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Showing results for "early childhood"
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It is well established that maternal mental illness is associated with an increased risk of poor development for children. However, inconsistencies in findings regarding the nature of the difficulties children experience may be explained by methodological or geographical differences.
Individuals with Fetal Alcohol Spectrum Disorder (FASD) are at risk of having adverse childhood experiences (ACEs), especially those with child protection or justice system involvement. The complex relationship between FASD and psychosocial vulnerabilities in the affected individual is an important clinical risk factor for comorbidity.
We did not find any associations between parental occupational extremely low-frequency magnetic fields exposure and childhood leukaemia
At the point of transition, the mechanistic pathway from sexual trauma to psychosis does not appear to operate through affective symptoms
Individuals identified as at ultra-high risk (UHR) for psychosis are at risk of poor functional outcome regardless of development of psychotic disorder.
The aetiology of childhood brain tumours (CBT) is largely unknown.
The aim of this analysis was to investigate whether maternal coffee or tea consumption during pregnancy was associated with the risk of CBT.
Caregiver-mediated supports in general have shown mixed evidence for enhancing language outcomes in infants at higher likelihood of autism. While caregivers play a substantial role in caregiver-mediated supports, little is known about whether caregivers' own subclinical autistic features - known as broader autism phenotype - may moderate infant language outcomes.
Myeloperoxidase is released by neutrophils in inflamed tissues. MPO oxidizes chloride, bromide, and thiocyanate to produce hypochlorous acid, hypobromous acid, and hypothiocyanous acid, respectively. These oxidants are toxic to pathogens, but may also react with host cells to elicit biological activity and potential toxicity. In cystic fibrosis and related diseases, increased neutrophil inflammation leads to increased airway MPO and airway epithelial cell exposure to its oxidants.