Background: Few studies have explored the association between circadian syndrome (CircS) and lung health.
Objective: To access the relationship between CircS and lung health.
Methods: This prospective cohort study enrolled 6,252 adults. Multivariable logistic and linear regression models were employed to examine the association between CircS and the prevalence of chronic lung disease, respiratory symptoms, and lung function, as appropriate. Receiver operating characteristic curve analysis was used to compare the predictive power of the number of metabolic syndrome (MetS) and CircS components for lung health. Kaplan-Meier survival and multiple Cox regression analyses were used to assess the relationship between CircS and all-cause mortality. The effects of CircS on health-related quality of life (HQL) and health care use were also evaluated.
Results: Participants with CircS were significantly associated with a higher prevalence of asthma, chronic bronchitis, cough, wheeze, phlegm production, and exertional dyspnea. The number of CircS components demonstrated better predictive power for the prevalence of asthma, chronic bronchitis, emphysema, cough, wheeze, phlegm production, and exertional dyspnea than the number of MetS components. Higher numbers of CircS components were significantly associated with decreased forced expiratory volume in the first second (FEV) and forced vital capacity (FVC), worse HQL, and increased health care use. Longitudinally, participants with CircS exhibited a higher risk of all-cause mortality than those without CircS.
Conclusions: Our results support the claim of that CircS is a better predictor of lung health than the Mets in adults in the United States. Elevated CircS levels are associated with poorer lung function, increased health care use, worse HQL, and a higher risk of mortality.
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http://dx.doi.org/10.1016/j.rmed.2025.108031 | DOI Listing |
Eur J Cardiothorac Surg
March 2025
Division of Thoracic Surgery, Department of Surgery, Taipei Veterans General Hospital, ; Taipei City, Taiwan.
Objectives: To assess the prognostic impact of adequate lymphadenectomy and determine the optimal nodal assessment for different clinical stages of lung cancer.
Methods: We retrospectively reviewed 1214 patients with clinical stage I-III non-small cell lung cancer who had preoperative PET/CT and curative surgery (2006-2017). Patients were categorized based on whether they had adequate [R0] or inadequate lymphadenectomy [R(un)].
Sci Adv
March 2025
Department of Radiation Oncology, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Lung cancer exhibits altered metabolism, influencing its response to radiation. To investigate the metabolic regulation of radiation response, we conducted a comprehensive, metabolic-wide CRISPR-Cas9 loss-of-function screen using radiation as selection pressure in human non-small cell lung cancer. Lipoylation emerged as a key metabolic target for radiosensitization, with lipoyltransferase 1 (LIPT1) identified as a top hit.
View Article and Find Full Text PDFJ Immunol
March 2025
Department of Environmental Health, Boston University School of Public Health, Boston, MA, United States.
While immunotherapy has shown some efficacy in lung adenocarcinoma (LUAD) patients, many respond only partially or not at all. One limitation in improving outcomes is the lack of a complete understanding of immune checkpoint regulation. Here, we investigated a possible link between an environmental chemical receptor implicated in lung cancer and immune regulation, the AhR, a known but counterintuitive mediator of immunosuppression (interferon (IFN)-γ), and regulation of two immune checkpoints (PD-L1 and IDO).
View Article and Find Full Text PDFProc Natl Acad Sci U S A
March 2025
Laboratorio 1. Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas-Universidad de Salamanca and Centro de Investigación Biomédica en Red Cáncer (CIBERONC), Salamanca 37007, Spain.
We evaluated the in vivo therapeutic efficacy and tolerability of BI-3406-mediated pharmacological inhibition of SOS1 in comparison to genetic ablation of this universal Ras-GEF in various KRAS-dependent experimental tumor settings. Contrary to the rapid lethality caused by SOS1 genetic ablation in SOS2 mice, SOS1 pharmacological inhibition by its specific inhibitor BI-3406 did not significantly affect animal weight/viability nor cause noteworthy systemic toxicity. Allograft assays using different KRAS cell lines showed that treatment with BI-3406 impaired RAS activation and RAS downstream signaling and decreased tumor burden and disease progression as a result of both tumor-intrinsic and -extrinsic therapeutic effects of the drug.
View Article and Find Full Text PDFUnited European Gastroenterol J
March 2025
University Hospital RWTH Aachen, Aachen, Germany.
Background And Aims: The severe alpha-1 antitrypsin deficiency (AATD) genotype Pi*ZZ increases the risk of liver disease (AATD-LD) and lung disease. While non-invasive tests (NITs) are widely used for fibrosis stage and monitoring of all liver diseases, the consensus for use in AATD-LD is limited. A Delphi panel study was conducted to address this need.
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