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IntroductionThe fundamentals of endoscopic surgery (FES) program has considerable validity evidence for its use in measuring the knowledge, skills, and abilities required for competency in endoscopy. Beginning in 2018, the American Board of Surgery will require all candidates to have taken and passed the written and performance exams in the FES program. Recent work has shown that the current ACGME/ABS required case volume may not be enough to ensure trainees pass the FES skills exam. The aim of this study was to investigate the feasibility of a simulation-based mastery-learning curriculum delivered on a novel physical simulation platform to prepare trainees to pass the FES manual skills exam.MethodsThe newly developed endoscopy training system (ETS) was used as the training platform. Seventeen PGY 1 (10) and PGY 2 (7) general surgery residents completed a pre-training assessment consisting of all 5 FES tasks on the GI Mentor II. Subjects then trained to previously determined expert performance benchmarks on each of 5 ETS tasks. Once training benchmarks were reached for all tasks, a post-training assessment was performed with all 5 FES tasks.ResultsTwo subjects were lost to follow-up and never returned for training or post-training assessment. One additional subject failed to complete any portion of the curriculum, but did return for post-training assessment. The group had minimal endoscopy experience (median 0, range 0–67) and minimal prior simulation experience. Three trainees (17.6%) achieved a passing score on the pre-training FES assessment. Training consisted of an average of 48 ± 26 repetitions on the ETS platform distributed over 5.1 ± 2 training sessions. Seventy-one percent achieved proficiency on all 5 ETS tasks. There was dramatic improvement demonstrated on the mean post-training FES assessment when compared to pre-training (74.0 ± 8 vs. 50.4 ± 16, p < 0.0001, effect size = 2.4). The number of ETS tasks trained to proficiency correlated moderately with the score on the post-training assessment (r = 0.57, p = 0.028). Fourteen (100%) subjects who trained to proficiency on at least one ETS task passed the post-training FES manual skills exam.ConclusionsThis simulation-based mastery learning curriculum using the ETS is feasible for training novices and allows for the acquisition of the technical skills required to pass the FES manual skills exam. This curriculum should be strongly considered by programs wishing to ensure that trainees are prepared for the FES exam.

Immune-mediated tissue regeneration driven by a biomaterial scaffold is emerging as an innovative regenerative strategy to repair damaged tissues. We investigated how biomaterial scaffolds shape the immune microenvironment in traumatic muscle wounds to improve tissue regeneration. The scaffolds induced a pro-regenerative response, characterized by an mTOR/Rictor-dependent T helper 2 pathway that guides interleukin-4–dependent macrophage polarization, which is critical for functional muscle recovery. Manipulating the adaptive immune system using biomaterials engineering may support the development of therapies that promote both systemic and local pro-regenerative immune responses, ultimately stimulating tissue repair.

Background Each year in the USA, over 2.4 million people experience mild traumatic brain injury (TBI), which can induce long-term neurological deficits. The dentate gyrus of the hippocampus is notably susceptible to damage following TBI, as hilar mossy cell changes in particular may contribute to post-TBI dysfunction. Moreover, microglial activation after TBI may play a role in hippocampal circuit and/or synaptic remodeling; however, the potential effects of chronic microglial changes are currently unknown. The objective of the current study was to assess neuropathological and neuroinflammatory changes in subregions of the dentate gyrus at acute to chronic time points following mild TBI using an established model of closed-head rotational acceleration induced TBI in pigs. Methods This study utilized archival tissue of pigs which were subjected to sham conditions or rapid head rotation in the coronal plane to generate mild TBI. A quantitative assessment of neuropathological changes in the hippocampus was performed via immunohistochemical labeling of whole coronal tissue sections at 3 days post-injury (DPI), 7 DPI, 30 DPI, and 1 year post-injury (YPI), with a focus on mossy cell atrophy and synaptic reorganization, in context with microglial alterations (e.g., density, proximity to mossy cells) in the dentate gyrus. Results There were no changes in mossy cell density between sham and injured animals, indicating no frank loss of mossy cells at the mild injury level evaluated. However, we found significant mossy cell hypertrophy at 7 DPI and 30 DPI in anterior (> 16% increase in mean cell area at each time; p  = <  0.001 each) and 30 DPI in posterior (8.3% increase; p  = <  0.0001) hippocampus. We also found dramatic increases in synapsin staining around mossy cells at 7 DPI in both anterior (74.7% increase in synapsin labeling; p  = <  0.0001) and posterior (82.7% increase; p  = <  0.0001) hippocampus. Interestingly, these morphological and synaptic alterations correlated with a significant change in microglia in proximity to mossy cells at 7 DPI in anterior and at 30 DPI in the posterior hippocampus. For broader context, while we found that there were significant increases in microglia density in the granule cell layer at 30 DPI (anterior and posterior) and 1 YPI (posterior only) and in the molecular layer at 1 YPI (anterior only), we found no significant changes in overall microglial density in the hilus at any of the time points evaluated post-injury. Conclusions The alterations of mossy cell size and synaptic inputs paired with changes in microglia density around the cells demonstrate the susceptibility of hilar mossy cells after even mild TBI. This subtle hilar mossy cell pathology may play a role in aberrant hippocampal function post-TBI, although additional studies are needed to characterize potential physiological and cognitive alterations.

