Objective Regenerating genes express mainly in gastrointestinal tissues and the injured regenerating pancreatic tissues,which can promote the regeneration of pancreatic β cells and other tissue cells.In recent years,researches on Reg family mainly involved the gene structure of various subtypes of Reg,and its role in diabetes,gastrointestinal cancer,inflammation,anti-microbial and the related mechanisms.Among the various subtypes of Reg,regenerating geneⅢ(Reg3) plays a particularly crucial role in these diseases.Therefore,Reg3 is a promising target for the treatment of these diseases.Based on the relationships of Reg3 with a variety of diseases,our group devote to the role of Reg3 [human REG3A,and mouse Reg3γ(Reg3g)] in type 1 diabetes,inflammation-linked pancreatic carcinogenesis,and the immunological changes participated in these processes.Hence,this review will summarize serial studies on Reg3 and the feasibility of it as drug targets.

Objective To construct luciferase reporter plasmid containing synthetic CArG elements and to investigate their radiation-inducible property in tumor cells. Methods Insert chimeric regulation elements consisting of nine tandem-repeat copies of CArG sequence (CCATATAAGG) and CMV IE basal gene promoters into pGL3-Basic vectors to construct luciferase reporter plasmids. Tumor cells(HeLa, A549 and HepG2) were transiently transfected by reporter plasmids using lipofectamine, and transfected cells were irradiated by ?-ray with different doses. After 36 h, we assayed the level of reporter gene expression. Results The CArG elements could successfully induce the expression of a downstream reporter gene following irradiation, with maximal expression seen after 3 Gy irradiation. Conclusion The synthetic CArG elements are responsive to low dose of radiation and are able to enhance down-stream gene expression. It is expected to be the essential potential for future application of radiogenetic cancer therapy.

· AlM:To investigate the effect of compound anisodine on fundus blood circulation after vitrectomy with face-down position.
· METHODS: Sixty patients ( 60 eyes ) with rhegmatogenous retinal detachment received vitrectomy with silicone oil tamponade operation, who were randomized divided into treatment group ( 30 eyes ) and control group ( 30 eyes ) .The patients in the treatment group received the subcutaneously injection of compound anisodine hydrobromide by the superficial temporal artery once daily for 14d since postoperative first day.Retinal microcirculation blood flow parameters were recorded with Heidelberg retinal flowmeter postoperative 1d, 1 and 2wk, and were compared between two groups.
·RESULTS: The blood flow parameters ( Vol, Flw, Vel) of control group postoperative 1 and 2wk were significantly less than those postoperative 1d.Otherwise the parameters of treatment postoperative 1 and 2wk were significantly more than those postoperative 1d. The parameters between two groups were significant different ( P<0.01) .
· CONCLUSlON: Facing down after vitrectomy with
silicone oil tamponade may reduce retinal blood supply, consequently lead to retinal ischemia; compound anisodine can effectively improve the retinal and choroidal microcirculation after vitrectomy with face-down posture, reduce retinal ischemia, and enhance the visual function.

Objective:To observe the the effects of sustained-release coatings of HU-308 on the biological characteristics of rat oste-oblasts(ROBs)on Ti surface.Methods:The heparin/chitosan sustained release coatings containing HU-308 at different concentra-tions were prepared by layer-by-layer assembly technology on the alkali-and heat-treated Ti surface.The alkali-and heat-treated Ti samples were randomly divided into six groups,the samples in C group were used as control,in P group were treated by heparin/chi-tosan coatings and in T1,T2,T3 and T4 groups were treated by heparin/chitosan sustained-release coating containing HU-308 at dif-ferent concentrations.The adhesion,proliferation and ALP activity of ROBs cultured on the coatings were assessed at different times. Results:The adhesion,proliferation and ALP activity of ROBs of T4 group (the impregnating concentration of HU-308 was 0.025 mg/L)were the highest.Conclusion:The sustained-release coating with low concentration of HU-308 may improve the adhesion , proliferation and ALP activity of ROBs.

