1. {{White matter microstructure, cognition, and molecular markers in fragile X premutation females}}. {Neurology}. 2017; 89(13): 1430.
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2. Crawford H, Moss J, Oliver C, Riby D. {{Differential effects of anxiety and autism on social scene scanning in males with fragile X syndrome}}. {J Neurodev Disord}. 2017; 9(1): 9.
BACKGROUND: Existing literature draws links between social attention and socio-behavioural profiles in neurodevelopmental disorders. Fragile X syndrome (FXS) is associated with a known socio-behavioural phenotype of social anxiety and social communication difficulties alongside high social motivation. However, studies investigating social attention in males with FXS are scarce. Using eye tracking, this study investigates social attention and its relationship with both anxiety and autism symptomatology in males with FXS. METHODS: We compared dwell times to the background, body, and face regions of naturalistic social scenes in 11 males with FXS (M age = 26.29) and 11 typically developing (TD) children who were matched on gender and receptive language ability (M age = 6.28). Using informant-report measures, we then investigated the relationships between social scene scanning and anxiety, and social scene scanning and social communicative impairments. RESULTS: Males with FXS did not differ to TD children on overall dwell time to the background, body, or face regions of the naturalistic social scenes. Whilst males with FXS displayed developmentally ‘typical’ social attention, increased looking at faces was associated with both heightened anxiety and fewer social communication impairments in this group. CONCLUSIONS: These results offer novel insights into the mechanisms associated with social attention in FXS and provide evidence to suggest that anxiety and autism symptomatology, which are both heightened in FXS, have differential effects on social attention.
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3. Hara Y, Ago Y, Higuchi M, Hasebe S, Nakazawa T, Hashimoto H, Matsuda T, Takuma K. {{Oxytocin attenuates deficits in social interaction but not recognition memory in a prenatal valproic acid-induced mouse model of autism}}. {Horm Behav}. 2017; 96: 130-6.
Recent studies have reported that oxytocin ameliorates behavioral abnormalities in both animal models and individuals with autism spectrum disorders (ASD). However, the mechanisms underlying the ameliorating effects of oxytocin remain unclear. In this study, we examined the effects of intranasal oxytocin on impairments in social interaction and recognition memory in an ASD mouse model in which animals are prenatally exposed to valproic acid (VPA). We found that a single intranasal administration of oxytocin restored social interaction deficits for up to 2h in mice prenatally exposed to VPA, but there was no effect on recognition memory impairments. Additionally, administration of oxytocin across 2weeks improved prenatal VPA-induced social interaction deficits for at least 24h. In contrast, there were no effects on the time spent sniffing in control mice. Immunohistochemical analysis revealed that intranasal administration of oxytocin increased c-Fos expression in the paraventricular nuclei (PVN), prefrontal cortex, and somatosensory cortex, but not the hippocampal CA1 and CA3 regions of VPA-exposed mice, suggesting the former regions may underlie the effects of oxytocin. These findings suggest that oxytocin attenuates social interaction deficits through the activation of higher cortical areas and the PVN in an ASD mouse model.
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4. Hong ER, Gong LY, Ninci J, Morin K, Davis JL, Kawaminami S, Shi YQ, Noro F. {{A meta-analysis of single-case research on the use of tablet-mediated interventions for persons with ASD}}. {Res Dev Disabil}. 2017.
BACKGROUND: There is a growing amount of single-case research literature on the benefits of tablet-mediated interventions for individuals with autism spectrum disorder (ASD). With the development of tablet-based computers, tablet-mediated interventions have been widely utilized for education and treatment purposes; however, the overall quality and evidence of this literature-base are unknown. AIMS: This article aims to present a quality review of the single-case experimental literature and aggregate results across studies involving the use of tablet-mediated interventions for individuals with ASD. METHODS AND PROCEDURES: Using the Tau nonoverlap effect size measure, the authors extracted data from single-case experimental studies and calculated effect sizes differentiated by moderator variables. The moderator variables included the ages of participants, participants’ diagnoses, interventions, outcome measures, settings, and contexts. OUTCOMES AND RESULTS: Results indicate that tablet-mediated interventions for individuals with ASD have moderate to large effect sizes across the variables evaluated. The majority of research in this review used tablets for video modeling and augmentative and alternative communication. CONCLUSIONS AND IMPLICATIONS: To promote the usability of tablet-mediated interventions for individuals with ASD, this review indicates that more single-case experimental studies should be conducted with this population in naturalistic home, community, and employment settings.
