The effectiveness of a self-reporting bedside pain assessment tool for oncology inpatients.

BACKGROUND: Pain is common during cancer treatment, and patient self-reporting of pain is an essential first step for ideal cancer pain management. However, many studies on cancer pain management report that, because pain may be underestimated, it is often inadequately managed. OBJECTIVE: The aim of this study was to evaluate the effectiveness of bedside self-assessment of pain intensity for inpatients using a self-reporting pain board. METHODS: Fifty consecutive inpatients admitted to the Oncology Department of Chungbuk National University Hospital were included in this observational prospective study from February 2011 to December 2011. The medical staff performed pain assessments by asking patients questions and using verbal rated scales (VRS) over 3 consecutive days. Then, for 3 additional days, patients used a self-reporting pain board attached to the bed, which had movable indicators representing 0-10 on a numeric rating scale (NRS) and the frequency of breakthrough pain. RESULTS: Patient reliability over the medical staff's pain assessment increased from 74% to 96% after applying the self-reporting pain board (p=0.004). The gap (mean±standard deviation [SD]) between the NRS reported by patients and the NRS recorded on the medical records decreased from 3.16±2.08 to 1.00±1.02 (p<0.001), and the level of patient satisfaction with pain management increased from 54% to 82% (p=0.002). CONCLUSION: This study suggests that the self-reporting bedside pain assessment tool provides a reliable and effective means of assessing pain in oncology inpatients.

A more appropriate cardiac troponin T level that can predict outcomes in end-stage renal disease patients with acute coronary syndrome.

PURPOSE: Cardiac troponin T (cTnT), a useful marker for diagnosing acute myocardial infarction (AMI) in the general population, is significantly higher than the usual cut-off value in many end-stage renal disease (ESRD) patients without clinically apparent evidence of AMI. The aim of this study was to evaluate the clinical usefulness of cTnT in ESRD patients with acute coronary syndrome (ACS). MATERIALS AND METHODS: Two hundred eighty-four ESRD patients with ACS were enrolled between March 2002 and February 2008. These patients were followed until death or June 2009. Medical records were reviewed retrospectively. The cut-off value of cTnT for AMI was evaluated using a receiver operating characteristic (ROC) curve. We calculated Kaplan-Meier survival curves, and potential outcome predictors were determined by Cox proportional hazard analysis. RESULTS: AMIs were diagnosed in 40 patients (14.1%). The area under the curve was 0.98 in the ROC curve (p<0.001; 95% CI, 0.95-1.00). The summation of sensitivity and specificity was highest at the initial cTnT value of 0.35 ng/mL (sensitivity, 0.95; specificity, 0.97). Survival analysis showed a statistically significant difference in all-cause and cardiovascular mortalities for the group with an initial cTnT ≥0.35 ng/mL compared to the other groups. Initial serum cTnT concentration was an independent predictor for mortality. CONCLUSION: Because ESRD patients with an initial cTnT concentration ≥0.35 ng/mL have a poor prognosis, it is suggested that urgent diagnosis and treatment be indicated in dialysis patients with ACS when the initial cTnT levels are ≥0.35 ng/mL.

Pre-treatment of mesenchymal stem cells with a combination of growth factors enhances gap junction formation, cytoprotective effect on cardiomyocytes, and therapeutic efficacy for myocardial infarction.

OBJECTIVES: The goal of this study was to investigate the effect of pre-treatment of mesenchymal stem cells (MSCs) with growth factors (GFs) on cardiomyogenic differentiation, cytoprotective action on cardiomyocytes (CMCs), and their therapeutic efficacy in myocardial infarction. BACKGROUND: Mechanisms of myocardial repair with MSC transplantation have not been fully elucidated, and therapeutic efficacy needs to be enhanced. METHODS: The MSCs obtained from the bone marrow of Fisher344 rats were treated with fibroblast growth factor-2, insulin-like growth factor-1, and bone morphogenetic protein-2. The expression of cardiac specific markers and the cytoprotective effect of MSCs with its mechanism were evaluated. Efficacy of MSCs transplantation was studied in rat myocardial infarction model. RESULTS: Treatment of MSCs with cocktails of GFs enhanced expression of cardiac transcription factors and survival. Induction of cardiac specific markers by coculture with CMCs and gap junctional communication with CMCs was more active in GF-treated MSCs than untreated MSCs. The GF-treated MSCs reduced apoptosis of neighboring CMCs in a hypoxic condition and enhanced the phosphorylated Akt and phosphorylated c-AMP response element binding protein expression of CMCs, which was markedly reduced by gap junction blockade. In a rat myocardial infarction model, transplantation of GF-treated MSCs resulted in smaller infarct size and better cardiac function than transplantation of untreated MSCs. Additionally, GF treatment enhanced gap junction formation of transplanted MSCs, which did not aggravate arrhythmia. CONCLUSIONS: Pre-treatment of MSCs with GFs enhanced cytoprotective effects on neighboring CMCs through gap junction and improved the therapeutic efficacy of MSC transplantation for myocardial repair. "Priming of MSCs with GFs" before transplantation might improve the therapeutic efficacy of cell therapy.