A Mendelian randomization study revealed a causal link between napping and deep vein thrombosis (DVT).

BACKGROUND: Numerous individuals opt for napping to achieve adequate rest, and several studies have linked napping to various health conditions. Consequently, we aimed to investigate the potential effect of napping on the development of deep vein thrombosis (DVT). METHODS: We used the publicly available summary statistics data sets of genome-wide association studies (GWAS) meta-analyses for napping in individuals included in the UK Biobank as the exposure and a GWAS for DVT from the individuals included in the FinnGen Biobank as the outcome. The two-sample MR research approach was utilized to explore the causative link between napping and DVT. Single nucleotide polymorphisms (SNPs) data strongly related to napping were found and used as instrumental factors. Inverse variance weighting (IVW), weighted median and MR-Egger regression, and weighted mode approaches were four statistical techniques. RESULTS: There were 86 SNPs in all that were discovered to be strongly related to napping (P < 5 × 10-8, linkage disequilibrium r2 < 0.1). Consistent association between napping and DVT (IVW: odds ratio (OR) 0.508, 95% confidence interval (CI) 0.280-0.921; MR-Egger regression: OR 0.988, 95% CI 0.118-8.303; weighted median estimates: OR 0.419, 95% CI 0.181-0.974; weighted mode: OR 0.442, 95% CI 0.080-2.427) suggested that napping correlated with decreased risk of DVT. There was no evidence that genetic pleiotropy affected the link between napping and DVT (MR-Egger intercept - 6.7 × 10-3; P = 0.525). CONCLUSION: The results of the Mendelian randomization study suggested a potential causal relationship between napping and a reduced incidence of DVT.

Causal relationships between gut microbiota and lymphoma: a bidirectional Mendelian randomization study.

Background: Multiple studies have suggested a possible connection between the gut microbiota and the development of lymphoma, though the exact nature of this relationship remains unclear. This study aimed to explore whether a causal association exists between gut microbiota and lymphoma. Methods: A bidirectional two-sample Mendelian randomization (MR) approach was conducted to investigate potential causal effects between gut microbiota and various lymphoma subtypes. The primary method employed for MR analysis was inverse variance weighted (IVW), supplemented by additional methods including MR-Egger, weighted median, and weighted mode approaches. The Cochrane Q test, MR-PRESSO global test and MR-Egger intercept test were performed to assess pleiotropy and heterogeneity. Furthermore, a reverse MR analysis was performed to explore potential reverse causal effect. Results: The primary MR analysis identified 36 causal relationships between genetic liabilities in gut microbiota and different lymphoma subtypes. Neither the MR-PRESSO test nor the MR-Egger regression detected any pleiotropy, and Cochran's Q test indicated no significant heterogeneity. Conclusions: Our MR analysis revealed substantial causal associations between gut microbiota and lymphoma, offering new insights into lymphoma prevention and management microbiota.

Comprehensive analysis of single-cell RNA and bulk RNA sequencing based on M2 tumor-associated macrophage and angiogenesis-related genes to assess prognosis and therapeutic response in lung adenocarcinoma.

M2 tumor-associated macrophage (M2 TAM), a crucial component of the tumor microenvironment, has a significant impact on tumor invasion and metastasis in the form of angiogenesis for lung adenocarcinoma (LUAD). In this study, both single-cell RNA and bulk RNA sequencing data were analyzed to identify 12 M2 TAM and angiogenesis-related genes (OLR1, CTSL, HLA-DPB1, NUPR1, ALOX5, DOCK4, CSF2RB, PTPN6, TNFSF12, HNRNPA2B1, NCL, and BIRC2). These genes were used to construct a prognostic signature, which was subsequently validated using an external cohort. Moreover, the immune profile analysis indicated that the low-risk group exhibited a distinct immune cell infiltration and relatively active status. Importantly, the prognostic signature was closely associated with PD-1, CTLA4, tumor mutation burden, and anti-cancer drug sensitivity. In summary, this study proposes a new prognostic signature for patients with LUAD based on M2 TAM and angiogenesis-related genes. The signature forecasts the prognosis of LUAD by an independent manner, reveals the potential molecular mechanisms involved in tumor immune-related functions, and offers appropriate clinical strategies for the treatment of patients with LUAD.

Novel insights into causal associations of body mass index or height with pneumothorax: a two-sample Mendelian randomization study.

Background: Observational studies have reported an association between body mass index (BMI) as well as height and the risk of pneumothorax. However, it has long been unclear whether BMI or height are causally associated with pneumothorax. Methods: Genetic summary data for BMI, height and pneumothorax were retrieved from multiple independent large genome-wide association studies (GWAS). A series of quality control steps were conducted to select instruments. Four independent two-sample Mendelian randomization (MR) analyzes were performed to adequately assess the causal relationship between BMI or height on pneumothorax, and the robustness of the results was assessed by a series of sensitivity analyzes. Results: Height increased the risk of pneumothorax with an OR of 1.5181 (95%CI 1.3092-1.7604; p = 3.28e-08); there was no evidence of a causal effect of BMI on the risk of pneumothorax with an OR of 0.8979 (95%CI 0.7417-1.0869; p = 0.269). Height increased the risk of spontaneous pneumothorax with an OR of 1.0010 (95%CI 1.0002-1.0018; p = 0.012); the results showed no significant causal relationship between BMI and spontaneous pneumothorax either with an OR of 0.9992 (95%CI 0.9983-1.0002; p = 0.112). Conclusion: Our results supported a genetic association between height and pneumothorax. We found that height increased the risk of pneumothorax. However, no evidence was found to suggest a causal relationship between BMI and pneumothorax risk. The relationship between BMI and pneumothorax requires further in-depth analysis.

A predictive molecular signature consisting of lncRNAs associated with cellular senescence for the prognosis of lung adenocarcinoma.

The role of long noncoding RNAs (lncRNAs) has been verified by more and more researches in recent years. However, there are few reports on cellular senescence-associated lncRNAs in lung adenocarcinoma (LUAD). Therefore, to explore the prognostic effect of lncRNAs in LUAD, 279 cellular senescence-related genes, survival information and clinicopathologic parameters were derived from the CellAge database and The Cancer Genome Atlas (TCGA) database. Then, we constructed a novel cellular senescence-associated lncRNAs predictive signature (CS-ALPS) consisting of 6 lncRNAS (AC026355.1, AL365181.2, AF131215.5, C20orf197, GAS6-AS1, GSEC). According to the median of the risk score, 480 samples were divided into high-risk and low-risk groups. Furthermore, the clinicopathological and biological functions, immune characteristics and common drug sensitivity were analyzed between two risk groups. In conclusion, the CS-ALPS can independently forecast the prognosis of LUAD, which reveals the potential molecular mechanism of cellular senescence-associated lncRNAs, and provides appropriate strategies for the clinical treatment of patients with LUAD.