RESUMEN
Despite strong empirical support for treatments of eating disorders, research has demonstrated a trend of clinicians deviating from protocols outlined in empirically supported manuals. The present study used a convergent mixed-methods design to understand clinicians' use of and drift from empirically supported treatments in a sample of 114 licensed clinicians in the US who had substantial experience (i.e. one-third of caseload) working with patients with eating disorders and training in cognitive-behavioral therapy (CBT), family-based therapy (FBT), and/or interpersonal therapy (IPT) for eating disorders. Results revealed that 63.7-76.3% of clinicians drift from empirically supported treatments and 71.8% were aware they deviated from empirically supported treatments. Qualitative analyses identified client differences (57.2%) to be the primary reason why clinicians drift, with less participants describing therapist factors (20.4%), treatment shortcomings (12.6%), treatment setting (11.7%), logistic constraints (4.9%) and family factors (4.9%) as reasons why they drift. These findings suggest that drift for most clinicians may be better explained under the umbrella of evidence-based practice. Clinicians also identified a number of ways in which treatment and access to treatment can be improved. This broadened understanding of the use of empirically supported treatments within evidence-based practice may serve to help bridge the gap between research and practice.
Asunto(s)
Terapia Cognitivo-Conductual , Trastornos de Alimentación y de la Ingestión de Alimentos , Humanos , Terapia Cognitivo-Conductual/métodos , Terapia Familiar , Práctica Clínica Basada en la Evidencia , Trastornos de Alimentación y de la Ingestión de Alimentos/terapia , ConcienciaciónRESUMEN
Telomere length regulation is essential for cell viability in eukaryotes. While many pathways that affect telomere length are known, we do not yet have a complete understanding of the mechanism of length regulation. To identify new pathways that might regulate telomere length, we carried out a genetic screen in yeast and identified the cyclin-dependent kinase complex Bur1/2 as a regulator of telomere length. Mutations in either BUR1 cyclin-dependent kinase or the associated BUR2 cyclin resulted in short telomeres. This regulation did not function through the known role of BUR1 in regulating histone modification as bur1∆ set2∆ and bur2∆ set2∆ double mutants rescued cell growth but did not rescue the telomere shortening effects. We found that both bur1∆ and bur2∆ set2∆ were also defective in de novo telomere addition, and deletion of SET2 did also not rescue this elongation defect. The Bur1/2 cyclin-dependent kinase regulates transcription of many genes. We found that TLC1 RNA levels were reduced in bur2∆ set2∆ mutants; however, overexpression of TLC1 restored the transcript levels but did not restore de novo telomere elongation or telomere length. These data suggest that the Bur1/2 kinase plays a role in telomere elongation separate from its role in transcription of telomerase components. Dissecting the role of the Bur1/2 kinase pathway at telomeres will help complete our understanding of the complex network of telomere length regulation.