Relationship Between Physical Activity and Adult Asthma Control Using NHANES 2011-2020 Data.

BACKGROUND The purpose of this study was to determine whether PA is associated with asthma control using data from the National Health and Nutrition Examination Survey (NHANES) for 2011-2020. We did not find a relationship between physical activity (PA) and asthma control. MATERIAL AND METHODS In this study, we measured asthma control by counting asthma attacks and emergency room visits for asthma in the past year. Physical activity was divided into recreational physical activity and work physical activity. A total of 3158 patients (≥20 years old) were included in the study, of which 2375 were in the asthma attack group and 2844 were in the emergency care group, with indicators of asthma control and physical activity as dichotomous variables. Multiple sets of covariates were selected, such as age, gender, and race. Multiple logistic regression analysis and subgroup analysis were used to analyze the data. RESULTS Active workload was significantly correlated with acute asthma attacks, but the relationship with emergency care was not statistically significant. We found that the relationship between physical activity and emergency care was influenced by race, education, and economic level. CONCLUSIONS The amount of work activity was correlated with acute asthma attacks, and the relationship between physical activity and emergency case was influenced by race, education, and economic level.

CircRNA circHIPK3 serves as a prognostic marker to promote glioma progression by regulating miR-654/IGF2BP3 signaling.

Emerging evidences show RNA back-splicing produces a new type of noncoding RNA, namely circular RNA (circRNA). Many reports demonstrate that circRNA circHIPK3 exerts oncogenic or anti-tumor roles in different cancers, such as ovarian cancer, bladder cancer, osteosarcoma, colorectal cancer and liver cancer. However, no study about circHIPK3 function in glioma exists until today. In this study, we showed that circHIPK3 was upregulated in glioma tissues. Elevated level of circHIPK3 was linked to poor prognosis. Functional investigation indicated that circHIPK3 promotes glioma cell proliferation and invasion, and tumor propagation in vivo. Furthermore, miR-654 was identified as a target of circHIPK3 while IGF2BP3 was targeted by miR-654. CircHIPK3 could promote IGF2BP3 expression via interacting with miR-654 in glioma cells. Finally, CCK8 and transwell assays illustrated that IGF2BP3 overexpression could reverse the effects of IGF2BP3 depletion. Altogether, our findings demonstrated that circHIPK3 contributes to glioma progression through targeting miR-654 from IGF2BP3 and implies circHIPK3 might be a potential target for glioma therapy.

Application of mendelian randomization to study the causal relationship between smoking and the risk of chronic obstructive pulmonary disease.

BACKGROUND: Smoking is a risk factor for chronic obstructive pulmonary disease (COPD). Few studies have assessed the causal relationship between smoking and COPD using Mendelian randomization. METHODS: Exposure and outcome datasets were obtained from the IEU Open GWAS project (https://gwas.mrcieu.ac.uk/). The exposure data set includes smoking (ever smoke, smoking/smokers in household, exposure to tobacco smoke at home). The outcome data set includes COPD susceptibility and acute COPD admissions. The main methods of Mendelian randomization analysis are weighted median method and MR-Egger method. Heterogeneity and polymorphism analyses were performed to ensure the accuracy of the results. RESLUTS: ever smoke increased the risk of COPD prevalence, and ever smoke and smoking/smokers in household increased the risk of acute COPD admission. Conclusion Therefore, we should enhance the management of nonpharmacological prescription of COPD to reduce the individual incidence.

Cuproptosis-related gene signatures for predicting prognosis of lung adenocarcinoma.

Lung cancer (LC) is a common malignancy with high mortality rate, and lung adenocarcinoma (LUAD) is one of the common pathological types. Cuproptosis is a recently discovered new type of cell death dependent on mitochondria. However, the role of cuproptosis in LUAD is unknown. We obtained LUAD transcriptome data from the Cancer Genome Atlas (TCGA). Long-stranded non-coding RNA (LncRNAs) based on cuproptosis prognosis associated with LUAD were constructed for prognostic multi-LncRNA characterization. We divided TCGA-LUAD into training set and validation set to prove feasibility, and all samples were divided into high-risk group or low risk group. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to evaluate potential biological functions and explore the relationship between risk models and immunity. We identified 3 differentially expressed LncRNAs associated with LUAD prognosis and constructed prognostic model. Kaplan-Meier (K-M) analysis revealed prognostic model and LUAD prognosis. Our risk assessment model has a good reliability in predicting the prognosis of LUAD and was able to improve predictive ability of tumor mutational burdern. Single sample gene enrichment analysis (ssGSEA) revealed risk subgroups were associated with immune-related functions. The prognostic model based on cuproptosis lncRNA has important value in predicting the survival of LUAD patients.

Protective role of JNK inhibitor SP600125 in sepsis-induced acute lung injury.

BACKGROUND: Whether the c-Jun N-terminal kinase (JNK) pathway mediates apoptosis in sepsis-induced acute lung injury is not known. Here we investigated the effect of JNK inhibition in a rat model of sepsis-induced lung injury, and assessed expression of JNK and endoplasmic reticulum stress-related proteins. METHODS: Sepsis was established by cecal ligation and puncture (CLP) in 48 male Sprague-Dawley rats. 32 additional rats underwent sham surgery. 24 CLP rats and 24 sham rats received tail vein injection of 30 mg/kg SP600125. The rest received saline injection. At 6, 12 and 24 h after surgery, blood, bronchoalveolar lavage fluid (BALF) and lung tissue were collected. p-JNK, XBP-1, ATF-4 and CHOP levels of the lung tissue were measured by western blot; and the JNK mRNA levels were measured by qPCR. RESULTS: The W/D ratios of lungs in the CLP group were significantly higher than those in the sham group, but lower those in the CLP+JNK inhibitor group (P<0.05). TUNEL staining revealed significantly more apoptotic cells in the lungs of the CLP group than the sham group, and in the CLP+JNK inhibitor group the apoptotic index was significantly reduced (P<0.05). XBP-1, ATF-4, CHOP and p-JNK protein levels and JNK mRNA levels were significantly elevated in the CLP group (P<0.05), but significantly ameliorated in the CLP+JNK inhibitor group (P<0.05). CONCLUSIONS: Inhibition of the JNK signaling pathway mitigates sepsis-induced lung injury. Our results suggest that JNK signaling promotes endoplasmic reticulum stress and thus apoptosis in sepsis-induced lung injury.

LncRNA LOC728196/miR-513c axis facilitates glioma carcinogenesis by targeting TCF7.

Numerous long noncoding RNAs (lncRNAs) are reported to be dysregulated in glioma. However, how lncRNA participates in the process of glioma development and progression still remains elusive. Here, we identified a novel lncRNA LOC728196 highly expressed in glioma tissues. LOC728196 high expression predicts low survival rate in patients. Our data proved that LOC728196 knockdown repressed cellular growth, migration and invasion in vitro. Silencing LOC728196 led to impaired growth of glioma in vivo. Mechanistic studies further demonstrated that LOC728196 acts as the sponge for miR-513c to upregulate TCF7 expression. We observed a reciprocal inhibition between LOC728196 and miR-513c. Rescue assay showed that either inhibition of miR-513c or TCF7 overexpression restored the abilities of proliferation, migration and invasion in LOC728196-silenced glioma cells. Taken together, our study provides a comprehensive investigation on the role of LOC728196 in glioma progression and contributes to understanding the vital role of competing endogenous RNA (ceRNA).