Social Support as a Mediator of the Relationship between Hope and Decisional Conflict in Patients Deciding Whether to Receive Dialysis.

Background: The incidence rate of end-stage renal disease (ESRD) in Taiwan is the highest worldwide. Patients often hesitate and feel helpless when deciding whether to receive dialysis. However, the resulting delay in starting dialysis can potentially threaten patients' lives. Purpose: This study aimed to understand the current situation and correlations between hope, social support, and decisional conflict among patients with ESRD deciding whether to receive dialysis. In addition, the role of social support as a mediating variable of the relationship between hope and decisional conflict was investigated. Methods: This study was a cross-sectional, descriptive correlation study. Data, including demographic information, were collected from 85 patients with ESRD who were deciding whether to receive dialysis. Research tools included the Chinese versions of the Herth Hope Index, the Interpersonal Support Evaluation List, and the Decisional Conflict Scale. Results: When deciding whether to receive dialysis, patients with ESRD felt a low sense of hope, a moderate degree of social support, and a moderate degree of decisional conflict. Hope was significantly correlated with social support and decisional conflict. Social support demonstrated a full mediating effect of 47.7% (P < 0.001). Conclusions: Patients with ESRD facing the decision to receive dialysis felt a low sense of hope and exhibited decisional conflict. Social support was found to be a mediating variable of the relationship between hope and decisional conflict; therefore, medical personnel should increase the social support of patients with ESRD who are deciding whether to commence dialysis to promote patients' hope and reduce their decisional conflict.

Myeloid Zinc Finger 1 (MZF1) Maintains the Mesenchymal Phenotype by Down-regulating IGF1R/p38 MAPK/ERα Signaling Pathway in High-level MZF1-expressing TNBC cells.

BACKGROUND/AIM: Signaling regulation of myeloid zinc finger 1 (MZF1) has been implicated in the progression of many human malignancies; however, the mechanistic action of MZF1 in triple-negative breast cancer (TNBC) progression remains elusive. In this study, the aim was to investigate the molecular mechanisms of MZF1 and its functional role in TNBC cellular migration and invasion. MATERIALS AND METHODS: Hs578T and MDA-MB-231 cells were transfected to stably express the acidic domain of MZF1 (MZF160-72), or were transfected with MZF1-specific or ELK1-specific short hairpin RNA (shRNA). Changes in cell morphology and distributions of cellular proteins were observed and subsequently migration and invasion were measured by wound healing and transwell assays. Expression levels of epithelial-mesenchymal transition (EMT)-related genes were carried out using immunoblotting and quantitative reverse transcription-polymerase chain reaction (RT-PCR) assays. Data of transcriptional regulation were obtained from promoter-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. RESULTS: Herein, we found that MZF1 in high-level MZF1-expressing TNBC cells is associated with cell migration, invasion, and mesenchymal phenotype. MZF1 interacted with the promoter region of insulin-like growth factor 1 receptor (IGF1R) to drive invasion and metastasis of high-level MZF1-expressing TNBC cells. Exogenous expression of the acidic domain of MZF1 repressed the binding of endogenous MZF1 to IGF1R promoter via blocking the interaction with ETS-like gene 1 (ELK1). This blockage not only caused MZF1 protein degradation, but also restrained ELK1 nuclear localization in high-level MZF1-expressing TNBC cells. MZF1, but not ELK1, was necessary for the retention of mesenchymal phenotype by repressing IGF1R promoter activity in TNBC cells expressing high levels of MZF1. Activation of the IGF1R-driven p38MAPK-ERα-slug-E-cadherin signaling axis mediated the conversion of mesenchymal cell to epithelial phenotype, caused by MZF1 destabilization. These results suggest that MZF1 is an oncogenic inducer. CONCLUSION: Blocking of the MZF1/ELK1 interaction to reduce MZF1 protein stability by saturating the endogenous MZF1/ELK1 binding domains might be a promising therapeutic strategy for the treatment of high-level MZF1-expressing TNBC.

Cetrimonium Bromide Inhibits Cell Migration and Invasion of Human Hepatic SK-HEP-1 Cells Through Modulating the Canonical and Non-canonical TGF-ß Signaling Pathways.

BACKGROUND/AIM: Cetrimonium bromide (CTAB), a quaternary ammonium surfactant, is an antiseptic agent against bacteria and fungi. However, the mechanisms by which its pharmacological actions affect epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma (HCC) cells, such as adenocarcinoma in SK-HEP-1 cells, have not been investigated. We, thereby, investigated whether CTAB inhibits cellular mobility and invasiveness of human hepatic adenocarcinoma in SK-HEP-1 cells. MATERIALS AND METHODS: SK-HEP-1 cells were treated with CTAB, and subsequent migration and invasion were measured by wound healing and transwell assays. Protein expression was detected by immunoblotting analysis. RESULTS: Our data revealed that treatment of SK-HEP-1 cells with CTAB altered their mesenchymal spindle-like morphology. CTAB exerted inhibitory effects on the migration and invasion of SK-HEP-1 cells dose-dependently, and reduced protein levels of matrix metalloproteinase-2 (MMP-2), MMP-9, snail, slug, twist, vimentin, fibronectin, N-cadherin, Smad2, Smad3, Smad4, phosphoinositide-3-kinase (PI3K), p-PI3K, Akt, p-Akt, ß-catenin, mammalian target of rapamycin (mTOR), p-mTOR, p-p70S6K, p-extracellular signal-regulated kinases (ERK)1/2, p-p38 mitogen-activated protein kinase (MAPK) and p-c-Jun N-terminal kinase (JNK), but increased protein levels of tissue inhibitor matrix metalloproteinase-1 (TIMP-1), TIMP-2, claudin-1 and p-GSK3ß. Based on these observations, we suggest that CTAB not only inhibits the canonical transforming growth factor-ß (TGF-ß) signaling pathway though reducing SMADs (an acronym from the fusion of Caenorhabditis elegans Sma genes and the Drosophila Mad, Mothers against decapentaplegic proteins), but also restrains the non-canonical TGF-ß signaling including MAPK pathways like ERK1/2, p38 MAPK, JNK and PI3K. CONCLUSION: CTAB is involved in the suppression of TGF-ß-mediated mesenchymal phenotype and could be a potent medical agent for use in controlling the migration and invasion of hepatic adenocarcinoma.

[Applying the Diffusion of Innovation Theory to Improve the Prevalence of Use of a Disease Management Information System].

BACKGROUND & PROBLEMS: The unit promoted the use of a disease management information system, but lacked consensus regarding its use. The problems that were identified included: the business-oriented design of the information system, lack of education and training, dual-track operations, and awkward operation interface. Use of the information system among nurses in the unit had thus decreased over time. PURPOSE: To increase the prevalence of use of the disease management information system. RESOLUTIONS: The diffusion of innovation theory was applied to strengthen the innovative characteristics of the disease management information system. The improvement measures adopted included: incorporation of recommendations, revision of the information system, provision of testing, arranging education and training sessions for the nurses, implementation of a regular audit system, and the revision of standard operating procedures. RESULTS: The prevalence of use of the disease management information system increased from 33.3% pretest to 100% posttest. CONCLUSIONS: This project applied the diffusion of innovation theory to strengthen the innovative characteristics of the disease management information system, guide the nurses to adapt and change, and improve their use of and satisfaction with the disease management information system.