Creating a culturally responsive online personal health course

Many Americans face critical barriers to living a healthy lifestyle because of their status as members of marginalized social groups (Gill, 2007; Harrison & Clark, 2016; Robert Wood Johnson Foundation, 2018). Factors such as race/ethnicity and income affect educational attainment, which can negatively influence health outcomes for people from underserved groups, and ultimately contribute to health inequities (Egerter, Braveman, Sadegh-Nobari, Grossman-Kahn, & Dekker, 2011). Blacks and Latinos between the ages of 18 and 24 are less likely than Whites to go to college (Musu-Gillette et al., 2016) and are more likely than Whites to first enroll in community colleges rather than 4-year colleges (Ma & Baum, 2016). Over twice as many students with yearly family incomes less than $20,000 attend community colleges compared with students with family incomes over$50,000 (Radwin, Wine, Siegal, & Bryan, 2013). People from marginalized groups and those living in poverty are less likely to enroll in and complete higher education, and the degrees they do attain tend to be lower, which negatively affects many health outcomes. Culturally responsive pedagogy (CRP) is a theoretical framework for teaching based on the recognition that if students from marginalized groups are to have better lives, they must (a) learn academic content (academic success), (b) understand and appreciate their own cultural beliefs and values (cultural competence), and (c) be able to see and evaluate how social conditions affect their positions in society (sociopolitical consciousness; Ladson-Billings, 2006). The purpose of this study was to design and evaluate an online personal health course that incorporates CRP to provide students with health information that was personally applicable and engaging. Using principles from the CRP literature, an online personal health course was designed to meet the health and learning needs of diverse community college students at a community college in the United States. The course was evaluated using open-ended faculty interviews, Likert-type open-ended questions of students, and narrative reviews of the course provided by experts in online teaching and learning and CRP. Quantitative data were analyzed using frequencies. Qualitative data were analyzed using an iterative process of quotation identification, sorting quotes into related topics, and interpreting the meaning of topics related to the study objectives. Students, faculty, and experts generally agreed that the course was designed to be personally meaningful and engaging for diverse students and promoted academic success. Opportunities for cultural competence exist in the course but need to be more clearly articulated. In line with the literature, sociopolitical consciousness was the aspect of CRP that needs the most development in the future. Suggestions are included for improving the design and cultural responsiveness of the course, thereby increasing its value for student learning

Molecular and cytologic studies of Ehlers-Danlos syndrome type VIII

We present a family with findings of Ehlers-Danlos syndrome type VIII and a presenile appearance due to decreased subcutaneous tissue with drawn skin, defective wound healing, contractures, and thin hair. To investigate this syndrome, we studied collagen production and the growth properties of cultured fibroblasts taken from affected relatives. We could not find evidence of a collagen defect or premature senescence of cultured fibroblasts, although the fibroblasts may have a decreased growth rate. We conclude that this family has findings of EDS VIII and premature aging and propose that this overlapping phenotype is due to a single pathogenetic mechanism. Our studies of collagen production and fibroblast replication did not discern this mechanism.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/38257/1/1320410305_ftp.pd

Mapping of human and murine genes for latent TGF-β binding protein-2 (LTBP2)

A novel gene, isolated because of structural similarities to fibrillin, was called LTBP2 when its 4.6-kb transcript was found to encode a protein sequence related to the latent TGF-β binding protein (LTBP1), which is encoded on human chromosome (Chr) 2, region p12-q22. We have assigned the human and murine LTBP2 loci to regions of conserved synteny on human Chr 11 and mouse Chr 19. By PCR analysis of somatic cell hybrid DNA and fluorescence in situ hybridization, LTBP2 was mapped to human Chr band 11q12 and Ltbp2 to mouse Chr band 19B. Differences between inbred strains were discovered by single-strand conformation analysis of PCR products from the 3′ untranslated region. Analysis of BXD and AKXL recombinant inbred strains have placed Ltbp2 between D19Rp19 and Ly10 on proximal mouse Chr 19.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47013/1/335_2004_Article_BF00350892.pd

Positive predictive value of automated database records for diabetic ketoacidosis (DKA) in children and youth exposed to antipsychotic drugs or control medications: a tennessee medicaid study

<p>Abstract</p> <p>Background</p> <p>Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of treatment with some atypical antipsychotic drugs in children and <b>youth</b>. Because drug-associated DKA is rare, large automated health outcomes databases may be a valuable data source for conducting pharmacoepidemiologic studies of DKA associated with exposure to individual antipsychotic drugs. However, no validated computer case definition of DKA exists. We sought to assess the positive predictive value (PPV) of a computer case definition to detect incident cases of DKA, using automated records of Tennessee Medicaid as the data source and medical record confirmation as a "gold standard."</p> <p>Methods</p> <p>The computer case definition of DKA was developed from a retrospective cohort study of antipsychotic-related type 2 diabetes mellitus (1996-2007) in Tennessee Medicaid enrollees, aged 6-24 years. Thirty potential cases with any DKA diagnosis (ICD-9 250.1, ICD-10 E1x.1) were identified from inpatient encounter claims. Medical records were reviewed to determine if they met the clinical definition of DKA.</p> <p>Results</p> <p>Of 30 potential cases, 27 (90%) were successfully abstracted and adjudicated. Of these, 24 cases were confirmed by medical record review (PPV 88.9%, 95% CI 71.9 to 96.1%). Three non-confirmed cases presented acutely with severe hyperglycemia, but had no evidence of acidosis.</p> <p>Conclusions</p> <p>Diabetic ketoacidosis in children and youth can be identified in a computerized Medicaid database using our case definition, which could be useful for automated database studies in which drug-associated DKA is the outcome of interest.</p

