Objective A comparison of the quality of life and present status of happiness between AIDS patients in Provinces A and B helps to analyze the impact of the prevention and control mechanism on choice of the AIDS patient care mode.Methods The quality of the life questionnaire designed by WHO for AIDS patients and the Subjective Well-being questionnaire from the Memorial University of Newfoundland were called into play to describe the quality of life and present subjective wellbeing of 93 and 57 AIDS patients respectively from Province A and Province B;these patients were interviewed to understand the systematic arrangements of AIDS control in the two provinces and their AIDS patient care models.Results Differences found in the scores of the total quality of life and subjective wellbeing between the two provinces are significant statistically (P＜0.05);differences found in the scores of respective dimensions of quality of life,except for social relations,are significant statistically (P＜0.05).Results of interview found that the prevention and control mechanism of Province A feature a combination of medical administration and disease control departments,management by level of city,county,township and village.The care mode is characteristic of that centering on village doctors.The patient care mechanism in Province B features sectionalized management,and its model is characteristic of that centering on local CDC aided by infectious disease hospitals.Conclusion Establishment of the AIDS prevention and control mechanism should take into account features of local resources,and different regions should provide care models to fit the needs of local AIDS patients.

Triple positive breast cancer overexpress ER (estrogen receptor), PR and HER2 (human epidermal growth factor receptor 2, HER2), accounting for about 50%-60% of the HER2 positive breast cancer patients. Based on the data from clinical trials, the crosstalk between the ER signaling pathway and the HER2 signaling pathway in triple-positive breast cancer may weaken the efficacy of anti-HER2 therapy and endocrine therapy, and this feature has attracted widespread attention. Emerging evidence shows that while blocking HER2 signaling pathway, together with enhancing blocking of ER signaling pathway, such as anti-HER2 dual-targeting + endocrine therapy ± CDK4 / 6 inhibitors, could effectively overcome drug resistance, and improve the efficacy. Predictive biomarkers including Ki67, intrinsic subtypes, and multi-gene assay, which have the potential benefit for personalized treatment.

Objective Non-small cell lung cancer(NSCLC)is the leading cause of cancer-related death worldwide.This stud-y aimed to investigate the effects of the long noncoding RNA(lncRNA)MALAT1 on the proliferation and invasion of NSCLC through the regulation of glutathione peroxidase 3(GPx3)and its mechanism.Methods By analyzing the mRNA expression in-formation,methylation data,and clinical information of NSCLC patients in the TCGA database,the differences in the expression of the key genes MALAT1 and GPx3 and their relationships with patient prognosis were identified.The expression level of GPx3 in lung adenocarcinoma tissue was evaluated via immunohistochemical staining.Moreover,cell culture,real-time quantita-tive PCR,MTT assays for cell proliferation,colony formation,and migration and invasion experiments were used to study the effects of inhibiting the lncRNA MALAT1 on the proliferation and invasion of A549 cells.In addition,Western blotting was used to detect changes in related protein expression.Results In NSCLC tissue,MALAT1 expression was significantly increased and associated with poor prognosis,whereas GPx3 expression was significantly decreased,and patients with low GPx3 expres-sion had significantly lower overall survival rates than those with high GPx3 expression.High levels of MALAT1 methylation are closely associated with the occurrence and development of lung adenocarcinoma.Silencing the lncRNA MALAT1 significant-ly inhibited the proliferation,colony formation ability,migration,and invasion ability of lung cancer cells while promoting the ex-pression of GPx3.Protein level analysis further confirmed that silencing MALAT1 reduced the expression of tumor stem cell markers and inhibited the epithelial-mesenchymal transition(EMT)process.The lncRNA MALAT1 plays a key role in the de-velopment of NSCLC by recruiting LSD2 to regulate GPx3 expression.Conclusion The novel mechanism by which the lncRNA MALAT1 promotes tumor cell proliferation and invasion in NSCLC by regulating GPx3 expression provides new biomarkers for the early diagnosis,treatment,and prognostic assessment of NSCLC,highlighting the relationship between the expression levels and methylation levels of MALAT1 and GPx3 and their relationship with the prognosis of NSCLC patients.