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Kim, Bung-Nyun,Kim, Jae-Won,Cummins, Tarrant D.R.,Bellgrove, Mark A.,Hawi, Ziarih,Hong, Soon-Beom,Yang, Young-Hui,Kim, Hyo-Jin,Shin, Min-Sup,Cho, Soo-Churl,Kim, Ji-Hoon,Son, Jung-Woo,Shin, Yun-Mi,Chun Lippincott Williams Wilkins, Inc. 2013 JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY Vol.33 No.3
ABSTRACT: Noradrenergic dysfunction may be associated with cognitive impairments in attention-deficit/hyperactivity disorder (ADHD), including increased response time variability, which has been proposed as a leading endophenotype for ADHD. The aim of this study was to examine the relationship between polymorphisms in the α-2A-adrenergic receptor (ADRA2A) and norepinephrine transporter (SLC6A2) genes and attentional performance in ADHD children before and after pharmacological treatment.One hundred one medication-naive ADHD children were included. All subjects were administered methylphenidate (MPH)–OROS for 12 weeks. The subjects underwent a computerized comprehensive attention test to measure the response time variability at baseline before MPH treatment and after 12 weeks. Additive regression analyses controlling for ADHD symptom severity, age, sex, IQ, and final dose of MPH examined the association between response time variability on the comprehensive attention test measures and allelic variations in single-nucleotide polymorphisms of the ADRA2A and SLC6A2 before and after MPH treatment.Increasing possession of an A allele at the G1287A polymorphism of SLC6A2 was significantly related to heightened response time variability at baseline in the sustained (P = 2.0 × 10) and auditory selective attention (P = 1.0 × 10) tasks. Response time variability at baseline increased additively with possession of the T allele at the DraI polymorphism of the ADRA2A gene in the auditory selective attention task (P = 2.0 × 10). After medication, increasing possession of a G allele at the MspI polymorphism of the ADRA2A gene was associated with increased MPH-related change in response time variability in the flanker task (P = 1.0 × 10).Our study suggested an association between norepinephrine gene variants and response time variability measured at baseline and after MPH treatment in children with ADHD. Our results add to a growing body of evidence, suggesting that response time variability is a viable endophenotype for ADHD and suggesting its utility as a surrogate end point for measuring stimulant response in pharmacogenetic studies.
Prediction Models for Suicide Attempts among Adolescents Using Machine Learning Techniques
Jae Seok Lim(Jae Seok Lim),Chan-Mo Yang(Chan-Mo Yang),Ju-Won Baek(Ju-Won Baek),Sang-Yeol Lee(Sang-Yeol Lee),Bung-Nyun Kim(Bung-Nyun Kim) 대한정신약물학회 2022 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.20 No.4
Objective: Suicide attempts (SAs) in adolescents are difficult to predict although it is a leading cause of death among adolescents. This study aimed to develop and evaluate SA prediction models based on six different machine learning (ML) algorithms for Korean adolescents using data from online surveys. Methods: Data were extracted from the 2011−2018 Korea Youth Risk Behavior Survey (KYRBS), an ongoing annual national survey. The participants comprised 468,482 nationally representative adolescents from 400 middle and 400 high schools, aged 12 to 18. The models were trained using several classic ML methods and then tested on internal and external independent datasets; performance metrics were calculated. Data analysis was performed from March 2020 to June 2020. Results: Among the 468,482 adolescents included in the analysis, 15,012 cases (3.2%) were identified as having made an SA. Three features (suicidal ideation, suicide planning, and grade) were identified as the most important predictors. The performance of the six ML models on the internal testing dataset was good, with both the area under the receiver operating characteristic curve (AUROC) and area under the precision−recall curve (AUPRC) ranging from 0.92 to 0.94. Although the AUROC of all models on the external testing dataset (2018 KYRBS) ranged from 0.93 to 0.95, the AUPRC of the models was approximately 0.5. Conclusion: The developed and validated SA prediction models can be applied to detect high risks of SA. This approach could facilitate early intervention in the suicide crisis and may ultimately contribute to suicide prevention for adolescents.
Atomoxetine and Fluoxetine Activate AMPK-ACC-CPT1 Pathway in Human SH-SY5Y and U-87 MG Cells
Songhee Jeon(Songhee Jeon),Jeong-Eun Park(Jeong-Eun Park),Young Ho Do(Young Ho Do),Renata Santos(Renata Santos ),Seong Mi Lee(Seong Mi Lee),Bung-Nyun Kim(Bung-Nyun Kim),Jae Hoon Cheong(Jae Hoon Cheong 대한신경정신의학회 2023 PSYCHIATRY INVESTIGATION Vol.20 No.3
Objective Atomoxetine and fluoxetine are psychopharmacologic agents associated with loss of appetite and weight. Adenosine monophosphate-activated protein kinase (AMPK) is the cellular energy sensor that regulate metabolism and energy, being activated by fasting and inhibited by feeding in the hypothalamus. Methods Human brain cell lines (SH-SY5Y and U-87 MG cells) were used to study the outcome of atomoxetine and fluoxetine treatment in the activity of AMPK-acetyl-CoA carboxylase (ACC)- carnitine palmitoyl transferase 1 (CPT1) pathway and upstream regulation by calcium/calmodulin-dependent kinase kinase β (CaMKKβ) using immunoblotting and CPT1 enzymatic activity measures. Results Phosphorylation of AMPK and ACC increased significantly after atomoxetine and fluoxetine treatment in the first 30-60 minutes of treatment in the two cell lines. Activation of AMPK and inhibition of ACC was associated with an increase by 5-fold of mitochondrial CPT1 activity. Although the neuronal isoform CPT1C could be detected by immunoblotting, activity was not changed by the drug treatments. In addition, the increase in phospho-AMPK and phospho-ACC expression induced by atomoxetine was abolished by treatment with STO-609, a CaMKKβ inhibitor, indicating that AMPK-ACC-CPT1 pathway is activated through CaMKKβ phosphorylation. Conclusion These findings indicate that at the cellular level atomoxetine and fluoxetine treatments may activate AMPK-ACC-CPT1 pathways through CaMKKβ in human SH-SY5Y and U-87 MG cells.