autism/hypoxia

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Autism spectrum disorders and fetal hypoxia in a population-based cohort: accounting for missing exposures via Estimation-Maximization algorithm.

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BACKGROUND Autism spectrum disorders (ASD) are associated with complications of pregnancy that implicate fetal hypoxia (FH); the excess of ASD in male gender is poorly understood. We tested the hypothesis that risk of ASD is related to fetal hypoxia and investigated whether this effect is greater

Combined fetal inflammation and postnatal hypoxia causes myelin deficits and autism-like behavior in a rat model of diffuse white matter injury.

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Diffuse white matter injury (WMI) is a serious problem in extremely preterm infants, and is associated with adverse neurodevelopmental outcome, including cognitive impairments and an increased risk of autism-spectrum disorders. Important risk factors include fetal or perinatal inflammatory insults

[Case of infantile autism with pediatric Wernicke's encephalopathy due to severe eating disorder].

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Wernicke's encephalopathy (WE) or thiamine deficiency is fatal if left untreated. We report a case of a 3-year-old boy with infantile autism and a severe eating disorder who developed WE after 3 weeks of starvation without thiamine supplementation. The eating disorder started when he entered

Proposed toxic and hypoxic impairment of a brainstem locus in autism.

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Electrophysiological findings implicate site-specific impairment of the nucleus tractus solitarius (NTS) in autism. This invites hypothetical consideration of a large role for this small brainstem structure as the basis for seemingly disjointed behavioral and somatic features of autism. The NTS is

Autism Spectrum Disorder Screening at 18-36 Months in Infants with Moderate and Severe Neonatal Encephalopathy: Is Routine Screening Required?

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Background: Hypoxia, acidosis, and inflammation cause impairment of neuronal development due to lack of sufficient oxygen and nutrition, and there may be an increased risk of ASD in neonates with Neonatal Encephalopathy (NE). To evaluate

Perinatal anoxia degrades auditory system function in rats.

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Little is known about the neural bases of the reduced auditory and cortical processing speeds that have been recorded in language-impaired, autistic, schizophrenic, and other disabled human populations. Although there is strong evidence for genetic contributions to etiologies, epigenetic factors

Impaired Gas Exchange at Birth and Risk of Intellectual Disability and Autism: A Meta-analysis.

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We conducted meta-analyses of 67 studies on the association between neonatal proxies of impaired gas exchange and intellectual disability (ID) or autism spectrum disorders (ASD). Neonatal acidosis was associated with an odds ratio (OR) of 3.55 [95 % confidence interval (95 % CI) 2.23-5.49] for ID

Prenatal influences on brain dopamine and their relevance to the rising incidence of autism.

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The incidence of autism has risen 10-fold since the early 1980s, with most of this rise not explainable by changing diagnostic criteria. The rise in autism is paradoxical in that autism is considered to be one of the most genetically determined of the major neurodevelopmental disorders and should

Autism genes and the leukocyte transcriptome in autistic toddlers relate to pathogen interactomes, infection and the immune system. A role for excess neurotrophic sAPPα and reduced antimicrobial Aβ.

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Prenatal and early childhood infections have been implicated in autism. Many autism susceptibility genes (206 Autworks genes) are localised in the immune system and are related to immune/infection pathways. They are enriched in the host/pathogen interactomes of 18 separate microbes (bacteria/viruses

Preeclampsia, placental insufficiency, and autism spectrum disorder or developmental delay.

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OBJECTIVE Increasing evidence suggests that autism spectrum disorder (ASD) and many forms of developmental delay (DD) originate during fetal development. Preeclampsia may trigger aberrant neurodevelopment through placental, maternal, and fetal physiologic mechanisms. OBJECTIVE To determine whether

Hypoxia affects Slc7a5 expression through HIF-2α in differentiated neuronal cells.

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An imbalance of branched-chain amino acids (BCAAs) in the brain may result in neuropathological conditions, such as autism spectrum disorders. The L-type amino acid transporter 1 (LAT1), encoded by the solute carrier transporter 7a5 (Slc7a5) gene, is critical for maintaining normal levels of

In utero exposure to transient ischemia-hypoxemia promotes long-term neurodevelopmental abnormalities in male rat offspring

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The impact of transient ischemic-hypoxemic insults on the developing fetal brain is poorly understood despite evidence suggesting an association with neurodevelopmental disorders such as schizophrenia and autism. To address this, we designed an aberrant uterine hypercontractility paradigm with

Reptilian behavioural patterns in childhood autism.

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Childhood autism may be caused by damage to three phylogenetically distinct regions of the brain, or their major pathways and connections. Injury to the neocortex results in loss of language and cognitive function, while injury to the limbic cortex results in autistic withdrawal and abolition of

Autism in India: a case-control study to understand the association between socio-economic and environmental risk factors.

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Autism spectrum disorder is a neurodevelopmental disorder and the cause of autism is still unclear. The aim of this study was to investigate the association of socioeconomic, environmental, pregnancy and newborn-related risk factors among children with autism spectrum disorders. This was a

GeneAnalytics Pathway Analysis and Genetic Overlap among Autism Spectrum Disorder, Bipolar Disorder and Schizophrenia.

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Bipolar disorder (BPD) and schizophrenia (SCH) show similar neuropsychiatric behavioral disturbances, including impaired social interaction and communication, seen in autism spectrum disorder (ASD) with multiple overlapping genetic and environmental influences implicated in risk and course of

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