Objective:To observe the clinical efficacy and safety of Bianyan oral liquids in the treatment of acute pharyngitis. Methods:The clinical data of 200 patients with acute pharyngitis in the outpatient department of traditional Chinese medicine in our hospital from September 2010 to June 2012 were analyzed. They were divided into the control group with 100 cases and the observation group with another 100 cases. The control group was given Jinlianhua granules, while the observation group was received Bianyan oral liquids. After 5 days, the symptom score, effective rate, changes in accompanied symptoms and safety index were observed and com-pared. Results:The symptom score and effective rate of the observation group were better than those of the control group (P<0. 05), and the improvement in defecation was better than that of the control group (P<0. 05) as well. There were two cases in the observation group suffered nausea and stomachache, and one case in the control group suffered diarrhea while no untoward effect emerged. Conclu-sion:Bianyan oral liquids with the effects of heat-clearing and detoxicating, nourishing yin and fluid and treatment both manifestation and root cause show significant effect in the treatment of acute pharyngitis.

Objective To study the activity of the survivin gene promoter in several tumor cell lines and evaluate the possible application of this promoter in tumor gene therapy. Methods ①The expressions of survivin gene in A549,MDA-MB231 and HepG2 cell lines were detected by RT-PCR and Western blotting.②Tumor cells(A549,MDA-MB231,HepG2) were transiently transfected by reporter plasmids containing different length of survivin promoter using lipofectamine.And 48 h later,the level of reporter gene expression was analyzed.Results There were different levels of survivin expression in A549,MDA-MB231 and HepG2 cell lines.Transient transfection assay approved that pLuc-surP-987,pLuc-surP-596,pLuc-surP-269 and pLuc-surP-158 showed high activity and 269 bp survivin promoter demonstrated the highest activity. Conclusion In transcriptional level,survivin promoter can activate the reporter gene in several tumor cell lines.It is a potential candidate promoter in tumor gene therapy.

Objective To observe the influences of stemona alkaloids on esterase isozymes activities and glycogen content of Oncomelania hupensis in order to explore the molluscicidal mechanism of stemona alkaloids.Methods O.hupensis snails were immersed in the liquid of stemona alkaloids at the concentration of 6.5 mg/L(72 h LC50),the surviving ones were picked out and sampled after being immersed for 12,24,48,72,96 h,then PAGE and anthrone colorimetry methods were used to observe the changes of liver esterase isozymes activities and tissue glycogen content of O.hupensis during the immersion period.A group of snails immersed in de-chlorinous water served as control.Results Esterase isozymes activities firstly increased,and then decreased until almost lost completely during the 96 h immersion period.Meanwhile,glycogen content gradually decreased as the immersion time extended.After being immersed for 96 h,glycogen content decreased by 72.00% compared with the control group.Conclusion Stemona alkaloids could inhibit the viability of O.hupensis by causing decrease of esterase isozymes activities and glycogen content.

OBJECTIVE To investigate enhanced immune function of methionine encephalin (MENK) and its anti-tumor mechanism in CT26 colon cancer mouse model. METHODS 3×106 CT26 cells were implanted subcutaneously in BALB/c mice. Four days after, MENK was peritoneally administrated at the concentration of 20 mg·kg-1 for 14 d. The percentage of MDSCs in bone marrow, spleen, blood, tumor and liver were detected by flow cytometry. Non- esterified fatty acid (NEFA), triglycerides (TG) and total cholesterol (T-CHO) in liver homogenate were tested by a NEFA test kit, a TG test kit and a T- CHO test kit respectively. qRT- PCR and Western blot were used to measure mRNA and protein levels of inflammation-, glycometabolsim- and lipometabolsim-associated indexes in liver. RESULTS MENK decreased percentages of MDSCs in bone marrow, spleen, blood and tumor in colon cancer mice. MENK-treated mice displayed elevated ratio of CD4+T and CD8+T cells in spleen as well as increased T and B lymphocytes proliferation. Meanwhile, MENK also ameliorated liver damage reflected by lower levels of GPT and GOT in serum and reduced risks of cancer- associated index including inflammation, high lipid and high glucose. Furthermore, MENK lowered down the levels of NEFA, TG and T- CHO in liver homogenate. MENK treatment decreased expression of p- STAT3, increased expression of p-AKT, IRS1 and Glut4 at protein level as well as reduced lipogenesis-associated genes and elevated glycolysis-associated genes in liver of tumor bearing mice. Also, abated expression of genes associated with MDSCs generation (M-CSF, GM-CSF, IL-6, IL-1β) and migration (S100A9, KC) was observed within shrunken subcutaneous tumor by MENK intervention. CONCLUSION MENK has the ability to strength immune function against colon cancer by reducing MDSCs and improving liver metabolism.

OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) onpromotion of IR and HCC, and explore its underlying mechanisms. METHODS Lentivirus were used to mediate the knockdown of PID1 in HFD induced IR mouse model as well as ob/ob mice. Intraperitoneal glucose and insulin tolerance were performed 4 weeks after lentivirus injection. Hydrodynamics-based transfection was applied to induce the liver specific overexpression of PID1. Flow cytometry was exerted to detect the proportion and function of immune cells.qRT-PCR and Western blot were used to detect the expression of downstream pathways of PID1. Liquid chromatography-mass spectrometry (LC-MS) and co-immunoprecipitation (Co-IP) were conducted to identify proteins interacting with PID1.Chromatin immunoprecipitation(ChIP)was operated to measure the modification of H3K4me3 of PID1 promoter.RESULTS PID1 restriction improved insulin resistance,hyperglycemia and fatty liver. Conversely, hepatic knockdown of PID1 attenuated liver xenografted tumor growth. Moreover,PID1 liver-specific protooncogenes via hydrodynamics-based transfection established a primary hepatocellular carcinoma mouse model,induced an immunosuppressive environment,with the reduction of CD3+,CD4+,CD8+T cells,retarded maturation of dendritic cells(DCs),pronounced differentiation of regulatory T cells(Tregs),and recruitment of MDSC.In addition,PID1 overexpression activated prolifer-ation related genes, promoted anti-inflammatory genes, suppressed pro-inflammatory genes, induced glycolysis and lipid metabolism genes to facilitate tumorigenesis in liver. Importantly, PID1 exerted its tumor-promoting function through binding to epidermal growth factor receptor(EGFR)and activation of downstream KRAS/ERK pathway.As such,PID1 exist trimethylation of histone H3 at lysine 4(H3K4me3) modification and IR up-regulated the expression of PID1 by activation the H3K4me3 modification. CONCLUSION PID1 is a new gene that exerts both liver cancer-promoting and insulin resistance inducing function.IR accelerates liver cancer development and progression partially dependent on the activation of PID1.

OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) on promotion of IR and HCC, and explore its underlying mechanisms. METHODS Lentivirus were used to mediate the knockdown of PID1 in HFD induced IR mouse model as well as ob/ob mice. Intraperitoneal glucose and insulin tolerance were performed 4 weeks after lentivirus injection. Hydrodynamics-based transfection was applied to inducethe liver specific overexpression of PID1. Flow cytometry was exerted to detect the proportion and function of immune cells. qRT-PCR and Western blot were used to detect the expression of downstream pathways of PID1.Immunoprecipitation was used to determine the receptor of PID1. Chromatin immunoprecipitation (ChIP) was operated to measure the modification of H3K4me3 of PID1 promoter. RESULTS PID1 restriction improved insulin resistance, hyperglycemia and fatty liver. Conversely, hepatic knockdown of PID1 attenuated liver xenografted tumor growth. Moreover, PID1 liver- specific protooncogenes via hydrodynamics- based transfection established a primary hepatocellular carcinoma mouse model, induced an immunosuppressive environment, with the reduction of CD3 +, CD4 +, CD8 +T cells, retarded maturation of dendritic cells (DCs), pronounced differentiation of regulatory T cells (Tregs), and recruitment of MDSC. In addition, PID1 overexpression activated proliferation related genes, promoted anti- inflammatory genes, suppressed pro-inflammatory genes, induced glycolysis and lipid metabolism genes to facilitate tumorigenesis in liver. Importantly, PID1 exerted its tumor-promoting function through binding to epidermal growth factor receptor (EGFR) and activation of downstream MAPK pathway. As such, PID1 exist trimethylation of histone H3 at lysine 4 (H3K4me3) modification and IR up-regulated the expression of PID1 by activation the H3K4me3 modification. CONCLUSION PID1 is a new gene that exerts both liver cancer-promoting and insulin resistance inducing function. IR accelerates liver cancer development and progression partially dependent on the activation of PID1.