Novel variants continue to emerge in the SARS-CoV-2 pandemic. University testing programs may provide timely epidemiologic and genomic surveillance data to inform public health responses. We conducted testing from September 2021 to February 2022 in a university population under vaccination and indoor mask mandates. A total of 3,048 of 24,393 individuals tested positive for SARS-CoV-2 by RT-PCR; whole genome sequencing identified 209 Delta and 1,730 Omicron genomes of the 1,939 total sequenced. Compared to Delta, Omicron had a shorter median serial interval between genetically identical, symptomatic infections within households (2 versus 6 days, P  = 0.021). Omicron also demonstrated a greater peak reproductive number (2.4 versus 1.8), and a 1.07 (95% confidence interval: 0.58, 1.57; P  < 0.0001) higher mean cycle threshold value. Despite near universal vaccination and stringent mitigation measures, Omicron rapidly displaced the Delta variant to become the predominant viral strain and led to a surge in cases in a university population. This study presents results from a SARS-CoV-2 genomic surveillance study at a university campus in which ~2,000 samples were sequenced over five months. The authors document the replacement of Delta with Omicron as the dominant variant, and describe clinical characteristics and transmission dynamics.

ObjectiveWe aimed to evaluate the feasibility and utility of an unsupervised testing mechanism, in which participants pick up a swab kit, self-test (unsupervised) and return the kit to an on-campus drop box, as compared with supervised self-testing at staffed locations.DesignUniversity SARS-CoV-2 testing cohort.SettingHusky Coronavirus Testing provided voluntary SARS-CoV-2 testing at a university in Seattle, USA.Outcome measuresWe computed descriptive statistics to describe the characteristics of the study sample. Adjusted logistic regression implemented via generalised estimating equations was used to estimate the odds of a self-swab being conducted through unsupervised versus supervised testing mechanisms by participant characteristics, including year of study enrolment, pre-Omicron versus post-Omicron time period, age, sex, race, ethnicity, affiliation and symptom status.ResultsFrom September 2021 to July 2022, we received 92 499 supervised and 26 800 unsupervised self-swabs. Among swabs received by the laboratory, the overall error rate for supervised versus unsupervised swabs was 0.3% vs 4%, although this declined to 2% for unsupervised swabs by the spring of the academic year. Results were returned for 92 407 supervised (5% positive) and 25 836 unsupervised (4%) swabs from 26 359 participants. The majority were students (79%), 61% were female and most identified as white (49%) or Asian (34%). The use of unsupervised testing increased during the Omicron wave when testing demand was high and stayed constant in spring 2022 even when testing demand fell. We estimated the odds of using unsupervised versus supervised testing to be significantly greater among those <25 years of age (p<0.001), for Hispanic versus non-Hispanic individuals (OR 1.2, 95% CI 1.0 to 1.3, p=0.01) and lower among individuals symptomatic versus asymptomatic or presymptomatic (0.9, 95% CI 0.8 to 0.9, p<0.001).ConclusionsUnsupervised swab collection permitted increased testing when demand was high, allowed for access to a broader proportion of the university community and was not associated with a substantial increase in testing errors.

