55 research outputs found
Smartphone viewing distance and sleep: an experimental study utilizing motion capture technology
No full textMichitaka Yoshimura,1,* Momoko Kitazawa,1–3,* Yasuhiro Maeda,2 Masaru Mimura,4 Kazuo Tsubota,1 Taishiro Kishimoto,4,5 1Department of Ophthalmology, Keio University School of Medicine, Tokyo, 2RIKEN Center for Advanced Photonics, Wako, Saitama, 3Department of Nursing, Aino University Junior College, 4Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan; 5Department of Psychiatry, Hofstra Northwell School of Medicine, NY, USA *These authors contributed equally to this work Abstract: There are studies reporting the negative impact of smartphone utilization on sleep. It is considered that reduction of melatonin secretion under the blue light exposure from smartphone displays is one of the causes. The viewing distance may cause sleep disturbance, because the viewing distance determines the screen illuminance and/or asthenopia. However, to date, there has been no study closely investigating the impact of viewing distance on sleep; therefore, we sought to determine the relationship between smartphone viewing distance and subjective sleep status. Twenty-three nursing students (mean age ± standard deviation of 19.7±3.1 years) participated in the study. Subjective sleep status was assessed using the Pittsburgh Sleep Quality Index, morningness–eveningness questionnaire, and the Epworth sleepiness scale. We used the distance between the head and the hand while holding a smartphone to measure the viewing distance while using smartphones in sitting and lying positions. The distance was calculated using the three-dimensional coordinates obtained by a noncontact motion-sensing device. The viewing distance of smartphones in the sitting position ranged from 13.3 to 32.9 cm among participants. In the lying position, it ranged from 9.9 to 21.3cm. The viewing distance was longer in the sitting position than in the lying position (mean ± standard deviation: 20.3±4.7 vs 16.4±2.7, respectively, P<0.01). We found that the short viewing distance in the lying position had a positive correlation to a poorer sleep state (R2=0.27, P<0.05), lower sleep efficiency (R2=0.35, P<0.05), and longer sleep latency (R2=0.38, P<0.05). Moreover, smartphone viewing distances in lying position correlated negatively with subjective sleep status. Therefore, when recommending ideal smartphone use in lying position, one should take into account the viewing distances. Keywords: smartphone, sleep, blue light, distanc
Changes in Subjective Sleep, Physical Condition, and Mental Health during the COVID-19 Pandemic: A Nationwide Survey in Japan
No full text This study aimed to investigate how people’s subjective health changed after the coronavirus disease 2019 (COVID-19) pandemic. This survey was conducted in May 2021 as a nationwide online self-reported survey in Japan. The respondents indicated how their sleep, physical condition, and mental state altered after the pandemic. Furthermore, they answered questionnaires about their intention to get vaccinated, the means of gathering information, etc. A logistic regression analysis was performed. Of the 2,573 responses, there was a decline of approximately 13.6%, 14.0%, and 23.8% in subjective sleep, physical condition, and mental health after the pandemic, respectively. The logistic regression analysis demonstrated that regarding sleep, the affected group was younger, got vaccinated against influenza annually, had lower income, experienced poor sleep quality in the past month, and had worse physical and psychiatric symptoms than before the pandemic. Concerning the physical condition, the affected group lived alone, witnessed deficient sleep quality in the past month, and had deteriorated mental health status than before the COVID-19 pandemic. In terms of mental status, the affected group was younger, females, had access to more sources of information, and experienced worse sleep and physical conditions than the unchanged or improved group (p < 0.05). Each group indicated an association with the background factors, confirming that the subjective sleep, physical condition, and mental state affected each other. From a preventive perspective, the results of this study suggested that factors such as youth, gender, sleep quality, pregnancy, reduced income, and greater access to information, may be necessary for physical and mental support. The above-mentioned factors should be considered in light of community life and approached accordingly
Two days’ sleep debt causes mood decline during resting state via diminished amygdala-prefrontal connectivity
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Effects of a sleep hygiene education program on children in a Japanese elementary school
No full textOur objective in this study was to evaluate the effects of a Sleep Hygiene Education Program (SHEP) on sleep quality in students aged 9 to 11 in a Japanese elementary school. In the SHEP we gave a 75-minute lecture to the students. Both before and after the program, we distributed sleep-related questionnaires to 110 students and then collected and analyzed them. Three items concerning sleep quality; 'Time of going to bed', 'Feeling upon waking up' and 'Who wakes you up ?' were statistically analyzed using McNemar's Test. The results showed that there was no significant change in the items 'Time of going to bed' and 'Who wakes you up ?' comparing before and after the program. However, the item 'Feeling upon waking up' showed a significant positive change after the program. These results suggest that SHEP has the potential for improving sleep quality even in young students.departmental bulletin pape
p66Shc has a pivotal function in impaired liver regeneration in aged mice by a redox-dependent mechanism
