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IQ: intelligence quotient; SES: socioeconomic status; LDES: Learning Disability Evaluation Scale; LQ: learning quotient; DHA: docosahexaenoic acid; AA: arachidonic acid. ; Abstract Objective The majority of studies on the associations between breastfeeding and cognitive functioning have focused on IQ, with only a few investigating learning skills, and none of the latter adjusting for maternal IQ. We examined the association between breastfeeding and learning abilities in school-aged children using a cross-sectional design. Methods We recruited 868 children, aged 8–11 years and parents completed the Learning Disability Evaluation Scale (LDES). Multivariable linear regression models were used and age, gender, area of residence, annual family income, maternal education, and maternal age at delivery, were included as covariates. Maternal IQ was added to further adjust for the effects of maternal cognitive ability. Path analysis was conducted to investigate the mediation effect of maternal IQ between breastfeeding and learning skills. Results Children who were ever-breastfed had higher learning quotient scores on the LDES (p = 0.001) as well as higher scores on subscales related to speaking (p = 0.001), reading (p = 0.005), writing (p = 0.004), spelling (p = 0.003), and mathematical calculation (p = 0.003) than the never-breastfed participants. All of these variables remained significant after adjusting for gestational and socioeconomic factors and for maternal IQ as covariates. The path analysis showed that breastfeeding had both indirect and direct effects on the learning quotient. Conclusions The results suggest that breastfeeding is positively associated with learning skills in school-aged children. ; This work was supported by the Eco-technopia 21 project of Korea Institute of Environmental Science and Technology (091-081-059) and by the National Research Foundation of Korea (NRF) Grant funded by the Korea government (MSIP) (No. 2015M3C7A1028926). The funding source had no role in the study's design, the collection, analysis, or interpretation of the data, the writing of the report, or in the decision to submit the paper for publication.

Background: Neurobiologic studies have suggested that dysregulation of central noradrenergic systems may be involved in the pathophysiology of attention deficit hyperactivity disorder (ADHD), and it has been hypothesized that genetic changes in the norepinephrine pathways might contribute to dysfunction of the prefrontal cortex circuits in ADHD. We previously reported decreased cerebral blood flow in the right lateral prefrontal cortex and both orbitofrontal cortices in children with ADHD. Genetic investigations have shown that the alpha-2A-adrenergic receptor gene (ADRA2A) is associated with ADHD. Our aim was to examine whether the presence of a risk allele of the ADRA2A MspI polymorphism is associated with differences in regional cerebral blood flow in boys with ADHD. Methods: We recruited 21 Korean boys with ADHD (mean age 9.9, standard deviation [SD] 2.7 yr) and 11 age-and sex-matched controls (mean age 10.6 [SD 2.1] yr). Each participant underwent technetium-99m-hexamethylpropylene amine oxime ((99m)Tc-HMPAO) single-photon emission computed tomography. We performed image analyses with voxel-wise t statistics using SPM2. Results: We found regional hypoperfusion in the prefrontal regions, including the right orbitofrontal and right medial gyri, and the bilateral putamen and cerebellum in boys with ADHD relative to controls (p < 0.0005, uncorrected for multiple comparisons). Boys with ADHD who carried the C allele (n = 13) at the ADRA2A MspI polymorphism had reduced perfusion in the bilateral orbitofrontal regions compared with those without the C allele (n = 8) (p < 0.0005, uncorrected for multiple comparisons). Limitations: This study was limited by the small sample size, and we did not obtain genetic data from the controls. Conclusion: Our findings suggest that regional differences in cerebral perfusion in the