Publications by authors named "Uyen T Mai"

Introduction: Coaching interventions in graduate medical education have proven successful in increasing technical and communication skills, reducing errors, and improving patient care. Effective stakeholder engagement enhances the relevance, value, and long-term sustainability of interventions, yet specific strategies for stakeholder engagement remain uncertain. The purpose of this article is to identify strategies to foster engagement of diverse stakeholder groups in coaching interventions.

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A large proportion of the world's population harbors latent HSV type 1 (HSV-1). Cross-talk between antiviral CD8 T cells and HSV-1 appear to control latency/reactivation cycles. We found that compared with healthy asymptomatic individuals, in symptomatic (SYMP) patients, the CD8 T cells with the same HLA-A*0201-restricted HSV-1 epitope specificities expressed multiple genes and proteins associated to major T cell exhaustion pathways and were dysfunctional.

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While the role of CD8 T cells in the control of herpes simplex virus 1 (HSV-1) infection and disease is gaining wider acceptance, a direct involvement of effector CD4 T cells in this protection and the phenotype and function of HSV-specific human CD4 T cell epitopes remain to be fully elucidated. In the present study, we report that several epitopes from the HSV-1 virion tegument protein (VP11/12) encoded by UL46 are targeted by CD4 T cells from HSV-seropositive asymptomatic individuals (who, despite being infected, never develop any recurrent herpetic disease). Among these, we identified two immunodominant effector memory CD4 T cell epitopes, amino acids (aa) 129 to 143 of VP11/12 (VP11/12) and VP11/12, using , , and approaches based on the following: (i) a combination of the TEPITOPE algorithm and PepScan library scanning of the entire 718 aa of HSV-1 VP11/12 sequence; (ii) an peptide-protein docking analysis and binding assay that identify epitopes with high affinity to soluble HLA-DRB1 molecules; and (iii) an ELISpot assay and intracellular detection of gamma interferon (IFN-γ), CD107 degranulation, and CD4 T cell carboxyfluorescein succinimidyl ester (CFSE) proliferation assays.

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The crosstalk between the host's inflammasome system and the invading virulent/less-virulent viruses determines the outcome of the ensuing inflammatory response. An appropriate activation of inflammasomes triggers antiviral inflammatory responses that clear the virus and heal the inflamed tissue. However, an aberrant activation of inflammasomes can result in a harmful and overwhelming inflammation that could damage the infected tissue.

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