Objective:To compare the compressive strength of porcelain crown with Co-Cr,CAD/CAMpure titanium and CAD/CAM zirconia respectively.Methods:Metal models of simulating crown core of the ideal premolar were manufactured,digital data of the met-al model were obtained by CAD/CAMsystem,the basement crowns of Co-Cr,CAD/CAMpure titanium and CAD/CAMzirconia were respectively made(n =5),size of each crown was kept the same and the spcimens were set as group A,B and C respectively.Then masking porcelain and body porcelain were fired on basement crowns according to the instructions.The thickness of the porcelain was kept the same.All of the porcelain crowns were located on the Instron testing machine,the compression strength force values were measured.Data were statistically analysed by SPSS 1 3.0 software.The bonding surface of basement material and porcelain was observed by SEMafter compressive failure.Results:The compressive strength(N)of group A,B and C was 2 990 ±1 88,2 305 ±1 57,2 1 50 ± 1 31 ,A vs B or C,P <0.05,B vs C,P >0.05.Conclusion:All the 3 base materials with porcelain crown satisfy the clinical require-ments.The compressive strength of Co-Cr porcelain crown is stronger than that of CAD/CAMpure titanium porcelain crown and CAD/CAMzirconia porcelain crown.

Objective To study the feasibility of TNF-α promoting migration of rat mesenchymal stem cells (MSCs) to local damaged tissues. Methods The MSCs was exposed to TNF-α at different concentrations and the expression rate of surface adheslon molecules and specific markers as well as their adhesion to endothelial cells were detected.Based on the above steps,the MSCs stimulated with the optimal concentration of TNF-α were obtained and were injected intravenously to the rats whose hindlimbs experienced ischemia damage.The rats were executed for achieving the muscle samples in the ischemic area,which were made into frozen section to count the number of MSCs. Results ( 1 ) Twenty-four hours after the TNF-o stimulation,the expression of adhesion molecule (VCAM-1) of MSCs increased in a concentration-dependent manner,while the expression of adhesion molecules (ICAM-1,L-Selectin and VLA4) of MSCs showed no significant changes.Besides,the expression rate of specific markers of MSCs was also obscure.(2) Exposed to 10 ng/ml TNF-o,MSCs presented an obviously increased ability in adhesion to the endothelial cells.(3) MSCs stimulated with 10 ng/ml TNF-α showed a larger number in the ischemia-damaged tissue of rat hindlimbs than that in the control group. Conclusion TNF-α at concentration of 10 ng/ml is effective within a short term in increasing VCAM-1 expression in rat MSCs and promoting the adhesion of MSCs to endothelial cells without affecting their character.

The aim of this study is to establish a simple and stable model like poloxamer 407 (P-407)-induced dyslipidemia of golden hamster model, and investigate the mechanism of lipid metabolism disturbance in this model. PPARalpha agonist and HMG-CoA reductase inhibitor were administrated to validate the efficacy on regulating lipid metabolism in the dyslipidemia golden hamster model. Six weeks male golden hamsters were chosen to inject P-407 intraperitoneally at a bolus dose of 300 mg x kg(-1), an intermittent injection at a dose of 200 mg x kg(-1) every 72 hours after the bolus. The results showed that P-407-induced golden hamster model characterized as increased serum triglyceride (TG), total cholesterol (TC), free cholesterol (free-CHO), cholesteryl ester (CE), free fatty acids (FFA) and apoB levels, and the hyperlipidemia state maintained at a stable level persistently. Meanwhile, augmented malondialdehyde (MDA) and nitric oxide (NO) level was observed. LCAT and SR-B I mRNA levels in liver of model group were down-regulated (expression ratio is 0.426; 0.783), while HMG-CoA reductase mRNA level was up-regulated (expression ratio is 1.493) compared with those of the normal group. The serum cholesterol and triglyceride levels were significantly lower in P-407-induced dyslipidemia hamster model after treated with atorvastatin (Ato) at a dose of 50 mg x kg(1) or fenofibrate (Fen) at 100 mg x kg(-1) for two weeks. These findings suggest that serum lipid distribution in dyslipidemia golden hamster is similar to that of human, and which may be relevant to the disturbance of the enzymes expression involved in lipid metabolism in liver. Results obtained from this study support the concept that dyslipidemia golden hamster may be an adequate animal model to evaluate the efficacy of lipid-lowering agents.

AIM: To study the effects of cholecystokinin octapeptide (CCK-8) on T-lymphocyte subsets in keyhole limpet haemocyanin (KLH)-immunized mice.METHODS: Female BALB/c mice were immunized with KLH and injected with different dosages of CCK-8 or saline simultaneously. Positive CD4+and CD8+ T cells in peripheral blood or splenocytes were measured by flow cytometry. The production and mRNA level of Th1 cytokine, IFN-? and Th2 cytokine, IL-4 in the splenocytes were evaluated by ELISA and RT-PCR, respectively. In addition, lung tissue sections were made with HE staining.RESULTS: CCK-8 downregulated the positive CD4+and CD8+ T lymphocytes both in peripheral blood and in splenocytes in KLH-immunized mice, resulting in the reduction of CD4+/CD8+ ratio.CCK-8 improved the production of IFN-?, elevated IFN-? gene transcription, whereas cut down the production of IL-4, decreased IL-4 gene transcription. CCK-8 lightened the pulmonary inflammation induced by KLH.CONCLUSION: CCK-8 inhibits CD4+T lymphocytes activation, Th2 cytokine mRNA expression and protein production in KLH-immunized mice, indicating that CCK-8 modulates adaptive immune response.