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5. Kathuria A, Nowosiad P, Jagasia R, Aigner S, Taylor RD, Andreae LC, Gatford NJF, Lucchesi W, Srivastava DP, Price J. {{Stem cell-derived neurons from autistic individuals with SHANK3 mutation show morphogenetic abnormalities during early development}}. {Mol Psychiatry}. 2017.
Shank3 is a structural protein found predominantly at the postsynaptic density. Mutations in the SHANK3 gene have been associated with risk for autism spectrum disorder (ASD). We generated induced pluripotent stem cells (iPSCs) from control individuals and from human donors with ASD carrying microdeletions of SHANK3. In addition, we used Zinc finger nucleases to generate isogenic SHANK3 knockout human embryonic stem (ES) cell lines. We differentiated pluripotent cells into either cortical or olfactory placodal neurons. We show that patient-derived placodal neurons make fewer synapses than control cells. Moreover, patient-derived cells display a developmental phenotype: young postmitotic neurons have smaller cell bodies, more extensively branched neurites, and reduced motility compared with controls. These phenotypes were mimicked by SHANK3-edited ES cells and rescued by transduction with a Shank3 expression construct. This developmental phenotype is not observed in the same iPSC lines differentiated into cortical neurons. Therefore, we suggest that SHANK3 has a critical role in neuronal morphogenesis in placodal neurons and that early defects are associated with ASD-associated mutations.Molecular Psychiatry advance online publication, 26 September 2017; doi:10.1038/mp.2017.185.
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6. Kaushik G, Xia Y, Pfau JC, Thomas MA. {{Dysregulation of autism-associated synaptic proteins by psychoactive pharmaceuticals at environmental concentrations}}. {Neurosci Lett}. 2017.
Autism Spectrum Disorders (ASD) are complex neurological disorders for which the prevalence in the U.S. is currently estimated to be 1 in 50 children. A majority of cases of idiopathic autism in children likely result from unknown environmental triggers in genetically susceptible individuals. These triggers may include maternal exposure of a developing embryo to environmentally relevant minute concentrations of psychoactive pharmaceuticals through ineffectively purified drinking water. Previous studies in our lab examined the extent to which gene sets associated with neuronal development were up- and down-regulated (enriched) in the brains of fathead minnows treated with psychoactive pharmaceuticals at environmental concentrations. The aim of this study was to determine whether similar treatments would alter in vitro expression of ASD-associated synaptic proteins on differentiated human neuronal cells. Human SK-N-SH neuroblastoma cells were differentiated for two weeks with 10muM retinoic acid (RA) and treated with environmentally relevant concentrations of fluoxetine, carbamazepine or venlafaxine, and flow cytometry technique was used to analyze expression of ASD-associated synaptic proteins. Data showed that carbamazepine individually, venlafaxine individually and mixture treatment at environmental concentrations significantly altered the expression of key synaptic proteins (NMDAR1, PSD95, SV2A, HTR1B, HTR2C and OXTR). Data indicated that psychoactive pharmaceuticals at extremely low concentrations altered the in vitro expression of key synaptic proteins that may potentially contribute to neurological disorders like ASD by disrupting neuronal development.
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7. Kim SH, Bal VH, Lord C. {{Longitudinal follow-up of academic achievement in children with autism from age 2 to 18}}. {J Child Psychol Psychiatry}. 2017.
OBJECTIVE: This study examined early predictors of and changes in school-age academic achievement and class placement in children referred for autism spectrum disorder (ASD) at age 2. METHOD: Of 111 ASD referrals, 74 were diagnosed with ASD at age 18. Regression analyses were performed to identify age 3 predictors of achievement in arithmetic, passage comprehension, word reading, and spelling at ages 9 and 18. Linear Mixed Models were used to examine predictors of academic growth between ages 9 and 18. RESULTS: Academic skills varied widely at 9 and 18, but were mostly commensurate with or higher than expected given cognitive levels. However, 22% (age 9) and 32% (age 18) of children with average/above average IQ showed below/low average achievement in at least one academic domain. Children who remained in general education/inclusion classrooms had higher achievement than those who moved to special education classrooms. Stronger cognitive skills at age 3 and 9 predicted better academic achievement and faster academic growth from age 9 to 18. Parent participation in intervention by age 3 predicted better achievement at age 9 and 18. CONCLUSIONS: Many children with ASD achieve basic academic skills commensurate with or higher than their cognitive ability. However, more rigorous screening for learning difficulties may be important for those with average cognitive skills because a significant minority show relative academic delays. Interventions targeting cognitive skills and parent participation in early treatment may have cascading effects on long-term academic development.
