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Insomnia in North Korean Refugees: Association with Depression and Post-Traumatic Stress Symptoms
YuJin G. Lee,JinYong Jun,YuJin Lee,Juhyun Park,Soohyun Kim,SoHee Lee,SoYoung Yu,SeogJu Kim 대한신경정신의학회 2016 PSYCHIATRY INVESTIGATION Vol.13 No.1
Objective-We investigated the prevalence of insomnia and its clinical characteristics in North Korean refugees. Methods-North Korean refugees living in South Korea (48 males, 129 females; mean age 38.22±12.24 years) and South Koreans (112 males, 203 females; mean age 39.48±10.32 years) completed the following questionnaires: the Self-reported Questionnaire on Insomnia, Center for Epidemiological Studies-Depression Scale (CES-D), Trauma Exposure Check List for North Korean Refugees, and the Impact of Event Scale-Revised (IES-R). Results-North Korean refugees had insomnia more often than South Koreans did (38.42% vs. 8.89%). Depression combined with insomnia was also more prevalent in North Korean refugees (28.25% vs. 3.17%). Compared with South Koreans with insomnia, North Korean refugees with insomnia showed higher CES-D scores. The North Korean refugees with insomnia had experienced a larger number of traumatic events, and had higher CES-D and IES-R scores compared to North Korean refugees without insomnia. Insomnia in North Korean refugees was also associated with the presence of significant depressive and post-traumatic stress disorder (PTSD) symptoms. Conclusion-Insomnia was common in North Korean refugees and was closely associated with depressive and PTSD symptoms. Our study suggests that complaints of insomnia may indicate more severe psychopathology, especially in refugees.
JongBae Choi,YuJin G. Lee,DoUn Jeong 대한신경정신의학회 2017 PSYCHIATRY INVESTIGATION Vol.14 No.4
Objective-The effect of transdermal nicotine patch on sleep physiology is not well established. The current study aimed to examine the influence of nicotine patch on homeostatic sleep propensity and autonomic nervous system. Methods-We studied 16 non-smoking young healthy volunteers with nocturnal polysomnography in a double blind crossover design between sleep with and without nicotine patch. We compared the sleep variables, sleep EEG power spectra, and heart rate variability. Results-The night with nicotine patch showed significant increase in sleep latency, wake after sleep onset, and stage 1 sleep; and decrease in total sleep time, sleep efficiency, and percentage of REM sleep. Also, spectral analysis of the sleep EEG in the night with nicotine patch revealed decreased slow wave activity in stage 2 and REM sleep and increased alpha activity in the first NREM-REM sleep cycle. Heart rate variability showed no differences between the 2 nights, but the low to high ratio (a parameter indicative of sympathetic nervous system activity) positively correlated with wake after sleep onset in night with nicotine patch. Conclusion-Transdermal nicotine patch significantly disrupts sleep continuity, sleep architecture, and homeostatic sleep propensity. The overactivation of the sympathetic nervous system may be responsible for these changes.
Mitochondrial chaperone HSP ‐60 regulates anti‐bacterial immunity via p38 MAP kinase signaling
Jeong, Dae‐,Eun,Lee, Dongyeop,Hwang, Sun‐,Young,Lee, Yujin,Lee, Jee‐,Eun,Seo, Mihwa,Hwang, Wooseon,Seo, Keunhee,Hwang, Ara B,Artan, Murat,Son, Heehwa G,Jo, Jay‐,Hyun,Baek, Haes Published for the European Molecular Biology Organ 2017 The EMBO journal Vol.36 No.8
<P>Mitochondria play key roles in cellular immunity. How mitochondria contribute to organismal immunity remains poorly understood. Here, we show that HSP-60/HSPD1, a major mitochondrial chaperone, boosts anti-bacterial immunity through the up-regulation of p38 MAP kinase signaling. We first identify 16 evolutionarily conserved mitochondrial components that affect the immunity of Caenorhabditis elegans against pathogenic Pseudomonas aeruginosa (PA14). Among them, the mitochondrial chaperone HSP-60 is necessary and sufficient to increase resistance to PA14. We show that HSP-60 in the intestine and neurons is crucial for the resistance to PA14. We then find that p38 MAP kinase signaling, an evolutionarily conserved anti-bacterial immune pathway, is down-regulated by genetic inhibition of hsp-60, and up-regulated by increased expression of hsp-60. Overexpression of HSPD1, the mammalian ortholog of hsp-60, increases p38 MAP kinase activity in human cells, suggesting an evolutionarily conserved mechanism. Further, cytosol-localized HSP-60 physically binds and stabilizes SEK-1/MAP kinase kinase 3, which in turn up-regulates p38 MAP kinase and increases immunity. Our study suggests that mitochondrial chaperones protect host eukaryotes from pathogenic bacteria by up-regulating cytosolic p38 MAPK signaling.</P>