AIM: To investigate in vitro effects of cholecystokinin octapeptide(CCK-8) on the expressions of B7.1 and B7.2 and the costimulatory activity of T lymphocytes in unstimulated macrophages.METHODS: Mouse peritoneal macrophages were isolated and incubated with CCK-8(10-12-10-6 mol/L) for indicated time.The B7.1 and B7.2 expressions of murine peritoneal macrophages were analyzed by flow cytometry.CD4+T cells were isolated from mouse spleen using immunomagnetic beads,and cultured with 1/4 numbers of macrophages which were pretreated with CCK-8 and/or anti-B7.1 antibody,anti-B7.2 antibody,CCK1R antagonist CR1409,CCK2R antagonist CR2945 for 24 h.ConA was added into the culture medium to stimulate CD4+T cell proliferation.The proliferation was determined by measuring -TdR incorporation in a ?-scintillation counter.RESULTS: B7.1 and B7.2 expressions and costimulatory activity of peritoneal macrophages were enhanced by CCK-8 in a dose-dependent manner,and the maximal effects occurred at the concentrations of 10-9 mol/L to 10-7 mol/L.Anti-B7.2 antibody,but not anti-B7.1 antibody,reduced the modulatory role of CCK-8 on costimulatory activity.Both CR1409 and CR2945 reversed the effect of CCK-8 on costimulation,and the role of CR1409 was more significant.CONCLUSION: CCK-8 enhances macrophage costimulatory activity by upregulating B7.2 expression,which is mediated by CCK1R and CCK2R.CCK1R might be the major receptor responsible for the modulation of CCK-8 on costimulation.

BACKGROUND:Establishing a characteristic.stable and repeatable model of Th1/Th2 imbalance in animals,is the key of studying the mechanism of Th1/Th2 imbalance.OBJECTIVE:To observe the characteristics of Th1/Th2 imbalance in splenocytes derived from Balb/C mice immnnized by keyhole limpet hemocyanin(KLH).DESIGN:A randomized control exploratory experiment.SETTING:Hebei Provincial Forensic Laboratory.Institute of Basic Medicine,Hebei Medical University.MATERLALS:The experiment was carried out in the Hebei Provincial Forensic Laboratory,Institute of Basic Medicine,Hebei Medical University from September 2005 to January 2007.Balb/C mice were adopted in this study.and all the disposals were in accordance with the guidance of animal ethics.METHODS:Balb/C mice were immunized with KLH emulsified in complete Freund's adjuvant(CFA),splenocytes were acquired,and the peak of cytokine secretion was determined in 3 groups:KLH groups of 6.25 mg,kg.12.5 mg,kg and 25 mg/kg.According to the immunizing dose and immunizing frequency.mice were divided into 7 groups:KLH groups of 6.25 mg/kg,12.5 mg/kg and 25 mg/kg,secondary immunity groups of 6.25 mg/kg,12.5 mg/kg and 25 mg/kg,as well as control group.According to the determined levels of IgG1 and IgG2a in blood serum.mice were divided into KLH group of 6.25 mg/kg and control group.MAIN OUTCOME MEASURES:Mice splenocytes supematant was detected with enzyme linked immunosorbent assay (ELISA)for the production of Th1 cytokines interferon (IFN)-γ,interleukin(IL)-2.IL-12 p40 and Th2 cytokines IL-4 and IL-5.The levels of Th1 antibody IgG2a and Th2 antibody IgG1 in blood serum were also detected by ELISA.RESULTS:The spleen derived from KLH-immunized mice appeared hypertrophy,and the number of splenocytes was manifold.Splenocytes restimulated with KLH in vitro produced much more IFN-γ,IL-2,IL-4,IL-5,but not IL-12p40.IL-2 secretion was obviously elevated after incubated for 24 hours and achieved pinnacle at 48 hours;productions of IL-4,IL-5 and IFN-γ were elevated after 24 hours,and increased gradually to 96 hours;IL-12p40 production was very low at every time point.Using different doses of KLH inlmunity once or twice,could all lead to the elevated productions of IL-2,IL-4,IL-5,IFN-γ,and the elevation of IL-4/IFN-γ ratio,but the secondary immunity group of 6.25 mg/kg KLH showed obviously higher levels than other groups(P＜0.01).The level of KLH specific antibody IgG2a and IgG1,especially IgG1 was elevated in blood serum of KLH-immunized mice.CONCLUSION:Balb/C mice immunizad with KLH emulsified in CFA can indce a Th2 predominant imbalance in splenocytes.

The potential medicinal value of Ma bamboo (Dendrocalamus latiflorus), one of the most popular and economically important bamboo species in China, has been underestimated. In the present study, we found that D. latiflorus leaf extract (DLE) reduced fasting blood glucose levels, body weight, and low-density lipoprotein cholesterol with low liver toxicity in db/db mice. In addition, gene expression profiling was performed and pathway enrichment analysis showed that DLE affected metabolic pathways. Importantly, DLE activated the AKT signaling pathway and reduced glucose production by downregulating glucose-6-phosphatase (G6PC) and phosphoenolpyruvate carboxykinase 1 (PCK1) expression. Moreover, network pharmacology analysis identified rutin as an active component in DLE through targeting insulin growth factor 1 receptor (IGF1R), an upstream signaling transducer of AKT. Due to its hypoglycemic effects and low toxicity, DLE may be considered an adjuvant treatment option for type 2 diabetes patients.