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8. Krysta K, Krzystanek M, Cubala WJ, Wiglusz MS, Jakuszkowiak-Wojten K, Galuszko-Wegielnik M, Czarnowska-Cubala M, Szarmach J, Wlodarczyk A, Janas-Kozik M. {{Telepsychiatry and Virtual Reality an the Teatment of Patients with Intellectual and Developmental Disabilities}}. {Psychiatr Danub}. 2017; 29(Suppl 3): 656-9.
BACKGROUND: Treatment and rehabilitation of people with intellectual and developmental disabilities is a multidisciplinary challenge, which require implementing new attitudes. The use of modern technology solutions like telepsychiatry or virtual reality may be a valuable addition to the traditional methods. OBJECTIVE: The objective of this review was to explore the usability of new technological solutions in this special population of patients. METHODS: The search in the PubMed was conducted using the following terms: (intellectual disability (Title/Abstract) OR developmental disability OR learning disorder (Title/Abstract)) AND virtual reality (Title/Abstract) OR telepsychiatry OR telemedicine OR e-mental health AND English (lang) AND (1995/01/01(PDAT): 2017/07/31(PDAT)). RESULTS: Telepsychiatry may be a useful tool in situations, when the direct access to professional assistance is limited, in solving particular problems like e.g. managing challenging behavior, also to support patients’ parents and for diagnostic and educational purposes. Virtual reality can be a safe and effective method of improving different skills, developing physical fitness, and enriching the ways of spending the leisure time. CONCLUSIONS: Using modern technology is a relatively new and promising field in which new ideas may develop to support the already existing services for patients with intellectual and developmental disabilities.
9. Lappe M. {{The maternal body as environment in autism science}}. {Soc Stud Sci}. 2016; 46(5): 675-700.
Research on autism and environmental risk factors has expanded substantially in recent years. My analysis draws attention to the regimes of perceptibility that shape how the environment is materialized in post-genomic science. I focus on how more complex narratives of autism’s causes and social anxieties surrounding child development have helped situate autism risk in women’s bodies before and during pregnancy. This has resulted in what I call the maternal body as environment in autism science. I show that this figure involves three characteristics: the molecularization of the environment, an individualization of risk, and the internalization of responsibility. I argue that these three features point to a new spatial and temporal politics of risk and responsibility that may heighten social and medical surveillance of women’s bodies and decisions, eclipsing larger questions about the uneven distribution of exposures in society and more holistic understandings of health that include neurodiversity. I conclude by considering what the maternal body as environment signals for women, social justice, and the politics of environmental health in the post-genomic era.
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10. Lebrun N, Parent P, Gendras J, Billuart P, Poirier K, Bienvenu T. {{Autism spectrum disorder recurrence, resulting of germline mosaicism for a CHD2 gene missense variant}}. {Clin Genet}. 2017.
Germline mosaicism for a novel missense variant p.Thr645Met located in the SNF2-related ATP dependent helicase domain of CHD2 in 2 affected siblings with autism spectrum disorder.
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11. Liu T, Liu X, Li Y, Zhu C, Markey PS, Pelowski M. {{Assessing autism at its social and developmental roots: A review of Autism Spectrum Disorder studies using functional near-infrared spectroscopy}}. {Neuroimage}. 2017.
We review a relatively new method for studying the developing brain in children and infants with Autism Spectrum Disorder (ASD). Despite advances in behavioral screening and brain imaging, due to paradigms that do not easily allow for testing of awake, very young, and socially-engaged children-i.e., the social and the baby brain-the biological underpinnings of this disorder remain a mystery. We introduce an approach based on functional near-infrared spectroscopy (fNIRS), which offers a noninvasive imaging technique for studying functional activations by measuring changes in the brain’s hemodynamic properties. This further enables measurement of brain activation in upright, interactive settings, while maintaining general equivalence to fMRI findings. We review the existing studies that have used fNIRS for ASD, discussing their promise, limitations, and their technical aspects, gearing this study to the researcher who may be new to this technique and highlighting potential targets for future research.
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12. Macova L, Bicikova M, Ostatnikova D, Hill M, Starka L. {{Vitamin D, neurosteroids and autism}}. {Physiol Res}. 2017; 66(Supplementum 3): S333-S40.
