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Background Telemedicine holds promise to bridge the transition of care between inpatient and outpatient settings. Despite this, the unique communication and technical skills required for virtual encounters are not routinely taught or practiced in graduate medical education (GME) programs. Objective To develop an objective structured clinical examination (OSCE) case to assess residents' telemedicine-specific skills and identify potential gaps in our residency program's curriculum. Methods As part of a multi-station OSCE in 2019, we developed a case simulating a remote encounter between a resident and a recently discharged standardized patient. We developed an assessment tool comprising specific behaviors anchored to “not done,” “partly done,” and “well done” descriptors to evaluate core communication and telemedicine-specific skills. Results Seventy-eight NYU internal medicine residents participated in the case. Evaluations from 100% of participants were obtained. Residents performed well in Information Gathering and Relationship Development domains. A mean 95% (SD 3.3%) and 91% (SD 4.9%) of residents received “well done” evaluations across these domains. A mean 78% (SD 14%) received “well done” within Education/Counseling domain. However, only 46% (SD 45%) received “well done” evaluations within the Telemedicine domain; specific weak areas included performing a virtual physical examination (18% well done) and leveraging video to augment history gathering (17% well done). There were no differences in telemedicine-specific skill evaluations when stratified by training track or postgraduate year. Conclusions We simulate a post-discharge virtual encounter and present a novel assessment tool that uncovers telemedicine-specific knowledge gaps in GME trainees.

Virtual urgent care (VUC) provides real-time evaluation, triage, and treatment of low-acuity medical problems; however, VUC physicians have varying levels of telemedicine training. We created a workplace-based experiential onboarding program that deployed standardized patients (SPs) into a VUC clinic to evaluate and deliver feedback to independently practicing physicians, providing quality assurance and identifying areas for improvement.We simulated evaluation of an adult with upper respiratory symptoms. To replicate a real-life encounter, we developed a mock electronic medical entry with demographic and medical information and scheduled SPs into the clinic's actual patient queue. SPs provided seamless, realistic training within the real-world virtual clinic environment. Using an adapted assessment tool anchored toTwenty-one physicians participated. All performed well in core communication and disease management domains. Ninety-three percent of behaviors (This workplace-based experiential onboarding program uncovered knowledge gaps within telemedicine skills and patient education domains. Identification of these gaps can help drive new virtual care curricula.

The COVID-19 pandemic has dramatically disrupted the educational experience of medical trainees. However, a detailed characterization of exactly how trainees’ clinical experiences have been affected is lacking. Here, we profile residents’ inpatient clinical experiences across the four training hospitals of NYU’s Internal Medicine Residency Program during the pandemic’s first wave. We mined ICD-10 principal diagnosis codes attributed to residents from February 1, 2020, to May 31, 2020. We translated these codes into discrete medical content areas using a newly developed “crosswalk tool.” Residents’ clinical exposure was enriched in infectious diseases (ID) and cardiovascular disease content at baseline. During the pandemic’s surge, ID became the dominant content area. Exposure to other content was dramatically reduced, with clinical diversity repopulating only toward the end of the study period. Such characterization can be leveraged to provide effective practice habits feedback, guide didactic and self-directed learning, and potentially predict competency-based outcomes for trainees in the COVID era.

PROBLEM Internal medicine training programs operate under the assumption that the three-year residency training period is sufficient for trainees to achieve the depth and breadth of clinical experience necessary for independent practice; however, the medical conditions to which residents are exposed in clinical practice are not easily measured. As a result, residents' clinical educational experiences are poorly understood. APPROACH A crosswalk tool (a repository of international classification of diseases [ICD]-10 codes linked to medical content areas) was developed to query routinely collected inpatient principal diagnosis codes and translate them into an educationally meaningful taxonomy. This tool provides a robust characterization of residents' inpatient clinical experiences. OUTCOMES This pilot study has provided proof of principle that the crosswalk tool can effectively map one year of resident-attributed diagnosis codes to both the broad content category level (for example "Cardiovascular Disease") and to the more specific condition category level (for example "Myocardial Disease"). The authors uncovered content areas in their training program that are overrepresented and some that are underrepresented relative to material on the American Board of Internal Medicine (ABIM) Certification Exam. NEXT STEPS The crosswalk tool introduced here translated residents' patient care activities into discrete, measurable educational content and enabled one internal medicine residency training program to characterize residents' inpatient educational experience with a high degree of resolution. Leaders of other programs seeking to profile the clinical exposure of their trainees may adopt this strategy. Such clinical content mapping drives innovation in the experiential curriculum, enables comparison across practice sites, and lays the groundwork to test associations between individual clinical exposure and competency-based outcomes, which, in turn, will allow medical educators to draw conclusions regarding how clinical experience reflects clinical competency.

