Despite difficulties measuring parenting styles, many studies have demonstrated a significant relationship between disruptive children and certain parenting practices. One of the most frequently used scales to measure parenting styles is the Alabama Parenting Questionnaire (APQ). This scale was originally defined based on theoretical dimensions and using samples from the USA. Therefore, both factor analysis studies and its adaptation to other countries have been proposed to improve and widen its use. The aim of this study was to adapt the APQ to the Italian population. A community sample of 258 mothers and children (94 %) and 192 fathers (70 %) from 274 families with children from 10- to 14-years-old who agreed to participate and met the inclusion criteria completed the APQ. Principal components and exploratory factor analyses resulted in a unique 19-item version of the APQ for mothers, fathers, and children. This unified version has resulted in two factor categories: positive (12 items) and negative parenting (7 items). The internal consistency and goodness of fit of the model were satisfactory. Moderate and significant convergent validity were found for mothers and fathers but not for children. In fact, we found differences in validity rates among the participants. Children perceived less positive and more negative parenting than did fathers and mothers, and mothers believed that they provided more positive parenting than did other parents. In conclusion, the APQ Italian version of the parents and children global report forms are considered a suitable measure for positive and negative parenting styles with acceptable validity and reliability indice
We identified a 14q21.2 microdeletion in a 16-year-old boy with autism spectrum disorder (ASD), IQ in the lower part of normal range but high-functioning memory skills. The deletion affects a gene desert, and the non-deleted gene closest to the microdeletion boundaries is LRFN5, which encodes a protein involved in synaptic plasticity and implicated in neuropsychiatric disorders. LRFN5 expression was significantly decreased in the proband's skin fibroblasts. The deleted region includes the pseudogene chr14.232.a, which is transcribed into a long non-coding RNA (lncLRFN5-10), whose levels were also significantly reduced in the proband's fibroblasts compared to controls. Transfection of the patient's fibroblasts with a plasmid expressing chr14.232.a significantly increased LRFN5 expression, while siRNA targeting chr14.232.a-derived lncLRFN5-10 reduced LRFN5 levels. In summary, we report on an individual with ASD carrying a microdeletion encompassing the pseudogene chr14.232.a encoding for lncLRFN5-10, which was found to affect the expression levels of the nearby, non-deleted LRFN5. This case illustrates the potential role of long non-coding RNAs in regulating expression of neighbouring genes with a functional role in ASD pathogenesis.
We report on a 21-year old woman with intellectual disability, autistic features, severe obesity, and facial dysmorphisms suggestive of Wolf-Hirschhorn syndrome (WHS). Array-CGH analysis showed a 2.89 Mb deletion on chromosome 14q11.2 containing 47 known genes. The most interesting genes included in this deletion are CHD8, a chromodomain helicase DNA binding protein that is associated with autism spectrum disorders, and MMP14, a matrix metalloproteinase that has been linked to obesity and type 2 diabetes. This report shows that 14q11.2 microdeletions can mimic WHS and suggests that gene(s) in the deleted interval that may be responsible for a phenocopy of WHS.
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