Vitamin D had been for a long time investigated for its effects on bone metabolism. Recently has been observed that the incidence of some neurodevelopmental disorders (including autism) increases hand in hand with vitamin D deficiency. Indeed, vitamin D was reported to modulate the biosynthesis of neurotransmitters and neurotrophic factors; moreover, its receptor was found in the central nervous system. Vitamin D deficiency was therefore assessed as a risk factor for autism, however the biological mechanism has not yet been revealed. In our review we focused on potential connections among vitamin D, steroids and autism. Potential mechanisms of vitamin D action are also discussed.
13. McDuffie A, Banasik A, Bullard L, Nelson S, Feigles RT, Hagerman R, Abbeduto L. {{Distance delivery of a spoken language intervention for school-aged and adolescent boys with fragile X syndrome}}. {Dev Neurorehabil}. 2017: 1-16.
A small randomized group design (N = 20) was used to examine a parent-implemented intervention designed to improve the spoken language skills of school-aged and adolescent boys with FXS, the leading cause of inherited intellectual disability. The intervention was implemented by speech-language pathologists who used distance video-teleconferencing to deliver the intervention. The intervention taught mothers to use a set of language facilitation strategies while interacting with their children in the context of shared story-telling. Treatment group mothers significantly improved their use of the targeted intervention strategies. Children in the treatment group increased the duration of engagement in the shared story-telling activity as well as use of utterances that maintained the topic of the story. Children also showed increases in lexical diversity, but not in grammatical complexity.
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14. Qualls LR, Corbett BA. {{Examining the relationship between social communication on the ADOS and real-world reciprocal social communication in children with ASD}}. {Res Autism Spectr Disord}. 2017; 33: 1-9.
BACKGROUND: While many children with autism spectrum disorders (ASDs) communicate better with adults than peers, diagnostic measures are given by adult examiners. These measures may not accurately capture the deficits that children with ASD have in communicating with their peers. METHOD: This study examined the ability of the Autism Diagnostic Observation Schedule (ADOS) Social Communication scale to predict reciprocal communication in children with ASD during natural play with peers using the Peer Interaction Paradigm (PIP). Thirty participants with ASD were given the ADOS and then participated in the PIP, after which their behavior was analyzed. RESULTS: Using linear regression, we found that Social Communication was the primary significant predictor for reciprocal communication during play, and that reciprocal communication was not predicted by Verbal IQ or the Restrictive and Repetitive Behaviors scale on the ADOS. CONCLUSIONS: The findings suggest that the ADOS measures naturally-occurring social communication patterns with peers and can be used to inform treatment options for children with ASD based on an accurate measure of their level of impairment in social communication.
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15. Robertson CE, Baron-Cohen S. {{Sensory perception in autism}}. {Nat Rev Neurosci}. 2017.
Autism is a complex neurodevelopmental condition, and little is known about its neurobiology. Much of autism research has focused on the social, communication and cognitive difficulties associated with the condition. However, the recent revision of the diagnostic criteria for autism has brought another key domain of autistic experience into focus: sensory processing. Here, we review the properties of sensory processing in autism and discuss recent computational and neurobiological insights arising from attention to these behaviours. We argue that sensory traits have important implications for the development of animal and computational models of the condition. Finally, we consider how difficulties in sensory processing may relate to the other domains of behaviour that characterize autism.
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16. Rodriguez NM, Levesque MA, Cohrs VL, Niemeier JJ. {{Teaching children with autism to request help with difficult tasks}}. {J Appl Behav Anal}. 2017.
We taught three children diagnosed with autism spectrum disorder to request help using an interrupted chain procedure during which we manipulated task materials such that the child was either incapable or capable of independently completing a link of a behavior chain. We initially observed undesirable generalization of requests for help during capable trials when teaching was introduced during incapable trials for two participants and to a lesser extent for the third participant. However, with repeated exposure to differential prompting and reinforcement across incapable and capable trials, differential responding was observed across EO-present and EO-absent trials for all three participants during both teaching sets and one generalization set that was never exposed to teaching procedures. These findings suggest that it is important to consider the antecedent conditions under which the response should occur when teaching children to request help.
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17. Rutten AX, Vermeiren R, Van Nieuwenhuizen C. {{Autism in adult and juvenile delinquents: a literature review}}. {Child Adolesc Psychiatry Ment Health}. 2017; 11: 45.
