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1.
BMC Emerg Med ; 23(1): 23, 2023 03 01.
Artigo em Inglês | MEDLINE | ID: mdl-36859177

RESUMO

BACKGROUND: The use of point-of-care ultrasound (POCUS) is increasing. Numerous investigators have evaluated the learning curves in POCUS, but there are no published studies on how emergency physicians perceive their own competence level with this skill. METHODS: A nationwide survey amongst Finnish emergency physicians was conducted. The respondents reported their use of POCUS and how it has affected their clinical decision-making. The number of POCUS examinations performed was compared to the self-assessed skill level with different applications. Cut-off values were determined for the number of examinations required to acquire a good self-assessed skill level in each POCUS application. The correlation between self-confidence and the self-estimated skill level was analyzed. Several different statistical methods were used, such as Student's t-test, Pearson's correlation test, Loess method and ROC curve analysis. RESULTS: A total of 134 out of 253 Finnish emergency medicine specialists and residents (52%) responded to the survey. The most commonly used POCUS applications were POCUS-assisted procedures, pleural effusion and pneumothorax, inferior vena cava and lower extremity deep venous thrombosis. The initial rate of perceived skill acquisition was very steep with the curve flattening with greater skill and more experience. The number of examinations performed to reach a self-assessed good competence varied from seven to 75 with different applications. The lowest cut-off point for self-assessed good competence was obtained for rapid ultrasound for the shock and hypotension-protocol and the highest for focused cardiac examinations. There was an excellent correlation between self-confidence and the self-assessed skill level. CONCLUSIONS: The Finnish emergency practitioners' self-assessed development of POCUS skills parallels the previously published learning curves of POCUS. The correlation of self-confidence and the self-assessed skill level was found to be excellent. These findings add information on the development of perceived POCUS skills amongst emergency physicians and could complement a formal performance assessment.


Assuntos
Médicos , Sistemas Automatizados de Assistência Junto ao Leito , Humanos , Autorrelato , Estudos Transversais , Finlândia
2.
Respir Res ; 12: 2, 2011 Jan 04.
Artigo em Inglês | MEDLINE | ID: mdl-21205293

RESUMO

BACKGROUND: Asthma leads to structural changes in the airways, including the modification of extracellular matrix proteins such as tenascin-C. The role of tenascin-C is unclear, but it might act as an early initiator of airway wall remodelling, as its expression is increased in the mouse and human airways during allergic inflammation. In this study, we examined whether Th1 or Th2 cells are important regulators of tenascin-C in experimental allergic asthma utilizing mice with impaired Th1 (STAT4-/-) or Th2 (STAT6-/-) immunity. METHODS: Balb/c wildtype (WT), STAT4-/- and STAT6-/- mice were sensitized with intraperitoneally injected ovalbumin (OVA) followed by OVA or PBS airway challenge. Airway hyperreactivity (AHR) was measured and samples were collected. Real time PCR and immunohistochemistry were used to study cytokines and differences in the expression of tenascin-C. Tenascin-C expression was measured in human fibroblasts after treatment with TNF-α and IFN-γ in vitro. RESULTS: OVA-challenged WT mice showed allergic inflammation and AHR in the airways along with increased expression of TNF-α, IFN-γ, IL-4 and tenascin-C in the lungs. OVA-challenged STAT4-/- mice exhibited elevated AHR and pulmonary eosinophilia. The mRNA expression of TNF-α and IFN-γ was low, but the expression of IL-4 was significantly elevated in these mice. OVA-challenged STAT6-/- mice had neither AHR nor pulmonary eosinophilia, but had increased expression of mRNA for TNF-α, IFN-γ and IL-4. The expression of tenascin-C in the lungs of OVA-challenged STAT4-/- mice was weaker than in those of OVA-challenged WT and STAT6-/- mice suggesting that TNF-α and IFN-γ may regulate tenascin-C expression in vivo. The stimulation of human fibroblasts with TNF-α and IFN-γ induced the expression of tenascin-C confirming our in vivo findings. CONCLUSIONS: Expression of tenascin-C is significantly attenuated in the airways of STAT4-/- mice, which may be due to the impaired secretion of TNF-α and IFN-γ in these mice.


Assuntos
Remodelação das Vias Aéreas , Asma/metabolismo , Pulmão/metabolismo , Fator de Transcrição STAT4/deficiência , Tenascina/metabolismo , Animais , Asma/genética , Asma/imunologia , Asma/fisiopatologia , Hiper-Reatividade Brônquica , Células Cultivadas , Modelos Animais de Doenças , Feminino , Fibroblastos/imunologia , Fibroblastos/metabolismo , Humanos , Interferon gama/metabolismo , Pulmão/imunologia , Pulmão/fisiopatologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Knockout , Ovalbumina , RNA Mensageiro/metabolismo , Fator de Transcrição STAT4/genética , Fator de Transcrição STAT6/deficiência , Fator de Transcrição STAT6/genética , Tenascina/genética , Células Th1/imunologia , Células Th2/imunologia , Fator de Necrose Tumoral alfa/metabolismo , Regulação para Cima
3.
Respiration ; 75(4): 450-8, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18230951

RESUMO

BACKGROUND: Smoking alters the inflammatory cell balance in the airways, often leading to repeated respiratory infections and, eventually, chronic obstructive pulmonary disease (COPD) in susceptible individuals. OBJECTIVE: It was the aim of this study to evaluate alterations in the airway inflammatory balance caused by chronic cigarette smoke exposure. METHODS: We compared results of biopsy and bronchoalveolar lavage (BAL) samples from non-smoking (n = 8) and smoking (n = 5; pack years 25.06 +/- 11.75, range 7.13-36.8) subjects without COPD. RESULTS: In BAL samples, we found a significantly higher number of total cells (353 +/- 96 million vs. 114 +/- 52 million; p = 0.003) and macrophages (331 +/- 100 million vs. 84 +/- 36 million; p = 0.002) in asymptomatic smoking subjects in comparison with never-smokers. Macrophages correlated negatively with the forced expiratory volume in 1 s as percent of the predicted value (rho = -0.75, p = 0.003). Of 23 mediators examined, mRNA expression of cytokines interleukin (IL)-6, interferon-gamma, tumor necrosis factor-beta, IL-13 and chemokines CCL5, CCL3, CCL4 and CCL20 was significantly lowered in BAL cells of smokers compared with never-smokers and was negatively correlated with macrophages and positively correlated with the forced expiratory volume in 1 s as percent of the predicted value. Differential cell counts were similar between smokers and never-smokers in the bronchial biopsies. CONCLUSION: We conclude that in a susceptible population, smoking suppresses inflammatory defense by inhibiting expression of inflammatory mediators in the airways on a large scale.


Assuntos
Brônquios/patologia , Líquido da Lavagem Broncoalveolar/química , Quimiocinas/metabolismo , Fumar/metabolismo , Fumar/patologia , Adulto , Biópsia , Brônquios/metabolismo , Líquido da Lavagem Broncoalveolar/citologia , Contagem de Células , Quimiocinas/análise , Feminino , Humanos , Macrófagos/citologia , Macrófagos/metabolismo , Masculino , Pessoa de Meia-Idade , RNA Mensageiro/análise , RNA Mensageiro/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa
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