Copycat Suicide Induced by Entertainment Celebrity Suicides in South Korea

SooAh Jang,JiMin Sung,JinYoung Park,WooTaek Jeon 대한신경정신의학회 2016 PSYCHIATRY INVESTIGATION Vol.13 No.1

Objective-Throughout the past several years, there have been a number of entertainment celebrity suicides in South Korea. The aim of this study was to investigate the clustering of suicides following celebrities’ suicides in South Korea from 2005 to 2008, particularly according to certain characteristics. Methods-Seven celebrity suicides were examined and defined using the Korean Integrated Newspaper Database System (KINDS) and from these, we considered four affected periods occurring 28 days after each celebrity’s suicide. A Poisson time-series autoregression model was used to estimate the relative risk of the total suicide number for each affected period from 2005 to 2008. Logistic regression analysis was performed to investigate whether there were specific increases in the numbers of suicides in subgroups matching each celebrity. Results-There were significant increases in the risk of suicide during the affected periods. Remarkable increases were found in the subgroups matching each celebrity, especially in the group in which all factors (sex, age, and method) were similar. Conclusion-This study provides confirmation that a significant copycat effect was induced by these celebrities’ suicides, especially among people who identified more with the celebrities. This implies that countermeasures for upright media coverage of celebrity suicides should be discussed and practiced properly in South Korea.

Long-Term Culture of Organotypic Hippocampal Slice from Old 3xTg-AD Mouse: An ex vivo Model of Alzheimer’s Disease

Sooah Jang,Hyunjeong Kim,Hyejin Kim,SuKyoung Lee,EunWoo Kim,KeeNam koong,Eosu Kim 대한신경정신의학회 2018 PSYCHIATRY INVESTIGATION Vol.15 No.2

Objective-Conventional methods for organotypic hippocampal tissue slice culture (OHSC) have shown several disadvantages or limitations regarding age of animals used, duration of culture and difficulty using neurodegenerative models. Therefore, we tried to establish OHSC from old 3xTg-Alzheimer’s disease (AD) mice for longer period (over 4 weeks) and to validate utility of this system as a valid platform for translational neuroscience of AD. Methods-OHSC was performed with old 3xTg-AD mice (12-14 months), old wild type mice (12-14 months) and young 3xTg-AD mice (2-4 months) using serum-free medium for 4 weeks. Hippocampal structure was evaluated by 4’, 6-diamidino-2-phenylindole (DAPI) intensity and neuronal metabolism was measured by Alamarblue assay. Pathologic characteristics of AD were also investigated; β-amyloid levels by ELISA, amyloid plaque deposition by Thioflavin-S staining, and glial activation by immunohistochemistry. Results-Following 4-week culture in serum-free media, hippocampal cells and layers were well preserved in cultured slices from old AD mice as was in those from young AD and old wild type mice. On the contrary, excessive regression of total visible cells was observed in conventional serum-containing medium regardless of genotype of mice. In parallel with this well preserved structure, major pathologic characteristics of AD were also well manifested in hippocampal slices from old AD mice. Conclusion-Our findings suggest that long-term OHSC from old 3xTg-AD mouse can serve as a promising ex vivo system for studies on pathophysiology of AD, especially with the minimum number of sacrifice of experimental animals.

Suppression of AIMP1 protects cognition in Alzheimer’s disease model mice 3xTg-AD

Jang, Sooah,Lee, Jung Ho,Sohn, Bo Kyung,Kim, Eosu,Park, Sang Gyu,Yoon, Kang Jun,Park, Minsun,Kim, Eun Woo,Jeong, Jihyeon,Lee, Jun-Young,Kim, Chul Hoon,Namkoong, Kee Wolters Kluwer Health | Lippincott Williams Wilkin 2017 NEUROREPORT - Vol.28 No.2

<P>Neuroinflammation has been raised as a candidate of unifying pathogenesis and a target of a disease-modifying strategy for Alzheimer's disease (AD). Aminoacyl-tRNA synthetase complex (ARS)-interacting multifunctional protein 1 (AIMP1) is a cytokine that is known to amplify the actions of tumor necrosis factor-a and to be involved in microglial activation and neuronal death. In this respect, AIMP1 could be a plausible target for the treatment of AD. Therefore, we aimed to examine whether anti-AIMP1 antibody could exert therapeutic effects against cognitive impairment using 3xTg-AD mice. Through the passive avoidance test, we found that an intraperitoneal injection of anti-AIMP1 antibody over 4 weeks was effective in protecting memory function in 3xTg-AD mice (16 weeks old). In addition, to address the translational implications of AIMP1, we measured blood AIMP1 levels in patients with AD (n=22), mild cognitive impairment (n=25), and normal cognition (n=23). Blood AIMP1 levels were associated negatively with global cognitive function and were significantly higher in individuals with a higher degree of medial temporal lobe atrophy, which is one of the representative clinical markers of AD. Our results suggested a possible association of AIMP1 with AD pathogenesis, as well as the potential of the anti-AIMP1 antibody as a novel therapeutic option for AD. Copyright (C) 2017 Wolters Kluwer Health, Inc. All rights reserved.</P>

