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1.
Laryngoscope ; 134(2): 795-802, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-37602761

RESUMO

OBJECTIVES: Vocal process granulomas (VPGs) are benign laryngeal lesions that may manifest as ulcerated regions of the vocal fold or nodular polypoid lesions. Gold standard treatments for idiopathic VPG are yet to be established at this time. This study evaluated clinical decision-making and outcomes in the treatment of VPG patients based on experiences of academic laryngologists across the United States. METHODS: A 21-question survey was developed to evaluate each respondent's specific VPG patient population, clinical decision-making in treating VPG, and corresponding treatment outcomes. The survey was distributed to 168 laryngologists at academic institutions across the United States. Data were analyzed through the Qualtrics platform. RESULTS: A total of 106 responses were analyzed, with a completion rate of 63.1%. Etiology of VPG was most commonly attributed to phonotrauma (96.2%) and reflux (71.8%). Primary first-line treatment was most commonly antireflux medications (92%). Other common first line treatments included voice therapy (58.8%) and inhaled steroids (42.5%). With these treatments, the majority of laryngologists report that recurrence is uncommon (68.4%). Dysphonia was cited as the most frequent long-term sequelae at 27.8%. CONCLUSIONS: VPG treatment strategies continue to be controversial across the United States with many treatments described in the literature with variable application in the practice of academic laryngologists today. Based on survey results, antireflux medications and voice therapy may be the most widely used and most effective treatment options. Establishment of gold standard therapy for VPG as well as further research into recurrent or persistent VPG despite antireflux and voice therapy should be explored. LEVEL OF EVIDENCE: 5 Laryngoscope, 134:795-802, 2024.


Assuntos
Disfonia , Laringe , Voz , Humanos , Granuloma , Prega Vocal , Disfonia/complicações
2.
Endocrinology ; 157(11): 4351-4363, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27631552

RESUMO

The etiology for half of congenital hypopituitarism cases is unknown. Our long-term goal is to expand the molecular diagnoses for congenital hypopituitarism by identifying genes that contribute to this condition. We have previously shown that the forkhead box transcription factor, FOXO1, is present in approximately half of somatotropes at embryonic day (e) 18.5, suggesting it may have a role in somatotrope differentiation or function. To elucidate the role of FOXO1 in somatotrope differentiation and function, Foxo1 was conditionally deleted from the anterior pituitary (Foxo1Δpit). Uncommitted progenitor cells are maintained and able to commit to the somatotrope lineage normally based on the expression patterns of Sox2, a marker of uncommitted pituitary progenitors, and Pou1f1 (also known as Pit1), which marks committed progenitors. Interestingly, Foxo1Δpit embryonic mice exhibit delayed somatotrope differentiation as evidenced by an almost complete absence of GH immunoreactivity at e16.5 and reduced expression of Gh at e18.5 and postnatal day (P) 3. Consistent with this conclusion, expression of GHRH receptor, a marker of terminally differentiated somatotropes, is significantly reduced at e18.5 and P3 in the absence of FOXO1. The mechanism of FOXO1 regulation of somatotrope differentiation may involve the basic helix-loop-helix transcription factor, Neurod4, which has been implicated in somatotrope differentiation and is significantly reduced in Foxo1Δpit mice. Foxo1Δpit mice do not exhibit growth defects, and at P21 their pituitary glands exhibit a normal distribution of somatotropes. These studies demonstrate that FOXO1 is important for initial somatotrope specification embryonically but is dispensable for postnatal somatotrope expansion and growth.


Assuntos
Proteína Forkhead Box O1/metabolismo , Somatotrofos/citologia , Somatotrofos/metabolismo , Animais , Diferenciação Celular/genética , Diferenciação Celular/fisiologia , Embrião de Mamíferos/metabolismo , Éxons/genética , Feminino , Hormônio Foliculoestimulante/genética , Hormônio Foliculoestimulante/metabolismo , Proteína Forkhead Box O1/genética , Imuno-Histoquímica , Hibridização In Situ , Hormônio Luteinizante/genética , Hormônio Luteinizante/metabolismo , Camundongos , Hipófise/citologia , Hipófise/metabolismo , Gravidez , Células-Tronco/citologia , Células-Tronco/metabolismo , Fatores de Tempo
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