Pubmed du 05/07/15

Pubmed du jour

2015-07-05 12:03:50

1. Pulcini CD, Perrin JM, Houtrow AJ, Sargent J, Shui A, Kuhlthau K. {{Examining Trends and Coexisting Conditions Among Children Qualifying for SSI Under ADHD, ASD, and ID}}. {Acad Pediatr};2015 (Jul-Aug);15(4):439-443.

OBJECTIVE: To examine the prevalence trends and coexisting conditions in attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and intellectual disability (ID) in the pediatric Supplemental Security Income (SSI) population and general population. METHODS: The Social Security Administration (SSA) provided data on primary and secondary diagnoses of children qualifying for SSI for years 2000 to 2011. We compared SSA data with 2000-2011 National Health Interview Survey data on the prevalence of mental health diagnoses among children in the general population living between 0 and 199% of the federal poverty line. We utilized linear regression analysis to test the statistical significance of differences in the trends of the conditions’ prevalence. RESULTS: Over this time period, the SSI population experienced increases in ADHD (5.8%) and ASD (7.2%) and a decrease in ID (-10.3%). Comparison with change in the general population indicated no significant difference in ADHD but significant differences in ASD and ID. Relative percentage changes reflect similar changes. The SSI population qualifying for SSI with ADHD (70.8%) had higher rates of coexisting conditions than the general population (66.1%), but lower rates of coexisting conditions for ASD and ID. CONCLUSIONS: ADHD is on the rise among children receiving SSI and in the general population. This suggests that the rise of ADHD in the SSI population is expected and does not represent a misallocation of resources. Changes described among the SSI population in ASD and ID may allude to diagnostic/coding trends and/or true changes in prevalence. Limitations arise from the comparability of the 2 data sets.

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2. Rossler OE, Theis C, Heiter J, Fleischer W, Anonymous S. {{Is it ethical to heal a young white elephant from his physiological autism?}}. {Prog Biophys Mol Biol};2015 (Jun 30)
Forty years ago a causal therapy of autism was offered which has never been tried out by the therapeutic profession. It predictably is so effective that even members of other mirror-competent bonding species can be healed from their « physiological autism. » Niklas Luhmann belonged to the therapy’s supporters and Leo Szilard had anticipated it in fiction 30 years earlier. The Ottersberg Lectures on Philosophy revived it through the enthusiasm and cooperation of the youthful audience.

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3. Searing BM, Graham F, Grainger R. {{Support Needs of Families Living with Children with Autism Spectrum Disorder}}. {J Autism Dev Disord};2015 (Jul 4)
This study examined the perceived availability and helpfulness of supports used by caregivers of children with Autism Spectrum Disorder in New Zealand, particularly for caregivers who are Maori, and who live rurally. Caregivers (N = 92) completed the Family Support Scale with comparisons analysed using t tests. Free text comments were invited and analysed using a general inductive approach. More support was perceived as available by Non-Maori than Maori p = 0.03, 95 % CI (0.21, 3.88). Spouses were rated as the most helpful support. Professional helpers were rated as ‘somewhat helpful’. Helpful support emphasised caring, knowledge and accessibility. Ethnic differences in perceptions of support endorse calls for culturally tailored supports. Informal supports are highly valued however professional supports require development to better meet caregiver needs.

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4. Steinman G. {{Plausible etiology of brain dysconnectivity in autism – Review and prospectus}}. {Med Hypotheses};2015 (Jun 27)
This report summarizes recent findings related to the neuropathology of autism. Combining the relevant observations assessed here, a comprehensive, coherent hypothesis explaining the etiology of juvenile autism may be deduced. This proposed mechanism describes a process initiated by insulin-like growth factor deficiency, resulting in brain dysconnectivity as central to the behavioral manifestations of this disease.

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5. Takada Y, Hirano M, Kiyonaka S, Ueda Y, Yamaguchi K, Nakahara K, Mori MX, Mori Y. {{Rab3 interacting molecule 3 mutations associated with autism alter regulation of voltage-dependent Ca channels}}. {Cell Calcium};2015 (Jun 23)
Autism is a neurodevelopmental psychiatric disorder characterized by impaired reciprocal social interaction, disrupted communication, and restricted and stereotyped patterns of interests. Autism is known to have a strong genetic component. Although mutations in several genes account for only a small proportion of individuals with autism, they provide insight into potential biological mechanisms that underlie autism, such as dysfunction in Ca2+ signaling, synaptic dysfunction, and abnormal brain connectivity. In autism patients, two mutations have been reported in the Rab3 interacting molecule 3 (RIM3) gene. We have previously demonstrated that RIM3 physically and functionally interacts with voltage-dependent Ca2+ channels (VDCCs) expressed in neurons via the beta subunits, and increases neurotransmitter release. Here, by introducing corresponding autism-associated mutations that replace glutamic acid residue 176 with alanine (E176A) and methionine residue 259 with valine (M259V) into the C2B domain of mouse RIM3, we demonstrate that both mutations partly cancel the suppressive RIM3 effect on voltage-dependent inactivation of Ba2+ currents through P/Q-type CaV2.1 recombinantly expressed in HEK293 cells. In recombinant N-type CaV2.2 VDCCs, the attenuation of the suppressive RIM3 effect on voltage-dependent inactivation is conserved for M259V but not E176A. Slowing of activation speed of P/Q-type CaV2.1 currents by RIM3 is abolished in E176A, while the physical interaction between RIM3 and beta subunits is significantly attenuated in M259V. Moreover, increases by RIM3 in depolarization-induced Ca2+ influx and acetylcholine release are significantly attenuated by E176A in rat pheochromocytoma PC12 cells. Thus, our data raise the interesting possibility that autism phenotypes are elicited by synaptic dysfunction via altered regulation of presynaptic VDCC function and neurotransmitter release.

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