Objective To investigate the clinical significance of H2A histone family member(H2AX)gene in human lung adenocarcinoma,and to explore its biological role in lung adenocarcinoma.Methods The tran-scriptome data of lung adenocarcinoma were downloaded from the Cancer Genome Atlas and Gene Expression database.The expression of H2AX mRNA in lung adenocarcinoma tissues and adjacent normal lung tissues was extracted by R 4.3.1 software,and the relationship between the expression of H2AX and the clinicopath-ological parameters of the patients was analyzed.Kaplan-Meier and Cox regression analysis were used to ana-lyze the prognostic value of H2AX gene expression.The expression of H2AX gene in lung adenocarcinoma cell lines and normal bronchial epithelial cells was verified by quantitative real-time PCR(qPCR).Gene set enrich-ment analysis,gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were used to explore the biological role of H2AX gene.Results The expression of H2AX mRNA in lung adenocarcinoma tissues was significantly higher than that in adjacent normal tissues(P<0.001).qPCR results showed that compared with normal bronchial epithelial cells,the expression levels of H2AX mRNA in lung adenocarcinoma cell lines A549 and SPC-A1 were significantly increased(P<0.05).H2AX expression was associated with tumor stage(P=0.029)and N stage(P=0.016).Kaplan-Meier curve analysis showed that high expression of H2AX was associated with a lower overall survival rate of patients(P<0.001).Cox regression analysis showed that H2AX was an independent prognostic factor for lung adenocarcinoma patients(HR=1.011,95%CI 1.003-1.020,P=0.006).The results of functional enrichment analysis showed that H2AX gene was involved in molecular functions such as cell cycle,DNA replication,mismatch repair,and P53 signaling pathway.Conclusion H2AX gene is highly expressed in human lung adenocarcinoma,which is relat-ed to the malignant progression of tumor patients.H2AX gene can affect the progression of lung adenocarcino-ma through a variety of pathways,and may be used as a molecular marker for lung adenocarcinoma patients.

Under the new situation of rapid development of medical science and technology, how to effectively cultivate medical students’ humanistic spirit and comprehensively improve medical quality is an important responsibility of medical college teachers. Blend-learning can guide students to immersive learning in multiple dimensions and forms. Obstetrics and Gynecology is one of the main compulsory courses for clinical medical students, which is faced more sensitive and vulnerable female patients, and required higher humanistic quality training for medical students. Through the construction of the blend-learning platform, medical humanities can be better integrated into the content and teaching design of medical education, and students can be more appropriately imperceptibly trained in medical humanities in obstetrics and gynecology teaching, so as to enhance medical students’ medical humanities quality in the process of obstetrics and gynecology diagnosis and treatment, and improve doctor-patient relationship.

Colorectal cancer (CRC) and hepatocellular carcinoma (HCC) are the second and third most common causes of death by cancer, respectively. The etiologies of the two cancers are either infectious insult or due to chronic use of alcohol, smoking, diet, obesity and diabetes. Pathological changes in the composition of the gut microbiota that lead to intestinal inflammation are a common factor for both HCC and CRC. However, the gut microbiota of the cancer patient evolves with disease pathogenesis in unique ways that are affected by etiologies and environmental factors. In this review, we examine the changes that occur in the composition of the gut microbiota across the stages of the HCC and CRC. Based on the idea that the gut microbiota are an additional "lifeline" and contribute to the tumor microenvironment, we can observe from previously published literature how the microbiota can cause a shift in the balance from normal → inflammation → diminished inflammation from early to later disease stages. This pattern leads to the hypothesis that tumor survival depends on a less pro-inflammatory tumor microenvironment. The differences observed in the gut microbiota composition between different disease etiologies as well as between HCC and CRC suggest that the tumor microenvironment is unique for each case.