Food Sanitation Law which was issued for many years has no longer been congruent with the current development of socio-economy. Under this situation,Food Safety Law came into being. Although the promulgation of the law is important,the task of carrying out the law is more difficult. On the basis of concluding the problems in carrying out the food sanitation law and the analysis of its causes,it is significant to discuss the Food Safety Law from the viewpoint of Food Sanitation Law enforcement.

Objective:To study the changes of NKG2C/NKG2A expressed on T cells in HIV chronically infected individuals and HAART-treatment AIDS patients and the relationship with disease progression of HIV. Methods: We collected peripheral blood from HIV chronically infected individuals,HAART-treatment AIDS patients and healthy human and used the flow cytometry by staining fluorescent antibody to detect the NKG2C/NKG2A receptors expressed on T cells. Results:NKG2C+,NKG2A+ and NKG2C+NKG2A-expressed on T cells in HIV chronically infected individuals were significantly higher than the healthy control group ( P=0. 025,P=0. 032,P=0. 029),while in HAART-treatment AIDS patients were significantly lower than that in HIV chronically infected individuals (P=0. 033,P=0. 037,P=0. 018),returned to the normal levels with no significant difference compared with the healthy control group. The absolute number of peripheral blood CD4+ T lymphocytes in HIV chronically infected individuals was negative correlation with T cells which expressing NKG2A+,NKG2C+NKG2A+ and NKG2C-NKG2A+( r=-0. 697,P<0. 000 1;r=-0. 463,P=0. 015;r=-0. 693,P<0. 000 1). What was more,the absolute number of peripheral blood CD4+ T lymphocytes had positive correlation with the ratio of NKG2C and NKG2A expressed on T cells receptor in HIV chronically infected individuals(r=0. 476,P=0. 012). Conclusion:Studying the expression of NKG2C and NKG2A receptors on T cell has great significance in HIV infected individuals, which may provide a scientific basis for clinical prognosis of HIV infection.

[Abstract] Objective: To investigate the expression level of lncRNA (long non-coding RNA) SNHG1 in endometrial cancer tissues, and to analyze its mechanism of action as well as its clinical significance. Methods: NCBI-GEO and TCGA database were used to analyze the expression level of SNHG1 in endometrial cancer. A total of 53 cases of endometrial cancer tissue samples and 41 cases of normal endometrial tissue samples were collected from January 2016 to March 2019 at Zhongxin Ecocity Hospital of Tianjin Medical University; in addition, endometrial cancer cell lines Ishikawa and HEC-1A as well as normal endometrial ESC cells were also collected for this study. qPCR was used to detect the expression level of SNHG1 in tissues and cells, and its correlation with the clinical characteristics of patients were statistically analyzed. The effect of SNHG1 on cell proliferation and apoptosis of HEC-1A cells was measured by MTT assay and Annexin V/PI double staining Flow cytometry, respectively. The migration and invasion of HEC-1A cells were measured by Transwell assay. StarBase was used to predict the regulatory relationship between SNHG1 and RELA, which was then verified by qPCR and Western blotting. Dual fluorescent reporter gene system and qPCR were adopted to identify the influence of SNHG1 on NF-κB pathway. Results: The expression of SNHG1 was significantly up-regulated in endometrial cancer tissues compared with normal endometrial tissues (P<0.01), and its expression was related to tumor size, TNM staging, histological grade and lymph node metastasis (all P<0.05). The expression level of SNHG1 in Ishikawa and HEC-1A cells was significantly higher than that in ESC cells (all P<0.01). Overexpression of SNHG1 notably promoted the proliferation, migration and invasion and inhibited cell apoptosis of HEC-1A cells. By promoting the expression of RELA, SNHG1 activated the NF-κB pathway and promoted the expressions of downstream gene IL-6 and CCL19 (all P<0.01). Conclusion: Up-regulated SNHG1 in endometrial cancer functions as an oncogene by activating the NF-κB pathway through promoting the RELA expression.