PURPOSE: Impairments in word finding, language skills and memory in dementia patients increase the obstacles for health professionals to provide effective care. Although some research on communication with dementia patients has been done, no research that pre-assessed nurses' difficulties in communicating with dementia patients has been identified. This study aims to explore nurses' difficulties in communicating with patients who have dementia. METHODS: This was a qualitative research using the phenomenological approach. Data were collected through in-depth interviews. Fifteen nurses with at least 6 months of dementia care experience participated in this study. Each interview was audio-taped and transcribed within 48 hours after each interview. Participants were asked to respond to the question, "Please describe the difficulties in communicating with patients who have dementia." RESULTS: Through content analysis, two themes, each with two subthemes emerged: Different language, including repetitive responses and lack of language consensus; blocked messages, including difficulty in accessing emotions and in understanding needs. Ineffective language refers to a lack of agreement dialect between the nurse and the patient while blocked messages refer to the inability of nurses to understand the true underlying meaning of messages the patients send out through verbal or nonverbal behaviors or expression. CONCLUSION: The results can serve as reference for planning dementia communication education for school curriculum to enhance student nurses' communication abilities and for junior nurses working in long-term or acute care settings to increase nurses' patient-centered communication abilities with the ultimate goal of improving quality of care for patients with dementia.
Communication ; Consensus ; Curriculum ; Dementia* ; Education ; Health Occupations ; Humans ; Long-Term Care* ; Memory ; Qualitative Research ; Taiwan*

Purpose: sThe study aimed to translate the Exercise Self-Efficacy Scale (ESES) into Indonesian and test the cultural equivalence, reliability, and validity of the new version for university students. Methods: The cross-sectional study recruited 379 Indonesian university students using convenience sampling. Phase 1, a culturally appropriate version of the ESES was developed in the Indonesian language. Phase 2, the psychometric properties were determined through exploratory factor analysis, bootstrap factor analysis, and confirmatory factor analysis. The internal consistency reliability was tested using Cronbach's α, whereas the stability using intraclass correlation coefficient to assess. Results: The students' ages ranged from 17 to 39 years, and 65.0% were women. For translation equivalence, the mean item content validity indexes ranged from 3.5 to 4, and all items were understandable. The 16-item scale exhibited cross-cultural appropriateness and readability, with a three-factor model explaining 62.3% of the variance in exercise self-efficacy. A bootstrap analysis using 100 resamples further confirmed the three-factor model. The indices of the good-fit model that used the three-factor by two-stage least squares method were satisfactory, with χ2/df = 3.3, goodness of fit index = .88, and root mean-square error of approximation = .05 (p < .001). The Cronbach's α was .78, .80, and .92 for factors 1, 2, and 3, respectively. The test--retest reliability was demonstrated with an intraclass correlation coefficient of .91, indicating adequate measurement stability. Conclusion The 16-item ESES-I has acceptable validity and reliability; however, a broader application of the scale requires further testing in different populations to confirm its external validity.

Purpose: sThe study aimed to translate the Exercise Self-Efficacy Scale (ESES) into Indonesian and test the cultural equivalence, reliability, and validity of the new version for university students. Methods: The cross-sectional study recruited 379 Indonesian university students using convenience sampling. Phase 1, a culturally appropriate version of the ESES was developed in the Indonesian language. Phase 2, the psychometric properties were determined through exploratory factor analysis, bootstrap factor analysis, and confirmatory factor analysis. The internal consistency reliability was tested using Cronbach's α, whereas the stability using intraclass correlation coefficient to assess. Results: The students' ages ranged from 17 to 39 years, and 65.0% were women. For translation equivalence, the mean item content validity indexes ranged from 3.5 to 4, and all items were understandable. The 16-item scale exhibited cross-cultural appropriateness and readability, with a three-factor model explaining 62.3% of the variance in exercise self-efficacy. A bootstrap analysis using 100 resamples further confirmed the three-factor model. The indices of the good-fit model that used the three-factor by two-stage least squares method were satisfactory, with χ2/df = 3.3, goodness of fit index = .88, and root mean-square error of approximation = .05 (p < .001). The Cronbach's α was .78, .80, and .92 for factors 1, 2, and 3, respectively. The test--retest reliability was demonstrated with an intraclass correlation coefficient of .91, indicating adequate measurement stability. Conclusion The 16-item ESES-I has acceptable validity and reliability; however, a broader application of the scale requires further testing in different populations to confirm its external validity.

Eupafolin, a constituent of the aerial parts of Phyla nodiflora, has neuroprotective property. Because reducing the synaptic release of glutamate is crucial to achieving pharmacotherapeutic effects of neuroprotectants, we investigated the effect of eupafolin on glutamate release in rat cerebrocortical synaptosomes and explored the possible mechanism. We discovered that eupafolin depressed 4-aminopyridine (4-AP)-induced glutamate release, and this phenomenon was prevented in the absence of extracellular calcium. Eupafolin inhibition of glutamate release from synaptic vesicles was confirmed through measurement of the release of the fluorescent dye FM 1-43. Eupafolin decreased 4-AP-induced [Ca2+ ] i elevation and had no effect on synaptosomal membrane potential. The inhibition of P/Q-type Ca2+ channels reduced the decrease in glutamate release that was caused by eupafolin, and docking data revealed that eupafolin interacted with P/Q-type Ca2+ channels. Additionally, the inhibition of calcium/calmodulindependent protein kinase II (CaMKII) prevented the effect of eupafolin on evoked glutamate release. Eupafolin also reduced the 4-AP-induced activation of CaMK II and the subsequent phosphorylation of synapsin I, which is the main presynaptic target of CaMKII. Therefore, eupafolin suppresses P/Q-type Ca2+ channels and thereby inhibits CaMKII/synapsin I pathways and the release of glutamate from rat cerebrocortical synaptosomes.

Diabetic nephropathy (DN) is a hyperglycemia-induced progressivedevelopment of renal insufficiency. Excessive glucose can increase mitochondrialreactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction.Our previous study indicated that cilostazol (CTZ) can reduce ROS levelsand decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes.This study investigated the potential mechanisms of CTZ in rats with DN and in highglucose-treated mesangial cells. Male Sprague–Dawley rats were fed 5 mg/kg/day ofCTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealedthat CTZ reduced the thickness of the glomerular basement membrane and improvedmitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatmentreduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemiaand interacted with the intrinsic pathway for regulating cell apoptosis as anantiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROSproduction, altered the apoptotic status, and down-regulated transforming growthfactor beta (TGF-) and nuclear factor kappa light chain enhancer of activated B cells(NF-B). Base on the results of our previous and current studies, CTZ decelerationof hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenanceof the mitochondrial function and reduction in TGF- and NF-B levels.

Diabetic nephropathy (DN) is a hyperglycemia-induced progressivedevelopment of renal insufficiency. Excessive glucose can increase mitochondrialreactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction.Our previous study indicated that cilostazol (CTZ) can reduce ROS levelsand decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes.This study investigated the potential mechanisms of CTZ in rats with DN and in highglucose-treated mesangial cells. Male Sprague–Dawley rats were fed 5 mg/kg/day ofCTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealedthat CTZ reduced the thickness of the glomerular basement membrane and improvedmitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatmentreduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemiaand interacted with the intrinsic pathway for regulating cell apoptosis as anantiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROSproduction, altered the apoptotic status, and down-regulated transforming growthfactor beta (TGF-) and nuclear factor kappa light chain enhancer of activated B cells(NF-B). Base on the results of our previous and current studies, CTZ decelerationof hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenanceof the mitochondrial function and reduction in TGF- and NF-B levels.