There is strong relationship between self-efficacy and health promotion.And the researches about applying self-efficacy to promoting health behavior of the older adults increase as aging.This paper reviewed the self-efficacy and its relationship with health-promoting behavior of older adults.

BACKGROUND: There are pressure sensors in carotid-sinus, which are very sensitive to blood pressure regulated by ions and play an important role in the regulation of blood pressure. But it is yet not very clear how different ions regulate the blood pressure through pressure sensors in carotidsinus.OBJECTIVE: To observe the effect of different ions at various concentrations outside the carotid-sinus.DESIGN: Self-control experiment.SETTING: Preclinical Experiment Center, Fourth Military Medical University of Chinese PLA.MATERIALS: The experiment was accomplished in the Preclinical Experiment Center, Fourth Military Medical University of Chinese PLA from December 2000 to June 2001. Totally 18 New Zealand pure strain rabbits were provided by the Aninal Experimenting Center of Fourth Military Medical University of Chinese PLA. They were standard grade Ⅱ, of either gender and body mass was (2.0±0.2) kg.METHODS: The rabbits were divided into Na+, K+ and Ca2+ groups according to random numbers, and each group consisted of 6 rabbits. After anaesthesia, tracheal intubatton was performed on the rabbit, and bilateral carotid arteries were separated with carotid-sinus separated on one side and vessel intubatton performed in the other side for blood pressure measurement. Then various concentrations of Na+, K+ and Ca2+ ions were added outside the carotid-sinus with the pipette to make the carotid-sinus completed immersed in the ion solutions. The basal blood pressure and the peak value after ions addition were recorded respectively.MAIN OUTCOME MEASURES: The basal blood pressure and the peak value after ions addition.RESULTS: After Na+ (0.15, 1.5 mol/L) was added the blood pressure was(97±12), (83±17) mm Hg. It was decreased significantly compared with the basal value (106±14), (105±12) mm Hg (t=2.946, P ＜ 0.05). K+ (0.4 mol/L)decreased the blood pressure significantly [(106±12), (64±13) mm Hg, (t=13.496, P ＜ 0.01)], but other concentrations of K+ were not effective. Ca2+(0.07 mol/L) increased the blood pressure to (113±16) mm Hg compared with the basal value (103±12) mm Hg (t=-3.627, P ＜ 0.01).CONCLUSION: Na+, K+ and Ca2+ regulate the blood pressure by acting on the carotid-sinus directly. High concentrations of Na+ and K+ possess the effect of decreasing the blood pressure, while high concentrations of Ca2+increases it, which may be an important mechanism of blood pressure regulation.

AIM To investigate the effects and mechanism of cardiomyocyte hypertrophy induced by urocortin. METHODS The cardiomyocytes were divided into 8 groups: normal control, urocortin, staurosporine(Sta), verapamil(Ver), H89, urocortin+Sta, urocortin+Ver, and urocortin+H89 groups. The cardiomyocytes diameter was measured by computer photograph analysis system. The protein synthetic rate was obtained through measuring the incorporation of [~3H]-leucine into myocyte protein by liquid scintillation method. The total protein content was assayed by Lowry method. The expression of atrial natriuretic peptide (ANP) was determined by Western blot. [Ca~(2+)]_i transient was measured by Till image system by cell loading Fura-2/AM. RESULTSUrocortin group enhanced cardiomyocyte volume, protein synthesis, total protein content and expression of ANP by 30.9%, 36.3%, 35.5% and 34.7%;urocortin+Sta group decreased cardiomyocyte diameter, protein synthesis, total protein content and expression of ANP by 16.5%, 22.1%, 18.1% and 21.3%;urocortin+H89 group decreased the cardiomyocyte diameter, the protein synthesis,total protein content and expression of ANP by 16.6%, 21.5%, 19.5% and 20.6%;urocortin+Ver decreased the cardiomyocyte diameter, the protein synthesis, total protein content and the expression of ANP by 17.1%, 20.9%, 17.9% and 19.9%;Sta, H89 and Ver could decrease the [Ca~(2+)]_i transient induced by urocortin. CONCLUSION The hypertrophic effect of urocortin in rat neonatal cardiomyocytes is mediated via activation of protein kinase C and protein kinase A pathway and L-type calcium channels.

