ABSTRACT
PURPOSE: Cystoscopy is the most common procedure used to diagnose urological diseases; however, it is invasive and can be associated with pain and anxiety. Although pain relieving medications, such as lidocaine lubricants, are used during cystoscopy, the procedure still causes discomfort. Therefore, non-medical intervention is needed to reduce pain and anxiety during the procedure and increase patient satisfaction. The aim of this study was to evaluate the effect of heating therapy on pain, anxiety, physiologic measures, and satisfaction during cystoscopy. METHODS: This was a single-blinded, single-center, randomized controlled trial. A total of 145 participants who underwent cystoscopy between August 2017 and October 2017 were recruited and randomly assigned to an experimental or control group. Before and after cystoscopy, all the participants self-reported the degree of pain they felt, while pain was objectively assessed by trained nurses. Anxiety was evaluated using the validated Korean version of the State-Trait Anxiety Inventory. Blood pressure and pulse rate were also recorded as physiologic measures. After cystoscopy, satisfaction was measured in the experimental group only using the Korean version of the Client Satisfaction Questionnaire. RESULTS: Heating therapy reduced both subjective and objective pain and anxiety in the experimental group compared to the control group. Heating therapy also decreased the systolic and diastolic blood pressure and pulse rate in the experimental group compared to the control group. Women reported significantly greater satisfaction than men. CONCLUSION: Heating therapy during cystoscopy is a convenient and effective nursing intervention that decreases pain and anxiety and enhances patient satisfaction. The study has been registered with the Clinical Research Information Service Registry, and the trial registration number is [12616000803493].
Subject(s)
Cystoscopy , Pain Management , Anxiety/etiology , Cystoscopy/adverse effects , Cystoscopy/methods , Female , Heating , Humans , Male , Pain/diagnosis , Pain/etiology , Pain Management/methods , Patient Satisfaction , Personal SatisfactionABSTRACT
After primary infection of B cells with Epstein-Barr virus (EBV), infected B cells express several viral homologs of human genes that promote activation (LMP1 and CD40) or survival (BHRF and BCL2). EBV-infected B cells also express germinal center phenotype markers, such as CD77, PNA, CD95, and CD38. This transformation of B cells by EBV infection resembles normal B-cell activation and differentiation arising in the germinal center. In the present study, we found that EBV-transformed B cells expressed centrocyte/centroblast marker 1 (CM1), a possible marker of GC B cells and an inducer of their apoptosis. Moreover, ligation of CM1 on EBV-transformed B cells by immobilized anti-CM1 monoclonal antibody induced cell death. The ligation of CM1 immediately increased the generation of intracellular reactive oxygen species (ROS) and disrupted the mitochondrial membrane potential. Pretreatment with N-acetyl cystein (an ROS inhibitor) almost completely blocked this cell death, but Z-VAD-fmk (a caspase inhibitor) did not. We further investigated whether apoptosis-inducing factor (AIF) and endonuclease G (EndoG), which are both related to caspase-independent cell death, would be translocated to the nucleus during the ligation of CM1. We found that AIF and EndoG were released to the cytosplam but not translocated to the nucleus. Moreover, cytochalasin D, a cytoskeleton disruptor, rescued the cells from CM1-mediated cell death and blocked ROS generation. Therefore, it is conceivable that CM1 signaling might provoke cytoskeleton polymerization and trigger ROS generation. Taking these observations together, we conclude that the ligation of CM1 on EBV-transformed B cells can cause cell death via the ROS produced by F-actin polymerization in a caspase-independent manner, although this cell death might be unrelated to AIF and EndoG release from the mitochondria.
