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1.
AEM Educ Train ; 8(1): e10948, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38510726

RESUMO

Objectives: The role of biological sex in interprofessional relationships is an important factor in collaborative health care settings such as the emergency department (ED) but one that has been sparsely studied. While there is anecdotal evidence on gender-based differences in communication, little research has focused on this topic. The goal of this study was to determine whether there are differences in paging frequency between nurses and male and female residents. Methods: We conducted a retrospective review of patient visits to our urban, tertiary care academic ED between January 1 and April 1, 2021. Only pages from nurses to emergency medicine (EM) residents were included. Outcome variables included number of pages received by sex, number of unique ED visits, and mean number of pages per unique visit. Pearson's chi-square tests were used to analyze differences between observed and expected results. Results: A total of 15,617 pages from nurses to residents over 6843 unique patient visits to the ED were analyzed. This included 187 nurses, 162 (87%) of whom were female and 25 (13%) were male. Of the 39 residents, 12 (31%) were female and 27 (69%) were male. Female residents received 4500 pages over 2228 unique patient ED visits, or a mean of two pages per patient with a mean of 186 unique ED visits per female resident. Male residents received 11,117 pages over 4615 unique patient ED visits, or a mean of 2.4 pages per patient, with a mean of 171 unique ED visits per male resident. This difference in pages per patient was statistically significant (χ2(1) = 369, p < 0.001). Conclusions: We found that male residents received significantly more pages per patient than their female colleagues. Overall, further research is required to understand the factors, such as characteristics of patients or preferred communication methods of providers, that drive this disparity and what the implications are for patient outcomes.

2.
Ultrasound J ; 13(1): 6, 2021 Feb 14.
Artigo em Inglês | MEDLINE | ID: mdl-33586112

RESUMO

OBJECTIVES: Point-of-care ultrasound (POCUS) has become increasingly integrated into medical education given the growing role of evaluative and procedural techniques in practice today. Tele-ultrasound is a new and promising venture that aims to expand medical knowledge and education to previously unreached or underserved areas. This study aimed to determine the non-inferiority of teaching ultrasound remotely using tele-ultrasound via the Philips Lumify (Philips Medical Systems, Bothell, WA) system, which utilizes video conferencing technology and real-time imaging that can be viewed by the operator and educator simultaneously. METHODS: Three commonly used ultrasound exams were taught and evaluated in 56 ultrasound-naive medical participants: Focused Assessment with Sonography in Trauma (FAST), Lower Extremity Deep Venous Thrombosis (LEDVT) screening, and ultrasound-guided vascular access. The participants were randomized into either in-person traditional learning or tele-ultrasound learning with the Philips Lumify (Philips Medical Systems, Bothell, WA) units. The primary outcome of interest was the ability to perform certain tasks for each exam RESULTS: Competency on each exam was tested across all exams and no inferiority was found between in-person and remote learning (p < 0.05). CONCLUSIONS: Our findings support the use of tele-ultrasound in beginner ultrasound education.

3.
Am J Physiol Gastrointest Liver Physiol ; 307(9): G871-82, 2014 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-25234043

RESUMO

Tumor necrosis factor-induced protein 3 (TNFAIP3; also known as A20) negatively regulates NF-κB and MAPK signals to control inflammatory responses. TNFAIP3 also protects against TNF-induced cell death. Intestinal epithelial cell (IEC) expression of TNFAIP3 improves barrier function and tight junction integrity and prevents dextran sulfate sodium (DSS)-induced IEC death and colitis. We therefore investigated the effects of TNFAIP3 expression in IEC on immune homeostasis in the intestines of immune-compromised mice. Villin-TNFAIP3 (v-TNFAIP3) transgenic mice were interbred with IL-10(-/-) mice (v-TNFAIP3 × IL-10(-/-)) and incidence, onset, and severity of colitis was assessed. v-TNFAIP3 × IL-10(-/-) mice displayed severe, early onset, and highly penetrant colitis that was not observed in IL-10(-/-) or v-TNFAIP3 mice. V-TNFAIP3 mice displayed altered expression of mucosal cytokines, increased numbers of mucosal regulatory T cells, and altered expression of mucosal antimicrobial peptides (AMPs). Microbial colonization of the inner mucus layer of v-TNFAIP3 mice was observed, along with alterations in the microbiome, but this was not sufficient to induce colitis in v-TNFAIP3 mice. The relative sterility of the inner mucus layer observed in wild-type and IL-10(-/-) mice was lost in v-TNFAIP3 × IL-10(-/-) mice. Thus IEC-derived factors, induced by signals that are inhibited by TNFAIP3, suppress the onset of inflammatory bowel disease in IL-10(-/-) mice. Our results indicate that IEC expression of TNFAIP3 alters AMP expression and allows microbial colonization of the inner mucus layer, which activates an IL-10-dependent anti-inflammatory process that is necessary to prevent colitis.


Assuntos
Colite Ulcerativa/metabolismo , Cisteína Endopeptidases/metabolismo , Interleucina-10/genética , Mucosa Intestinal/metabolismo , Peptídeos e Proteínas de Sinalização Intracelular/metabolismo , Microbiota , Animais , Antígenos de Neoplasias/genética , Antígenos de Neoplasias/metabolismo , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Colite Ulcerativa/genética , Colite Ulcerativa/microbiologia , Cisteína Endopeptidases/genética , Deleção de Genes , Mucosa Intestinal/microbiologia , Mucosa Intestinal/patologia , Peptídeos e Proteínas de Sinalização Intracelular/genética , Lectinas Tipo C/genética , Lectinas Tipo C/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Proteínas Associadas a Pancreatite , Ribonuclease Pancreático/genética , Ribonuclease Pancreático/metabolismo , Proteína 3 Induzida por Fator de Necrose Tumoral alfa
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