Canadian respiratory journal最新文献

Introduction: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrotic lung disease with a poor prognosis and no effective pharmacological treatments. Cytokines are a class of small-molecule proteins with diverse biological activities. Many cytokines-most notably transforming growth factor β-have been demonstrated to play an important role in IPF. However, a few studies have systematically described the relationship between cytokines and IPF.

Methods: Lung tissues from controls and patients with IPF were collected during lung transplantation. The expression profiles of 440 cytokines in lung tissues were obtained using protein microarrays. Proteomic analysis was performed, and differentially expressed proteins (DEPs) were identified. Furthermore, an integrative bioinformatics analysis was performed and included functional enrichment analysis, protein-protein interaction (PPI) network construction, hub protein determination, immune cell infiltration analysis, potential drug prediction, and single-cell analysis. The hub protein expression was validated through Gene Expression Omnibus (GEO) database evaluation and immunochemical analysis.

Results: 32 DEPs were identified from the two groups. They were mainly enriched in cell chemotaxis, basal part of cell, and growth factor binding and were involved in PI3K-Akt signaling. The PPI network was constructed for the DEPs, and five hub proteins (FGF2, HGF, HBEGF, ERBB3, and ANGPT2) were identified. The immune infiltration analysis demonstrated a significantly higher percentage of resting NK cells in IPF lung tissue. The drug prediction analyses identified 13 potential candidates targeting the five hub proteins. The single-cell analysis predicted the cellular localization of each key cytokine.

Conclusions: Using protein microarrays, we obtained comprehensive cytokine expression profiles in control and IPF lung tissues and conducted an integrated bioinformatics analysis of the proteomic data. Our findings may improve the comprehension of the role of cytokines in IPF and the underlying mechanisms. Moreover, they provide novel targets for developing safe and efficacious drugs for treating IPF.

Objective: This study aims to investigate the relationship between the difference in hematocrit and albumin (HCT-ALB) and ventilator-associated pneumonia (VAP) among patients undergoing continuous mechanical ventilation.

Methods: This research utilized the data from the Medical Information Mart for Intensive Care IV database. The primary outcome was VAP occurred. HCT-ALB levels were divided into three groups according to the quantile: < -1.10; -1.10-5.30; ≥ 5.30. All patients with continuous mechanical ventilation were categorized into two groups: those who developed VAP and those who did not. Univariate and multivariate logistic regression analyses were used to assess the relationship between HCT-ALB and VAP risk. Receiver operating characteristic (ROC) curves were used to evaluate the predictive ability. To further assess the robustness of the findings, subgroup analyses were performed.

Results: In our study, a total of 3021 patients were enrolled, and among them, 361 patients experienced VAP. Multivariate logistic regression showed that taking HCT-ALB < -1.10 as reference, HCT-ALB ≥ 5.30 was linked to an increased risk of VAP in patients undergoing continuous mechanical ventilation (odds ratio = 1.36, 95% confidence interval: 1.02-1.81). The ROC curve demonstrated approximately moderate predictive ability. This association remained robust in subgroups of male, quick Sepsis-Related Organ Failure Assessment score ≤ 2, not using antibiotics, having oral care, and no history of trauma injury, chronic obstructive pulmonary disease, or respiratory failure.

Conclusion: HCT-ALB, as an easily measurable indicator, was associated with the risk of VAP in patients with continuous mechanical ventilation.

Objective: This study aimed to explore the potential of LINC01214 in providing prognostic and therapeutic insights, thereby offering valuable references for the research of non-small cell lung cancer (NSCLC).

Methods: 122 NSCLC subjects were recruited. The molecular level was quantified by qPCR and WB. Kaplan-Meier estimated the prognostic effects and Cox regression analyses the hazard ratio. The cell activities including proliferation, apoptosis, and migration/invasion were evaluated by CCK-8, flow cytometry, and Transwell. The regulatory axis of LINC01214/miR-497-3p/HSP90AB1 was verified by the dual luciferase reporter assay and rescue experiments.

