Efficacy of combined surgery and pembrolizumab for the treatment of pulmonary large cell carcinoma: a case report.

Pulmonary large cell carcinoma (LCC) is a rare and aggressive subtype of non-small cell lung cancer (NSCLC) with poor prognosis. Surgical resection remains the cornerstone of treatment for resectable LCC; however, its efficacy is limited in advanced stages, necessitating adjuvant therapies to reduce postoperative recurrence risk. Recent advances in immunotherapy have shown promising survival benefits.

Development of a urine-based metabolomics approach for multi-cancer screening and tumor origin prediction.

Background: Cancer remains a leading cause of mortality worldwide. A non-invasive screening solution was required for early diagnosis of cancer. Multi-cancer early detection (MCED) tests have been considered to address the challenge by simultaneously identifying multiple types of cancer within a single test using minimally invasive blood samples.

DsbA-L activates TGF-β1/SMAD3 signaling and M2 macrophage polarization by stimulating AKT1 and NLRP3 to promote pulmonary fibrosis.

Background: Pulmonary fibrosis (PF) is a progressive and difficult-to-heal lung disease that poses a significant threat to human life and health. This study aimed to investigate the potential pathological mechanisms of PF and to identify new avenues for the treatment of PF.

Methods: Clinical samples were collected to assess the effect of disulfide-bond A oxidoreductase-like protein (DsbA-L) on PF.

Molecular characterization of PANoptosis-related genes associated with immune infiltration and prognosis in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic pulmonary disease with unknown pathogenesis and poor prognosis. PANoptosis, a newly identified form of inflammatory programmed cell death, has been implicated in various inflammatory lung diseases. This study aimed to identify differentially expressed PANoptosis-related genes (PRDEGs) associated with immune infiltration and prognosis in IPF, while also establishing a novel prognostic prediction model.

PTPRZ1 dephosphorylates and stabilizes RNF26 to reduce the efficacy of TKIs and PD-1 blockade in ccRCC.

Clear cell renal cell carcinoma (ccRCC), the most common subtype of renal cell carcinoma, often exhibits resistance to tyrosine kinase inhibitors (TKIs) when used as monotherapy. However, the integration of PD-1 blockade with TKIs has significantly improved patient survival, making it a leading therapeutic strategy for ccRCC. Despite these advancements, the efficacy of this combined therapy remains suboptimal, necessitating a deeper understanding of the underlying regulatory mechanisms.

Meta-analysis of the association between sex hormones and pulmonary fibrosis.

Background: This study aimed to investigate the association between sex hormones and the risk of pulmonary fibrosis by conducting a meta-analysis of previously published studies.

Methods: We executed a comprehensive search of the PubMed, Embase, Cochrane Library, and Web of Science databases to locate pertinent studies published up to April 2024. We included studies that reported the association between sex hormones and the risk of pulmonary fibrosis.

HDAC8 Enhances the Function of HIF-2α by Deacetylating ETS1 to Decrease the Sensitivity of TKIs in ccRCC.

Drug resistance after long-term use of Tyrosine kinase inhibitors (TKIs) has become an obstacle for prolonging the survival time of patients with clear cell renal cell carcinoma (ccRCC). Here, genome-wide CRISPR-based screening to reveal that HDAC8 is involved in decreasing the sensitivity of ccRCC cells to sunitinib is applied. Mechanically, HDAC8 deacetylated ETS1 at the K245 site to promote the interaction between ETS1 and HIF-2α and enhance the transcriptional activity of the ETS1/HIF-2α complex.

Airway epithelial-derived exosomes induce acute asthma exacerbation after respiratory syncytial virus infection.

Acute asthma exacerbation refers to the progressive deterioration of asthma symptoms that is always triggered by virus infection represented by respiratory syncytial virus (RSV). After RSV infection, exaggerated Th2-mediated pulmonary inflammation is the critical pathological response of asthmatic patients with acute exacerbation. Significantly, airway epithelial cells, being the primary targets of RSV infection, play a crucial role in controlling the pulmonary inflammatory response by releasing airway epithelial cell-derived exosomes (AEC-Exos), which potentially influence the development of asthma.

Airway epithelial overexpressed cathepsin K induces airway remodelling through epithelial-mesenchymal trophic unit activation in asthma.

Background And Purpose: Airway epithelial cells (AECs) regulate the activation of epithelial-mesenchymal trophic units (EMTUs) during airway remodelling through secretion of signalling mediators. However, the major trigger and the intrinsic pathogenesis of airway remodelling is still obscure.

Experimental Approach: The differing expressed genes in airway epithelia related to airway remodelling were screened and verified by RNA-sequencing and signalling pathway analysis.

Analysis of necroptosis-related prognostic genes and immune infiltration in idiopathic pulmonary fibrosis.

Background: IPF is an undetermined, progressive lung disease. Necroptosis is a type of programmed apoptosis, which involved in the pathogenesis of lung diseases like COPD and ARDS. However, necroptosis in IPF have not been adequately studied.

A Comprehensive Mass Spectrometry-Based Workflow for Clinical Metabolomics Cohort Studies.

