Negative perceptions result in the belief that such children are so troubled it would be impossible to adopt them and create "normal" families. A 2004 report from the Pew Commission on Children in Foster Care has shown that the number of children waiting in foster care doubled since the 1980s and now remains steady at about a half-million a year. "Attitude toward Adoption Questionnaire (ATAQ): this questionnaire was first developed by Abdollahzadeh, Chaloyi and Mahmoudi(2019). Preliminary Edition: This questionnaire has 23 items based on the Likert scale of 1 (totally Disagree), up to 5 (Totally Agree) being obtained after refining the items designed to construct the present tool and per-study study. The analysis of item and initial psychometric analyses indicate that there are two factors in it. Items 3-10-11-12-14-15-16-17-19-20-21 are reversed and the rest are graded positively. The results of exploratory factor analysis by main components with varimax rotation indicated two components of attitude toward adoption being named respectively cognitive as the aspects of attitude toward adoption and behavioral-emotional aspects of attitude toward adoption. These two components explained 43.25% of the variance of the total sample. Cronbachs alpha coefficient was used to measure the reliability of the questionnaire. Cronbachs alpha coefficient was 0.709 for the whole questionnaire, 0.71 for the first component, and 0.713 for the second one. In addition, there was a significant positive relationship between desired social tendencies and the cognitive aspect of attitude toward adoption as well as the behavioral -emotional aspects of attitude toward adoption (P ≤ 0.01).
This can be due to genetic errors such as the deletion or mutation of a segment of chromosome 15, uniparental disomy, or translocation. While Angelman syndrome can be caused by a single mutation in the UBE3A gene, the most common genetic defect leading to Angelman syndrome is a 5- to 7-Mb (megabase) maternal deletion in chromosomal region 15q11.2-q13.Specifically, the paternal copy of UBE3A is known to be imprinted within the hippocampus, cortex, thalamus, olfactory bulb, and cerebellum. Therefore, in these areas of the brain, a functioning maternal copy of UBE3A is essential for proper development.Region 15q11-13 is implicated in both Angelman syndrome and Prader–Willi syndrome (PWS). While AS results from mutation, loss or abnormal imprinting involving the UBE3A gene within this region on the maternal chromosome, loss of a different cluster of genes within the same region on the paternal chromosome causes PWS.The methylation test that is performed for Angelman syndrome looks for methylation on the genes neighbor SNRPN, which is silenced by methylation on the maternal copy of the gene. Neurophysiology
The electroencephalogram (EEG) in AS is usually abnormal, more so than clinically expected. This EEG facilitates the differential diagnosis of AS, but is not pathognomonic. Three distinct interictal patterns are seen in these patients. The most common pattern is a very large amplitude 2–3 Hz rhythm most prominent in prefrontal leads. Next most common is a symmetrical 4–6 Hz high voltage rhythm. The third pattern, 3–6 Hz activity punctuated by spikes and sharp waves in occipital leads, is associated with eye closure.