Objective To investigate illness uncertainty state and explore its influencing factors in hospitalized children and adolescents with cancer.Methods A cross-sectional survey was performed in 112 children and adolescents with cancer aged 7～18 years old from two hospitals with the Chinese version of Uncertainty Scale for Kids-20 and the self-designed demographic questionnaire.Results The mean total scores of illness uncertainty was (45.16±6.67) points.The results of single-factor analysis showed that the factors influencing the uncertainty in illness of children and adolescents with cancer were as follows:age,personality characteristics,course of disease,the methods of treatment,current disease status,absence from school or not,the times of hospitalization,family monthly income,and the extent of parents' understanding about the disease-related knowledge.Multi-factor stepwise regression analysis showed that the main influencing factors of the uncertainty in illness were the current condition,family monthly income,absence from school or not and the extent of parents' understanding about the disease-related knowledge.Conclusions Illness uncertainty is common in children and adolescents with cancer.Nurses should attach importance to the impacts of illness uncertainty,and take effective interventions to decrease it,alleviate psychological pressure and improve quality of life in children and adolescents with cancer.

Objective To discuss the effect of QGY/CDDP hepatoma lines multi-drug resistance (MDR) reversed by gene transfection of mdr1,mrp-ASODN+ultrasound contrast agent+ultrasound.Methods The QGY/CDDP cells were transfected by mdr1,mrp ASODN+ultrasound contrast agent+ultrasound irradiation respectively and detected of the various indicators:cell adhesion rate,cell sensitivity to cell drug-resistance,the mRNA expression of mdr1 and mrp gene,the expression of P-gp and MRP protein. Results After mdr1-ASODN transfection,the drug sensitivity and expression of P-gp,MRP protein of QGY/CDDP cells were smaller changes(P＞0.05),and the rate of cells adherent and expression of resistance gene mRNA were obvious changes(P＜0.05).After mrp-ASODN transfection,the cells adherent rate,the drug sensitivity,the expression of resistance gene mRNA and P-gp,MRP protein were obvious changes respectively(P＜0.05),the experiment group(group 2')had bigger effects(P＜0.05).Conclusions mdr1. mrp-ASODN+ultrasound contrast agent+ultrasound irradiation could safely partly reverse MDR of hepatoma cells,which is a potential new approach for gene therapy.

Objective To investigate the effects of simvastatin (SV) on the proliferation,differentiation and apoptosis of human promyelocytic leukemia cell line NB4.Methods NB4 cells were incubated with SV at different concentration with or without all-trans retinoic acid (ATRA),and NB4 cells without any treatment were taken as normal control.Cells of different groups were collected at 24 h,48 h and 72 h after incubation for further detection.Morphological changes by Wright stain were performed.MTT method was used to assay the growth inhibition rate and flow cytometry was used to detect the surface CD11b expression levels,the early stage apoptosis ratio and cell necrosis ratio.Results Treated with 15 μ mol/L SV,10 μ mol/L SV and 5 μ mol/L SV respectively,with the NB4 cells growth,the cell inhibition rates gradually increased (F =7.15,P =0.000),as well as CD11b expression levels (F =3.41,P =0.014) and AnnexinVexpression levels (F =43.38,P =0.000).Furthermore the NB4 cells treated with 15 μ mol/L SV exhibited the most significant changes with cell inhibition rate of 0.96±0.02,CD11b expression level increased to (62.41±6.37) ％ and AnnexinV expression level increased to (87.38±2.94) ％ after 72 h incubation.Combination of 15 μmol/L SV with 0.5 μmol/L ATRA displayed obvious interaction for increasing CD11b expression levels (F =4.093,P =0.025),while no significant interaction for cell inhibition rates and Annexin V expression levels were observed.After 72 h incubation,the CD11b expression levels (89.46±9.13) ％ in NB4 cells treated with 15 μ mol/L SV in combination with 0.5 μ mol/L ATRA were significantly higher than those treated with ATRA (71.27±7.27) ％ and SV (62.41±6.37) ％ (t =2.71,P =0.054; t =4.37,P =0.017)' solely.Conclusion Simvastatin in vitro inhibits NB4 cell proliferation,promotes cell apoptosis,and synergistically induces cell differentiation with ATRA dose-dependently in vitro,which indicates that SV may have the effect of synergistic anti-promyelocytic potency with ATRA.

Objective To investigate the effect of simvastatin (SV) in combination with cytosine arabinoside (ARA-C) on the proliferation and apoptosis of K562 cells. Methods Human K562 cells were incubated with SV and cytosine arabinoside alone or in combination and K562 cells without any treatment were taken as normal control. Cells in different groups were collected at 24, 48 and 72 h after incubation for further detections. Morphological changes by Wright stain were performed. MTT method was used to assay the growth inhibition rate and cytoflowmetry was used to detect the early stage apoptosis ratio and cell necrosis ratio. Results Compared with Ara-C group and SV group, cells in the group treated with SV combined with Ara-C showed obvious karyopyknosis,apoptosis bodies formation and significant cell growth inhibition, which were positively correlated with culture time. Combination of 15 μmol/L SV and Ara-C showed the most significant cell growth inhibition with a inhibition rate of (72±1) % at 72 h of culture, as was significantly higher than that of 15 μmol/L SV group (45±2) % and 20 μmol/L Ara-C group (44±0) % (P ＜0.01),furthermore, combination of 15 μmol/L simvastatin and Ara-C showed synergistic inhibition with Q value of 1.24 and 1.19 at 24 h and 48 h in each. The apoptosis rates at early stage (AnnexinV) detected by flow cytometry in 20 μmol/L, 15 μmol/L and 10 μmol/L SV treated K562 cells were significantly higher than that in normal K562 cells (P ＜0.01), as were positively correlated with culture time and SV dose (P ＜0.05). There were no significant difference of early apoptosis rate between the 20 μmol/L SV and 15 μmol/L SV groups (P ＞0.05), yet the very two were both higher than that of 10 μmol/L SV group (P ＜0.05). There were no statistic differences of late apoptosis rate (PI) amongdifferent treated groups (P ＞0.05). Conclusion SV inhibited K562 cell proliferation and induced cell apoptosis in vitro, and combination of SV and Ara-C exhibited obvious synergistic inhibition and apoptosis, which may increase the sensitivity of K562 cell to chemotherapy. SV at 15 μmol/L may be the best concentration for K562 cells in vitro.