By using SWOT method, we analyze the strengthen, weakness, existing opportunity and challenging of applying Mini-CEX which is named Mini Clinical Evaluation Exercise in theOrgan-system-based curriculum modelclinical nursing teaching, and propose related development strategy of Mini-CEX.

Objective: To investigate the effect of ginsenoside Rg3 combined with TRAIL on the apoptosis of lung cancer H358 cells and its possible mechanism. Methods: After the completion of cell culture, H538 cells were treated with TRAIL (0, 50, 100, 200 ng/ ml ) or Rg3 (0, 25, 50, 100 μmol/L) for 48 h, and the cells were grouped according to different treatments, namely control group, 50 μmol/LRg3 group, 100 ng/ml TRAILgroup and 50 μmol/LRg3+100 ng/ml TRAILgroup. The effects of Rg3 and/or TRAILon the proliferation of H358 cells were detected by MTT assay. The effects of Rg3 and/or TRAIL on the morphological changes of H358 cells were observed by DAPI staining. Theapoptosis of H358 cells in each group was detected by flow cytometry. The effects of Rg3 and/or TRAIL on the expressions of death receptor 5 (DR5) and caspase-8 in H358 cells were detected by WB. Results: Compared with the other groups, the proliferation of lung cancer H358 cells was significantly inhibited, while the apoptosis was significantly elevated in the 50 μmol/LRg3+100 ng/ml TRAILgroup (P<0.05).After color developing, cells in 50 μmol/LRg3+100 ng/ml TRAILgroup had nuclear shrinkage, chromatin condensation, increased fluorescence intensity, and late morphological changes such as saturation fragmentation. Compared with the other groups, the expression levels of DR5 and caspase-3 ,8 in the cells of 50 μmol/L Rg3+100 ng/ml TRAIL group were significantly increased (P<0.05). Conclusion: Ginsenoside Rg3 combined with TRAIL can synergistically inhibit the proliferation and induce apoptosis of lung cancer H358 cells. The mechanism may be related to the up-regulation of DR5 and caspase-8 by ginsenoside Rg3.

Objective:To investigate the effect of sorafenib on the proliferation of human oral cancer TCA8113 cells and to explore the underlying mechanisms.Methods:Mter treated with sorafenib at 2.5,5,10,20 μg/ml respectively for48 h,TCA8113 cell proliferation was examined by MTT and colony formation assay.Western blotting was employed to examine the p38MAPK expression in the cells.TCA8113 cells were pretreated with 10 μmol/L of SB203580 (a specific inhibitor of p38MAPK) for 30 min,and then by different concentrations of sorafenib for 48 h,cell proliferation was tested by MTT assay.Results:Sorafenib significantly inhibited the proliferation of TCA8113 cells in a concentration dependent fashion.Sorafenib also remarkably promoted the activation of p38MAPK of the cells.SB203580 significantly alleviated soiafenib induced TCA8113 cell viability decrease.Conclusion:Sorafenib can inhibit the proliferation of TCA8113 cells,which may be related to the activation of p38MAPK.

Objective To identify the interaction between nuclear localization signal-retinoic acid receptor α (NLS-RARα) and Ubiquilin 1(UBQLN1). Methods The recombination expression plasmids pGBKT7-NLS-RAR and pACT2-UBQLN1, which expressed bait-protein NLS-RARα and target protein UBQLN1 respectively, were cotransformated into yeast AH109. The interaction of the expression plasmids in the living cells was investigated by yeast two-hybrid assay. HA-tagged fusion protein (pCMV-HA-NLS-RARα) expression vector and Myc-tagged fusion protein (pCMV-Myc-JTV1) expression vector were constructed, identified, and cotransfected respectively into human embryo kidney 293 cells(HEK293). The interaction was detected by co-immunoprecipitation.Results Blue clones were found on yeast AH109 plate cotransformated with pGBKT7-NLS-RARα and pACT2-UBQLN1. Double restriction enzyme digestion showed that pCMV-HA-NLS-RARα and pCMV-Myc-JTV1 were successfully constructed. Then HA-NLS-RAR protein was immunoprecipitated by anti-HA polyclonal antibody and the expression of Myc-UBQLN1 was tested by Western blot with anti-Myc monoclonal antibody from immunoprecipitated complex. Conclusion The interaction between NLS-RARα and UBQLN1 can be verified by yeast two-hybrid assay and co-immunoprecipitation.

