<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mimura, M.</style></author><author><style face="normal" font="default" size="100%">Hoeft, F.</style></author><author><style face="normal" font="default" size="100%">Kato, M.</style></author><author><style face="normal" font="default" size="100%">Kobayashi, N.</style></author><author><style face="normal" font="default" size="100%">Sheau, K.</style></author><author><style face="normal" font="default" size="100%">Piggot, J.</style></author><author><style face="normal" font="default" size="100%">Mills, D.</style></author><author><style face="normal" font="default" size="100%">Galaburda, A.</style></author><author><style face="normal" font="default" size="100%">Korenberg, J. R.</style></author><author><style face="normal" font="default" size="100%">Bellugi, U.</style></author><author><style face="normal" font="default" size="100%">Reiss, A. L.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A preliminary study of orbitofrontal activation and hypersociability in Williams Syndrome</style></title><secondary-title><style face="normal" font="default" size="100%">J Neurodev Disord</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Journal of neurodevelopmental disorders</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">Jan 26</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21304831</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">2</style></number><edition><style face="normal" font="default" size="100%">2011/02/10</style></edition><volume><style face="normal" font="default" size="100%">2</style></volume><pages><style face="normal" font="default" size="100%">93-98</style></pages><isbn><style face="normal" font="default" size="100%">1866-1955 (Electronic)18</style></isbn><language><style face="normal" font="default" size="100%">Eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Individuals with Williams syndrome (WS) demonstrate an abnormally positive social bias. However, the neural substrates of this hypersociability, i.e., positive attribution bias and increased drive toward social interaction, have not fully been elucidated. METHODS: We performed an event-related functional magnetic resonance imaging study while individuals with WS and typically developing controls (TD) matched positive and negative emotional faces. WS compared to TD showed reduced right amygdala activation during presentation of negative faces, as in the previous literature. In addition, WS showed a unique pattern of right orbitofrontal cortex activation. While TD showed medial orbitofrontal cortex activation in response to positive, and lateral orbitofrontal cortex activation to negative, WS showed the opposite pattern. In light of the general notion of a medial/lateral gradient of reward/punishment processing in the orbitofrontal cortex, these findings provide an additional biological explanation for, or correlate of positive attribution bias and hypersociability in WS.&lt;/p&gt;</style></abstract><notes><style face="normal" font="default" size="100%">&lt;p&gt;&lt;span role=&quot;menubar&quot;&gt;J Neurodev Disord.&lt;/span&gt;&amp;nbsp;2010 Jan 26;2(2):93-98.&lt;/p&gt;</style></notes><custom2><style face="normal" font="default" size="100%">3034146</style></custom2><auth-address><style face="normal" font="default" size="100%">Department of Neuropsychiatry, Showa University School of Medicine, Tokyo, Japan; Center for Interdisciplinary Brain Sciences Research (CIBSR), Stanford University, School of Medicine, Stanford, CA, USA.</style></auth-address></record></records></xml>