Infections caused by foodborne enteric pathogens including typhoidal and non-typhoidal Salmonella species can mimic symptoms of acute appendicitis. The association between such bacterial pathogens and pathology-proven acute appendicitis has been described, but this link is poorly understood. Here we describe a case of a young man with typhoid fever presenting with histology-proven acute appendicitis requiring urgent appendectomy, and provide a brief review of relevant literature to prompt more widespread recognition of this rare cause of a common surgical emergency.

Antithrombotic therapy for stroke prevention in patients with atrial fibrillation (AF) has dramatically shifted from warfarin, a vitamin K antagonist, to the direct oral anticoagulants (DOACs) such as dabigatran, apixaban, and rivaroxaban. In patients with contraindications to oral anticoagulation, left atrial appendage occlusion (LAAO) devices, such as the Watchman™ device, may be considered; however, temporary postimplantation antithrombotic therapy is still a recommended practice. We present a case of complex antithrombotic management, post LAAO device implantation, designed to avoid drug interactions with concomitant rifampin use and remained necessary secondary to subsequent device leak. This case highlights the challenges of antithrombotic therapy post LAAO device placement in a complex, but representative, patient.

Background: During the rapid onset of the pandemic, clinicians transitioned from traditional outpatient practice to virtual modalities for providing routine care to patient panels. Like training programs nationwide, telemedicine training and assessment had not been systematically incorporated into our residency. In response, a scheduled Internal Medicine (IM) Objective Structured Clinical Examination (OSCE) was adapted to a remote modality to become virtual care-focused learning experience for trainees and to provide valuable feedback to educators. Methods: Standardized Patients (SPs) rated residents on their communication (including information gathering, relationship development and patient education), patient activation and satisfaction, and telemedicine skills. Analyses included a comparison of domain scores for residents who participated in both the 2020 remote and 2019 in-person OSCEs, and a review of written resident comments about the virtual OSCE. Results: During 2020’s video visit OSCE (VOSCE), residents (n = 23) excelled at nonverbal communication but struggled with virtual physical exams and information gathering. In debrief, residents expressed substantial interest in more opportunity to practice virtual visit skills going forward. In comparing scores of the virtual care (2020) OSCE with the in-person (2019) version, the small subset of residents who participated in both assessments (n = 9) performed similarly on communication skills, patient satisfaction and activation. Patient education scores were significantly lower during the virtual care OSCE ( P = .008). Conclusion: Our reformulated OSCE accomplished 3 goals including; (1) physically distancing residents from SPs per COVID regulations, (2) providing residents with the opportunity to practice critical virtual visit skills, and (3) alerting our educators to curricular improvement areas. Our methods are useful for other institutions and have applications to the larger medical education community.

Pancreatic β-cell survival remains poorly understood despite decades of research. GATA transcription factors broadly regulate embryogenesis and influence survival of several cell types, but their role in adult β-cells remains undefined. To investigate the role of GATA factors in adult β-cells, we derived β-cell-inducible Gata4- and Gata6-knockout mice, along with whole-body inducible Gata4 knockouts. β-Cell Gata4 deletion modestly increased the proportion of dying β-cells in situ with ultrastructural abnormalities suggesting endoplasmic reticulum (ER) stress. Notably, glucose homeostasis was not grossly altered in Gata4- and Gata6-knockout mice, suggesting that GATA factors do not have essential roles in β-cells. Several ER stress signals were up-regulated in Gata4 and Gata6 knockouts, most notably CHOP, a known regulator of ER stress-induced apoptosis. However, ER stress signals were not elevated to levels observed after acute thapsigargin administration, suggesting that GATA deficiency only caused mild ER stress. Simultaneous deletion of Gata4 and CHOP partially restored β-cell survival. In contrast, whole-body inducible Gata4 knockouts displayed no evidence of ER stress in other GATA4-enriched tissues, such as heart. Indeed, distinct GATA transcriptional targets were differentially expressed in islets compared with heart. Such β-cell-specific findings prompted study of a large meta-analysis dataset to investigate single nucleotide polymorphisms harbored within the human GATA4 locus, revealing several variants significantly associated with type 1 diabetes mellitus. We conclude that GATA factors have important but nonessential roles to promote ER integrity and β-cell survival in a tissue-specific manner and that GATA factors likely contribute to type 1 diabetes mellitus pathogenesis.

