Reliability and Validation of the Japanese Version of the Patient Empowerment Scale

Empowerment scales for inpatients have been developed worldwide, but their validity and reliability have not been adequately tested and applied to the health promotion and care among older adults during hospitalization. In this study, the Patient Empowerment Scale developed by Faulkner was translated into Japanese, and Japanese patients were surveyed to test its clinical applicability. To test its applicability, 151 patients in rehabilitation wards were surveyed in four municipalities. After considering ceiling/floor effects and validating the structure, the Patient Empowerment Scale—Japanese comprised 37 items and six factors: subject–staff interaction, environmental adjustment through collaboration, necessary information gathering and problem awareness, proactive behavioral practices, self-disclosure, and self-management of activities. Criteria-related validity assessment confirmed the scale’s correlation with the Health Locus of Control Scale, General Self-Efficacy Scale, 13-item Sense of Coherence Scale, Rosenberg Self-Esteem Scale, and Philadelphia Geriatric Center Morale Scale. Regarding internal consistency, the Cronbach’s alpha was 0.93 for all 37 items. The Cronbach’s alphas for the six factors were 0.93, 0.91, 0.92, 0.92, 0.91, and 0.75, respectively. In our test/re-test of reliability, Spearman’s rank correlation coefficient between the first and second total scores was ρ = 0.96, p < 0.01. These results confirm the scale’s validity and reliability, and its applicability to older hospitalized patients

Human neutrophil peptide-1 promotes alcohol-induced hepatic fibrosis and hepatocyte apoptosis

<div><p>Background and aims</p><p>Neutrophil infiltration of the liver is a typical feature of alcoholic liver injury. Human neutrophil peptide (HNP)-1 is an antimicrobial peptide secreted by neutrophils. The aim of this study was to determine if HNP-1 affects ethanol-induced liver injury and to examine the mechanism of liver injury induced by HNP-1.</p><p>Methods</p><p>Transgenic (TG) mice expressing HNP-1 under the control of a β-actin-based promoter were established. Ethanol was orally administered to HNP-1 TG or wild-type C57BL/6N (WT) mice. SK-Hep1 hepatocellular carcinoma cells were used to investigate the effect of HNP-1 on hepatocytes <i>in vitro</i>.</p><p>Results</p><p>After 24 weeks of ethanol intake, hepatic fibrosis and hepatocyte apoptosis were significantly more severe in TG mice than in WT mice. Levels of CD14, TLR4, and IL-6 in liver tissues were higher in TG mice than in WT mice. Apoptosis was accompanied by higher protein levels of caspase-3, caspase-8, and cleaved PARP in liver tissue. In addition, phosphorylated ASK1, ASK1, phosphorylated JNK, JNK1, JNK2, Bax, Bak and Bim were all more abundant in TG mice than in WT mice. In contrast, the level of anti-apoptotic Bcl2 in the liver was significantly lower in TG mice than in WT mice. Analysis of microRNAs in liver tissue showed that miR-34a-5p expression was significantly higher in TG mice than in WT mice. Furthermore, in the presence of ethanol, HNP-1 increased the apoptosis with the decreased level of Bcl2 in a concentration-dependent manner <i>in vitro</i>.</p><p>Conclusions</p><p>HNP-1 secreted by neutrophils may exacerbate alcohol-induced hepatic fibrosis and hepatocyte apoptosis with a decrease in Bcl2 expression and an increase in miR-34a-5p expression.</p></div

Evaluation of apoptosis-related protein using Western blot analysis in liver tissue in the 24-week model.

<p>Results are shown as means ± SD Results are shown as means ± SD (<i>n</i> = 11 in TG mice and <i>n</i> = 6 in WT mice). <i>*P<0</i>.<i>05</i>, <i>**P<0</i>.<i>01</i>, <i>***P<0</i>.<i>001</i>.</p

Expression of F4/80, CD68, CD14 and toll-like receptor 4 in liver tissue.

<p>(A) Semi-quantification of positive cells for immunostaining using anti-F4/80 or anti-CD68 antibody. (B) Semi-quantification of CD14 and toll-like receptor 4 protein expression assessed by Western blot analysis. Results are shown as means ± SD (<i>n</i> = 11 in TG mice and <i>n</i> = 6 in WT mice). <i>*P<0</i>.<i>05</i>.</p

Apoptosis in human hepatic adenocarcinoma cell line SK-Hep-1 by ethanol and HNP-1 assessed by caspase 3/7 activity and DNA fragmentation.

<p>(A) Activity of caspase 3/7. (B) DNA fragmentation. <i>*P<0</i>.<i>05</i>, ^§A405 nm-A480 nm. Results are shown as means ± SD (<i>n</i> = 4 for each group).</p

Expression of α-smooth muscle actin in liver tissue.

<p>(A) Semi-quantification for positive area of immunostaining using anti-α-smooth muscle actin antibody in the 24-week model. (B) α-smooth muscle actin expression assessed by Western blot analysis. Results are shown as means ± SD (<i>n</i> = 11 in TG mice and <i>n</i> = 6 in WT mice). SMA, smooth muscle actin. <i>*P = 0</i>.<i>001</i>, <i>**P<0</i>.<i>05</i></p

NFκB and IL-6 expression in liver tissue.

<p>(A) Semi-quantification of positive cells for immunostaining using anti-NFκB-p65 antibody in the 8- and 24-week model. (B) Semi-quantification of the nuclear NFκB-p65 activities in liver tissue. (C) Protein levels of NFκB-p65 and interleukin-6 in liver tissue assessed by Western blot analysis. Results are shown as means ± SD (7 TG mice and 6 WT mice in the 8-week intake group, and 11 TG mice and 6 WT mice in the 24-week intake group). <i>*P<0</i>.<i>05</i>, <i>**P<0</i>.<i>01</i>, <i>***P<0</i>.<i>001</i>.</p

Expression of mRNA levels of Bcl2 and microRNA 34a-5p in the human hepatic adenocarcinoma cell line SK-Hep-1.

<p>(A) In the absence of ethanol. (B) In the presence of 100 mM ethanol. Results are shown as means ± SD (n = 4 for each group). <i>*P<0</i>.<i>05</i>, <i>**P<0</i>.<i>01</i>.</p