BACKGROUND: Here we present an overview of the literature on autism in adult and juvenile delinquents. We analyzed both the prevalence of autism spectrum disorders (ASD) in groups of delinquents and the prevalence of offending in people with ASD. There is a high prevalence of psychiatric disorders amongst people in custody, but there is disagreement about the prevalence of ASD in this population. Some studies have found overrepresentation of people with ASD in forensic populations whereas others have found that people with ASD have a similar rate of offending to the general population. METHODS: We carried out a systematic search of literature published between 1990 and 2016 and identified studies on the co-occurrence of autism and delinquency using standard search engines. RESULTS: The prevalence of delinquency in the ASD population varied from 5 to 26%, whilst ASD was found in 2-18% of the forensic populations studied. The reported prevalence of ASD in delinquents and of offending in people with ASD varied widely. This might be due to the use of different diagnostic instruments, the diversity of the samples, the high rate of comorbid psychiatric disorders and the various types of offending behavior. CONCLUSIONS: We cannot conclude from our analysis that people with ASD are more likely to offend than the general population.
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18. Sbardella D, Tundo GR, Campagnolo L, Valacchi G, Orlandi A, Curatolo P, Borsellino G, D’Esposito M, Ciaccio C, Cesare SD, Pierro DD, Galasso C, Santarone ME, Hayek J, Coletta M, Marini S. {{Retention of Mitochondria in Mature Human Red Blood Cells as the Result of Autophagy Impairment in Rett Syndrome}}. {Sci Rep}. 2017; 7(1): 12297.
Rett Syndrome (RTT), which affects approximately 1:10.000 live births, is a X-linked pervasive neuro-developmental disorder which is caused, in the vast majority of cases, by a sporadic mutation in the Methyl-CpG-binding protein-2 (MeCP2) gene. This is a transcriptional activator/repressor with presumed pleiotropic activities. The broad tissue expression of MeCP2 suggests that it may be involved in several metabolic pathways, but the molecular mechanisms which provoke the onset and progression of the syndrome are largely unknown. In this paper, we report that primary fibroblasts that have been isolated from RTT patients display a defective formation of autophagosomes under conditions of nutrient starvation and that the mature Red Blood Cells of some RTT patients retain mitochondria. Moreover, we provide evidence regarding the accumulation of the p62/SQSTM1 protein and ubiquitin-aggregated structures in the cerebellum of Mecp2 knockout mouse model (Mecp2 -/y ) during transition from the non-symptomatic to the symptomatic stage of the disease. Hence, we propose that a defective autophagy could be involved in the RTT clinical phenotype, which introduces new molecular perspectives in the pathogenesis of the syndrome.
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19. Silbaugh BC, Falcomata TS, Ferguson RH. {{Effects of a lag schedule of reinforcement with progressive time delay on topographical mand variability in children with autism}}. {Dev Neurorehabil}. 2017: 1-12.
OBJECTIVE: Evaluate the effects of a Lag 1 schedule of reinforcement and progressive time delay (TD) on topographical mand variability in children with autism. METHODS: Using single-subject design methodology, a multiple baseline across behaviors with embedded reversal design was employed. During Lag 0, reinforcement was delivered contingent on any independent instances of manding. During Lag 1 + TD, prompts were faded and reinforcement was delivered contingent on independent or prompted variant mand topographies. RESULTS: Higher levels of topographical mand variability were observed during Lag 1 + TD for both participants. CONCLUSIONS: A Lag 1 schedule of reinforcement with progressive TD increased variability across functionally equivalent vocal mand topographies for both participants. This finding extends prior literature by providing a novel model for studying reinforced mand variability in children, and by demonstrating how practitioners could use prompts and differential reinforcement to increase topographical mand variability in children with autism.
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20. Strom M, Granstrom C, Lyall K, Ascherio A, Olsen SF. {{Research Letter: Folic acid supplementation and intake of folate in pregnancy in relation to offspring risk of autism spectrum disorder}}. {Psychol Med}. 2017: 1-7.
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21. Taylor T, Kozlowski AM, Girolami PA. {{Comparing behavioral treatment of feeding difficulties and tube dependence in children with cerebral palsy and autism spectrum disorder}}. {NeuroRehabilitation}. 2017.