Results: LINC01214 increased both in the malignant tissues and cell lines of NSCLC. Mortality was increased in NSCLC patients with high LINC01214 levels. LINC01214 was an independent risk predictor of prognosis in NSCLC. Silencing of LINC01214 inhibited the NSCLC cell proliferation, migration, and invasion and promoted apoptosis. The abundance of miR-497-3p showed an opposite trend to LINC01214. LINC01214 could target miR-497-3p and negatively correlate with miR-497-3p. The inhibitory effect of LINC01214 on cell activity was reversed by miR-497-3p. HSP90AB1 was predicted and further confirmed as the target of miR-497-3p. The LINC01214/miR-497-3p/HSP90AB1 axis regulated NSCLC cell proliferation, migration, and invasion.

Conclusion: LINC01214, a potential biomarker, contributed to the progression of NSCLC through the miR-497-3p/HSP90AB1 axis by promoting cell proliferation and motility.

Background: Lung cancer is the predominant cause of cancer-related mortality globally. Computed tomography (CT) scanning is employed to enhance the early diagnosis of lung cancer by screening for risk factors. This study aimed to examine the impact of CT scanning on the incidence of lung cancer detection in a group with unidentified risk factors for the disease.

Methods: Data from two patient cohorts were analyzed: the "study group," comprising individuals with a CT-detected pulmonary nodule of ≥ 8 mm and unknown lung cancer risk factors, and the "control group," consisting of individuals with a pulmonary nodule of ≥ 8 mm identified by CT scan due to known lung cancer risk factors.

Results: No significant difference was seen between the groups regarding malignancy frequency (p=0.155) and early-stage occurrence (p=0.842).

Conclusions: The incidence of lung cancer in pulmonary nodules measuring ≥ 8 mm is not influenced by the presence of lung cancer risk factors.

Background: In 2022, new guidelines for the diagnosis and treatment of pulmonary hypertension (PH) revised the hemodynamic definition, reducing the mean pulmonary artery pressure threshold from ≥ 25 to > 20 mmHg. The optimal threshold of transthoracic echocardiography (TTE) parameters and the predictive capability require further validation. This study aims to investigate the diagnostic value of TTE parameters under the new hemodynamic criteria.

Methods: Retrospective analysis of PH patients who underwent right heart catheterization and TTE examination between 2017 and 2022 in a single center. Logistic regression was employed to ascertain the predictive capacity of parameters across various conditions. Receiver operating characteristic curves were used to determine the optimal cutoff values based on the new criteria.

Results: In a cohort of 213 patients, the optimal cutoff values identified were a tricuspid annular plane systolic excursion (TAPSE) to systolic pulmonary arterial pressure (sPAP) ratio of < 0.50 mm/mmHg, a right ventricular outflow tract acceleration time (RVOT-AT) of < 93 ms, and a right atrial area (RAA) > of 14.5 cm². Regardless of the inclusion of tricuspid regurgitation velocity (TRV) and related parameters, RVOT-AT < 93 ms manifested as an effective predictive parameter. A combination of RVOT-AT < 93 ms, main pulmonary artery diameter > 25 mm and RAA > 14.5 cm² exhibited better specificity.

Conclusion: The threshold values for TAPSE/sPAP, RVOT-AT, and RAA should be adjusted to improve the predictive capacity of PH based on revised criteria in this single-center dataset. RVOT-AT was a promising indirect parameter, and the utilization of combined indirect indicators may enhance diagnostic accuracy, particularly in instances where satisfactory TRV measurements are unavailable.

Hypoxic pulmonary hypertension (HPH) lacks effective treatments. The research is designed to examine the effectiveness of Notoginsenoside R1 (NGR1) in addressing HPH and to explore its molecular mechanisms. Under hypoxic conditions, we created a rat model of HPH and treated the animals with NGR1. We assessed the therapeutic effects of NGR1 on HPH through hemodynamic measurements and pulmonary artery vascular remodeling. We employed transcriptomic analysis to evaluate gene expression changes in HPH rats. We conducted untargeted metabolomics to examine how NGR1 influences the metabolic profile of HPH rats. NGR1 treatment significantly improved hemodynamic parameters and ameliorated pulmonary artery vascular remodeling in HPH rats. Transcriptomic analysis identified Pck1 as the most significantly altered gene. NGR1 intervention significantly improved the expression of vascular remodeling-related proteins. NGR1 reversed the expression of glycolysis-related genes. NGR1 reduced the levels of glycolysis-related metabolites. Further analysis revealed that NGR1 treatment decreased PFKL, HK2, and LDHA protein expression and lowered lactate levels in lung tissue. Our findings demonstrate that NGR1 effectively alleviates the pathological features of HPH in rats. NGR1 inhibits hypoxia-induced glycolysis-mediated pulmonary artery remodeling, mitigates vascular endothelial damage, and suppresses the abnormal proliferation of smooth muscle cells and fibroblasts.

