Objective:This study aimed to evaluate18F-fluorodeoxyglucose positron emission tomography-computed tomography (18F-FDG PET-CT) for diagnosis, targeted biopsy and therapy of relapsing polychondritis (RP).Methods:The literature pertaining to the use of 18F-FDG PET-CT in patients with RP was retrieved from the Cochrane Library, PubMed, EMBASE, CNKI and Wanfang databases until July 2015. Clinical characteristics, auxiliary examination results, chest CT findings, tracheoscopy and biopsy findings, high metabolic activity lesions, maximum standardized uptake values (SUVmax), 18F-FDG PET-CT-guided biopsy site, pathologic results of biopsy samples, and alteration in high 18F-FDG-uptake lesions after treatment were retrospectively analyzed.Results:Eighteen publications with 26 cases were enrolled. The 5 most common symptoms of RP patients diagnosed with 18F-FDG PET-CT were cough, fever, chest tightness, sore throat, and arthralgia. Of the 26 patients, 23 had multiple and symmetric cartilage lesions with high metabo...

Background: D-dimer is a fibrin-degrading substance that is soluble and whose degradation is produced by plasma protein-mediated degradation of cross-linked fibrin. Previous investigations have shown a link between D-dimer and the mortality in lung cancer patients. However, different investigations varied whether D-dimer could predict prognosis in these patients.Methods: A meta-analysis and systematic review of all available cohort studies were performed on the link between circulating D-dimer levels and survival of lung cancer patients. Relevant studies were searched in Embase, Cochrane Library, and PubMed databases. Data from 540 lung cancer patients from the First Hospital of Soochow University and Sichuan Cancer Hospital were used for external validation.Results: We finally obtained 19 eligible cohort studies with pooled HR showing that high D-dimer levels contribute to death in tumor group (HR 1.62, 95% CI: 1.39–1.88, I² = 75.0%). Further stratified analysis showed that higher circulating D-dimer in the advanced lung cancer group was linked to a 1.91-fold risk (HR = 2.91, 95% CI: 2.24–3.78, I² = 6.0%). Incorporation of other variables, including days of follow-up, country, design, public year, population, disease status, and quality score, into the meta-regression model, indicated that disease status was an additional source of heterogeneity (p < 0.001). External validation of 540 patients also showed that high levels of D-dimer showed a higher risk of overall mortality (HR 1.39, 95% CI: 1.13–1.72, p = 0.002) and VTE events (HR 3.98, 95% CI: 1.99–8.70, p = 0.002) in lung cancer patients.Conclusions: High circulating plasma D-dimer levels independently predict long-term prognosis and the risk of venous thromboembolism in lung cancer.

Background: Squamous cell carcinoma of the lung (LUSC) is a severe and highly lethal malignant tumor of the respiratory system, and its molecular mechanisms at the molecular level remain unc\lear.Methods: We acquired RNA-seq data from 8 surgical samples obtained from early-stage LUSC and adjacent non-cancerous tissues from 3 different centers. Utilizing Deseq2, we identified 1088 differentially expressed genes with |LogFC| > 1 and a p-value < 0.05 threshold. Furthermore, through MR analysis of Exposure Data for 26,153 Genes and 63,053 LUSC Patients, incorporating 7,838,805 SNPs as endpoints, we identified 213 genes as potential exposure factors.Results: After intersecting the results, we identified 5 differentially expressed genes, including GYPE, PODXL2, RNF182, SIRPG, and WNT7A. PODXL2 (OR 95% CI, 1.169 (1.040 to 1.313)) was identified as an exposed risk factor, with p-values less than 0.01 under the inverse variance weighted model. GO and KEGG analyses revealed enhanced ubiquitin-protein transferase activity and activation of pathways such as the mTOR signaling pathway and Wnt signaling pathway. Immune infiltration analysis showed downregulation of Plasma cells, T cells regulatory (Tregs), and Dendritic cells activated by the identified gene set, while an enhancement was observed in Macrophages M1. Furthermore, we externally validated the expression levels of these five genes using RNA-seq data from TCGA database and 11 GEO datasets of LUSC, and the results showed SIRPG could induce LUSC.Conclusion: SIRPG emerged as a noteworthy exposure risk factor for LUSC. Immune infiltration analysis highlighted Macrophages M1 and mTOR signaling pathway play an important role in LUSC.

Background: Poor air quality can result in a variety of respiratory disorders. However, the air quality index (AQI) and the level of fine particulate matter (PM2.5) on the progression and prognosis of nonsmall‐cell lung cancer (NSCLC) are unclear.Methods: We launched a cohort study focused on the relationship between air quality and overall survival as well as progression, incorporating data from 590 patients with NSCLC in our medical center between November 1, 2013 and March 1, 2016. Forty‐nine patients from Sichuan Cancer Hospital were used for validation.Results: Cases with poorer AQI 6 months before NSCLC diagnosis were more likely to progress to stage III to IV NSCLC than controls (OR = 2.61, 95% CI 1.35–5.24, p = 0.005). Similarly, if exposed to high levels of PM2.5 during these 6 months, overall survival was poor (HR [95% CI] = 1.53 [1.13, 2.07], p = 0.006). According to multivariate analysis, age, gender, KPS, PM2.5, hyperlipemia, and NSCLC stage were independent risk factors of overall survival. A predictive model developed by these factors above yielded a favorable agreement (C‐index = 0.758) on the calibration curve. External validation was conducted by 46 patients from Sichuan Cancer Hospital displaying an AUC of 0.724 (0.684–0.763).Conclusions: PM2.5 and AQI levels affect disease progression and long‐term survival in NSCLC patients. An overall survival prediction model based on the PM2.5 level can help clinicians predict the risk of death in NSCLC.

Background: Epigenetic regulation significantly affects immune responses in lung adenocarcinoma (LUAD). However, the role of RNA N6‐methyladenosine (m6A) modification, especially in obstructive sleep apnea‐hypopnea syndrome (OSAHS) within LUAD, is not well understood.Methods: This study examined m6A modification patterns in 973 LUAD patients using 23 regulatory genes. Unsupervised clustering categorized patients by m6A profiles, quantified by an m6A score. Associations with clinical outcomes, including survival, immune infiltration, tumor microenvironment, OSAHS incidence, and drug sensitivity, were analyzed.Results: m6A regulator mutations were linked to LUAD, revealing two distinct modification patterns and three gene clusters, all tied to immune phenotypes and clinical outcomes. Higher m6A scores correlated with lower survival, more frequent OSAHS, and increased immune activity. Patients with high m6A scores were more sensitive to PD‐L1/PD‐1 inhibitors and Phenformin, while those with low scores responded better to Cisplatin, Epothilone B, and Talazoparib.Conclusion: Analyses confirmed m6A modification's role in LUAD progression, immune regulation, and outcomes. The m6A score is a valuable prognostic marker associated with survival, OSAHS incidence, and drug sensitivity. These findings highlight m6A's potential as a therapeutic target and biomarker, particularly for LUAD patients with OSAHS.