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1.
Korean J Anesthesiol ; 77(2): 265-272, 2024 Apr.
Article in English | MEDLINE | ID: mdl-38556779

ABSTRACT

BACKGROUND: Although peer-assisted learning is known to be effective for reciprocal learning in medical education, it has been understudied in simulation. We aimed to assess the effectiveness of peer-led compared to instructor-led debriefing for non-technical skill development in simulated crisis scenarios. METHODS: Sixty-one undergraduate medical students were randomized into the control group (instructor-led debriefing) or an intervention group (peer debriefer or peer debriefee group). After the pre-test simulation, the participants underwent two more simulation scenarios, each followed by a debriefing session. After the second debriefing session, the participants underwent an immediate post-test simulation on the same day and a retention post-test simulation two months later. Non-technical skills for the pre-test, immediate post-test, and retention tests were assessed by two blinded raters using the Ottawa Global Rating Scale (OGRS). RESULTS: The participants' non-technical skill performance significantly improved in all groups from the pre-test to the immediate post-test, with changes in the OGRS scores of 15.0 (95% CI [11.4, 18.7]) in the instructor-led group, 15.3 (11.5, 19.0) in the peer-debriefer group, and 17.6 (13.9, 21.4) in the peer-debriefee group. No significant differences in performance were found, after adjusting for the year of medical school training, among debriefing modalities (P = 0.147) or between the immediate post-test and retention test (P = 0.358). CONCLUSIONS: Peer-led debriefing was as effective as instructor-led debriefing at improving undergraduate medical students' non-technical skill performance in simulated crisis situations. Peer debriefers also improved their simulated clinical skills. The peer debriefing model is a feasible alternative to the traditional, costlier instructor model.


Subject(s)
Simulation Training , Humans , Learning , Peer Group , Clinical Competence
2.
Resuscitation ; 138: 284-296, 2019 05.
Article in English | MEDLINE | ID: mdl-30928503

ABSTRACT

AIMS: To systematically evaluate the literature on interventions that improve skills retention following advanced structured resuscitation training programs designed for healthcare professionals. METHODS: A systematic review of MEDLINE, EMBASE, CENTRAL, CINAHL, PsycINFO, ERIC, and Scopus was performed. Only randomized controlled trials investigating skills retention following advanced structured resuscitation training programs for healthcare professionals between inception to November 21, 2018 were included. Publications that assessed only knowledge acquisition were excluded. Relevant data from included studies were extracted and study quality was critically appraised, both independently and in duplicate by multiple reviewers. The risk of bias was assessed with the Cochrane Risk of Bias tool and the Medical Education Research Study Quality Instrument (MERSQI). Due to significant clinical heterogeneity in SRT training, study designs and interventions, a qualitative synthesis was used to summarize findings. MAIN RESULTS: Sixteen studies, with a combined total of 1192 participants, were included in the final analysis. The majority of studies were conducted in North America and involved trainees or novice learners. ACLS was the most extensively studied, followed by NRP, ALS, and ATLS. Skills retention at 6 months was the most commonly used primary endpoint assessed using a simulated resuscitation checklist with either an adopted or created assessment tool. Most studies demonstrated a positive impact on skills retention when an interactive intervention or simulation was used. However, merely having a high-fidelity mannequin alone for simulation was found to have minimal effect on skills retention in the absence of other changes in content delivery. Booster sessions were found to be minimally effective in reinforcing long-term skills retention; however, most studies examining this intervention had small sample sizes and were underpowered. CONCLUSIONS: Simulation-based interventions, refresher courses and adjustments to the content delivery of advanced structured resuscitation training courses were found to have the greatest impact on skills retention. However, due to significant heterogeneity and methodological flaws in the available studies, no definitive conclusions can be made regarding other interventions. Overall, there is a paucity of skills retention research and further high-quality randomized controlled trials are needed to determine the optimal intervention and design for resuscitation training that would maximize skills retention.


