Development and validation of machine learning models for diagnosis and prognosis of lung adenocarcinoma, and immune infiltration analysis.

The aim of our study was to develop robust diagnostic and prognostic models for lung adenocarcinoma (LUAD) using machine learning (ML) techniques, focusing on early immune infiltration. Feature selection was performed on The Cancer Genome Atlas (TCGA) data using least absolute shrinkage and selection Operator (LASSO), random forest (RF), and support vector machine (SVM) algorithms. Six ML algorithms were employed to construct the diagnostic models, which were evaluated through receiver operating characteristic (ROC) curves, precision-recall curves (PRC), and classification error (CE), and validated on the GSE7670 dataset.

Identifying crucial lncRNAs and mRNAs in hypoxia-induced A549 lung cancer cells and investigating their underlying mechanisms via high-throughput sequencing.

Background: Rapid proliferation and outgrowth of tumor cells frequently result in localized hypoxia, which has been implicated in the progression of lung cancer. The present study aimed to identify key long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) involved in hypoxia-induced A549 lung cancer cells, and to investigate their potential underlying mechanisms of action.

Methods: High-throughput sequencing was utilized to obtain the expression profiles of lncRNA and mRNA in both hypoxia-induced and normoxia A549 lung cancer cells.

LncRNA RP11-58O9.2 predicts poor prognosis and promotes progression of non-small cell lung cancer.

Objective: Long non-coding RNAs (lncRNAs) play a crucial role in non-small cell lung cancer (NSCLC). This study aimed to investigate the novel biomarker, lncRNA RP11-58O9.2, in patients with NSCLC.

Analysis of Risk Factors for Thromboembolic Events in 88 Patients with COVID-19 Pneumonia in Wuhan, China: A Retrospective Descriptive Report.

BACKGROUND Since the outbreak of COVID-19 in December 2019, there have been 96 623 laboratory-confirmed cases and 4784 deaths by December 29 in China. We aimed to analyze the risk factors and the incidence of thrombosis from patients with confirmed COVID-19 pneumonia. MATERIAL AND METHODS Eighty-eight inpatients with confirmed COVID-19 pneumonia were reported (31 critical cases, 33 severe cases, and 24 common cases).

Circular RNA hsa_circ_0014130 Inhibits Apoptosis in Non-Small Cell Lung Cancer by Sponging miR-136-5p and Upregulating BCL2.

Previous studies indicated that circular RNAs (circRNA) played vital roles in the development of non-small cell lung cancer (NSCLC). Although hsa_circ_0014130 might be a potential NSCLC biomarker, its function in NSCLC remains unknown. Thus, this study aimed to investigate the role of hsa_circ_0014130 in the progression of NSCLC.

Identification of crucial microRNAs and genes in hypoxia-induced human lung adenocarcinoma cells.

Background: Variations of microRNA (miRNA) expression profile in hypoxic lung cancer cells have not been studied so far. Therefore, using miRNA microarray technology, this study aimed to study the miRNA expression profile and investigate the potential crucial miRNAs and their target genes in hypoxia-induced human lung adenocarcinoma cells.

Materials And Methods: Based on miRNA microarray, miRNA expression profiling of hypoxia-induced lung adenocarcinoma A549 cells was obtained.

Schedule-dependent cytotoxicity of sunitinib and TRAIL in human non-small cell lung cancer cells with or without EGFR and KRAS mutations.

Background: Non-small cell lung cancer (NSCLC) patients who do initially respond to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) may eventually develop resistance, which may at least partly be due to the acquisition of a secondary EGFR mutation (T790M). Additionally, it has been found that KRAS mutations may serve as poor prognostic biomarkers. Here, we aimed at establishing a suitable treatment regimen for the multi-target TKI sunitinib and the tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in NSCLC-derived cells with or without EGFR and KRAS mutations.

Effect of hirudin on the levels of acute lung injury rat tumor necrosis factor-α and matrix metalloproteinase-12.

The aim of this study was to observe the effect of hirudin on the expression of lung tissue protease activated receptor-1 (PAR-1) and the correlation between inflammation factors and the expression of PAR-1 after hirudin pre-treatment and to provide the theoretical basis for the treatment of lung injury by hirudin. Wistar rats of the model group were intraperitoneally administered endotoxin by injection (LPS 10 mg/kg) to copy acute lung injury (ALI) animal models, while the rats of the control group were injected with an equal amount of physiological saline. The rats of the hirudin groups were injected with hirudin and endotoxin intraperitoneally at the same time.

Association of ADAM33 gene with susceptibility to COPD in Tibetan population of China.

Chronic obstructive pulmonary disease (COPD) is a common, complex disorder associated with substantial morbidity and mortality, influenced by both environmental factor and genetic factor. ADAM33 gene was found to be associated with asthma, declined lung function and COPD. The purpose of the study was to test whether SNPs in ADAM33 were associated with COPD in Tibetan population of China.

[Effect of dexamethasone on expression of hypoxia inducible factor-1α and vascular endothelial growth factor in hypoxic mice].

Background: It has been proved that hypoxia is closely related to oncogenesis and development of tumor. The aim of this study is to observe the effect of dexamethasone on expression of hypoxia inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF) in lung tissues of hypoxic mice, and to investigate the relationship between hypoxia and angiogenesis and mechanism of dexamethasone.

Methods: The Kunming mice were randomly divided into control group and three experimental groups (3-day hypoxia group, 6-day hypoxia group, and hypoxia+dexamethasone group).

[Inhibitory effect of emodin on proliferation of human lung adenocarcinoma cells in vitro].

Objective: To investigate the anti-tumor mechanisms of emodin on human lung adenocarcinoma cell line Anip973 (LACC).

Methods: The influence of emodin of different concentration at different time on LACC proliferation were determined and compared using MTT colorimeric assay and cell growth curve assay. And the cell apoptotic rate was determined by flow cytometry and analyzed with electronic microscope.