Quality of life, depression, and productivity of city government employees in Japan : a comparison study using the Athens insomnia scale and insomnia severity index

Background:Insomnia has a high prevalence in modern society. Various tools have been developed to assess insomnia. We performed a direct comparison between the Insomnia Severity Index (ISI) and the Athens Insomnia Scale (AIS) in a Japanese population.Methods:A cross-sectional questionnaire-based study was conducted in September 2017 as part of the Night in Japan Home Sleep Monitoring Study. In addition to insomnia, assessed using the AIS and ISI, depression, sleepiness, quality of life, and work performance were assessed using the Patient Health Questionnaire (PHQ)-9, a Japanese version of the Epworth Sleepiness Scale, the Short Form-8 Health Survey Questionnaire (SF-8), and the World Health Organization Health and Work Performance Questionnaire, respectively. Receiver operating characteristic (ROC) curves were constructed to compare the outcomes of the AIS and the ISI.Results:A total of 1685 (81.9%) of all eligible employees were enrolled. The total scores of the AIS and ISI had a Pearson correlation coefficient (r) of 0.80 (p < 0.01). The area under the ROC curve for the AIS and ISI for the detection of depression (PHQ-9 ≥ 10) was 0.89 and 0.86, respectively. The prevalence of clinical insomnia (ISI ≥ 15) and definite insomnia (AIS ≥ 10) were 6.5 and 10.8%, respectively. Both the AIS and ISI showed a weak negative correlation with the physical component summary score of the SF-8 (r = − 0.37, p < 0.01 and r = − 0.32, p < 0.01, respectively) and absolute presenteeism (r = − 0.32, p < 0.01 and r = − 0.28, p < 0.01, respectively) and a moderate negative correlation with the mental component summary score of the SF-8 (r = − 0.53, p < 0.01 and r = − 0.43, p < 0.01, respectively).Conclusions:A strong positive correlation was found between the total scores of the AIS and ISI. Both the AIS and ISI were found to be associated with low physical and mental quality of life, depression, and productivity loss at work. Moreover, they had a moderate accuracy for detecting depression. Both the AIS and ISI may serve as useful screening tools for both insomnia and depression in the Japanese working population.Trial registration:UMIN-CTR (UMIN000028675, registered on 2017/8/15) and ClinicalTrials.gov (NCT03276585, registered on 2017/9/3)

AN AUTOPSY CASE OF SYSTEMIC AMYLOIDOSIS WITH MONOCLONAL GAMMOPATHY OF UNDETERMINED SIGNIFICANCE

A 56-year-old man had fever and cough ten days ago on death. He was admitted to hospital for increasing dyspnea. Acute interstitial pneumonia was suspected, and he was treated with steroid pulse and some symptomatic therapies, but finally he died of respiratory insufficiency. An autopsy study revealed amyloid deposition in the lungs, spleen，and other organs. Systemic amyloidosis was diagnosed. In serum preserved, he was diagnosed with monoclonal gammopathy of undetermined significance (MGUS

Protective role of podocyte autophagy against glomerular endothelial dysfunction in diabetes.

To examine the cell-protective role of podocyte autophagy against glomerular endothelial dysfunction in diabetes, we analyzed the renal phenotype of tamoxifen (TM)-inducible podocyte-specific Atg5-deficient (iPodo-Atg5-/-) mice with experimental endothelial dysfunction. In both control and iPodo-Atg5-/- mice, high fat diet (HFD) feeding induced glomerular endothelial damage characterized by decreased urinary nitric oxide (NO) excretion, collapsed endothelial fenestrae, and reduced endothelial glycocalyx. HFD-fed control mice showed slight albuminuria and nearly normal podocyte morphology. In contrast, HFD-fed iPodo-Atg5-/- mice developed massive albuminuria accompanied by severe podocyte injury that was observed predominantly in podocytes adjacent to damaged endothelial cells by scanning electron microscopy. Although podocyte-specific autophagy deficiency did not affect endothelial NO synthase deficiency-associated albuminuria, it markedly exacerbated albuminuria and severe podocyte morphological damage when the damage was induced by intravenous neuraminidase injection to remove glycocalyx from the endothelial surface. Furthermore, endoplasmic reticulum stress was accelerated in podocytes of iPodo-Atg5-/- mice stimulated with neuraminidase, and treatment with molecular chaperone tauroursodeoxycholic acid improved neuraminidase-induced severe albuminuria and podocyte injury. In conclusion, podocyte autophagy plays a renoprotective role against diabetes-related structural endothelial damage, providing an additional insight into the pathogenesis of massive proteinuria in diabetic nephropathy