1. {{Assistance with treatment choices related to autism}}. {Nurse Educ};2012 (Mar);37(2):49.
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2. Lindberg S, von Post I, Eriksson K. {{The experiences of parents of children with severe autism in connection with their children’s anaesthetics, in the presence and absence of the perioperative dialogue: a hermeneutic study}}. {Scand J Caring Sci};2012 (Feb 13)
Scand J Caring Sci; 2012 The experiences of parents of children with severe autism in connection with their children’s anaesthetics, in the presence and absence of the perioperative dialogue: a hermeneutic study The aim of this study was to obtain an understanding of what parents of children with severe autism experience in connection with their child’s anaesthetics, in the presence and absence of the perioperative dialogue. Twelve parents who had experi ence of their child receiving anaesthetics on one or more occasions took part in this study, in which anaesthesia care was organized as a perioperative dialogue. Data were collected by means of conversational interviews, and the text was interpreted using a hermeneutic approach. The hermeneutic text interpretation led to a new understanding based on the knowledge that in the absence of the perioperative dialogue, previous anaesthetics had meant the suffering of care by the following: a hopeless struggle, unspeakable suffering and a disgraceful scenario. However, continuity in the perioperative dialogue provided to be a way out of the suffering by being received by warm hands, being received by a known face and a subtle interplay between the child and nurse. Although health and well-being may be unobtainable goals in this special context of care, the findings provided ample descriptions of the positive effects of the perioperative dialogue, which is all the more valuable when dealing with children who will need repeated anaesthetics in the future.
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3. Maher P. {{Methylglyoxal, advanced glycation end products and autism: Is there a connection?}}. {Med Hypotheses};2012 (Feb 8)
Autism is a complex and heterogeneous neurodevelopmental disorder of unknown etiology but very likely resulting from both genetic and environmental factors. Recent estimates suggest that it affects 1 in 100-150 individuals in the US. Oxidative stress, inflammation and mitochondrial dysfunction have all been suggested to play key roles in autism and may be linked via alterations in cellular redox homeostasis. The glutathione/glutathione disulfide (GSH/GSSG) redox pair forms the major redox couple in cells and as such plays a critical role in regulating redox-dependent cellular functions. A number of studies have shown that variations in genes involved in GSH metabolism are associated with autism. GSH also modulates the activity of glyoxalase 1 (Glo-1), the rate-limiting enzyme for the removal of reactive dicarbonyls such as methylglyoxal (MG). MG is the major precursor for the formation of advanced glycation end products (AGEs). Both MG and AGEs can induce oxidative stress, inflammation and mitochondrial dysfunction and are implicated in diabetic complications and multiple, age-related neurological diseases. Dietary consumption of AGEs and MG correlates with food intake which has increased 20-30% over the past 20years. Both MG and AGEs are orally absorbed, leading to increased levels in the blood. Furthermore, in humans, increased MG and AGE levels in maternal blood correlate with increased MG and AGE levels in newborn blood, potentially exposing infants to high oxidative stress and inflammation. It is hypothesized that diet derived MG and AGEs in combination with inborn genetic vulnerabilities that affect the cellular redox status are major contributors to the development of autism and provide a causal link between oxidative stress, inflammation and mitochondrial dysfunction. If future research supports this hypothesis, then by reducing the exposure to these diet-derived factors, it might be possible to decrease the prevalence of at least a subset of autism cases.
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4. Misaki M, Wallace GL, Dankner N, Martin A, Bandettini PA. {{Characteristic cortical thickness patterns in adolescents with autism spectrum disorders: Interactions with age and intellectual ability revealed by canonical correlation analysis}}. {Neuroimage};2012 (Feb 3)
To investigate patterns and correlates of cortical thickness in adolescent males with autism spectrum disorders (ASD) versus matched typically developing controls, we applied kernel canonical correlation analysis to whole brain cortical thickness with the explaining variables of diagnosis, age, full-scale IQ, and their interactions. The analysis found that canonical variates (patterns of cortical thickness) correlated with each of these variables. The diagnosis- and age-by-diagnosis-related canonical variates showed thinner cortex for participants with ASD, which is consistent with previous studies using a univariate analysis. In addition, the multivariate statistics found larger affected regions with higher sensitivity than those found using univariate analysis. An IQ-related effect was also found with the multivariate analysis. The effects of IQ and age-by-IQ interaction on cortical thickness differed between the diagnostics groups. For typically developing adolescents, IQ was positively correlated with cortical thickness in orbitofrontal, postcentral and superior temporal regions, and greater thinning with age was seen in dorsal frontal areas in the superior IQ (>120) group. These associations between IQ and cortical thickness were not seen in the ASD group. Differing relationships between IQ and cortical thickness implies independent associations between measures of intelligence and brain structure in ASD versus typically developing controls. We discuss these findings vis-a-vis prior results obtained utilizing univariate methods.
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5. Robinson LM, Dauenhauer J, Bishop KM, Baxter J. {{Growing health disparities for persons who are aging with intellectual and developmental disabilities: the social work linchpin}}. {J Gerontol Soc Work};2012 (Feb);55(2):175-190.