orbitofrontal cortex represent an intermediate neuroimaging phenotype associated with the ADRA2A MspI polymorphism; these data support the validity of the noradrenergic hypothesis regarding the pathophysiology of ADHD. ; This work was supported by the Korea Research Foundation Grant funded by the Korean Government (KRF- 2006–003-E00192). ; Varghese GI, 2009, BRAIN, V132, P2102, DOI 10.1093/brain/awp027 ; May A, 2009, NAT REV NEUROL, V5, P199, DOI 10.1038/nrneurol.2009.28 ; Makris N, 2009, DEV NEUROSCI-BASEL, V31, P36, DOI 10.1159/000207492 ; Cho SC, 2008, AM J MED GENET B, V147B, P957, DOI 10.1002/ajmg.b.30725 ; Durston S, 2008, DEV PSYCHOPATHOL, V20, P1133, DOI 10.1017/S0954579408000539 ; Prince J, 2008, J CLIN PSYCHOPHARM, V28, pS39, DOI 10.1097/JCP.0b013e318174f92a ; Brennan AR, 2008, ANN NY ACAD SCI, V1129, P236, DOI 10.1196/annals.1417.007 ; Wang M, 2007, CELL, V129, P397, DOI 10.1016/j.cell.2007.03.015 ; Arnsten AFT, 2006, NEUROPSYCHOPHARMACOL, V31, P2376, DOI 10.1038/sj.npp.1301164 ; Dickstein SG, 2006, J CHILD PSYCHOL PSYC, V47, P1051, DOI 10.1111/j.1469-7610.2006.01671.x ; Krain AL, 2006, CLIN PSYCHOL REV, V26, P433, DOI 10.1016/j.cpr.2006.01.005 ; Wang B, 2006, AM J MED GENET B, V141B, P130, DOI 10.1002/ajmg.b.30258 ; Waldman ID, 2006, COGN AFFECT BEHAV NE, V6, P18 ; Biederman J, 2005, LANCET, V366, P237 ; Bush G, 2005, BIOL PSYCHIAT, V57, P1273, DOI 10.1016/j.biopsych.2005.01.034 ; Madras BK, 2005, BIOL PSYCHIAT, V57, P1397, DOI 10.1016/j.biopsych.2004.10.011 ; Park L, 2005, MOL PSYCHIATR, V10, P572, DOI 10.1038/sj.mp.4001605 ; Sawyer SL, 2005, EUR J HUM GENET, V13, P677, DOI 10.1038/sj.ejhg.5201368 ; Lee JS, 2005, HUM BRAIN MAPP, V24, P157, DOI 10.1002/hbm.20067 ; Bobb AJ, 2005, AM J MED GENET B, V132B, P109, DOI 10.1002/ajmg.b.30086 ; Szobot C, 2005, AM J MED GENET B, V132B, P53, DOI 10.1002/ajmg.b.30096 ; Belfer I, 2005, J HUM GENET, V50, P12, DOI 10.1007/s10038-004-0211-y ; Kim YS, 2004, YONSEI MED J, V45, P81 ; Kim BN, 2002, EUR ARCH PSY CLIN N, V252, P219, DOI 10.1007/s00406-002-0384-3 ; PARK KS, 2002, KOREAN ED DEV I WECH ; Peyron R, 2000, NEUROPHYSIOL CLIN, V30, P263 ; Avery RA, 2000, NEUROPSYCHOPHARMACOL, V23, P240 ; Mao ZM, 1999, BIOL PSYCHIAT, V46, P1259 ; Jakala P, 1999, NEUROPSYCHOPHARMACOL, V20, P460 ; Berquin PC, 1998, NEUROLOGY, V50, P1087 ; May A, 1998, PAIN, V74, P61 ; Kaufman J, 1997, J AM ACAD CHILD PSY, V36, P980 ; Smalley SL, 1997, AM J HUM GENET, V60, P1276 ; Allen G, 1997, SCIENCE, V275, P1940 ; Lario S, 1997, CLIN GENET, V51, P129 ; AMEN DG, 1997, ANN CLIN PSYCHIAT, V9, P81 ; Arnsten AFT, 1996, ARCH GEN PSYCHIAT, V53, P448 ; HARVEY AS, 1993, EPILEPSIA, V34, P869 ; ZAMETKIN AJ, 1993, ARCH GEN PSYCHIAT, V50, P333 ; ARNSTEN AFT, 1988, J NEUROSCI, V8, P4287 ; HOEHE MR, 1988, NUCLEIC ACIDS RES, V16, P9070 ; TALAIRACH J, 1988, COPLANAR STEREOTAXIC ; CHANG LT, 1978, IEEE T NUCL SCI, V25, P638 ; 1

The first of its kind, this book helps readers better understand Korean American mental health issues and their ongoing implications. The editors offer culturally competent practices, program developments, and policies that will better address the Korean Americans who are dealing with mental health issues.

Background: The orbitofrontal cortex (OFC) has consistently been implicated in the pathology of both drug and behavioral addictions. However, no study to date has examined OFC thickness in internet addiction. In the current study, we investigated the existence of differences in cortical thickness of the OFC in adolescents with internet addiction. On the basis of recently proposed theoretical models of addiction, we predicted a reduction of thickness in the OFC of internet addicted individuals.Findings: Participants were 15 male adolescents diagnosed as having internet addiction and 15 male healthy comparison subjects. Brain magnetic resonance images were acquired on a 3T MRI and group differences in cortical thickness were analyzed using FreeSurfer. Our results confirmed that male adolescents with internet addiction have significantly decreased cortical thickness in the right lateral