Evaluation of Open Access Websites for Anesthesia Education.

BACKGROUND: While the prevalence of free, open access medical education resources for health professionals has expanded over the past 10 years, many educational resources for health care professionals are not publicly available or require fees for access. This lack of open access creates global inequities in the availability and sharing of information and may have the most significant impact on health care providers with the greatest need. The extent of open access online educational websites aimed for clinicians and trainees in anesthesiology worldwide is unknown. In this study, we aimed to identify and evaluate the quality of websites designed to provide open access educational resources for anesthesia trainees and clinicians. METHODS: A PubMed search of articles published between 2009 and 2020, and a Startpage search engine web search was conducted in May 2021 to identify websites using the following inclusion criteria: (1) contain educational content relevant for anesthesia providers or trainees, (2) offer content free of charge, and (3) are written in the English language. Websites were each scored by 2 independent reviewers using a website quality evaluation tool with previous validity evidence that was modified for anesthesia (the Anesthesia Medical Education Website Quality Evaluation Tool). RESULTS: Seventy-five articles and 175 websites were identified; 37 websites met inclusion criteria. The most common types of educational content contained in the websites included videos (66%, 25/37), text-based resources (51%, 19/37), podcasts (35%, 13/37), and interactive learning resources (32%, 12/37). Few websites described an editorial review process (24%, 9/37) or included opportunities for active engagement or interaction by learners (30%,11/37). Scores by tertile differed significantly across multiple domains, including disclosure of author/webmaster/website institution; description of an editorial review process; relevancy to residents, fellows, and faculty; comprehensiveness; accuracy; disclosure of content creation or revision; ease of access to information; interactivity; clear and professional presentation of information; and links to external information. CONCLUSIONS: We found 37 open access websites for anesthesia education available on the Internet. Many of these websites may serve as a valuable resource for anesthesia clinicians looking for self-directed learning resources and for educators seeking to curate resources into thoughtfully integrated learning experiences. Ongoing efforts are needed to expand the number and improve the existing open access websites, especially with interactivity, to support the education and training of anesthesia providers in even the most resource-limited areas of the world. Our findings may provide recommendations for those educators and organizations seeking to fill this needed gap to create new high-quality educational websites.

Improved heart function follows enhanced inflammatory cell recruitment and angiogenesis in 11betaHSD1-deficient mice post-MI.

AIMS: Mice unable to locally regenerate corticosterone due to deficiency of 11ß-hydroxysteroid dehydrogenase type 1 (11ßHSD1) have enhanced angiogenesis during acute myocardial infarct healing. The present study investigates the hypotheses that in these mice (i) inflammation and angiogenic signalling are promoted and (ii) longer-term remodelling and function are improved. METHODS AND RESULTS: Myocardial infarction (MI) was induced by coronary artery ligation in 11ßHSD1(-/-) and wild-type (C57BL/6) mice. Studies were terminated 2, 4, 7, and 28 days post-surgery. Increased vessel density (CD31 immunoreactivity) on the infarct border was confirmed 7 days after MI in 11ßHSD1(-/-) hearts (P < 0.05) and was accompanied by improved ejection fraction (ultrasound) compared with C57BL/6. During wound healing, recruitment of neutrophils (at 2 days after MI) and macrophages (from 4 days after MI) and expression of monocyte-chemoattractant protein-1 was increased in 11ßHSD1(-/-) compared with C57BL/6 hearts (P < 0.05). Recruitment of alternatively activated YM1-positive macrophages was particularly enhanced in the period preceding increased vessel density and was accompanied by increased expression of pro-angiogenic IL-8. By 28 days post-MI, when the infarct scar had matured, higher vessel density was maintained in 11ßHSD1(-/-) hearts and vessels were smooth-muscle coated. Infarct scars were thicker (P < 0.001) in 11ßHSD1(-/-) compared with C57BL/6 hearts and ejection fraction was higher (P < 0.05). CONCLUSION: Increased vessel density in healing infarcts of mice deficient in 11(-/-)HSD1 follows recruitment of pro-reparative macrophages and increased pro-angiogenic signalling. Mature infarcts show less thinning and cardiac function is improved relative to wild-type mice, suggesting that 11ßHSD1 may be a novel therapeutic target after MI.

Transcriptional and physiological responses to chronic ACTH treatment by the mouse kidney.

We investigated the effects on urinary steroid and electrolyte excretion and renal gene expression of chronic infusions of ACTH in the mouse. ACTH caused a sustained increase in corticosteroid excretion; aldosterone excretion was only transiently elevated. There was an increase in the excretion of deoxycorticosterone, a weak mineralocorticoid, to levels of physiological significance. Nevertheless, we observed neither antinatriuresis nor kaliuresis in ACTH-treated mice, and plasma renin activity was not suppressed. We identified no changes in expression of mineralocorticoid target genes. Water turnover was increased in chronic ACTH-treated mice, as were hematocrit and hypertonicity: volume contraction is consistent with high levels of glucocorticoid. ACTH-treated mice exhibited other signs of glucocorticoid excess, such as enhanced weight gain and involution of the thymus. We identified novel ACTH-induced changes in 1) genes involved in vitamin D (Cyp27b1, Cyp24a1, Gc) and calcium (Sgk, Calb1, Trpv5) metabolism associated with calciuria and phosphaturia; 2) genes that would be predicted to desensitize the kidney to glucocorticoid action (Nr3c1, Hsd11b1, Fkbp5); and 3) genes encoding transporters of enzyme systems associated with xenobiotic metabolism and oxidative stress. Although there is evidence that ACTH-induced hypertension is a function of physiological cross talk between glucocorticoids and mineralocorticoids, the present study suggests that the major changes in electrolyte and fluid homeostasis and renal function are attributable to glucocorticoids. The calcium and organic anion metabolism pathways that are affected by ACTH may explain some of the known adverse effects associated with glucocorticoid excess.