Over 2.8 million people experience mild traumatic brain injury (TBI) in the United States each year, which may lead to long‐term neurological dysfunction. The mechanical forces that are caused by TBI propagate through the brain to produce diffuse axonal injury (DAI) and trigger secondary neuroinflammatory cascades. The cascades may persist from acute to chronic time points after injury, altering the homeostasis of the brain. However, the relationship between the hallmark axonal pathology of diffuse TBI and potential changes in glial cell activation or morphology have not been established in a clinically relevant large animal model at chronic time points. In this study, we assessed the tissue from pigs subjected to rapid head rotation in the coronal plane to generate mild TBI. Neuropathological assessments for axonal pathology, microglial morphological changes, and astrocyte reactivity were conducted in specimens out to 1‐year post‐injury. We detected an increase in overall amyloid precursor protein pathology, as well as periventricular white matter and fimbria/fornix pathology after a single mild TBI. We did not detect the changes in corpus callosum integrity or astrocyte reactivity. However, detailed microglial skeletal analysis revealed changes in morphology, most notably increases in the number of microglial branches, junctions, and endpoints. These subtle changes were most evident in periventricular white matter and certain hippocampal subfields, and were observed out to 1‐year post‐injury in some cases. These ongoing morphological alterations suggest persistent change in neuroimmune homeostasis. Additional studies are needed to characterize the underlying molecular and neurophysiological alterations, as well as potential contributions to neurological deficits. In this study, pigs were subjected to mild TBI by rapid head rotation and neuropathologically assessed for axonal pathology, microglial morphological changes, and astrocyte reactivity out to one year post injury. We detected acute changes in axonal pathology, particularly in the periventricular white matter and fimbria/fornix, as well as changes to microglia morphology in the periventricular white matter and hippocampal subfields out to one year post injury. These ongoing morphological alterations suggest persistent changes in neuroimmune homeostasis after a single mild TBI.

•University testing programs provide an opportunity to estimate vaccine effectiveness in community populations of healthy young adults, a population not well-represented in routine vaccine effectiveness studies.•In a university population, a COVID-19 mRNA monovalent booster dose after primary series provided increased protection against symptomatic SARS-CoV-2 infection with the Omicron variant compared to primary series vaccination alone.•Relative vaccine effectiveness was greater for individuals without any known prior SARS-CoV-2 infection versus those with a history of infection. Vaccine effectiveness (VE) studies utilizing the test-negative design are typically conducted in clinical settings, rather than community populations, leading to bias in VE estimates against mild disease and limited information on VE in healthy young adults. In a community-based university population, we utilized data from a large SARS-CoV-2 testing program to estimate relative VE of COVID-19 mRNA vaccine primary series and monovalent booster dose versus primary series only against symptomatic SARS-CoV-2 infection from September 2021 to July 2022. We used the test-negative design and logistic regression implemented via generalized estimating equations adjusted for age, calendar time, prior SARS-CoV-2 infection, and testing frequency (proxy for test-seeking behavior) to estimate relative VE. Analyses included 2,218 test-positive cases (59 % received monovalent booster dose) and 9,615 test-negative controls (62 %) from 9,066 individuals, with median age of 21 years, mostly students (71 %), White (56 %) or Asian (28 %), and with few comorbidities (3 %). More cases (23 %) than controls (6 %) had COVID-19-like illness. Estimated adjusted relative VE of primary series and monovalent booster dose versus primary series only against symptomatic SARS-CoV-2 infection was 40 % (95 % CI: 33–47 %) during the overall analysis period and 46 % (39–52 %) during the period of Omicron circulation. Relative VE was greater for those without versus those with prior SARS-CoV-2 infection (41 %, 34–48 % versus 33 %, 9 %–52 %, P < 0.001). Relative VE was also greater in the six months after receiving a booster dose (41 %, 33–47 %) compared to more than six months (27 %, 8–42 %), but this difference was not statistically significant (P = 0.06). In this relatively young and healthy adult population, an mRNA monovalent booster dose provided increased protection against symptomatic SARS-CoV-2 infection, overall and with the Omicron variant. University testing programs may be utilized for estimating VE in healthy young adults, a population that is not well-represented by routine VE studies.

