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Objective To develop kinesthetic and visual imagery questionnaires applicable to Chinese stroke survivors and evaluate their test-retest reliability,inter-rater reliability and internal consistency.Methods The English version of a kinesthetic and visual imagery questionnaire (KVIQ) was translated into Chinese using wellaccepted questionnaire translation procedures.Thirty stroke survivors were each assessed twice using two versions of the translation (the KVIQ-20 and the KVIQ-10) by two experienced raters with an interval of 7 days between the tests.The test-retest reliability,inter-rater reliability and internal consistency of the visual imagery score (visual imagery subscale),the kinesthetic imagery score (kinesthetic imagery subscale) and the total scores for the KVIQ-20 and KVIQ-10 versions were analyzed.Results The test-retest coefficients,the inter-rater reliability correlation coefficients and Cronbach's alphas for the KVIQ-20 version ranged from 0.879 to 0.945,from 0.894 to 0.936 and from 0.867 to 0.919,respectively.The corresponding measurements for the KVIQ-10 vcrsion were 0.914 to 0.953,0.852 to 0.900 and 0.827 to 0.878.Conclusion Both the KVIQ-20 and KVIQ-10 Chinese instruments have shown good testretest and inter-rater reliability and good internal consistency in assessing stroke survivors.Either is an effective tool for assessing their motor imagery ability.
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Objective To investigate the effect of Atorvastatin on the proliferation and apoptosis of leukemic HL-60-cell line,and to explore the possible role of phosphatidylinositol 3-kinase/serine/threonine protein kinase /mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway in this process.Methods HL-60 cells were incubated with different concentrations of Atorvastatin (1,5,10 μmol/L),and HL-60 cells without any treatment were used as controls.The proliferation of HL-60 which was investigated by four methyl thiazolyl tetrazolium assay when cells were cultured for 12,24,48 hours.The apoptosis was detected by flow cytometry after cells were incubated for 48 hours.The mRNA and protein expressions of AKT,PI3K and mTOR were detected by reverse transcription-polymerase chain reaction and Western blot methods,respectively.Results The results indicated that Atorvastatin could inhibit the proliferation and induce the apoptosis of HL-60 cells.When treated with 10 μmol/L Atorvastatin after 48 h,the proliferation inhibition of HL-60 was observed most obviously,with a high rate of (39.77 ± 3.01) ％,compared with the control group,it had statistical significance (t =4.016,P ＜ 0.01),meanwhile,the apoptosis of HL-60 was most notable,at a rate of (43.29 ±3.91)％,compared with the control group,it had statistical significance (t =3.625,P ＜ 0.05).There were basal expression of AKT,PI3K and mTOR in the control group.When treated with 10 μmol/L Atorvastatin after 48 h,the mRNA expression of PI3K,AKT and mTOR were down-regulated most obviously,at a decrease of (37.05 ± 4.11) ％,(53.79 ± 3.27) ％,(40.63 ± 2.42) ％ (t =4.805,3.799,4.312,all P ＜ 0.05),respectively,in comparison with the control group.At the same condition,the protein expression of PI3K,AKT and mTOR were decreased most visibly,with a decline of (41.09 ± 3.17) ％,(45.67 ± 2.92) ％,(63.41 ± 3.59) ％ (t =3.576,4.727,4.902,all P ＜ 0.05) respectively in comparison with the control group.Conclusions Atorvastatin can inhibit the proliferation and induce the apoptosis of leukemic cell HL-60,and the mechanism may be associated with the PI3K/ AKT/mTOR signal pathway.
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Objective To observe the effect of cytokine-induced killer (CIK) cells on the apoptosis of human leukemia cells,and explore the role of miR-155 in this process.Methods The cytotoxicity of CIK cells against a variety of leukemic cell lines (NALM-6,Jurkat) was investigated by MTT technique,miR-155 was determined by real time quantitative PCR,and the apoptosis was detected by flow cytometry in NALM-6 and Jurkat cells induced by CIK cells.Psi CHECK2-CEBP/β 3'-UTR containing the binding site of miR-155 was constructed,and then it was transfected into NALM-6 and Jurkat cells.Luciferase activity of CEBP/β (CCAAT/enhancer binding protein beta) was determined with the assistance of dual luciferase report system.Results CIK cells possessed strong cytotoxicity against NALM-6 and Jurkat cells,which was time-dependent and dose-dependent (P ＜ 0.05).CIK cells could increase the expression of miR-155 in NALM-6 cells by (2.87±0.19) fold (t =2.787,P ＜ 0.05),and in Jurkat cells by (1.98±0.25) fold (t =3.513,P ＜ 0.05).Moreover,miR-155 mimics could promote the apoptosis of NALM-6 and Jurkat cells induced by CIK cells (t =4.239,P ＜ 0.05;t =3.565,P ＜ 0.05).However,miR-155 inhibitor might block this process (t =3.772,P ＜ 0.05;t =4.017,P ＜ 0.05).MiR-155 targeted at the site of CEBP/β3'-UTR,and CIK cells could decrease the luciferase activity of NALM-6 cells by (42.89±2.07) ％ (t =3.578,P ＜ 0.05),meanwhile,in Jurkat cells by (37.02±1.95) ％ (t =4.393,P ＜ 0.05).Conclusion CIK cells could enhance human leukemia NALM-6 and Jurkat cells apoptosis by upregulating miR-155,which may provide a new database to elucidate leukemia cell therapy using CIK cells.
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@#Mechanical loading provides an anabolic stimulus for bone. Low frequency vibration is a kind of mechanic stimulus, which can promote osteogenesis in certain frequency, mode and intensity. The osteogenesis promotion of low frequency vibration may be associated with the membrane ion channels, integrin-cytoskeleton complex triggering mitogen activated protein kinase (MAPK) signal and second messengers regulating RANK-RANKL-OPG axals.
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Objective To study the effect of lactate of differentconcentration on the action potential of ventricular papillary muscle cell (n=4) and contractile force (n=10).Method Using intracellular microelectrode technique and microtension depicting method.Result The Result showed the effect of lactated solution of a certain comcentration became obvious. After perfused with lactate solution of 4mmol/L,the vilocity maximum decreased significantly (p<0.05) showed the 4mmol/L lactate solution decreased the rate of depolarization: decreased the efficency of Na + channel; lactate solution decreased the contractile force of cardiac muscle. Conclusion The possible mechanism was: Ca+ influx and Na+ - H+ exchange were inhibited, resulted in the elevation of intracellular H+ concentration; through Na+-Ca2+ exchange, Ca2+ efflux decreased resulted in the intracellular Ca2+ decreased resulted in the intracellular Ca2+ overload.