Medicated diet has a long history in China. It is a special dietary form under the guidance of basic theo-ries of traditional Chinese medicine (TCM). This article discussed the characteristics, hot spots and methodological development of current study on medicated diet. It also discussed on current misunderstandings on the study of med-icated diet, such as lack of the guidance of systematic theory, not well-formed system, lack of professional personnel and their limitations, in order to promote the subject development of medicated diet.

Purpose To observe the effects of the intervention or prevention of astragalus polysaccharide(APS)on type 1 diabetes in non-obese diabetic(NOD) mice. Methods the APS group was compared withthe normal solution(NS)group by the incidence of diabetes, the serum C-peptide levels and GAD-Ab levels,the proportion of CD4 or CD8 T subsets in splencytes, pancreatic histopathology and immunocyto-chemistry.Results It shows that the APS group has lower incidence of diabetes, higher serum C-P levels, decreaseddegree of the lymphocytic inflammation of pancreatic islets, stronger proliferation of CD8 T subsets and lowerratio of CD4/CD8 subgroup in splencytes than those of the NS group. Conclusions It proves thepreventive effects of APS on the onset of type 1 diabetes in NOD mice.

Core-shell-type lipid-polymer hybrid nanoparticles (CSLPHNs) are composed by a biodegradable polymeric core coated with single or multiple layers of biomimetic lipids ,which combine the benefits of polymeric nanoparticles and lipo-somes .CSLPHNs have the advantages of small particle size ,high drug loading ,good biocompatibility and controlled release capability .It has wide applications as a novel drug delivery system .This review gives a brief introduction in characteristics , preparation methods and applications of CSLPHNs ,specifically summarizes the developments in the fields of ophthalmic drug delivery ,tumor therapy and medical diagnostic imaging .

Objective: To explore the action mechanism of miR-139-5p inhibiting proliferation and invasion of epithelial ovarian cancer (EOC) cells by targetedly regulatingNotch1.Methods: A total of 24 pairs of EOC tissues and its corresponding para-cancerous tissues from patients, who underwent surgical resection in the DepartmentofGynecology,Nanyang Central Hospital of Henan Province, were collected for this study; in addition, human ovarian cancer cell lines (SKOV3, ES2, HEY-T30) and human ovarian epithelial cell line IOSE80 were also collected. Real-time quantitative PCR (qPCR) was applied to detectmRNAexpressionofmiR-139-5pandNotch1 in EOC tissues and cell lines. The miR-139-5p over-expression vector and recombinant plasmid pLV-Notch1 were transfected into SKOV3 cells. Blank control group (Ctrl group) and negative control group (NC group) were set up. Dual luciferase reporter gene assay was applied to verify the targeting relationship between miR-139-5p and Notch1 3'-UTR. CCK-8, Transwell and Scratch healing experiments were applied to detect cell proliferationinvasionandmigration, respectively. Western blotting was applied to detect expressions of proliferation and migration related proteins in cells. Results: Compared with para-cancerous tissues and IOSE80 cells, the expression of miR-139-5p was significantly decreased in EOC tissues and cell lines, while the expression of Notch1 mRNA was significantly increased (all P<0.01). The results of Dual luciferase reporter showed that Notch1 was the downstream target gene of miR-139-5p. Compared with NC group, cell proliferation, invasion and migration ability, expression levels of Notch1, NICD, Cyclin D1, Cyclin A1, Snail1, β-catenin and N-cadherin were all significantly decreased on 3 d in miR-139-5p mimic group (all P<0.01), while expression of E-cadherin was significantly increased (P<0.01); meanwhile, over-expression of Notch1 could reverse the inhibitory effect of miR-1395p on proliferation, invasion and migration of SKOV3 cells. Conclusion: miR-139-5p can targetedly regulate Notch1 to inhibit proliferation, invasion and migration of EOC cells, which may be related to its down-regulation of NICD, Cyclin D1, Cyclin A1, Snail1, βcatenin and N-cadherin, and up-regulation of E-cadherin.