Increased risk of pathogen transmission through proximity and contact is a well-documented cost of sociality. Affiliative social contact, however, is an integral part of primate group life and can benefit health. Despite its importance to the evolution and maintenance of sociality, the tradeoff between costs and benefits of social contact for group-living primate species remains poorly understood. To improve our understanding of this interplay, we used social network analysis to investigate whether contact via association in the same space and/or physical contact measured through grooming were associated with helminth parasite species richness in a community of wild chimpanzees (Pan troglodytes schweinfurthii). We identified parasite taxa in 381 fecal samples from 36 individuals from the Kasekela community of chimpanzees in Gombe National Park, Tanzania, from November 1, 2006, to October 31, 2012. Over the study period, eight environmentally transmitted helminth taxa were identified. We quantified three network metrics for association and grooming contact, including degree strength, betweenness, and closeness. Our findings suggest that more gregarious individuals—those who spent more time with more individuals in the same space—had higher parasite richness, while the connections in the grooming network were not related to parasite richness. The expected parasite richness in individuals increased by 1.13 taxa (CI: 1.04, 1.22; p = 0.02) per one standard deviation increase in degree strength of association contact. The results of this study add to the understanding of the role that different types of social contact play in the parasite richness of group-living social primates.

Hydra genome Hydra , first described by Anton van Leeuwenhoek in a letter to the Royal Society in 1702, has been studied by biologists for centuries and now is an important model for work on axial patterning, stem cell biology and regeneration. Its genome, over half of which is made up of mobile elements, has now been sequenced, as has the genome of a Curvibacter sp. bacterium stably associated with Hydra magnipapillata . Comparisons of the Hydra genome with those of other animals provide insights into the evolution of epithelia, contractile tissues, developmentally regulated transcription factors, pluripotency genes and the neuromuscular junction, as well as the Spemann–Mangold organizer, the region in the early embryo that establishes the embryo's axis. The freshwater cnidarian Hydra is a significant model for studies of axial patterning, stem cell biology and regeneration. Its (A+T)-rich genome has now been sequenced. Comparison of this genome with those of other animals provides insights into the evolution of epithelia, contractile tissues, developmentally regulated transcription factors, pluripotency genes and more. The freshwater cnidarian Hydra was first described in 1702 1 and has been the object of study for 300 years. Experimental studies of Hydra between 1736 and 1744 culminated in the discovery of asexual reproduction of an animal by budding, the first description of regeneration in an animal, and successful transplantation of tissue between animals 2 . Today, Hydra is an important model for studies of axial patterning 3 , stem cell biology 4 and regeneration 5 . Here we report the genome of Hydra magnipapillata and compare it to the genomes of the anthozoan Nematostella vectensis 6 and other animals. The Hydra genome has been shaped by bursts of transposable element expansion, horizontal gene transfer, trans -splicing, and simplification of gene structure and gene content that parallel simplification of the Hydra life cycle. We also report the sequence of the genome of a novel bacterium stably associated with H. magnipapillata . Comparisons of the Hydra genome to the genomes of other animals shed light on the evolution of epithelia, contractile tissues, developmentally regulated transcription factors, the Spemann–Mangold organizer, pluripotency genes and the neuromuscular junction.

Mechanistic insights into photodissociation dynamics of transition metal carbonyls, like Fe(CO) 5 , are fundamental for understanding active catalytic intermediates. Although extensively studied, the structural dynamics of these systems remain elusive. Using ultrafast X-ray scattering, we uncover the photochemistry of Fe(CO) 5 in real space and time, observing synchronous oscillations in atomic pair distances, followed by a prompt rotating CO release preferentially in the axial direction. This behavior aligns with simulations, reflecting the interplay between the axial Fe-C distances’ potential energy landscape and non-adiabatic transitions between metal-to-ligand charge-transfer states. Additionally, we characterize a secondary delayed CO release associated with a reduction of Fe-C steady state distances and structural dynamics of the formed Fe(CO) 4 . Our results quantify energy redistribution across vibration, rotation, and translation degrees of freedom, offering a microscopic view of complex structural dynamics, enhancing our grasp on Fe(CO) 5 photodissociation, and advancing our understanding of transition metal catalytic systems. Metal carbonyl complexes show photoreactivity interesting for catalytic and biological applications. Here the authors capture the structural dynamics of the photodissociation of iron pentacarbonyl in real space and time using ultrafast X-ray scattering.