[A Review on the Use of Effect Size in Nursing Research].

PURPOSE: The purpose of this study was to introduce the main concepts of statistical testing and effect size and to provide researchers in nursing science with guidance on how to calculate the effect size for the statistical analysis methods mainly used in nursing. METHODS: For t-test, analysis of variance, correlation analysis, regression analysis which are used frequently in nursing research, the generally accepted definitions of the effect size were explained. RESULTS: Some formulae for calculating the effect size are described with several examples in nursing research. Furthermore, the authors present the required minimum sample size for each example utilizing G*Power 3 software that is the most widely used program for calculating sample size. CONCLUSION: It is noted that statistical significance testing and effect size measurement serve different purposes, and the reliance on only one side may be misleading. Some practical guidelines are recommended for combining statistical significance testing and effect size measure in order to make more balanced decisions in quantitative analyses.

Arsenic trioxide induces Hsp70 expression via reactive oxygen species and JNK pathway in MDA231 cells.

In the present study, we determined the molecular pathways that induce the heat shock proteins (Hsps) after treatment of cells with arsenic trioxide. Administration of arsenic trioxide to MDA231 cells leads to induce Hsp70, which is accompanied by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK). We showed that arsenic trioxide-induced Hsp70 expression was caused by activation of ROS and prevented by the antioxidant N-Acetyl-Cysteine (NAC). SP600125 and dominant-negative SEK suppressed Hsp70 promoter-driven reporter gene expression, suggesting that JNK would be preferentially associated with the protective heat shock response against arsenic trioxide stress. In addition, SP600125, a specific JNK inhibitor, significantly reduced the amount of phosphorylated HSF1 upon administration of arsenic trioxide. It is likely that Hsp70 expression against arsenic trioxide exposure protects cells from oxidative injury and apoptotic cell death by means of JNK activity.

Influence of p53 and p21Waf1 expression on G2/M phase arrest of colorectal carcinoma HCT116 cells to proteasome inhibitors.

Ubiquitin-mediated protein degradation in vertebrates has been implicated in cell cycle control. In this report we explored the effects of proteasome inhibitors (MG132, lactacystin and ALLN) on cell cycle distribution. Colorectal carcinoma HCT116 cells were treated with proteasome inhibitor MG132. The results showed that MG132 inhibited cell proliferation in a dose-dependent manner. MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21. MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest. The release experiments from nocodazole-induced mitotic phase cells indicated that MG132 inhibits the proliferation of HCT116 cells via arrest in the G2 phase. In addition, when HCT116 cells were exposed to combination of sodium butyrate and MG132 enhanced cell growth inhibition and induction of apoptosis were observed.