Submitting to MedEdPORTAL: Do it right the first time

Presented as a Small Group/Roundtable Discussion at 2020 IUSM Education Day.Medical educators at Indiana University School of Medicine (IUSM) are encouraged to publish in MedEdPORTAL: The Journal of Teaching and Learning Resources. Published by the Association of American Medical Colleges (AAMC), MedEdPORTAL is a peer-reviewed, open-access journal for medical education scholarship. These publications contain complete curricula, including objectives, instructor guides, slides, and assessments, ready to be implemented in the classroom. When faculty members apply for promotion, MedEdPORTAL can demonstrate the quality of their work through peer-review, citation counts, and other usage reports. Despite submitting high quality learning modules, medical educators receive rejections from the MedEdPORTAL 62% of time. Reasons for rejection include insufficient educational context and assessment, mismatch of educational objectives and instructional content, and failure to build on existing curricula. Of immediately rejected submissions, 90% also have copyright issues. MedEdPORTAL is a member of the Open Access Scholarly Publishers Association (OASPA) and therefore has strict requirements for copyright and licensing images in the education materials. These requirements are difficult to navigate. For faculty who are not familiar with copyright and licensing, these barriers can be frustrating enough to deter them from submitting curricula. This workshop introduced MedEdPORTAL, described the submission process, and shared our strategies for putting together a successful submission. By the end of the workshop, participants were able to: • Identify curricula they have developed that would fit with the goals of MedEdPORTAL’s publishers • Use template to complete the Educational Summary Report (ESR) • Classify content as that which requires copyright permission, is in the public domain, or has a Creative Commons license • Navigate the process of manuscript submission and revisio

DOES AN EXTRA MASS IMPROVE THE ARM SWING SPEED?

This study investigated the effect of adding extra mass on individual segments during the performance of an arm swing task in the horizontal plane. The amount of extra mass was 0, 25, 50, 75, and 100% of the mass of the segment on which the extra mass was placed (upper arm or forearm). The variables studied were arm swing speed (hand speed), positive muscle impulse, and system moment of inertia (MOI). The purpose was to see if adding extra mass sped up or slowed down the arm swing and why. Twenty subjects were instructed to produce their maximum hand swing speed over the target point during the horizontal non-dominant arm swing. It was found that the forearm extra mass elicited a significant decrease in the arm swing speed, while the upper arm added mass did not cause decreases in arm speed. Rather, moderate amounts of extra mass at the upper arm (25 and 50% extra mass) induced slight, although not significant, increases in arm swing speed (0.66% and 1.41% increase, respectively). These increases in speed were accompanied by small increases in both the positive muscle impulse and the system MOI with the upper arm extra mass. Significant increases in the system MOI accounted for the significant swing speed drop caused by the forearm extra mass. It was concluded that extra mass is not always detrimental to the arm swing speed. Extra mass added close to the axis of rotation either makes no difference or may actually help swing speed

Are there mappable genes for family resemblance for the magnitude of intra-individual variation in systolic blood pressure?

BACKGROUND: The genetic regulation of variation in intra-individual fluctuations in systolic blood pressure over time is poorly understood. Analysis of the magnitude of the average fluctuation of a person's systolic blood pressure around his or her age-adjusted trend line, however, shows moderate, albeit significant, family resemblance in Cohort 1 of the Framingham Heart Study. To determine whether genomic regions affecting this phenotype could be identified, we pursued a "model-free" multipoint quantitative linkage analysis. RESULTS: Two different linkage methods revealed multiple nominally significant signals, two to four of which are "replicated" in Cohort 2. When both cohorts are assembled into extended pedigrees, three linkage signals remain nominally significant by one or both methods. CONCLUSION: Any or all of the genomic regions in the vicinity of D5S1456, D11S2359, and D20S470 may contain elements that regulate systolic blood pressure homeostasis

Identifying cryptic population structure in multigenerational pedigrees in a Mexican American sample

Cryptic population structure can increase both type I and type II errors. This is particularly problematic in case-control association studies of unrelated individuals. Some researchers believe that these problems are obviated in families. We argue here that this may not be the case, especially if families are drawn from a known admixed population such as Mexican Americans. We use a principal component approach to evaluate and visualize the results of three different approaches to searching for cryptic structure in the 20 multigenerational families of the Genetic Analysis Workshop 18 (GAW18). Approach 1 uses all family members in the sample to identify what might be considered "outlier" kindreds. Because families are likely to differ in size (in the GAW18 families, there is about a 4-fold difference in the number of typed individuals), approach 2 uses a weighting system that equalizes pedigree size. Approach 3 concentrates on the founders and the "marry-ins" because, in principle, the entire pedigree can be reconstructed with knowledge of the sequence of these unrelated individuals and genome-wide association study (GWAS) data on everyone else (to identify the position of recombinations). We demonstrate that these three approaches can yield very different insights about cryptic structure in a sample of families

Stratify or adjust? Dealing with multiple populations when evaluating rare variants

The unrelated individuals sample from Genetic Analysis Workshop 17 consists of a small number of subjects from eight population samples and genetic data composed mostly of rare variants. We compare two simple approaches to collapsing rare variants within genes for their utility in identifying genes that affect phenotype. We also compare results from stratified analyses to those from a pooled analysis that uses ethnicity as a covariate. We found that the two collapsing approaches were similarly effective in identifying genes that contain causative variants in these data. However, including population as a covariate was not an effective substitute for analyzing the subpopulations separately when only one subpopulation contained a rare variant linked to the phenotype

Detecting population stratification using related individuals

Although identification of cryptic population stratification is necessary for case/control association analyses, it is also vital for linkage analyses and family-based association tests when founder genotypes are missing. However, including related individuals in an analysis such as EIGENSTRAT can result in bias; using only founders or one individual per pedigree results in loss of data and inaccurate estimates of stratification. We examine a generalization of principal-component analyses to allow for the inclusion of related individuals by down-weighting the significance of individual comparisons