The OSSE: Development and validation of an "Objective Structured Supervision Evaluation".

Background: Trainee supervision and teaching are distinct skills that both require faculty physician competence to ensure patient safety. No standard approach exists to teach physician supervisory competence, resulting in variable trainee oversight and safety threats. The Objective Structured Teaching Evaluation (OSTE) does not adequately incorporate the specific skills required for effective supervision. To address this continuing medical education gap, the authors aimed to develop and identify validity evidence for an "Objective Structured Supervision Evaluation" (OSSE) for attending physicians, conceptually modeled on the historic OSTE. Methods: An expert panel used an iterative process to create an OSSE instrument, which was a checklist of key supervision items to be evaluated during a simulated endotracheal intubation scenario. Three trained "standardized residents" scored faculty participants' performance using the instrument. Validity testing modeled a contemporary approach using Kane's framework. Participants underwent simulation-based mastery learning (SBML) with deliberate practice until meeting a minimum passing standard (MPS). Results: The final instrument contained 19 items, including three global rating measures. Testing domains included supervision climate, participant control of patient care, trainee evaluation, instructional skills, case-specific measures, and overall supervisor rating. Reliability of the assessment tool was excellent (ICC range 0.84-0.89). The assessment tool had good internal consistency (Cronbach's α = 0.813). Out of 24 faculty participants, 17 (70.8%) met the MPS on initial assessment. All met the MPS after SBML and average score increased by 19.5% (95% CI of the difference 10.3%-28.8%, p = 0.002).

The Utility of Peers and Trained Raters in Technical Skill-based Assessments a Generalizability Theory Study.

OBJECTIVE: The gold standard for evaluation of resident procedural competence is that of validated assessments from faculty surgeons. A provision of adequate trainee assessments is challenged by a shortage of faculty due to increased clinical and administrative responsibilities. We hypothesized that with a well constructed assessment instrument and training, there would be minimal differences in procedural assessments made by near-peer resident raters (RR), faculty raters (FR), and trained raters (TR). DESIGN: Deidentified videos of residents performing hand-sewn (HA) and stapled (SA) anastomoses were distributed to blinded reviewers of 3 types. Intra-class correlation (ICC) of RR, FR and TR assessments was determined for each procedure. A fully-crossed design was used to examine the internal structure validity in a generalizability study. A Decision study was performed to make projections on the number of raters needed for a g-coefficient > 0.70. SETTING: This study was conducted within a private academic institution, using the creation of intestinal anastomoses as the procedural model. PARTICIPANTS: Raters consisted of residents who were untrained to the assessment (UTA) tool, UTA faculty surgeons, and individuals with training. RESULTS: Twenty nine videos were reviewed (15 HA and 14 SA) by a total of 9 video reviewers (4 RR, 2 FR, and 3 TR). HA ICC values were 0.84 (Confidence Interval [CI]:0.81-0.87) for RR, 0.89 (CI:0.86-0.92) for FR, and 0.88 (CI:0.86-0.90) for TR. SA ICC values were 0.77 (CI:0.72-0.80) for RR, 0.79 (CI:0.75-0.83) for FR, and 0.86 (CI:0.83-0.88) for TR. The g-coefficient was RR = 0.72, FR = 0.85, and TR = 0.77 for HA; and RR = 0.33, FR = 0.38, and TR = 0.4 for SA. The D-study indicated that at least 2 raters of any type were needed for HA and > 11 FR for SA. CONCLUSIONS: Faculty without training have high assessment agreement. Peers for surgical skills assessment is an option for formative evaluation without training. Training to assessment tools should be performed for any assessment, formative or summative, for the optimal evaluation of procedural competence.

The Prevalence of Disability Health Training and Residents With Disabilities in Emergency Medicine Residency Programs.

