ABSTRACT
The Department of Emergency Medicine at Queen's University developed, implemented, and evaluated an interprofessional simulation-based competition called the Simulation Olympics with the purpose of encouraging health care providers to practice resuscitation skills and foster strong team-based attitudes. Eleven teams (N â=â 45) participated in the competition. Teams completed three standardized resuscitation scenarios in a high-fidelity simulation laboratory with teams composed of nurses, respiratory therapists, and undergraduate and postgraduate medical trainees. Trained standardized actors and a dedicated technician were used for all scenarios. Judges evaluated team performance using standardized assessment tools. All participants (100%) completed an anonymous two-page questionnaire prior to the competition assessing baseline characteristics and evaluating participant attitudes, motivation, and barriers to participation. The majority of participants (71%) completed an evaluation form following the event focusing on highlights, barriers to participation, and desired future directions. Evaluations were uniformly positive in short-answer feedback and attitudinal scoring measures. To our knowledge, the Simulation Olympics competition is the first of its kind in Canada to be offered at an academic teaching hospital.
Subject(s)
Clinical Competence , Curriculum , Education, Medical, Continuing/methods , Emergency Medicine/education , Patient Simulation , Resuscitation/education , Humans , Ontario , Retrospective StudiesABSTRACT
Evidence from both human and animal studies implicates the serotonergic system in the development of attention-deficit hyperactivity disorder (ADHD) including positive association studies for several key serotonergic genes. The serotonin transporter (HTT) regulates the availability of serotonin by reuptake of the neurotransmitter from the synaptic cleft. Several studies have reported an association of this gene to ADHD, specifically the long variant of a common insertion/deletion polymorphism located in the promoter of this gene that results in increased transcription and higher HTT expression. An additional study found no evidence for an association with this polymorphism. Recently, an A/G single nucleotide polymorphism (SNP) was found within the promoter polymorphism with functional studies indicating that the long variant containing the G allele at this site behaves like the short variant. This previously unidentified functional change may have confounded earlier association studies. We investigated the relationship of several variants to ADHD: the promoter polymorphisms, SNP in the 3' untranslated region (3'UTR) with a reported association to ADHD and a rare, non-synonymous coding SNP. These polymorphisms were genotyped in 209 ADHD families identified through an affected proband. We did not find evidence for an association of these polymorphisms, or haplotypes of these polymorphisms, to ADHD in this sample.