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1.
Ann Otol Rhinol Laryngol ; 129(2): 115-121, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31526031

RESUMO

OBJECTIVE: Identify knowledge deficits about alternate airways (AAs) (tracheostomy and laryngectomy) among physicians across multiple specialties a tertiary institution and to assess the impact of an educational lecture on improving deficits. METHODS: Study Design: Cross-sectional assessment. Setting: Academic medical center. Subjects and Methods: An anonymous 10-item, multiple choice assessment was given to physicians at a tertiary care center in the departments of Otolaryngology, Emergency Medicine, Family Medicine, General Surgery, Internal Medicine, and Pediatrics. An educational lecture on AAs was presented. Scores between a pre-lecture and a 3-month post-lecture assessment were compared. Data was analyzed using ANOVA and chi-squared analysis. RESULTS: Otolaryngology physicians scored an average of 97.8%, while non-otolaryngology physicians scored 58.3% (P < .05). Non-otolaryngology surgical physicians scored 68.4% while non-surgical physicians were lower at 55.1% (P < .0001). Comparing pre-lecture to post-lecture scores, all non-otolaryngology physicians improved their scores significantly from 58.3% to 86.5% (P < .005). Non-surgical physicians had significant improvement after the instructional lecture, closing the score gap with surgical physicians for the post-lecture assessment. DISCUSSION: The care of patients with AAs requires an understanding of their basic principles. Our findings identify significant knowledge deficits among non-otolaryngologists. Through an instructional lecture, we demonstrated improvement in knowledge among non-otolaryngology physicians and durability of the knowledge after 3 months. CONCLUSIONS: Through an instructional lecture, we found tracheostomy and laryngectomy knowledge deficits can be identified and improved upon. Periodic reinforcement of basic principles for non-otolaryngology physicians may be a promising strategy to ensure the proper care of patients with AAs.


Assuntos
Competência Clínica , Conhecimentos, Atitudes e Prática em Saúde , Laringectomia/educação , Traqueostomia/educação , Estudos Transversais , Humanos , Medicina , Autorrelato , Centros de Atenção Terciária
2.
Cell Rep ; 17(12): 3233-3245, 2016 12 20.
Artigo em Inglês | MEDLINE | ID: mdl-28009292

RESUMO

Neural circuits involving midbrain dopaminergic (DA) neurons regulate reward and goal-directed behaviors. Although local GABAergic input is known to modulate DA circuits, the mechanism that controls excitatory/inhibitory synaptic balance in DA neurons remains unclear. Here, we show that DA neurons use autocrine transforming growth factor ß (TGF-ß) signaling to promote the growth of axons and dendrites. Surprisingly, removing TGF-ß type II receptor in DA neurons also disrupts the balance in TGF-ß1 expression in DA neurons and neighboring GABAergic neurons, which increases inhibitory input, reduces excitatory synaptic input, and alters phasic firing patterns in DA neurons. Mice lacking TGF-ß signaling in DA neurons are hyperactive and exhibit inflexibility in relinquishing learned behaviors and re-establishing new stimulus-reward associations. These results support a role for TGF-ß in regulating the delicate balance of excitatory/inhibitory synaptic input in local microcircuits involving DA and GABAergic neurons and its potential contributions to neuropsychiatric disorders.


Assuntos
Neurônios Dopaminérgicos/metabolismo , Proteínas Serina-Treonina Quinases/genética , Receptores de Fatores de Crescimento Transformadores beta/genética , Reversão de Aprendizagem/fisiologia , Fator de Crescimento Transformador beta1/genética , Animais , Dendritos/genética , Dendritos/fisiologia , Neurônios Dopaminérgicos/fisiologia , Neurônios GABAérgicos/metabolismo , Neurônios GABAérgicos/fisiologia , Regulação da Expressão Gênica , Humanos , Mesencéfalo/crescimento & desenvolvimento , Mesencéfalo/metabolismo , Camundongos , Receptor do Fator de Crescimento Transformador beta Tipo II , Transdução de Sinais/genética , Sinapses/genética , Sinapses/metabolismo , Fator de Crescimento Transformador beta1/metabolismo
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