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Objective Attention deficit hyperactivity disorder (ADHD) is a common neuropsychological disorder primarily diagnosed in childhood. Early intervention was found to significantly improve developmental outcomes, implicating on the role of early identification of ADHD markers. In the current study, we explored the developmental history of children referred to neurological assessment to identify early ADHD predictors. Methods A total of 92 children and adolescents (41 females) recruited at a pediatric neurology clinic, with suspected ADHD (n = 39) or other neurological difficulties (n = 53) such as headaches, seizures, tic disorders, orthostatic hypotension, postischemic stroke, intermittent pain, and vasovagal syncope. Developmental history information was obtained from caregivers, and evaluation for possible ADHD was performed. Developmental details were compared between children with and without current ADHD diagnosis. Results Word-finding difficulties (WFDs) in preschool age was reported in 30.4% of the sample. Among children diagnosed with ADHD, 43% had WFDs history, compared with only 5% in children without ADHD. Among children with WFDs history, 93% were later diagnosed with ADHD compared with 42% in children without WFDs history. The relationship between WFDs and ADHD was significant (chi-square test [1, N = 92] = 20.478, p < 0.0001), and a logistic regression model demonstrated that asides from a family history of ADHD, the strongest predictor for ADHD in school age children was a history of WFDs. Conclusion Preliminary evidence supports a predictive link between preschool WFDs and later ADHD diagnosis, highlighting the importance of early WFDs clinical attention. [ABSTRACT FROM AUTHOR]

On the basis of previous findings suggesting that in human embryonic stem cell-derived cardiomyocytes (hESC-CM) the sarcoplasmic reticulum Ca(2+)-induced release of calcium machinery is either absent or immature, in the present study we tested the hypothesis that hESC-CM contain fully functional 1,4,5-inositol trisphosphate (1,4,5-IP(3))-operated intracellular Ca(2+) ([Ca(2+)](i)) stores that can be mobilized upon appropriate physiological stimuli. To test this hypothesis we investigated the effects of angiotensin-II (AT-II) and endothelin-1 (ET-1), which activate the 1,4,5-IP(3) pathway, on [Ca(2+)](i) transients and contractions in beating clusters of hESC-CM. Our major findings were that in paced hESC-CM both AT-II and ET-1 (10(-9) to 10(-7) M) increased the contraction amplitude and the maximal rates of contraction and relaxation. In addition, AT-II (10(-9) to 10(-7) M) increased the [Ca(2+)](i) transient amplitude. The involvement of 1,4,5-IP(3)-dependent intracellular Ca(2+) release in the inotropic effect of AT-II was supported by the findings that (a) hESC-CM express AT-II, ET-1, and 1,4,5-IP(3) receptors determined by immunofluorescence staining, and (b) the effects of AT-II were blocked by 2 microM 2-aminoethoxyphenyl borate (a 1,4,5-IP(3) receptor blocker) and U73122 (a phospholipase C blocker). In conclusion, these findings demonstrate for the first time that hESC-CM exhibit functional AT-II and ET-1 signaling pathways, as well as 1,4,5-IP(3)-operated releasable Ca(2+) stores.