This study examined whether children with symptoms of attention-deficit/hyperactivity disorder (ADHD) demonstrate positive illusory perceptions of their own competence and others' competence. Participants (67 children with ADHD symptoms; 40 non-ADHD children) completed the Self-Perception Profile for Children and rated actors' competence in videos clips where inconsistent cues of performance had to be integrated in order to determine the actor's competence. Teachers completed the Teacher Rating Scale of Child's Actual Behavior. Children with ADHD symptoms overestimated their own competence relative to teachers' estimates in all domains significantly more than non-ADHD children. There were no significant group differences in perceptions of others' competence. Findings suggest that positive illusions are exclusive to perceptions of self and do not extend to perceptions of others.

We investigated whether symptoms of attention-deficit/hyperactivity disorder (ADHD) are pathways through which deficits in inhibition and working memory are associated with teacher- and parent-rated social impairment in children. Participants were 64 children (55% males; 53% with ADHD) in grades 3-6. Consistent with our hypotheses, the association between inhibition and social impairment was mediated by hyperactivity/impulsivity and the association between working memory and social impairment was mediated by inattention. Support was not obtained for alternative models wherein the association between inhibition and social impairment was mediated by inattention, and the association between working memory and social impairment was mediated by hyperactivity/impulsivity. Further, tests of hierarchical models suggest that neither inhibition nor working memory is primary but, rather, that these cognitive processes are related to one another and that they collectively (but not uniquely) contribute to hyperactivity/impulsivity and inattention. These findings have implications for conceptual models of ADHD, for understanding factors that influence and sustain social impairment among youth with symptoms of the disorder, and for interventions aimed to addressing such impairment.

Ether-à-go-go-related gene (ERG) K channels have been implicated in the generation of pacemaker activities in the heart. To study the presence and function of ERG K channels in the pacemaker cells of the small intestine [the interstitial cells of Cajal (ICC)], a combination of patch-clamp techniques, tissue and live cell immunohistochemistry, RT-PCR, and in vitro functional studies were performed. Nonenzymatically isolated ICC in culture were identified by vital staining and presence of rhythmic inward currents. RT-PCR showed the presence of ERG mRNA in the intestinal musculature, and immunohistochemistry on tissue and cultured cells demonstrated that protein similar to human ERG was concentrated on ICC in the Auerbach's plexus region. Whole cell ERG K+ currents were evoked on hyperpolarization from 0 mV (but not from -70 mV) up to -120 mV and showed strong inward rectification. The currents were inhibited by E-4031, cisapride, La3+, and Gd3+ but not by 50 microM Ba2+. The ERG K+ inward current had a typical transient component with fast activation and inactivation kinetics followed by significant steady-state current. E-4031 also inhibited tetraethylammonium (TEA)-insensitive outward current indicating that the ERG K+ current is operating at depolarizing potentials. In contrast to TEA, blockers of the ERG K+ currents caused marked increase in tissue excitability as reflected by an increase in slow-wave duration and an increase in superimposed action potential activity. In summary, ERG K channels in ICC contribute to the membrane potential and play a role in regulation of pacemaker activity of the small intestine.

Interstitial cells of Cajal (ICC) are involved in generation of gut pacemaker activity, neurotransmission and stretch sensation. Pacemaker ICC exhibit spontaneous cyclic calcium oscillations that are in synchrony with its pacemaker activity. The spontaneous rhythmic inward currents in ICC that underlie gut pacemaker activity are linked to this calcium oscillation. It is probable that more than one type of channel contributes to the inward current with a high conductance chloride channel and a nonselective cation channel being the main candidates. The activation of these channels is linked to intracellular calcium cycling mechanism and involves inositol 1,4,5-trisphosphate (IP3)-mediated calcium release from the sarcoplasmic reticulum, and calcium uptake into mitochondria. This ion channel activity is modulated by signalling through neurotransmitter receptors, including the NK1 receptor. This finding and the presence of other neurotransmitter receptor mRNA transcripts indicates that ion channels in ICC are targets for neurotransmitter action. The ether-a-go-go-related (ERG) K channel is probably the most important K channel contributing to the resting membrane potential and excitability of the ICC. Many ion channels in ICC are regulated by second messenger systems which makes them highly susceptible to neurotransmitter modulation.

Decapentaplegic (Dpp) is a Drosophila member of the Transforming Growth Factor-beta (TGF-beta)/Bone Morphogenetic Protein (BMP) superfamily of growth factors. Dpp serves as a classical morphogen, where concentration gradients of this secreted factor control patterning over many cell dimensions. Regulating the level of Dpp signaling is therefore critical to its function during development. One type of molecule proposed to modulate growth factor signaling at the cell surface are integral membrane proteoglycans. We show here that division abnormally delayed (dally), a Drosophila member of the glypican family of integral membrane proteoglycans is required for normal Dpp signaling during development, affecting cellular responses to this morphogen. Ectopic expression of dally+ can alter the patterning activity of Dpp, suggesting a role for dally+ in modulating Dpp signaling strength. These findings support a role for members of the glypican family in controlling TGF-beta/BMP activity in vivo by affecting signaling at the cell surface.