Objective To explore the current status and influencing factors of returning to work among breast cancer patients by Meta-analysis.Methods Literatures studies on the current status and influencing factors of returning to work among breast cancer patients were systematically searched in databases.The literature was sorted,screened and evaluated,and a total of 15 articles were included,involving 3975 breast cancer patients after surgery.Results After Meta-analysis,the return-to-work rate among breast cancer patients was 48.49％.Age,treatment method,social support,surgical method,and self-efficacy were influencing factors.Conclusion Clinically,early evaluation and intervention should be carried out for patients with relevant factors to improve the quality of life after breast cancer surgery and improve the level of patients' readiness to return to work.

Objective To explore the current status and influencing factors of returning to work among breast cancer patients by Meta-analysis.Methods Literatures studies on the current status and influencing factors of returning to work among breast cancer patients were systematically searched in databases.The literature was sorted,screened and evaluated,and a total of 15 articles were included,involving 3975 breast cancer patients after surgery.Results After Meta-analysis,the return-to-work rate among breast cancer patients was 48.49％.Age,treatment method,social support,surgical method,and self-efficacy were influencing factors.Conclusion Clinically,early evaluation and intervention should be carried out for patients with relevant factors to improve the quality of life after breast cancer surgery and improve the level of patients' readiness to return to work.

Objective:To identify species type and analyze the homology of Brucella in a family cluster infection. Methods:Two patients with brucellosis from the same family who were treated at the First People's Hospital of Lianyungang City, Jiangsu Province in May 2022 were selected as the research subjects. Brucella strains (H4LYG01 and H2LYG02) were isolated through blood culture. The isolated strains were identified for species type and homology analysis using a fully automated microbial mass spectrometry detection system. Molecular typing of the isolated strains was performed using multiple locus variable-number tandem-repeat analysis (MLVA) and multilocus sequence typing (MLST). Results:H4LYG01 and H2LYG02 were both Brucella Maltese, and the credibility scores were 9.745 and 9.627, respectively, and the homology was 100%. The MLVA results showed that the gene loci of H4LYG01 and H2LYG02 were completely identical, with the same genotype. The MLST results showed that the sequence type (ST) of H4LYG01 and H2LYG02 were both ST8 types. Conclusion:The two isolated strains of Brucella from a family with clustered infections are both Brucella Maltese and from the same source.

Objective : To construct a knockdown recombinant adeno⁃associated virus (AAV⁃shCTSK) targeting the mouse Cathepsin K(CTSK) gene and assess the knockdown efficiency of AAV⁃shCTSK in mice , and to investigate its impact on lipid storage within adipose tissue. Methods : ShRNA primers specific to both the negative control (NC) and CTSK were designed , annealed , and integrated into the backbone vector. Following clone selection and sequencing for validation , recombinant plasmids were purified. Adeno⁃associated viral vectors , along with packaging and helper plasmids , were co⁃transfected into 293T cells using the transfection reagent PEI for adeno⁃associat⁃ed viral packaging and amplification. The resultant AAV⁃shNC and AAV⁃shCTSK were injected into the epididymal adipose tissue of mice via in situ injection. Two weeks post⁃injection , the expression of CTSK protein was evaluated through immunoblotting assay and the size of intracellular lipid droplets in mouse adipose tissue was detected by HE staining. Results : Successful acquisition of AAV⁃shNC and AAV⁃shCTSK adeno⁃associated viruses was achieved. In mice subjected to in situ injection of AAV⁃shCTSK , effective knockdown of CTSK in adipose tissue was confirmed , accompanied by a significant reduction in the size of white adipocytes. Conclusion A knockdown adeno-associated virus targeting CTSK in mice is successfully constructed , and CTSK knockdown in adipose tissue leads to a notable decrease in lipid content.