Subject(s)
Clinical Competence , Health Personnel/education , Qualitative Research , Randomized Controlled Trials as Topic/methods , Resuscitation/education , Humans , Learning
3.
PLoS One ; 9(2): e90439, 2014.
Article in English | MEDLINE | ID: mdl-24587363

ABSTRACT

Indoleamine 2,3-dioxygenase (IDO) is a tryptophan-degrading enzyme known to suppress antitumor CD8(+) T cells (TCD8). The role of IDO in regulation of antiviral TCD8 responses is far less clear. In addition, whether IDO controls both immunodominant and subdominant TCD8 is not fully understood. This is an important question because the dominance status of tumor- and virus-specific TCD8 may determine their significance in protective immunity and in vaccine design. We evaluated the magnitude and breadth of cross-primed TCD8 responses to simian virus 40 (SV40) large T antigen as well as primary and recall TCD8 responses to influenza A virus (IAV) in the absence or presence of IDO. IDO(-/-) mice and wild-type mice treated with 1-methyl-D-tryptophan, a pharmacological inhibitor of IDO, exhibited augmented responses to immunodominant epitopes encoded by T antigen and IAV. IDO-mediated suppression of these responses was independent of CD4(+)CD25(+)FoxP3(+) regulatory T cells, which remained numerically and functionally intact in IDO(-/-) mice. Treatment with L-kynurenine failed to inhibit TCD8 responses, indicating that tryptophan metabolites are not responsible for the suppressive effect of IDO in our models. Immunodominant T antigen-specific TCD8 from IDO(-/-) mice showed increased Ki-67 expression, suggesting that they may have acquired a more vigorous proliferative capacity in vivo. In conclusion, IDO suppresses immunodominant TCD8 responses to tumor and viral antigens. Our work also demonstrates that systemic primary and recall TCD8 responses to IAV are controlled by IDO. Inhibition of IDO thus represents an attractive adjuvant strategy in boosting anticancer and antiviral TCD8 targeting highly immunogenic antigens.


Subject(s)
CD8-Positive T-Lymphocytes/immunology , Immune Tolerance/genetics , Indoleamine-Pyrrole 2,3,-Dioxygenase/immunology , Animals , Antigens, Polyomavirus Transforming/immunology , Antigens, Viral/immunology , CD4 Antigens/genetics , CD4 Antigens/immunology , CD8-Positive T-Lymphocytes/cytology , CD8-Positive T-Lymphocytes/drug effects , CD8-Positive T-Lymphocytes/metabolism , Forkhead Transcription Factors/genetics , Forkhead Transcription Factors/immunology , Gene Expression , Immunity, Innate , Indoleamine-Pyrrole 2,3,-Dioxygenase/antagonists & inhibitors , Indoleamine-Pyrrole 2,3,-Dioxygenase/deficiency , Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics , Influenza A virus/immunology , Interleukin-2 Receptor alpha Subunit/genetics , Interleukin-2 Receptor alpha Subunit/immunology , Kynurenine/pharmacology , Lymphocyte Activation , Mice , Mice, Knockout , T-Lymphocytes, Regulatory/cytology , T-Lymphocytes, Regulatory/immunology , T-Lymphocytes, Regulatory/metabolism , Tryptophan/analogs & derivatives , Tryptophan/pharmacology
4.
Trends Mol Med ; 17(2): 65-77, 2011 Feb.
Article in English | MEDLINE | ID: mdl-21087900

ABSTRACT

Invariant natural killer T (iNKT) cells are innate lymphocytes with unique specificity for glycolipid antigens and remarkable immunomodulatory properties. The role of costimulatory interactions in iNKT cell responses has recently come under scrutiny. Although iNKT cells and their prototype glycolipid agonist α-galactosylceramide (α-GalCer) have shown promise in several clinical trials conducted in patients with cancer or viral diseases, current iNKT cell-based therapies are far from effective. The concomitant targeting of T cell receptors (TCRs) and costimulatory molecules on iNKT cells represents an exciting new opportunity to optimize such therapeutic approaches. Here, we review recent advances in our understanding of iNKT cell costimulation and discuss potential treatment modalities based on the responsiveness of iNKT cells to disease-tailored glycolipids and select costimulatory ligands.


Subject(s)
Immunotherapy , Natural Killer T-Cells/immunology , Animals , Antigens, Differentiation/genetics , Antigens, Differentiation/immunology , Gene Expression Regulation/immunology , Humans , Lymphocyte Activation/immunology , Proto-Oncogene Proteins/genetics , Proto-Oncogene Proteins/immunology , Signal Transduction/genetics , Signal Transduction/immunology
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