Chinese medical journal pulmonary and critical care medicine最新文献

{"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}

{"title":"Light at night and lung cancer risk: A worldwide interdisciplinary and time-series study","authors":"Runchen Wang ,&nbsp;Qixia Wang ,&nbsp;Jianfu Li ,&nbsp;Jianrong Zhang ,&nbsp;Shixuan Lyu ,&nbsp;Wenhao Chi ,&nbsp;Zhiming Ye ,&nbsp;Xuanzhuang Lu ,&nbsp;Ying Shi ,&nbsp;Yubin Wang ,&nbsp;Xinjian Wu ,&nbsp;Ruiyu Hu ,&nbsp;Mónica Pérez-Ríos ,&nbsp;Jianxing He ,&nbsp;Wenhua Liang","doi":"10.1016/j.pccm.2024.02.004","DOIUrl":"10.1016/j.pccm.2024.02.004","url":null,"abstract":"<div><h3>Background</h3><p>Light at night (LAN) has become a concern in interdisciplinary research in recent years. This global interdisciplinary study aimed to explore the exposure–lag–response association between LAN exposure and lung cancer incidence.</p></div><div><h3>Methods</h3><p>LAN data were obtained from the Defense Meteorological Satellite Program's Operational Linescan System. Data of lung cancer incidence, socio-demographic index, and smoking prevalence of populations in 201 countries/territories from 1992 to 2018 were collected from the Global Burden of Disease Study. Spearman correlation tests and population-weighted linear regression analysis were used to evaluate the correlation between LAN exposure and lung cancer incidence. A distributed lag nonlinear model (DLNM) was used to assess the exposure–lag effects of LAN exposure on lung cancer incidence.</p></div><div><h3>Results</h3><p>The Spearman correlation coefficients were 0.286–0.355 and the population-weighted linear regression correlation coefficients were 0.361–0.527. After adjustment for socio-demographic index and smoking prevalence, the Spearman correlation coefficients were 0.264–0.357 and the population-weighted linear regression correlation coefficients were 0.346–0.497. In the DLNM, the maximum relative risk was 1.04 (1.02–1.06) at LAN exposure of 8.6 with a 2.6-year lag time. After adjustment for socio-demographic index and smoking prevalence, the maximum relative risk was 1.05 (1.02–1.07) at LAN exposure of 8.6 with a 2.4-year lag time.</p></div><div><h3>Conclusion</h3><p>High LAN exposure was associated with increased lung cancer incidence, and this effect had a specific lag period. Compared with traditional individual-level studies, this group-level study provides a novel paradigm of effective, efficient, and scalable screening for risk factors.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 56-62"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000057/pdfft?md5=f8267d7354f962060e92df54ff77d169&pid=1-s2.0-S2772558824000057-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140274869","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":"Dysregulated bidirectional epithelial–mesenchymal crosstalk: A core determinant of lung fibrosis progression","authors":"Liudi Yao ,&nbsp;Zijian Xu ,&nbsp;Donna E. Davies ,&nbsp;Mark G. Jones ,&nbsp;Yihua Wang","doi":"10.1016/j.pccm.2024.02.001","DOIUrl":"10.1016/j.pccm.2024.02.001","url":null,"abstract":"<div><p>Progressive lung fibrosis is characterized by dysregulated extracellular matrix (ECM) homeostasis. Understanding of disease pathogenesis remains limited and has prevented the development of effective treatments. While an abnormal wound-healing response is strongly implicated in lung fibrosis initiation, factors that determine why fibrosis progresses rather than regular tissue repair occur are not fully explained. Within human lung fibrosis, there is evidence of altered epithelial and mesenchymal populations as well as cells undergoing epithelial–mesenchymal transition (EMT), a dynamic and reversible biological process by which epithelial cells lose their cell polarity and down-regulate cadherin-mediated cell–cell adhesion to gain migratory properties. This review will focus on the role of EMT and dysregulated epithelial–mesenchymal crosstalk in progressive lung fibrosis.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 27-33"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000021/pdfft?md5=d7dbdd75f10d4ca33e99d4859869ee0b&pid=1-s2.0-S2772558824000021-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140281509","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":"Impact of corticosteroids on initiation and half-year durability of humoral response in COVID-19 survivors","authors":"Yeming Wang ,&nbsp;Li Guo ,&nbsp;Guohui Fan ,&nbsp;Yang Han ,&nbsp;Qiao Zhang ,&nbsp;Lili Ren ,&nbsp;Hui Zhang ,&nbsp;Geng Wang ,&nbsp;Xueyang Zhang ,&nbsp;Tingxuan Huang ,&nbsp;Weiyang Wang ,&nbsp;Lan Chen ,&nbsp;Lixue Huang ,&nbsp;Xiaoying Gu ,&nbsp;Xinming Wang ,&nbsp;Jingchuan Zhong ,&nbsp;Ying Wang ,&nbsp;Hui Li ,&nbsp;Jiapei Yu ,&nbsp;Zhibo Liu ,&nbsp;Jianwei Wang","doi":"10.1016/j.pccm.2024.02.005","DOIUrl":"10.1016/j.pccm.2024.02.005","url":null,"abstract":"<div><h3>Background</h3><p>The impact of corticosteroids on humoral responses in coronavirus disease 2019 (COVID-19) survivors during the acute phase and subsequent 6-month period remains unknown. This study aimed to determine how the use of corticosteroids influences the initiation and duration of humoral responses in COVID-19 survivors 6 months after infection onset.</p></div><div><h3>Methods</h3><p>We used kinetic antibody data from the lopinavir–ritonavir trial conducted at Jin Yin-Tan Hospital in January 2020, which involved adults hospitalized with severe COVID-19 (LOTUS, ChiCTR2000029308). Antibody samples were collected from 192 patients during hospitalization, and kinetic antibodies were monitored at all available time points after recruitment. Additionally, plasma samples were collected from 101 COVID-19 survivors for comprehensive humoral immune measurement at the half-year follow-up visit. The main focus was comparing the humoral responses between patients treated with systemic corticosteroid therapy and the non-corticosteroid group.