OBJECTIVES: Individuals with disabilities experience significant health care disparities due to a multitude of barriers to effective care, which include a lack of adequate physician training on this topic and negative attitudes of physicians. This results in disparities through inadequate physical examination and diagnostic testing, withholding or inferior treatment, and neglecting preventative care. While much has been published about disability education in undergraduate medical education, little is known about the current state of disability education in emergency medicine (EM) residency programs. METHODS: In 2019, a total of 237 EM residency program directors (PDs) in the United States were surveyed about the actual and desired number of hours of disability health instruction, perceived barriers to disability health education, prevalence of residents and faculty with disabilities, and confidence in providing accommodations to residents with disabilities. RESULTS: A total of 104 surveys were completed (104/237, 43.9% response rate); 43% of respondents included disability-specific content in their residency curricula for an average of 1.5 total hours annually, in contrast to average desired hours of 4.16 hours. Reported barriers to disability health education included lack of time and lack of faculty expertise. A minority of residency programs have faculty members (13.5%) or residents (26%) with disabilities. The prevalence of EM residents with disabilities was 4.02%. Programs with residents with disabilities reported more hours devoted to disability curricula (5 hours vs 1.54 hours, p = 0.017) and increased confidence in providing workplace accommodations for certain disabilities including mobility disability (p = 0.002), chronic health conditions (p = 0.022), and psychological disabilities (p = 0.018). CONCLUSIONS: A minority of EM PDs in our study included disability health content in their residency curricula. The presence of faculty and residents with disabilities is associated with positive effects on training programs, including a greater number of hours devoted to disability health education and greater confidence in accommodating learners with disabilities. To reduce health care disparities for patients with disabilities, we recommend that a dedicated disability health curriculum be integrated into all aspects of the EM residency curriculum, including lectures, journal clubs, and simulations and include direct interaction with individuals with disabilities. We further recommend that disability be recognized as an aspect of diversity when hiring faculty and recruiting residents to EM programs, to address this training gap and to promote a diverse and inclusive learning environment.

Emergency Medicine Resident Education on Caring for Patients With Disabilities: A Call to Action.

People with disabilities constitute a marginalized population who experience significant health care disparities resulting from structural, socioeconomic, and attitudinal barriers to accessing health care. It has been reported that education on the care of marginalized groups helps to improve awareness, patient-provider rapport, and patient satisfaction. Yet, emergency medicine (EM) residency education on care for people with disabilities may be lacking. The goal of this paper is to review the current state of health care for patients with disabilities, review the current state of undergraduate and graduate medical education on the care of patients with disabilities, and provide suggestions for an improved EM residency curriculum that includes education on the care for patients with disabilities.

Ocular Dominance Plasticity in Binocular Primary Visual Cortex Does Not Require C1q.

C1q, the initiator of the classical complement cascade, mediates synapse elimination in the postnatal mouse dorsolateral geniculate nucleus of the thalamus and sensorimotor cortex. Here, we asked whether C1q plays a role in experience-dependent synaptic refinement in the visual system at later stages of development. The binocular zone of primary visual cortex (V1b) undergoes spine loss and changes in neuronal responsiveness following the closure of one eye during a defined critical period [a process referred to as ocular dominance plasticity (ODP)]. We therefore hypothesized that ODP would be impaired in the absence of C1q, and that V1b development would also be abnormal without C1q-mediated synapse elimination. However, when we examined several features of V1b development in mice lacking C1q, we found that the densities of most spine populations on basal and proximal apical dendrites, as well as firing rates and ocular dominance, were normal. C1q was only transiently required for the development of spines on apical, but not basal, secondary dendrites. Dendritic morphologies were also unaffected. Although we did not observe the previously described spine loss during ODP in either genotype, our results reveal that the animals lacking C1q had normal shifts in neuronal responsiveness following eye closure. Experiments were performed in both male and female mice. These results suggest that the development and plasticity of the mouse V1b is grossly normal in the absence of C1q.SIGNIFICANCE STATEMENT These findings illustrate that the development and experience-dependent plasticity of V1b is mostly normal in the absence of C1q, even though C1q has previously been shown to be required for developmental synapse elimination in the mouse visual thalamus as well as sensorimotor cortex. The V1b phenotypes in mice lacking C1q are more similar to the mild defects previously observed in the hippocampus of these mice, emphasizing that the contribution of C1q to synapse elimination appears to be dependent on context.

Automated dendritic spine detection using convolutional neural networks on maximum intensity projected microscopic volumes.

BACKGROUND: Dendritic spines are structural correlates of excitatory synapses in the brain. Their density and structure are shaped by experience, pointing to their role in memory encoding. Dendritic spine imaging, followed by manual analysis, is a primary way to study spines. However, an approach that analyses dendritic spines images in an automated and unbiased manner is needed to fully capture how spines change with normal experience, as well as in disease. NEW METHOD: We propose an approach based on fully convolutional neural networks (FCNs) to detect dendritic spines in two-dimensional maximum-intensity projected images from confocal fluorescent micrographs. We experiment on both fractionally strided convolution and efficient sub-pixel convolutions. Dendritic spines far from the dendritic shaft are pruned by extraction of the shaft to reduce false positives. Performance of the proposed method is evaluated by comparing predicted spine positions to those manually marked by experts. RESULTS: The averaged distance between predicted and manually annotated spines is 2.81 ± 2.63 pixels (0.082 ± 0.076 microns) and 2.87 ± 2.33 pixels (0.084 ± 0.068 microns) based on two different experts. FCN-based detection achieves F scores > 0.80 for both sets of expert annotations. COMPARISON WITH EXISTING METHODS: Our method significantly outperforms two well-known software, NeuronStudio and Neurolucida (p-value < 0.02). CONCLUSIONS: FCN architectures used in this work allow for automated dendritic spine detection. Superior outcomes are possible even with small training data-sets. The proposed method may generalize to other datasets on larger scales.