Islet amyloidosis by IAPP contributes to pancreatic β-cell death in diabetes, but the nature of toxic IAPP species remains elusive. Using concurrent time-resolved biophysical and biological measurements, we define the toxic species produced during IAPP amyloid formation and link their properties to induction of rat INS-1 β-cell and murine islet toxicity. These globally flexible, low order oligomers upregulate pro-inflammatory markers and induce reactive oxygen species. They do not bind 1-anilnonaphthalene-8-sulphonic acid and lack extensive β-sheet structure. Aromatic interactions modulate, but are not required for toxicity. Not all IAPP oligomers are toxic; toxicity depends on their partially structured conformational states. Some anti-amyloid agents paradoxically prolong cytotoxicity by prolonging the lifetime of the toxic species. The data highlight the distinguishing properties of toxic IAPP oligomers and the common features that they share with toxic species reported for other amyloidogenic polypeptides, providing information for rational drug design to treat IAPP induced β-cell death. DOI: http://dx.doi.org/10.7554/eLife.12977.001

Germ line PERK mutations are associated with diabetes mellitus and growth retardation in both rodents and humans. In contrast, late embryonic excision of PERK permits islet development and was found to prevent onset of diabetes, suggesting that PERK may be dispensable in the adult pancreas. To definitively establish the functional role of PERK in adult pancreata, we generated mice harboring a conditional PERK allele in which excision is regulated by tamoxifen administration. Deletion of PERK in either young adult or mature adult mice resulted in hyperglycemia associated with loss of islet and β cell architecture. PERK excision triggered intracellular accumulation of proinsulin and Glut2, massive endoplasmic reticulum (ER) expansion, and compensatory activation of the remaining unfolded-protein response (UPR) signaling pathways specifically in pancreatic tissue. Although PERK excision increased β cell death, this was not a result of decreased proliferation as previously reported. In contrast, a significant and specific increase in β cell proliferation was observed, a result reflecting increased cyclin D1 accumulation. This work demonstrates that contrary to expectations, PERK is required for secretory homeostasis and β cell survival in adult mice.

Accurate measurement of cell division is a fundamental challenge in experimental biology that becomes increasingly complex when slowly dividing cells are analyzed. Established methods to detect cell division include direct visualization by continuous microscopy in cell culture, dilution of vital dyes such as carboxyfluorescein di-aetate succinimidyl ester (CFSE), immuno-detection of mitogenic antigens such as ki67 or PCNA, and thymidine analogues. Thymidine analogues can be detected by a variety of methods including radio-detection for tritiated thymidine, immuno-detection for bromo-deoxyuridine (BrdU), chloro-deoxyuridine (CldU) and iodo-deoxyuridine (IdU), and chemical detection for ethinyl-deoxyuridine (EdU). We have derived a strategy to detect sequential incorporation of different thymidine analogues (CldU and IdU) into tissues of adult mice. Our method allows investigators to accurately quantify two successive rounds of cell division. By optimizing immunostaining protocols our approach can detect very low dose thymidine analogues administered via the drinking water, safe to administer to mice for prolonged periods of time. Consequently, our technique can be used to detect cell turnover in very long-lived tissues. Optimal immunofluoresent staining results can be achieved in multiple tissue types, including pancreas, skin, gut, liver, adrenal, testis, ovary, thyroid, lymph node, and brain. We have also applied this technique to identify oncogenic transformation within tissues. We have further applied this technique to determine if transit-amplifying cells contribute to growth or renewal of tissues. In this sense, sequential administration of thymidine analogues represents a novel approach for studying the origins and survival of cells involved in tissue homeostasis.

The molecular determinants of beta-cell mass expansion remain poorly understood. Cyclin D2 is the major D-type cyclin expressed in beta-cells, essential for adult beta-cell growth. We hypothesized that cyclin D2 could be actively regulated in beta-cells, which could allow mitogenic stimuli to influence beta-cell expansion. Cyclin D2 protein was sharply increased after partial pancreatectomy, but cyclin D2 mRNA was unchanged, suggesting posttranscriptional regulatory mechanisms influence cyclin D2 expression in beta-cells. Consistent with this hypothesis, cyclin D2 protein stability is powerfully regulated in fibroblasts. Threonine 280 of cyclin D2 is phosphorylated, and this residue critically limits D2 stability. We derived transgenic (tg) mice with threonine 280 of cyclin D2 mutated to alanine (T280A) or wild-type cyclin D2 under the control of the insulin promoter. Cyclin D2 T280A protein was expressed at much higher levels than wild-type cyclin D2 protein in beta-cells, despite equivalent expression of tg mRNAs. Cyclin D2 T280A tg mice exhibited a constitutively nuclear cyclin D2 localization in beta-cells, and increased cyclin D2 stability in islets. Interestingly, threonine 280-mutant cyclin D2 tg mice had greatly reduced beta-cell apoptosis, with suppressed expression of proapoptotic genes. Suppressed beta-cell apoptosis in threonine 280-mutant cyclin D2 tg mice resulted in greatly increased beta-cell area in aged mice. Taken together, these data indicate that cyclin D2 is regulated by protein stability in pancreatic beta-cells, that signals that act upon threonine 280 limit cyclin D2 stability in beta-cells, and that threonine 280-mutant cyclin D2 overexpression prolongs beta-cell survival and augments beta-cell mass expansion.