</p></div><div><h3>Results</h3><p>From illness onset to day 30, the median antibody titre areas under the receiver operating characteristic curve (AUCs) of nucleoprotein (N), spike protein (S), and receptor-binding domain (RBD) immunoglobulin G (IgG) were significantly lower in the corticosteroids group. The AUCs of N-, S-, and RBD-IgM as well as neutralizing antibodies (NAbs) were numerically lower in the corticosteroids group compared with the non-corticosteroid group. However, peak titres of N, S, RBD-IgM and -IgG and NAbs were not influenced by corticosteroids. During 6-month follow-up, we observed a delayed decline for most binding antibodies, except N-IgM (β −0.05, 95% CI [−0.10, 0.00]) in the corticosteroids group, though not reaching statistical significance. No significant difference was observed for NAbs. However, for the half-year seropositive rate, corticosteroids significantly accelerated the decay of IgA and IgM but made no difference to N-, S-, and RBD-IgG or NAbs. Additionally, corticosteroids group showed a trend towards delayed viral clearance compared with the non-corticosteroid group, but the results were not statistically significant (adjusted hazard ratio 0.71, 95% CI 0.50–1.00; <em>P</em> = 0.0508).</p></div><div><h3>Conclusion</h3><p>Our findings suggested that corticosteroid therapy was associated with impaired initiation of the antibody response but this did not compromise the peak titres of binding and neutralizing antibodies. Throughout the decay phase, from the acute phase to the half-year follow-up visit, short-term and low-dose corticosteroids did not significantly affect humoral responses, except for accelerating the waning of short-lived antibodies.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 48-55"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000069/pdfft?md5=84b16ab6fad66d96065793319e909241&pid=1-s2.0-S2772558824000069-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140279393","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":"Epithelial stem cells and niches in lung alveolar regeneration and diseases","authors":"Jilei Zhang ,&nbsp;Yuru Liu","doi":"10.1016/j.pccm.2023.10.007","DOIUrl":"10.1016/j.pccm.2023.10.007","url":null,"abstract":"<div><p>Alveoli serve as the functional units of the lungs, responsible for the critical task of blood–gas exchange. Comprising type I (AT1) and type II (AT2) cells, the alveolar epithelium is continuously subject to external aggressors like pathogens and airborne particles. As such, preserving lung function requires both the homeostatic renewal and reparative regeneration of this epithelial layer. Dysfunctions in these processes contribute to various lung diseases. Recent research has pinpointed specific cell subgroups that act as potential stem or progenitor cells for the alveolar epithelium during both homeostasis and regeneration. Additionally, endothelial cells, fibroblasts, and immune cells synergistically establish a nurturing microenvironment—or “niche”—that modulates these epithelial stem cells. This review aims to consolidate the latest findings on the identities of these stem cells and the components of their niche, as well as the molecular mechanisms that govern them. Additionally, this article highlights diseases that arise due to perturbations in stem cell–niche interactions. We also discuss recent technical innovations that have catalyzed these discoveries. Specifically, this review underscores the heterogeneity, plasticity, and dynamic regulation of these stem cell–niche systems. It is our aspiration that a deeper understanding of the fundamental cellular and molecular mechanisms underlying alveolar homeostasis and regeneration will open avenues for identifying novel therapeutic targets for conditions such as chronic obstructive pulmonary disease (COPD), fibrosis, coronavirus disease 2019 (COVID-19), and lung cancer.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 17-26"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558823000646/pdfft?md5=7c1408fc878897c86295b2adec9a4359&pid=1-s2.0-S2772558823000646-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139891416","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":"Omics approaches in asthma research: Challenges and opportunities","authors":"Molin Yue ,&nbsp;Shiyue Tao ,&nbsp;Kristina Gaietto ,&nbsp;Wei Chen","doi":"10.1016/j.pccm.2024.02.002","DOIUrl":"10.1016/j.pccm.2024.02.002","url":null,"abstract":"<div><p>Asthma, a chronic respiratory disease with a global prevalence of approximately 300 million individuals, presents a significant societal and economic burden. This multifaceted syndrome exhibits diverse clinical phenotypes and pathogenic endotypes influenced by various factors. The advent of omics technologies has revolutionized asthma research by delving into the molecular foundation of the disease to unravel its underlying mechanisms. Omics technologies are employed to systematically screen for potential biomarkers, encompassing genes, transcripts, methylation sites, proteins, and even the microbiome components. This review provides an insightful overview of omics applications in asthma research, with a special emphasis on genetics, transcriptomics, epigenomics, and the microbiome. We explore the cutting-edge methods, discoveries, challenges, and potential future directions in the realm of asthma omics research. By integrating multi-omics and non-omics data through advanced statistical techniques, we aspire to advance precision medicine in asthma, guiding diagnosis, risk assessment, and personalized treatment strategies for this heterogeneous condition.</p></div>","PeriodicalId":72583,"journal":{"name":"Chinese medical journal pulmonary and critical care medicine","volume":"2 1","pages":"Pages 1-9"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772558824000033/pdfft?md5=15b6c81a2559c1132b1d78b3893d97d1&pid=1-s2.0-S2772558824000033-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140089368","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}