OFC (p<0.05).Conclusion: This finding supports the view that the OFC alterations in adolescents with internet addiction reflect a shared neurobiological marker of addiction-related disorders in general. ; This work was supported by the Seoul National University Brain Fusion Program Research Fund. SBH was supported by a National Research Foundation of Korea (NRF) grant (Global Internship Program) funded by the Korean government (MEST). MY was supported by an NHMRC fellowship grant (#1021973). ; OAIID:oai:osos.snu.ac.kr:snu2013-01/102/0000003446/2 ; SEQ:2 ; PERF_CD:SNU2013-01 ; EVAL_ITEM_CD:102 ; USER_ID:0000003446 ; ADJUST_YN:Y ; EMP_ID:A072419 ; DEPT_CD:701 ; CITE_RATE:2.127 ; FILENAME:첨부된 내역이 없습니다. ; DEPT_NM:교육학과 ; EMAIL:cdkim@snu.ac.kr ; SCOPUS_YN:Y ; CONFIRM:Y

To determine the association between arginine vasopressin receptor 1A gene (AVPR1A)and autism spectrum disorders (ASDs), we examined 3 single nucleotide polymorphisms (SNPs), namely, rs7294536, rs3759292, and rs10877969, in the promoter region of AVPR1A by using a family-based association test (FBAT) in 151 Korean trios. Our results demonstrated a statistically significant association between autism and SNPs (additive model: rs7294536, chi(2)=9.328, df=2, P=0.002: rs10877969, chi(2)=11.529, df=2, P<0.001) as well as between autism and haplotype analysis (additive model: chi(2)=14.122, df=3,P=0.003). In addition, we found that ADI-R scores calculated by using a diagnostic algorithm for failure to develop peer relationships (A2) were higher in subjects having the AA genotype than in subjects having the AG and GG genotypes of rs7294536. Thus, our study provides evidence for a possible association between these SNPs and the phenotype of ASDs. (C) 2010 Elsevier Ireland Ltd. All rights reserved. ; This study was supported by grants from the Korea Healthcare Technology R&D Project, Ministry of Health &Welfare, Republic of Korea (A080651) and the Korea Research Foundation Grant funded by the Korean Government (MOEHRD, Basic Research Promotion Fund) (KRF-2008-331-C00226). ; Yang SY, 2010, PSYCHIAT RES, V178, P199, DOI 10.1016/j.psychres.2009.11.007 ; Nicholas JS, 2009, ANN EPIDEMIOL, V19, P808, DOI 10.1016/j.annepidem.2009.04.005 ; Levin R, 2009, PSYCHONEUROENDOCRINO, V34, P901, DOI 10.1016/j.psyneuen.2008.12.014 ; Baron-Cohen S, 2009, BRIT J PSYCHIAT, V194, P500, DOI 10.1192/bjp.bp.108.059345 ; Bora E, 2009, CURR OPIN PSYCHIATR, V22, P320, DOI 10.1097/YCO.0b013e328329e970 ; Yoo HJ, 2009, NEUROSCI RES, V63, P172, DOI 10.1016/j.neures.2008.11.007 ; Walum H, 2008, P NATL ACAD SCI USA, V105, P14153, DOI 10.1073/pnas.0803081105 ; Yoo HJ, 2008, NEUROSCI RES, V62, P66, DOI 10.1016/j.neures.2008.05.008 ; Chen J, 2008, EXP NEUROL, V211, P529, DOI 10.1016/j.expneurol.2008.02.023 ; Pardo CA, 2007, BRAIN PATHOL, V17, P434, DOI 10.1111/j.1750-3639.2007.00102.x ; Kim SA, 2007, NEUROSCI RES, V58, P332, DOI 10.1016/j.neures.2007.03.002 ; Ma DQ, 2007, MOL PSYCHIATR, V12, P376, DOI 10.1038/sj.mp.4001927 ; Cho IH, 2007, BRAIN RES, V1139, P34, DOI 10.1016/j.brainres.2007.01.002 ; YOO HJ, 2007, KOREAN VERSION AUTIS ; PRICHARD ZM, 2007, HUM MUTAT, V28, P1150 ; KNAFO A, 2007, GENES BRAIN BEHAV, V7, P266 ; Persico AM, 2006, TRENDS NEUROSCI, V29, P349, DOI 10.1016/j.tins.2006.05.010 ; Yirmiya N, 2006, MOL PSYCHIATR, V11, P488, DOI 10.1038/sj.mp.4001812 ; EGASHIRA N, 2006, NIHON SHINKEI SEISHI, V26, P101 ; Hammock EAD, 2005, GENES BRAIN BEHAV, V4, P289 ; Hammock EAD, 2005, SCIENCE, V308, P1630, DOI 10.1126/science.1111427 ; Wassink TH, 2004, MOL PSYCHIATR, V9, P968, DOI 10.1038/sj.mp.4001503 ; Kim SJ, 2002, MOL PSYCHIATR, V7, P503, DOI 10.1038/sj.mp.4001125 ; Chevaleyre V, 2002, J NEUROSCI, V22, P265 ; Folstein SE, 2001, NAT REV GENET, V2, P943 ; Son MC, 2001, NEUROBIOL LEARN MEM, V76, P388, DOI 10.1006/nlme.2001.4020 ; Horvath S, 2001, EUR J HUM GENET, V9, P301 ; Hurbin A, 1998, ENDOCRINOLOGY, V139, P4701 ; QIAO LY, 1998, ZHONGGUO YAO LI XUE, V19, P15 ; BAILEY A, 1995, PSYCHOL MED, V25, P63 ; *ASS AM PSYCH, 1994, DIAGN STAT MAN MENT ; VANDENHOOFF P, 1989, BRAIN RES, V505, P181 ; 3