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S¸ ü,heda Kaya,Filiz Ö,zsoy,Gü,lay Tas¸cı,Mehmet Kalaycı 대한신경정신의학회 2020 PSYCHIATRY INVESTIGATION Vol.17 No.9
Objective This study aims to investigate the levels of nesfatin-1-hormone in patients with Antisocial Personality Disorder (ASPD) and their relationship with clinical variables. Methods A total of 90 people (45 ASPD, 45 controls) were included in our study. Sociodemographic Data Form, Beck-Depression-Inventory (BDI), Beck-Anxiety-Inventory (BAI), Barratt Impulsivity Scale (BIS-11), Buss-Durkee-Hostility-Inventory (BDHI) were applied to all participants. Venous blood samples were taken from participants at the same time of the day when they were hungry. Results It was found that the BDI and BAI scores of the ASPD were higher than those of the controls (p<0.001, for both scales). The scores in BIS-11; motor and nonplanning-impulsivity subscales were higher than those of the controls (p<0.001, 0.036, respectively). The scores obtained by the ASPD were higher in all subscales of BDHI (p<0.001). For the nesfatin-1-hormone, the values of the ASPD were lower than those of the controls (p=0.044). No relationship was found between the nesfatin-1-hormone and any other laboratory parameters and applied scales (p>0.05). Conclusion This is the first study to examine the nesfatin-1-hormone levels in patients with any personality disorder. Further studies with more participants are needed in different types of personality disorders to understand the relationship between personality disorder and nesfatin-1-hormone levels.
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( Almira Aliyannissa ),( Rahmat Budi Kuswiyanto ),( Djatnika Setiabudi ),( Heda Melinda Nataprawira ),( Anggraini Alam ),( Nanan Sekarwana ) 대한신장학회 2020 Kidney Research and Clinical Practice Vol.39 No.1
Background: Studies on kidney complications in human immunodeficiency virus (HIV)-infected children are lacking. CD4 T lymphocytes are an important immune functions regulator and used as a basis for initiating antiretroviral therapy (ART) and monitoring disease progression. This study aims to determine the correlation between CD4 and estimated glomerular filtration rate (eGFR) or urine protein:creatinine ratio (uPCR) as markers of kidney complications. Methods: This cross sectional study was conducted on HIV-infected children aged 5 to 18 years who visited the Teratai HIV Clinic at Hasan Sadikin Hospital for monthly monitoring in June 2019. CD4 count, eGFR based on the Schwartz formula, and uPCR were obtained. Correlation analysis was performed with the Pearson test. Results: Subjects were 42 HIV-infected children, consisting of 23 males (54.8%) and 19 females (45.2%). Most children (65.0%) were in an advanced clinical stage and had been diagnosed with HIV for an average of 8 ± 3 years. All subjects had received ART, and six received tenofovir. Compliance to medications were good, and most subjects (79.0%) had normal nutritional status and CD4 count. All subjects had eGFR > 90 mL/min/1.73 ㎡, of which 21 (50.0%) were above normal value. Proteinuria was found in 12 patients (28.6%), and it was not significantly associated with clinical stages of HIV infection. CD4 count was correlated positively with eGFR (r = 0.473, P = 0.001) and negatively with uPCR (r = -0.284, P = 0.034). Conclusion: The degree of immunodeficiency appears to correlate with severity of renal injury. Screening at diagnosis and periodic monitoring of kidney functions are crucial in all childhood HIV patients.
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Potential role of orexin and sleep modulation in the pathogenesis of Alzheimer’s disease
Roh, Jee Hoon,Jiang, Hong,Finn, Mary Beth,Stewart, Floy R.,Mahan, Thomas E.,Cirrito, John R.,Heda, Ashish,Snider, B. Joy,Li, Mingjie,Yanagisawa, Masashi,de Lecea, Luis,Holtzman, David M. The Rockefeller University Press 2014 The Journal of experimental medicine Vol.211 No.13
<P>Age-related aggregation of amyloid-β (Aβ) is an upstream pathological event in Alzheimer’s disease (AD) pathogenesis, and it disrupts the sleep–wake cycle. The amount of sleep declines with aging and to a greater extent in AD. Poor sleep quality and insufficient amounts of sleep have been noted in humans with preclinical evidence of AD. However, how the amount and quality of sleep affects Aβ aggregation is not yet well understood. Orexins (hypocretins) initiate and maintain wakefulness, and loss of orexin-producing neurons causes narcolepsy. We tried to determine whether orexin release or secondary changes in sleep via orexin modulation affect Aβ pathology. Amyloid precursor protein (APP)/Presenilin 1 (PS1) transgenic mice, in which the orexin gene is knocked out, showed a marked decrease in the amount of Aβ pathology in the brain with an increase in sleep time. Focal overexpression of orexin in the hippocampus in APP/PS1 mice did not alter the total amount of sleep/wakefulness and the amount of Aβ pathology. In contrast, sleep deprivation or increasing wakefulness by rescue of orexinergic neurons in APP/PS1 mice lacking orexin increased the amount of Aβ pathology in the brain. Collectively, modulation of orexin and its effects on sleep appear to modulate Aβ pathology in the brain.</P>
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