As a comprehensive analysis of all metabolites in a biological system, metabolomics is being widely applied in various clinical/health areas for disease prediction, diagnosis, and prognosis. However, challenges remain in dealing with the metabolomic complexity, massive data, metabolite identification, intra- and inter-individual variation, and reproducibility, which largely limit its widespread implementation. This study provided a comprehensive workflow for clinical metabolomics, including sample collection and preparation, mass spectrometry (MS) data acquisition, and data processing and analysis.

Airway epithelial ITGB4 deficiency induces airway remodeling in a mouse model.

Background: Airway epithelial cells (AECs) with impaired barrier function contribute to airway remodeling through the activation of epithelial-mesenchymal trophic units (EMTUs). Although the decreased expression of ITGB4 in AECs is implicated in the pathogenesis of asthma, how ITGB4 deficiency impacts airway remodeling remains obscure.

Objective: This study aims to determine the effect of epithelial ITGB4 deficiency on the barrier function of AECs, asthma susceptibility, airway remodeling, and EMTU activation.

Maintains Cancer Stemness and Promotes Erlotinib Resistance in Lung Adenocarcinoma.

Erlotinib is a highly specific and reversible epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), but resistance inevitably develops as the disease progresses. Erlotinib resistance and cancer stem cells (CSCs) are poor factors hindering the prognosis of patients with lung adenocarcinoma (LUAD). Although studies have shown that erlotinib resistance and CSCs can jointly promote cancer development, the mechanism is currently unclear.

MiR-223-3p-loaded exosomes from bronchoalveolar lavage fluid promote alveolar macrophage autophagy and reduce acute lung injury by inhibiting the expression of STK39.

This study investigated the molecular mechanism by which bronchoalveolar lavage fluid exosomes (BALF-exo) alleviated acute lung injury (ALI). BALF-exo was isolated from mice. LPS was used to induce inflammation in rat alveolar macrophages (NR8383).

DNA Damage Response Gene-Based Subtypes Associated With Clinical Outcomes in Early-Stage Lung Adenocarcinoma.

DNA damage response (DDR) pathways play a crucial role in lung cancer. In this retrospective analysis, we aimed to develop a prognostic model and molecular subtype based on the expression profiles of DDR-related genes in early-stage lung adenocarcinoma (LUAD). A total of 1,785 lung adenocarcinoma samples from one RNA-seq dataset of The Cancer Genome Atlas (TCGA) and six microarray datasets of Gene Expression Omnibus (GEO) were included in the analysis.

The Core Role of Neutrophil-Lymphocyte Ratio to Predict All-Cause and Cardiovascular Mortality: A Research of the 2005-2014 National Health and Nutrition Examination Survey.

Objective: To further supplement the previous research on the relationship between neutrophil-lymphocyte ratio (NLR) and all-cause and cardiovascular mortality, and construct clinical models to predict mortality.

Methods: A total number of 2,827 observers were included from the National Health and Nutrition Examination Survey (NHANES) database in our research. NLR was calculated from complete blood count.

Early stage of antibody-mediated rejection after lung transplantation： A case report and literature review.

Antibody-mediated rejection (AMR) is a rare and serious complication after lung transplantation, with no characteristic of pathological manifestation, no systematic standard treatment, and the poor efficacy and prognosis. We reported a case of early AMR after lung transplantation and the relevant literature has been reviewed. A male patient presented with symptoms of cold 99 days after transplantation and resolved after symptomatic treatment.

A localization-independent approach for invisible and impalpable ground-glass opacity nodules detection in an lung specimen: two case reports.

A growing number of ground-glass opacity (GGO) nodules are screened out in lungs. Small GGOs are frequently neither visible nor palpable, thus undetectable during operation. Various nodule localization techniques have been developed to facilitate the intraoperative detection of GGO nodules; however, general localization techniques are infeasible or inappropriate in some cases.

Formation, contents, functions of exosomes and their potential in lung cancer diagnostics and therapeutics.

Lung cancer is the leading cause of cancer-related death worldwide due to diagnosis in the advanced stage and drug resistance in the subsequent treatments. Development of novel diagnostic and therapeutic methods is urged to improve the disease outcome. Exosomes are nano-sized vehicles which transport different types of biomolecules intercellularly, including DNA, RNA and proteins, and are implicated in cross-talk between cells and their surrounding microenvironment.

Downregulation of miR-223 promotes HMGB2 expression and induces oxidative stress to activate JNK and promote autophagy in an in vitro model of acute lung injury.

Background: Excessive autophagic activity in alveolar epithelial cells is one of the main causes of acute lung injury (ALI), but the underlying molecular mechanism has not been fully elucidated. Previous studies have shown that microRNAs (miRs) are involved in regulating autophagy in several diseases. This study aimed to determine the role of miR-223 in excessive autophagic activity in alveolar epithelial cells and the underlying mechanism to identify a novel therapeutic targets for the development of new drugs to treat acute respiratory distress syndrome (ARDS).

[Tumor infiltrating T lymphocyte components in malignant pleural effusion of lung adenocarcinoma and their killing activities to autologous tumor cells].

To analyze the components of tumor infiltrating T lymphocyte (TIL) cells in malignant pleural effusion of lung adenocarcinoma, and evaluate their killing activities to autologous tumor cells. 
 Methods: Malignant pleural effusions were collected from 17 patients with lung adenocarcinoma. Mononuclear cells were isolated by Ficoll density gradient centrifugation and flow cytometer was used to analyze TIL cell components.