The Japanese Workplace PERMA-Profiler: A validation study among Japanese workers.

OBJECTIVES: Although well-being at work is important for occupational health, multi-dimensional workplace well-being measures do not exist for Japanese workers. The purpose of this study was to investigate the validity of the Japanese version of the Workplace PERMA-Profiler. METHODS: Japanese workers completed online surveys at baseline (N = 310) and 1 month later (N = 100). The Workplace PERMA-Profiler was translated according to international guidelines. Job and life satisfaction, work engagement, psychological distress, work-related psychosocial factors, and work performance were measured as comparisons for convergent validity. Cronbach's alphas, Intra-class Correlation Coefficients (ICCs), and measurement errors were calculated for the reliability, and the validity of the measure was tested by correlational analyses and confirmatory factor analysis. RESULTS: A total of 310 (baseline) and 86 (follow-up) workers responded and were included in the analyses. Cronbach's alphas and ICCs of the Japanese Workplace PERMA-Profiler ranged from 0.75 to 0.96. Confirmatory factor analysis indicated that the 5-factor model demonstrated a marginally acceptable fit (χ2 (80) = 351.30, CFI = 0.892, TLI = 0.858, RMSEA = 0.105, SRMR = 0.051). Overall well-being and the five PERMA domains had moderate-to-strong correlations with job satisfaction, psychological distress (inversely), and work-related factors. CONCLUSIONS: The Japanese version of the Workplace PERMA-Profiler demonstrated adequate reliability and validity. This measure could be useful to assess well-being at work, promote well-being research among Japanese workers, and address the problem of definition for well-being in further studies.

The role of renal sympathetic nervous system in the pathogenesis of ischemic acute renal failure.

We investigated the role of renal sympathetic nervous system in the progression of ischemia/reperfusion-induced acute renal failure in rats. Acute renal failure was induced by clamping the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after the contralateral nephrectomy. Renal venous plasma norepinephrine concentrations markedly and significantly increased immediately after reperfusion, thereafter, the increased level declined but remained higher even at 24 h after reperfusion. Renal sympathetic nerve activity was significantly augmented during the renal ischemia. Renal denervation or the administration of pentolinium, a ganglion blocking agent, (5 mg/kg i.v.) at 5 min before ischemia attenuated the ischemia/reperfusion-induced renal dysfunction and histological damage, such as proteinaceous casts in tubuli and tubular necrosis. The elevation of renal venous norepinephrine levels after reperfusion was suppressed by renal denervation or pentolinium treatment. Thus, a surgical or pharmacological blockade of renal sympathetic nerve prevents the progression of ischemia/reperfusion-induced acute renal failure, thereby suggesting that renal sympathetic nervous system plays an important role in the development of the ischemic acute renal failure.

Preventive effect of L-carnosine on ischemia/reperfusion-induced acute renal failure in rats.

We investigated the effect of L-carnosine (beta-alanyl-L-histidine) on ischemic acute renal failure in rats. Ischemic acute renal failure was induced by occlusion of the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function in untreated acute renal failure rats markedly decreased at 1 day after reperfusion. Pre-ischemic treatment with L-carnosine dose-dependently (1, 10 microg/kg, i.v.) attenuated the ischemia/reperfusion-induced renal dysfunction. Histopathological examination of the kidney of untreated acute renal failure rats revealed severe renal damage, which was significantly suppressed by pre-treatment with L-carnosine, at each dose given. In untreated acute renal failure rats, norepinephrine concentrations in renal venous plasma remarkably increased within 2 min after reperfusion and thereafter rapidly decreased. Pre-ischemic treatment with L-carnosine at a dose of 10 microg/kg significantly depressed the elevated norepinephrine level. On the other hand, although the higher dose of L-carnosine given 5 min after reperfusion tended to ameliorate the renal dysfunction after reperfusion, the improvement was moderate compared with those seen in pre-ischemic treatment. These results indicate that L-carnosine prevents the development of ischemia/reperfusion-induced renal injury, and the effect is accompanied by suppression of the enhanced norepinephrine release in the kidney immediately after reperfusion. Thus, the preventing effect of L-carnosine on ischemic acute renal failure is probably through the suppression of enhanced renal sympathetic nerve activity induced by ischemia/reperfusion.