Correction to: Internal Medicine Point of Care Ultrasound: Indicators It's Here to Stay.

This editorial, "Internal Medicine Point of Care Ultrasound: Indicators It's Here to Stay" (DOI: 10.1007/s11606-019-05268-0), was intended to accompany "Education Indicators for Internal Medicine Point-of-Care Ultrasound: a Consensus Report from the Canadian Internal Medicine Ultrasound (CIMUS) Group".

Education Indicators for Internal Medicine Point-of-Care Ultrasound: a Consensus Report from the Canadian Internal Medicine Ultrasound (CIMUS) Group.

BACKGROUND: Curriculum development and implementation for internal medicine point-of-care ultrasound (IM POCUS) continues to be a challenge for many residency training programs. Education indicators may provide a useful framework to support curriculum development and implementation efforts across programs in order to achieve a consistent high-quality educational experience. OBJECTIVE: This study seeks to establish consensus-based recommendations for education indicators for IM POCUS training programs in Canada. DESIGN: This consensus study uses a modified nominal group technique for voting in the initial round, followed by two additional rounds of online voting, with consensus defined as agreement by at least 80% of the participants. PARTICIPANTS: Participants were 22 leaders with POCUS and/or education expertise from 13 Canadian internal medicine residency programs across 7 provinces. MAIN MEASURES: Education indicators considered were those that related to aspects of the POCUS educational system, could be presented by a single statistical measure, were readily understood, could be reliably measured to provide a benchmark for measuring change, and represented a policy issue. We excluded a priori indicators with low feasibility, are impractical, or assess learner reactions. Candidate indicators were drafted by two academic internists with post-graduate training in POCUS and medical education. These indicators were reviewed by two internists with training in quality improvement prior to presentation to the expert participants. KEY RESULTS: Of the 52 candidate education indicators considered, 6 reached consensus in the first round, 12 in the second, and 4 in the third round. Only 5 indicators reached consensus to be excluded; the remaining indicators did not reach consensus. CONCLUSIONS: The Canadian Internal Medicine Ultrasound (CIMUS) group recommends 22 education indicators be used to guide and monitor internal medicine POCUS curriculum development efforts in Canada.

The coxsackie-adenovirus receptor induces an inflammatory cardiomyopathy independent of viral infection.

The coxsackie-adenovirus receptor (CAR) is a viral receptor for Group B coxsackieviruses (CVBs) and adenoviruses. CAR has been linked with the innate immune response to CVB myocarditis, and with activation of inflammatory cells in vitro. We hypothesized that CAR activates signals that promote inflammation in the myocardium independent of viral infection. To test this we conditionally overexpressed murine CAR in cardiomyocytes of adult binary transgenic mice under the control of a tetracycline-responsive (tet-off) α-myosin heavy chain (αMtTA) promoter (mCAR(+)/αMtTA(+) mice). An inflammatory cardiomyopathy developed in both lines generated (6-mCAR(+)/αMtTA(+) and 12-mCAR(+)/αMtTA(+)) following withdrawal of doxycycline. Cardiac CAR was upregulated at 4weeks of age in 6-mCAR(+)/αMtTA(+) mice and induced a mild inflammatory infiltrate (score 1.3 of 4.0±0.3) at 6weeks, with 95% of mice surviving to that time. In the second line, 12-mCAR(+)/αMtTA(+) mice, CAR was upregulated in the majority of mice by 3weeks of age, and by 5weeks of age more severe cardiac inflammation (score 2.8 of 4.0±0.4) developed with only 56% of mice surviving. The cardiac inflammatory infiltrate was primarily natural killer cells and macrophages in both mCAR(+)/αMtTA(+) lines. A proinflammatory cytokine response with increased cardiac interferon-γ, interleukin (IL)-12, IL-1ß, tumor necrosis factor-α and IL-6 was detected by real-time RT-PCR. CAR has been linked to signaling via the inflammatory mitogen-activated protein kinase (MAPK) cascades; therefore, we evaluated the response of these pathways in hearts with upregulated CAR. Both stress-activated JNK and p38MAPK were activated in mCAR(+)/αMtTA(+) hearts prior to onset of inflammation and in isolated mCAR(+)/αMtTA(+) cardiomyocytes. In conclusion, we show for the first time that CAR upregulation in the adult mouse heart induces cardiac inflammation reminiscent of early viral myocarditis. CAR-induced stress-activated MAPK signaling may contribute to the development of cardiac inflammation unrelated to viral infection per se.

Acute exercise activates myocardial nuclear factor kappa B.

The myocardial stress response to exercise is dependent on exercise intensity and thus understanding the molecular responses between various exercise intensity levels might aid in exercise prescription. Nuclear factor kappa B (NF-κB) is a ubiquitous transcription factor that mediates a variety of cellular processes including inflammation, immune responses, apoptosis and cell growth/development. NF-κB can be comprised of homo- and/or heterodimers formed from five distinct proteins: p50 (NF-κB1), p52 (NF-κB2), RelA (p65), c-Rel, and RelB. NF-κB is located in the cytoplasm and kept inactive by inhibitory proteins but following the exposure to a myriad of stimuli, an activated NF-κB dimer translocates to the nucleus and exerts transcriptional effects on upwards of 150 genes. To examine the activation of NF-κB in the myocardium following exercise, male Sprague-Dawley rats (n = 24) were exercised by treadmill running at 20 m/min for 30 min or 30 m/min for 20 min. At 0, 2, or 24 h following exercise, animals were anesthetized, hearts excised and immediately frozen in liquid nitrogen. Portions of hearts were homogenized, protein concentrations determined and extracts assayed for NF-κB activation (DNA binding activity) using electrophoretic mobility shift assays (EMSA). Visual examination of EMSA autoradiographs revealed an enhanced NF-κB activation in the hearts from exercised animals when compared with non-running controls. Subsequent supershift analyses using antibodies specific for NF-κB subunits showed the higher intensity exercise was associated with p65 (RelA) in the activated NF-κB complex while the NF-κB complex in hearts from animals exercised at the lower intensity was comprised primarily of p50. These data suggest exercise is capable of activating myocardial NF-κB and that a threshold for the activation of specific NF-κB subunits may exist.