mechanism of NETs formation and pathophysiology associated with excessive NETs, aiming to provide insights for research and treatment of pulmonary infectious diseases.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 34-41"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558823000592/pdfft?md5=54cbede745bfc06ebe38fa9683577f62&pid=1-s2.0-S2772558823000592-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139884112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging role of cellular senescence in normal lung development and perinatal lung injury","authors":"Phyllis A. Dennery ,&nbsp;Hongwei Yao","doi":"10.1016/j.pccm.2024.01.001","DOIUrl":"10.1016/j.pccm.2024.01.001","url":null,"abstract":"<div><p>Cellular senescence is a status of irreversible growth arrest, which can be triggered by the p53/p21^cip1 and p16^INK4/Rb pathways via intrinsic and external factors. Senescent cells are typically enlarged and flattened, and characterized by numerous molecular features. The latter consists of increased surfaceome, increased residual lysosomal activity at pH 6.0 (manifested by increased activity of senescence-associated beta-galactosidase [SA-β-gal]), senescence-associated mitochondrial dysfunction, cytoplasmic chromatin fragment, nuclear lamin b1 exclusion, telomere-associated foci, and the senescence-associated secretory phenotype. These features vary depending on the stressor leading to senescence and the type of senescence. Cellular senescence plays pivotal roles in organismal aging and in the pathogenesis of aging-related diseases. Interestingly, senescence can also both promote and inhibit wound healing processes. We recently report that senescence as a programmed process contributes to normal lung development. Lung senescence is also observed in Down Syndrome, as well as in premature infants with bronchopulmonary dysplasia and in a hyperoxia-induced rodent model of this disease. Furthermore, this senescence results in neonatal lung injury. In this review, we briefly discuss the molecular features of senescence. We then focus on the emerging role of senescence in normal lung development and in the pathogenesis of bronchopulmonary dysplasia as well as putative signaling pathways driving senescence. Finally, we discuss potential therapeutic approaches targeting senescent cells to prevent perinatal lung diseases.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 10-16"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S277255882400001X/pdfft?md5=a703aae0752f78bff1506de9fd312029&pid=1-s2.0-S277255882400001X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140082645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Guide for Authors","authors":"","doi":"10.1016/S2772-5588(24)00012-4","DOIUrl":"https://doi.org/10.1016/S2772-5588(24)00012-4","url":null,"abstract":"","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages I-XI"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000124/pdfft?md5=ee8e5da0b0762adc5bc4ca2f7ec54f67&pid=1-s2.0-S2772558824000124-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140309535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small cell lung cancer transformations from non-small cell lung cancer: Biological mechanism and clinical relevance","authors":"Yang Yang,&nbsp;Songqing Fan","doi":"10.1016/j.pccm.2023.10.005","DOIUrl":"10.1016/j.pccm.2023.10.005","url":null,"abstract":"<div><p>Lung cancer is a leading cause of cancer deaths worldwide, consisting of two major histological subtypes: small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC). In some cases, NSCLC patients may undergo a histological transformation to SCLC during clinical treatments, which is associated with resistance to targeted therapy, immunotherapy, or chemotherapy. The review provides a comprehensive analysis of SCLC transformation from NSCLC, including biological mechanism, clinical relevance, and potential treatment options after transformation, which may give a better understanding of SCLC transformation and provide support for further research to define better therapy options.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 42-47"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558823000610/pdfft?md5=d9153284783970c63d5261c1466c3325&pid=1-s2.0-S2772558823000610-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139826150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}