Cell-Autonomous Regulation of Dendritic Spine Density by PirB.

Synapse density on cortical pyramidal neurons is modulated by experience. This process is highest during developmental critical periods, when mechanisms of synaptic plasticity are fully engaged. In mouse visual cortex, the critical period for ocular dominance (OD) plasticity coincides with the developmental pruning of synapses. At this time, mice lacking paired Ig-like receptor B (PirB) have excess numbers of dendritic spines on L5 neurons; these spines persist and are thought to underlie the juvenile-like OD plasticity observed in adulthood. Here we examine whether PirB is required specifically in excitatory neurons to exert its effect on dendritic spine and synapse density during the critical period. In mice with a conditional allele of PirB (PirBfl/fl), PirB was deleted only from L2/3 cortical pyramidal neurons in vivo by timed in utero electroporation of Cre recombinase. Sparse mosaic expression of Cre produced neurons lacking PirB in a sea of wild-type neurons and glia. These neurons had significantly elevated dendritic spine density, as well as increased frequency of miniature EPSCs, suggesting that they receive a greater number of synaptic inputs relative to Cre- neighbors. The effect of cell-specific PirB deletion on dendritic spine density was not accompanied by changes in dendritic branching complexity or axonal bouton density. Together, results imply a neuron-specific, cell-autonomous action of PirB on synaptic density in L2/3 pyramidal cells of visual cortex. Moreover, they are consistent with the idea that PirB functions normally to corepress spine density and synaptic plasticity, thereby maintaining headroom for cells to encode ongoing experience-dependent structural change throughout life.

Developmental Sculpting of Intracortical Circuits by MHC Class I H2-Db and H2-Kb.

Synapse pruning is an activity-regulated process needed for proper circuit sculpting in the developing brain. Major histocompatibility class I (MHCI) molecules are regulated by activity, but little is known about their role in the development of connectivity in cortex. Here we show that protein for 2 MHCI molecules H2-Kb and H2-Db is associated with synapses in the visual cortex. Pyramidal neurons in mice lacking H2-Kb and H2-Db (KbDb KO) have more extensive cortical connectivity than normal. Modified rabies virus tracing was used to monitor the extent of pyramidal cell connectivity: Horizontal connectivity is greater in the visual cortex of KbDb KO mice. Basal dendrites of L2/3 pyramids, where many horizontal connections terminate, are more highly branched and have elevated spine density in the KO. Furthermore, the density of axonal boutons is elevated within L2/3 of mutant mice. These increases are accompanied by elevated miniature excitatory postsynaptic current frequency, consistent with an increase in functional synapses. This functional and anatomical increase in intracortical connectivity is also associated with enhanced ocular dominance plasticity that persists into adulthood. Thus, these MHCI proteins regulate sculpting of local cortical circuits and in their absence, the excess connectivity can function as a substrate for cortical plasticity throughout life.

Blocking PirB up-regulates spines and functional synapses to unlock visual cortical plasticity and facilitate recovery from amblyopia.

During critical periods of development, the brain easily changes in response to environmental stimuli, but this neural plasticity declines by adulthood. By acutely disrupting paired immunoglobulin-like receptor B (PirB) function at specific ages, we show that PirB actively represses neural plasticity throughout life. We disrupted PirB function either by genetically introducing a conditional PirB allele into mice or by minipump infusion of a soluble PirB ectodomain (sPirB) into mouse visual cortex. We found that neural plasticity, as measured by depriving mice of vision in one eye and testing ocular dominance, was enhanced by this treatment both during the critical period and when PirB function was disrupted in adulthood. Acute blockade of PirB triggered the formation of new functional synapses, as indicated by increases in miniature excitatory postsynaptic current (mEPSC) frequency and spine density on dendrites of layer 5 pyramidal neurons. In addition, recovery from amblyopia--the decline in visual acuity and spine density resulting from long-term monocular deprivation--was possible after a 1-week infusion of sPirB after the deprivation period. Thus, neural plasticity in adult visual cortex is actively repressed and can be enhanced by blocking PirB function.