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Problem The University of Houston College of Medicine (UH COM) began its first admissions cycle after receiving preliminary accreditation in February 2020. With the advent of remote learning in response to the COVID-19 pandemic, the school moved its admissions process, including the multiple mini-interview (MMI), from an in-person to online format in mid-March 2020. Approach The UH COM selected Zoom as the video conferencing platform for its virtual admissions process, including the MMI. On each interview day (3-4 hours), 14-16 applicants joined administrators, faculty, and staff in a virtual meeting room. Applicants were divided into two groups: one viewed short presentations about the school, curriculum, and departments, while the other participated in 7 MMI stations (one-on-one interactions with interviewers) via virtual breakout rooms; the groups then switched. The MMI stations were the same as those used in person in early March. Applicants were able to ask questions at multiple points during the day. Technical support was provided for participants with connectivity issues or unfamiliar with Zoom. Outcomes Of the 180 applicants interviewed in March-April 2020, 134 (74%) participated in the virtual process and 46 (26%) in the on-site process. Twenty-five (83%) of the 30 members of the inaugural class of 2025 interviewed virtually. Advantages of the virtual format included ease of access for faculty and more flexibility and less expense for applicants. Challenges included the need for applicants to decide whether to accept an offer of admission from a new school without visiting and missed opportunities for faculty to have relatively unstructured interactions with applicants. Next steps This virtual admissions process was a feasible alternative for the inaugural class but is not sustainable. The UH COM plans to leverage lessons learned to refine the virtual format for use in future admissions cycles, even when in-person interviews are possible.

Long-term ethanol consumption at low to moderate levels exerts cardioprotective effects in the setting of ischemia and reperfusion (I/R). The aims of this study were to determine whether 1) a single orally administered dose of ethanol [ethanol preconditioning (EtOH-PC)] would induce a biphasic temporal pattern of protection (early and late phases) against the inflammatory responses to I/R and 2) adenosine and nitric oxide (NO) act as initiators of the late phase of protection. Ethanol was administered as a bolus to C57BL/6 mice at a dose that achieved a peak plasma concentration of ∼45 mg/dl 30 min after gavage and returned to control levels within 60 min of alcohol ingestion. The superior mesenteric artery was occluded for 45 min followed by 60 min of reperfusion beginning 10 min or 1, 2, 3, 4, or 24 h after ethanol ingestion, and the numbers of fluorescently labeled rolling and firmly adherent (stationary) leukocytes in single postcapillary venules of the small intestine were quantified using intravital microscopic approaches. I/R induced marked increases in leukocyte rolling and adhesion, effects that were attenuated by EtOH-PC 2–3 h before I/R (early phase), absent when assessed after 10 min, 1 h, and 4 h of ethanol ingestion, with an even more powerful late phase of protection reemerging when I/R was induced 24 h later. The anti-inflammatory effects of late EtOH-PC were abolished by treatment with adenosine deaminase, an adenosine A2(but not A1) receptor antagonist, or a NO synthase (NOS) inhibitor during the period of EtOH-PC. Preconditioning with an adenosine A2(but not an A1) receptor agonist in lieu of ethanol 24 h before I/R mimicked the protective actions of late phase EtOH-PC. Like EtOH-PC, the effect of preconditioning with an adenosine A2receptor agonist was abrogated by coincident NOS inhibition. These findings suggest that EtOH-PC induces a biphasic temporal pattern of protection against the proinflammatory effects of I/R. In addition, our observations are consistent with the hypothesis that the late phase of EtOH-PC is triggered by NO formed secondary to adenosine A2receptor-dependent activation of NOS during the period of ethanol exposure.

Ingestion of low levels of ethanol 24 h before [ethanol preconditioning (EPC)] ischemia and reperfusion (I/R) prevents postischemic leukocyte rolling (LR) and adhesion (LA), effects that were abolished by adenosine A2receptor (ADO-A2R) antagonists or nitric oxide (NO) synthase (NOS) inhibitors. The aims of this study were to determine whether NO derived from endothelial NOS (eNOS) during the period of ethanol exposure triggered entrance into this preconditioned state and whether these events were initiated by an ADO-A2R-dependent mechanism. Ethanol or distilled water vehicle was administered to C57BL/6J [wild type (WT)] or eNOS-deficient (eNOS−/−) mice by gavage. Twenty-four hours later, the superior mesenteric artery was occluded for 45 min. LR and LA were quantified by intravital microscopy after 30 and 60 min of reperfusion. I/R increased LR and LA in WT mice, effects that were abolished by EPC or NO donor preconditioning (NO-PC). NO-PC was not attenuated by coincident administration of an ADO-A2R antagonist. I/R increased LR and LA in eNOS−/− mice to levels comparable with those noted in WT animals. However, EPC only slightly attenuated postischemic LR and LA, whereas NO-PC remained effective as a preconditioning stimulus in eNOS−/− mice. Preconditioning with an ADO-A2R agonist (which we previously demonstrated prevents I/R-induced LR and LA in WT animals) failed to attenuate these postischemic adhesive responses in eNOS−/− mice. Our results indicate that EPC is triggered by NO formed secondary to ADO-A2R-dependent eNOS activation during the period of ethanol exposure 24 h before I/R.

Prolonged ischemia followed by reperfusion (I/R) results in impaired endothelial cell function in all segments of the microvasculature. Moreover, microcirculatory dysfunction plays a major role in the genesis of the reperfusion component of total tissue injury in I/R. Thus, preservation of endothelial function is an important therapeutic goal for ameliorating injury in tissues subjected to I/R. An accumulating body of evidence indicates that low to moderate ethanol consumption produces an adaptive transformation to a protected phenotype in both microvascular endothelium and parenchymal cells such that they are rendered resistant to the pathologic effects of I/R. The purpose of this review is to summarize our current understanding of the signaling pathways underlying the development of the preconditioned state induced by antecedent ethanol in arteriolar, capillary, and venular endothelium. In addition, we will highlight understudied areas with regard to microvascular protection afforded by antecedent ethanol in the hopes that this will stimulate investigation of its underlying mechanisms. Understanding these signaling pathways may provide a mechanistic rationale for the development of novel treatment interventions that target both the microcirculatory and parenchymal sequelae to I/R, thereby maximizing the therapeutic potential of the protected phenotypes produced by pharmacologic preconditioning.