Objective To monitor and compare the breathing mechanics on PC,VC and PRVC during pneumoperitoneum,and to discuss the significance of the clinic use of PRVC.Method Ninety laparoscopic cholecystectomy patients were equally divided into 3 groups (PC,VC,PRVC).Levels of PES,PAWM,PAP,PaCO2,ETCO2,TV MAP and HR were detected before pneumoperitoneum,and at 5,10,15 and 20 minutes postpneumoperitoneum.Results Pneumoperitoneum made three respiratory patterns with different levels of PAWM,PAP,and PES.PES post-pneumoperitoneum in the VC model was obviously higher than that in the PC and PRVC group.At 10 min post-pneumoperitoneum,levels of PaCO2 and ETCO2 increased obviously in the PC and VC group(P ＜ 0.05).Levels of PaCO2 and ETCO2 were increased in the PC group,but TV level post-pneumoperitoneum was significantly lower than that in the other two groups (P ＜ 0.05).Level of PaCO2 and ETCO2 were increased in the PC and VC group post-pneumoperitoneum,along with increases of MAP and HR (P ＜ 0.05).Levels of MAP and HR in the PRVC group post-pneumoperitoneum were significantly lower than those in the PC and VC group (P ＜ 0.05).Conclusion PRVC mode can effectively reduce the increases of pneumoperitoneum-induced PAWM,PAP,PES,without the unusual increase of PaCO2 and ETCO2 during surgeries,contributing to the stability of vital signs of perioperative patients.

AIM:To investigate the effect of genistein on the proliferation of human oral cancer TCA 8113 cells and to explore the underlying mechanisms .METHODS:The cell proliferation was examined by MTT assay , cell counting and colony formation assay .Western blotting was employed to examine the protein levels of vascular endothelial growth fac -tor (VEGF), extracellular signal-regulated kinase (ERK) and p-ERK.RESULTS: Genistein significantly inhibited the proliferation of TCA8113 cells in a concentration-dependent fashion .Moreover , genistein dose-dependently decreased the protein levels of VEGF, ERK and p-ERK.The expression of VEGF was also blunted by U 0126, a specific inhibitor of ERK.U0126 and axitinib, a VEGF receptor antagonist , both significantly inhibited the proliferation of TCA 8113 cells. CONCLUSION:Genistein inhibits the proliferation of TCA8113 cells, which may be related to its inhibitory effect on ERK expression and activation , thus subsequently decreasing the expression of VEGF .

AIM: To explore the effect of L-carnitine on nuclear factor of activated T-cells, cytoplasmic 3 (NFATc3) in cardiomyocytes under H2O2 stimulation.METHODS: Primary cultured neonatal rat myocardial cells were stimulated by H2 O2 at concentration of 200μmol/L for 12 h to induce oxidative stress injury.In treatment group, L-carni-tine and cyclosporin A ( CsA) , a specific inhibitor of calcineurin ( CaN) , were administered 30 min prior to H2 O2 stimula-tion.After treatment, total, cytoplasmic and nuclear NFATc3 protein levels were determined by Western blotting.The method of immunofluoresence was used to evaluate the distribution of NFATc3.RESULTS: H2 O2 treatment produced no effect on the expression of total NFATc3, but caused its translocation from the cytosolic to nuclear compartment, which was greatly blunted by L-carnitine pretreatment.CONCLUSION:L-carnitine antagonized oxidative stress injury via alleviating NFATc3 nuclear translocation.