Background and Objective: Given the involvement of neuropeptides in the pathophysiology of obstructive sleep apnea syndrome (OSAS), this study investigated the associations between plasma levels of β-endorphin (β-EP) and neuropeptide Y (NPY) and OSAS severity and evaluated their potential as predictive biomarkers. Methods: A total of 48 snoring patients undergoing polysomnography (PSG) were categorized into non-OSAS, mild, moderate, and severe OSAS groups (n = 12 per group) based on the apnea-hypopnea index (AHI). Plasma levels of β-EP and NPY were measured using ELISA. Statistical analyses included one-way ANOVA, Spearman's correlation, and receiver operating characteristic (ROC) curve analysis to assess predictive performance. Results: Plasma β-EP levels exhibited significant elevation in moderate (p=0.003) and severe OSAS groups (p=0.032) compared to the non-OSAS group. Notably, NPY levels demonstrated marked differences across all OSAS severity groups (p < 0.01), with significantly higher concentrations observed in mild, moderate, and severe OSAS patients versus non-OSAS controls (p < 0.01). A progressive increase in NPY levels was observed with advancing OSAS severity, accompanied by statistically significant intergroup differences (p < 0.01). Correlation analyses revealed strong positive associations between NPY levels and both BMI (p < 0.0001) and AHI (p < 0.0001). In contrast, β-EP correlated positively with AHI (p < 0.0001) but not with BMI (p=0.0931). ROC curve analysis identified β-EP (cutoff: 9.405 ng/L) as a moderate predictor of OSAS (AUC = 0.7986, p < 0.01; sensitivity: 72.22%, specificity: 83.33%). Strikingly, NPY (cutoff: 19.29 ng/L) exhibited perfect discriminative capacity (AUC = 1, p < 0.0001; sensitivity: 97.22%, specificity: 100%). Conclusions: Plasma β-EP and NPY levels are associated with OSAS severity and may serve as potential biomarkers. However, further validation in larger cohorts is needed to confirm their clinical utility.

Pulmonary embolism (PE) at high altitude (HA) is a potentially life-threatening but underrecognized condition. Unlike low-altitude PE, high-altitude pulmonary embolism (HA-PE) may result from unique hypoxia-driven mechanisms, including hemoconcentration, endothelial dysfunction, and a hypercoagulable state. In this narrative review, we summarize current evidence on the epidemiology, pathophysiology, diagnosis, management, and prognosis of HA-PE, based on the literature published between 2010 and 2025 retrieved from PubMed and CNKI. This review summarizes the epidemiological profile, clinical features, altitude-related diagnostic challenges, limitations of current therapeutic strategies, and the prognosis of HA-PE. A more comprehensive understanding of HA-PE is crucial for enhancing early detection and developing altitude-adapted management approaches.

Background: Polysomnography (PSG) is the traditional technique for diagnosing obstructive sleep apnea (OSA) with some limitations. Ultra-wideband radar (UWB) is a new method for diagnosing OSA that combines multiple techniques including radar technology, artificial intelligence (AI), and big data algorithms. The accuracy of UWB in OSA diagnosis needs further scientific verification, especially in southern China. Methods: Fifty patients from southern China wore UWB with oximetry and PSG simultaneously overnight. UWB generated automated reports; PSG was manually interpreted. Lowest oxygen saturation (LSpO2) and apnea-hypopnea index (AHI) from both methods were compared. Results: High correlation was found between UWB and PSG for AHI (r = 0.925, p < 0.001) and LSpO2 (r = 0.990, p < 0.001). The average bias of AHI (-3.09, p=0.98, 95% CI -15.48 - 9.31) and LSpO2 (-0.34, p > 0.99, 95% CI -3.68 - 3.04) between the two methods was small. ROC analysis showed good diagnostic performance of UWB versus PSG (AUC = 0.979, p < 0.001), with 95.8% sensitivity and 100% specificity. Conclusion: The study demonstrated UWB combined with oximetry could be a reliable alternative to PSG for diagnosing OSA in the south of China.