Particulate matter increases beta-amyloid and activated glial cells in hippocampal tissues of transgenic Alzheimer's mouse: Involvement of PARP-1

Jang, Sooah,Kim, Eun Woo,Zhang, Yinhua,Lee, Jimin,Cho, So Yeon,Ha, Junghee,Kim, Hyunjeong,Kim, Eosu Elsevier 2018 Biochemical and biophysical research communication Vol.500 No.2

<P><B>Abstract</B></P> <P>Exposure to air pollutants, such as particulate matter (PM), has been implicated in neurodegenerative disorders including Alzheimer's disease (AD). However, direct effects of PM on production of β-amyloid (Aβ), a key pathogenic molecule in AD, and its underlying mechanism are still elusive. Given PM's potential to induce oxidative stress in other tissues, we hypothesized that poly(ADP-ribose) polymerase (PARP-1) might be involved in PM-induced neurotoxicity. To address this, we used an <I>ex vivo</I> model of AD, the organotypic hippocampal slice tissue culture from old (12-14 months-of-age) triple transgenic 3xTg-AD mice. First, we observed that fine PM (aerodynamic diameter < 4 μm) can dose-dependently activate PARP-1 and decrease NAD<SUP>+</SUP> levels in Neuro2A cells. PARP-1 activation did occur under concentrations of PM which did not affect cell viability. Next, we observed that direct treatment of PM increased Aβ levels and activated glial cells in the <I>ex vivo</I> hippocampal tissues of 3xTg-AD mice. PM-induced glial activation was most prominent in CA1 region of the hippocampal tissue. Notably, we found that pharmacological inhibition of PARP-1 reversed both PM-induced Aβ increase and glial activation, arguing the possible involvement of PARP-1 in PM-induced AD pathogenesis. Our findings suggest that PARP-1 might be a potential molecular target, responsible for mediating negative effects of PM on the brain. Modulating PARP-1 activity could be a promising approach to prevent or alleviate PM-related environmental neurotoxicity which could initiate AD pathogenesis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Particulate matter (PM) activates PARP-1 in neuronal cells. </LI> <LI> PM increases beta-amyloid in <I>ex vivo</I> hippocampus of 3xTg-AD mouse. </LI> <LI> PM activates glial cells in <I>ex vivo</I> hippocampus of 3xTg-AD mouse. </LI> <LI> Pharmacological inhibition of PARP-1 reverses PM-induced AD pathologies. </LI> <LI> PARP-1 inhibition would be a promising approach counteracting PM's neurotoxicity. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Exploratory Clinical Trial of a Depression Diagnostic Software That Integrates Stress Biomarkers and Composite Psychometrics

Sooah Jang,In-Young Kim,Sun-Woo Choi,Anna Lee,Ju-Yeal Lee,Hyunkyung Shin,Junwoo Lee,Mikyeong Lee,Kyoung-Ryul Lee,Saeeun Jung,Jin Sun Ryu,Jihee Oh,Manjae Kwon,Joohan Kim,Ryunsup Ahn,Young-Chul Jung,Jeo 대한신경정신의학회 2024 PSYCHIATRY INVESTIGATION Vol.21 No.3

Objective This study evaluated the clinical effectiveness of Minds.NAVI, a depression screening kit combining psychometric measures and stress hormone biomarkers, in a prospective clinical trial. The objective was to assess its potential as a depression screening tool and investigate the associations between psychological assessments, salivary hormone staging, and depression severity.Methods Thirty-five participants with major depressive disorder and 12 healthy controls (HCs) were included. The Minds.NAVI software, utilizing the PROtective and Vulnerable factors battEry Test (PROVE) and salivary cortisol/dehydroepiandrosterone (DHEA) analysis, was employed. The PROVE test is a comprehensive self-report questionnaire that assesses depressive symptoms, suicide risk, attachment style, adverse childhood experiences, mentalization capacity, and resilience. In addition, salivary cortisol and DHEA levels were measured to evaluate the functional stage of the hypothalamic–pituitary–adrenal (HPA) axis.Results Minds.NAVI exhibited 100% sensitivity, 91.7% specificity, and 97.9% accuracy in distinguishing depression from HCs within an exploratory small group. Salivary stress hormone phases showed changes with depression stage (p=0.030), and the proportion of patients with “adrenal exhaustion stage” was higher in the moderate/severe depression group (p=0.038). Protective/vulnerable factors differed significantly between controls and depressed groups (p<0.001). Cortisol awakening response inversely correlated with depressive symptom severity (r=-0.31, p=0.034).Conclusion This study suggested possible clinical effectiveness of Minds.NAVI, a depression screening tool that integrates psychometric measures and stress hormone biomarkers. The findings support the potential association between depression, chronic stress, and HPA axis hyporesponsiveness.

국가 난제 해결을 위한 과학기술 관점의 경제・사회 시스템 혁신전략 연구 (3차년도) - 제3권: 재난안전관리 -

장진규(JinGyu Jang),손수아(SooAh Sohn) 과학기술정책연구원 2021 정책연구 Vol.- No.-