BACKGROUND: Feeding disorders are multifaceted with behavioral components often contributing to the development and continuation of food refusal. In these cases, behavioral interventions are effective in treating feeding problems, even when medical or oral motor components are also involved. Although behavioral interventions for feeding problems are frequently employed with children with autism, they are less commonly discussed for children with cerebral palsy. OBJECTIVE: The purpose of this study was to compare the effectiveness of using applied behavior analytic interventions to address feeding difficulties and tube dependence in children with autism and children with cerebral palsy. METHOD: Children ages 1 to 12 years who were enrolled in an intensive feeding program between 2003 and 2013, where they received individualized behavioral treatment, participated. RESULTS: Behavioral treatment components were similar across groups, predominately consisting of escape extinction (e.g., nonremoval of the spoon) and differential reinforcement. For both groups, behavioral treatment was similarly effective in increasing gram consumption and in decreasing refusal and negative vocalizations. A high percentage of individualized goals were met by both groups as well as high caregiver satisfaction reported. CONCLUSIONS: Behavioral interventions for food refusal are effective for children with cerebral palsy with behavioral refusal, just as they are for children with autism.
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22. Vidal S, Brandi N, Pacheco P, Gerotina E, Blasco L, Trotta JR, Derdak S, Del Mar O’Callaghan M, Garcia-Cazorla A, Pineda M, Armstrong J. {{The utility of Next Generation Sequencing for molecular diagnostics in Rett syndrome}}. {Sci Rep}. 2017; 7(1): 12288.
Rett syndrome (RTT) is an early-onset neurodevelopmental disorder that almost exclusively affects girls and is totally disabling. Three genes have been identified that cause RTT: MECP2, CDKL5 and FOXG1. However, the etiology of some of RTT patients still remains unknown. Recently, next generation sequencing (NGS) has promoted genetic diagnoses because of the quickness and affordability of the method. To evaluate the usefulness of NGS in genetic diagnosis, we present the genetic study of RTT-like patients using different techniques based on this technology. We studied 1577 patients with RTT-like clinical diagnoses and reviewed patients who were previously studied and thought to have RTT genes by Sanger sequencing. Genetically, 477 of 1577 patients with a RTT-like suspicion have been diagnosed. Positive results were found in 30% by Sanger sequencing, 23% with a custom panel, 24% with a commercial panel and 32% with whole exome sequencing. A genetic study using NGS allows the study of a larger number of genes associated with RTT-like symptoms simultaneously, providing genetic study of a wider group of patients as well as significantly reducing the response time and cost of the study.
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23. Wawrzynski P. {{ASD+M: Automatic parameter tuning in stochastic optimization and on-line learning}}. {Neural Netw}. 2017; 96: 1-10.
In this paper the classic momentum algorithm for stochastic optimization is considered. A method is introduced that adjusts coefficients for this algorithm during its operation. The method does not depend on any preliminary knowledge of the optimization problem. In the experimental study, the method is applied to on-line learning in feed-forward neural networks, including deep auto-encoders, and outperforms any fixed coefficients. The method eliminates coefficients that are difficult to determine, with profound influence on performance. While the method itself has some coefficients, they are ease to determine and sensitivity of performance to them is low. Consequently, the method makes on-line learning a practically parameter-free process and broadens the area of potential application of this technology.
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24. Whiteley P. {{Food and the gut: relevance to some of the autisms}}. {Proc Nutr Soc}. 2017: 1-6.
Complex, diverse and rarely appearing without comorbidity, the autism spectrum disorders continue to be a source of research interest. With core symptoms variably impacting on social communication skills, the traditional focus of many research efforts has centred on the brain and how genetic and environmental processes impact on brain structure, function and/or connectivity to account for various behavioural presentations. Alongside emerging ideas on autistic traits being present in various clinical states, the autisms, and the overrepresentation of several comorbid conditions impacting on quality of life, other research avenues have opened up. The central role of the brain in relation to autism may be at least partially influenced by the functions of other organs. The gastrointestinal (GI) tract represents an important biological system pertinent to at least some autism. The notion of a gut-brain-behaviour axis has garnered support from various findings: an overrepresentation of functional and pathological bowel states, bowel and behavioural findings showing bidirectional associations, a possible relationship between diet, GI function and autism and recently, greater focus on aspects of the GI tract such as the collected gut microbiota in relation to autism. Gaps remain in our knowledge of the functions of the GI tract linked to autism, specifically regarding mechanisms of action onward to behavioural presentation. Set however within the context of diversity in the presentation of autism, science appears to be moving towards defining important GI-related autism phenotypes with the possibility of promising dietary and other related intervention options onward to improving quality of life.