No full textLiver regeneration involves complicated processes and is affected by various patho-physiological conditions. The present study was designed to examine the molecular mechanisms underlying the aging-associated impairment of liver regeneration. Male C57BL/6J mice were used as young and aged mice (20 months old, respectively). These mice were subjected to 70% partial hepatectomy (PH). Liver regeneration and liver injury/stresses were evaluated chronologically after PH. Post-hepatectomy liver regeneration was markedly impaired in aged mice. Though the extent of hepatocyte proliferation in the regenerating liver was similar in aged and young mice, cell growth was absent in aged mice. Oxidative stress (OS) was observed immediately after hepatectomy, followed by marked apoptosis in aged mice. Signaling molecules regarding cell proliferation (MAPK, STAT-3, p46/52Shc) and anti-oxidation (catalase, SOD, Ref-1, GPx) were expressed/activated after hepatectomy in livers of both aged and young mice. Akt was not activated in aged-mouse liver, but its expression was similar to that in young mice. p66Shc, known as an age-/oxidant-associated protein, was strongly phosphorylated. By knocking-down p66Shc, the impairment of liver regeneration was normalized. OS immediately after hepatectomy induced subsequent liver injury (apoptosis), and deletion of p66Shc suppressed both OS and hepatocyte apoptosis in the regenerating liver of aged mice. Though we need additional data in other animal models to fully understand the mechanism, p66Shc may play a pivotal role in the impairment of liver regeneration in aged mice by triggering OS and subsequent apoptosis. The present data may provide a clue to understanding the mechanism underlying the association between aging and the impairment of liver regeneration
Mitochondrial delivery of Coenzyme Q(10) via systemic administration using a MITO-Porter prevents ischemia/reperfusion injury in the mouse liver
No full textWe herein report on a mitochondrial therapeutic effect based on the delivery of coenzyme Q(10) (CoQ(10)), an anti-oxidant, to in vivo mitochondria using a MITO-Porter, a liposome-based mitochondrial delivery system that functions via membrane fusion. To evaluate the effects, we used a mouse liver ischemia/reperfusion injury (I/R injury) model, in which mitochondrial reactive oxygen species are overexpressed. We packaged CoQ(10) in the lipid phase of a MITO-Porter and optimized the mitochondrial fusogenic activities to produce the CoQ(10)-MITO-Porter. A histological observation of the carriers in the liver by confocal laser scanning microscopy was done and the accumulation of the carrier labeled with a radio isotope in the liver confirmed that the CoQ(10)-MITO-Porter was delivered to liver mitochondria via systemic injection. These analytical results permitted us to optimize the compositions of the CoQ(10)-MITO-Porter so as to permit it to efficiently accumulate in mouse liver mitochondria. Finally, we applied the optimized CoQ(10) -MITO-Porter to mice via tail vein injection, and hepatic I/R injury was then induced, followed by measuring serum alanine aminotransferase (ALT) levels, a marker of liver injury. We confirmed that the use of the CoQ(10)-MITO-Porter resulted in a significant decrease in serum ALT levels, indicating that in vivo mitochondrial delivery of the CoQ(10) via MITO-Porter prevents I/R injury in mice livers. This provides a demonstration of the potential use of such a delivery system in mitochondrial therapies. (C) 2015 Elsevier B.V. All rights reserved
Extracts of bilberry (Vaccinium myrtillus L.) fruits improve liver steatosis and injury in mice by preventing lipid accumulation and cell death
No full textBilberry has been reported to have anti-oxidant and anti-inflammatory properties. We studied the effect of bilberry (Vaccinium myrtillus L.) fruits extracts (BEs) on the pathogenesis caused by lipid accumulation in fatty liver and non-alcoholic steatohepatitis (NASH). 5 mu g/ml of BEs was enough to suppress lipid accumulation in the fatty liver model of the mouse hepatic AML12 cells. BEs increased cell viability and anti-oxidant capacity, presumably by activating (phosphorylating) Akt/STAT3 and inducing MnSOD/catalase. BEs also significantly reduced Rubicon and induced p62/SQSTM1, possibly contributing to reduce cellular lipids (lipophagy). When the mice were fed supplemented with BEs (5% or 10%, w/w), hepatic steatosis, injury, and hypercholesterolemia/hyperglycemia were significantly improved. Furthermore, histological and cytokine studies indicated that BEs possibly suppress hepatic inflammation (hepatitis) and fibrosis. Therefore, BEs improved liver steatosis and injury, and potentially suppress fibrosis by suppressing inflammatory response, which therefore may prevent the progression of fatty liver to NASH
Poly(ADP-ribose) Polymerase (PARP) is Critically Involved in Liver Ischemia/Reperfusion-injury
No full textBackground: Poly(ADP-ribose) polymerase (PARP) is a DNA-repairing enzyme activated by extreme genomic stress, and therefore is potently activated in the remnant liver suffering from ischemia after surgical resection. However, the impact of PARP on post-ischemic liver injury has not been elucidated yet. Materials and methods: We investigated the impact of PARP on murine hepatocyte/liver injury induced by hypoxia/ischemia, respectively. Results: PJ34, a specific inhibitor of PARP, markedly protected against hypoxia/reoxygenation (H/R)-induced cell death, though z-VAD-fmk, a pan-caspase inhibitor similarly showed the protective effect. PJ34 did not affect H/R-induced caspase activity or caspase-mediated cell death. z-VAD-fmk also did not affect the production of PAR (i.e., PARP activity). Therefore, PARPand caspase-mediated cell death occurred in a mechanism independent of each other in H/R. H/R immediately induced activation of PARP and cell death afterwards, both of which were suppressed by PJ34 or Trolox, an antioxidant. This suggests that H/R-induced cell death occurred redox-dependently through PARP activation. H/R and OS induced nuclear translocation of apoptosis inducing factor (AIF, a marker of parthanatos) and RIP1-RIP3 interaction (a marker of necroptosis), both of which were suppressed by PJ34. H/R induced PARPmediated parthanatos and necroptosis redox-dependently. In mouse experiments, PJ34 significantly reduced serum levels of AST, ALT & LDH and areas of hepatic necrosis after liver ischemia/reperfusion, similar to z-VAD-fmk or Trolox. Conclusion: PARP, activated by ischemic damage and/or oxidative stress, may play a critical role in post-ischemic liver injury by inducing programmed necrosis (parthanatos and necroptosis). PARP inhibition may be one of the promising strategies against post-ischemic liver injury
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