ABSTRACT
PURPOSE: To develop and evaluate an individualised habituation programme for children with autism spectrum disorder (ASD) to enhance their cooperation during a routine dental examination. METHODS: In collaboration with school personnel, we developed and evaluated a research-based habituation programme comprising a toolbox with aids (pictures, videos, appliances, social stories) for preparations and gradual exposure to a 10-step dental examination. The habituation programme was subjected to a small-scale evaluation involving 17 children with ASD living in Rogaland, Norway. Changes in cooperation were registered using Frankl behaviour rating scale. Further, school personnel were interviewed using semi-structured interviews, and the data obtained were analysed through content analysis. RESULTS: Fourteen children (82%) completed the dental examination. Compared to previous accomplishments reported by the caregivers, an increased number of children completed the examination with a mirror and probe and were able to take an X-ray with good compliance following the habituation programme. The registration of cooperation (Frankl score) during each session indicated varying progression rates. Further, changing the dentist did not influence compliance, and most children showed a similar level of cooperation towards the dental examination one year later. Further, school personnel highlighted the need for preparations that could facilitate control and the importance of catering to individual needs. CONCLUSION: An individualised approach combining preparations and behavioural methods in close collaboration with school personnel can increase cooperation during a dental examination in children with ASD.
Subject(s)
Autism Spectrum Disorder , Humans , Child , Habituation, Psychophysiologic , Parents , Caregivers , NorwayABSTRACT
The IPC-81 cell line is derived from the transplantable BNML model of acute myelogenic leukemia (AML), known to be a reliable predictor of the clinical efficiency of antileukemic agents, like the first-line AML anthracycline drug daunorubicin (DNR). We show here that cAMP acted synergistically with DNR to induce IPC cell death. The DNR-induced death differed from that induced by cAMP by (1) not involving Bim induction, (2) being abrogated by GSK3ß inhibitors, (3) by being promoted by the HSP90/p23 antagonist geldanamycin and truncated p23 and (4) by being insensitive to the CRE binding protein (CREB) antagonist ICER and to cyclin-dependent protein kinase (CDK) inhibitors. In contrast, the apoptosis induced by cAMP correlated tightly with Bim protein expression. It was abrogated by Bim (BCL2L11) downregulation, whether achieved by the CREB antagonist ICER, by CDK inhibitors, by Bim-directed RNAi, or by protein synthesis inhibitor. The forced expression of BimL killed IPC-81(WT) cells rapidly, Bcl2-overexpressing cells being partially resistant. The pivotal role of CREB and CDK activity for Bim transcription is unprecedented. It is also noteworthy that newly developed cAMP analogs specifically activating PKA isozyme I (PKA-I) were able to induce IPC cell apoptosis. Our findings support the notion that AML cells may possess targetable death pathways not exploited by common anti-cancer agents.