Similar to the general population, adults with intellectual and developmental disabilities (IDD) are living into their 70s and beyond. Health care disparities have been well-documented for this vulnerable and underserved population. Social workers are often responsible for assessment, coordination of care, and negotiation of needed services for people with IDD. This article explores the challenges facing social workers in meeting the growing health and social needs of aging adults with IDD and their families. Trends in social work practice and gaps in education are discussed as they relate to addressing and reducing current health disparities.
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6. Santosh PJ. {{A neural systems approach in autism spectrum disorders}}. {Dev Med Child Neurol};2012 (Mar);54(3):206-207.
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7. Till SM, Wijetunge LS, Seidel VG, Harlow E, Wright AK, Bagni C, Contractor A, Gillingwater TH, Kind PC. {{Altered maturation of the primary somatosensory cortex in a mouse model of fragile X syndrome}}. {Hum Mol Genet};2012 (Feb 9)
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and results from loss of the fragile X mental retardation protein (FMRP). Many fragile X-related cognitive and behavioral features emerge during childhood and are associated with abnormal synaptic and cellular organization of the cerebral cortex. Identifying the roles of FMRP in cortical development will provide a basis for understanding the pathogenesis of the syndrome. However, how the loss of FMRP influences the developmental trajectory of cortical maturation remains unclear. We took advantage of the stereotyped and well-characterized development of the murine primary somatosensory cortex to examine cortical maturation during a time-window that corresponds to late embryonic and early postnatal development in the human. In the Fmr1 knockout mouse, we find a delay in somatosensory map formation, alterations in the morphology profile of dendrites and spines of layer 4 neurons, and a decrease in the synaptic levels of proteins involved in glutamate receptor signaling at times corresponding to the highest levels of FMRP expression. In contrast, cortical arealization, synaptic development in layer 4, and early postnatal regulation of mRNAs encoding synaptic proteins are not altered in Fmr1 knockout mice. The specificity of the developmental delay in Fmr1 knockout mice indicates that loss of FMRP does not result in a general stalling of cerebral cortex maturation. Instead, our results suggest that inaccurate timing of developmental processes caused by the loss of FMRP may lead to alterations in neural circuitry that underlie behavioral and cognitive dysfunctions associated with FXS.
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8. Treffert DA. {{Hyperlexia III: separating ‘autistic-like’ behaviors from autistic disorder; assessing children who read early or speak late}}. {WMJ};2011 (Dec);110(6):281-286; quiz 287.
Three conditions — Hyperlexia (children who read early), Einstein syndrome (children who speak late), and « Blindisms » (in children with impaired vision) — can present with « autistic-like » symptoms, traits, and behaviors that need to be differentiated from autistic disorder. Careful attention to that critical difference has important epidemiologic, etiologic, treatment, and outcome implications. This paper describes these conditions, makes suggestions for proper identification that can prevent unnecessary worry and distress for parents and other caregivers, and suggests appropriate management.
9. Wei H, Chadman KK, McCloskey DP, Sheikh AM, Malik M, Brown WT, Li X. {{Brain IL-6 elevation causes neuronal circuitry imbalances and mediates autism-like behaviors}}. {Biochim Biophys Acta};2012 (Feb 2)
Abnormal immune responses have been reported to be associated with autism. A number of studies showed that cytokines were increased in the blood, brain, and cerebrospinal fluid of autistic subjects. Elevated IL-6 in autistic brain has been a consistent finding. However, the mechanisms by which IL-6 may be involved in the pathogenesis of autism are not well understood. Here we show that mice with elevated IL-6 in the brain display many autistic features, including impaired cognitive abilities, deficits in learning, abnormal anxiety traits and habituations, as well as decreased social interactions. IL-6 elevation caused alterations in excitatory and inhibitory synaptic formations and disrupted the balance of excitatory/inhibitory synaptic transmissions. IL-6 elevation also resulted in an abnormal change in the shape, length and distributing pattern of dendritic spines. These findings suggest that IL-6 elevation in the brain could mediate autistic-like behaviors, possibly though the imbalances of neural circuitry and impairments of synaptic plasticity.
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10. Yoo HJ, Cho IH, Park M, Yang SY, Kim SA. {{Family based association of GRIN2A and GRIN2B with Korean autism spectrum disorders}}. {Neurosci Lett};2012 (Feb 3)
N-Methyl-d-aspartate (NMDA) receptor, one of the glutamate receptors, has a role in the regulation of synaptic activity. It functions as an ion channel in the central nervous system and its inappropriate activation has been implicated in several neurological conditions. To test the association between candidate genes related with NMDA receptors and autism spectrum disorders (ASDs), we examined single nucleotide polymorphisms (SNPs) for GRIN2A and GRIN2B by using the family-based association test (FBAT) in 151 Korean trios. There was a statistically significant associations between ASDs and haplotypes in GRIN2B (bi-allelic mode additive model P-value=0.003; FDR P-value=0.012). This study supports a possible role of GRIN2B as a candidate gene for the etiology of ASDs.