Genetic randomization reveals functional relationships among morphologic and tissue-quality traits that contribute to bone strength and fragility

We examined femora from adult AXB/BXA recombinant inbred (RI) mouse strains to identify skeletal traits that are functionally related and to determine how functional interactions among these traits contribute to genetic variability in whole-bone stiffness, strength, and toughness. Randomization of A/J and C57BL/6J genomic regions resulted in each adult male and female RI strain building mechanically functional femora by assembling unique sets of morphologic and tissue-quality traits. A correlation analysis was conducted using the mean trait values for each RI strain. A third of the 66 correlations examined were significant, indicating that many bone traits covaried or were functionally related. Path analysis revealed important functional interactions among bone slenderness, cortical thickness, and tissue mineral density. The path coefficients describing these functional relations were similar for both sexes. The causal relationship among these three traits suggested that cellular processes during growth simultaneously regulate bone slenderness, cortical thickness, and tissue mineral density so that the combination of traits is sufficiently stiff and strong to satisfy daily loading demands. A disadvantage of these functional interactions was that increases in tissue mineral density also deleteriously affected tissue ductility. Consequently, slender bones with high mineral density may be stiff and strong but they are also brittle. Thus, genetically randomized mouse strains revealed a basic biological paradigm that allows for flexibility in building bones that are functional for daily activities but that creates preferred sets of traits under extreme loading conditions. Genetic or environmental perturbations that alter these functional interactions during growth would be expected to lead to loss of function and suboptimal adult bone quality

Optimal resolution tomography with error tracking and the structure of the crust and upper mantle beneath Ireland and Britain

The classical Backus–Gilbert method seeks localized Earth-structure averages at the shortest length scales possible, given a data set, data errors, and a threshold for acceptable model errors. The resolving length at a point is the width of the local averaging kernel, and the optimal averaging kernel is the narrowest one such that the model error is below a specified level. This approach is well suited for seismic tomography, which maps 3-D Earth structure using large sets of seismic measurements. The continual measurement-error decreases and data-redundancy increases have reduced the impact of random errors on tomographic models. Systematic errors, however, are resistant to data redundancy and their effect on the model is difficult to predict. Here, we develop a method for finding the optimal resolving length at every point, implementing it for surface-wave tomography. As in the Backus–Gilbert method, every solution at a point results from an entire-system inversion, and the model error is reduced by increasing the model-parameter averaging. The key advantage of our method stems from its direct, empirical evaluation of the posterior model error at a point. We first measure inter- station phase velocities at simultaneously recording station pairs and compute phase-velocity maps at densely, logarithmically spaced periods. Numerous versions of the maps with varying smoothness are then computed, ranging from very rough to very smooth. Phase-velocity curves extracted from the maps at every point can be inverted for shear-velocity (V S ) profiles. As we show, errors in these phase-velocity curves increase nearly monotonically with the map roughness. We evaluate the error by isolating the roughness of the phase-velocity curve that cannot be explained by any Earth structure and determine the optimal resolving length at a point such that the error of the local phase-velocity curve is below a threshold. A 3-D V S model is then computed by the inversion of the composite phase-velocity maps with an optimal resolution at every point. The estimated optimal resolution shows smooth lateral variations, confirming the robustness of the procedure. Importantly, the optimal resolving length does not scale with the density of the data coverage: some of the best-sampled locations display relatively low lateral resolution, probably due to systematic errors in the data. We apply the method to image the lithosphere and underlying mantle beneath Ireland and Britain. Our very large data set was created using new data from Ireland Array, the Irish National Seismic Network, the UK Seismograph Network and other deployments. A total of 11 238 inter-station dispersion curves, spanning a very broad total period range (4–500 s), yield unprecedented data coverage of the area and provide fine regional resolution from the crust to the deep asthenosphere. The lateral resolution of the 3-D model is computed explicitly and varies from 39 km in central Ireland to over 800 km at the edges of the area, where the data coverage declines. Our tomography reveals pronounced, previously unknown variations in the lithospheric thickness beneath Ireland and Britain, with implications for their Caledonian assembly and for the mechanisms of the British Tertiary Igneous Province magmatism

Generalized Connective Tissue Disease in Crtap-/- Mouse

Mutations in CRTAP (coding for cartilage-associated protein), LEPRE1 (coding for prolyl 3-hydroxylase 1 [P3H1]) or PPIB (coding for Cyclophilin B [CYPB]) cause recessive forms of osteogenesis imperfecta and loss or decrease of type I collagen prolyl 3-hydroxylation. A comprehensive analysis of the phenotype of the Crtap-/- mice revealed multiple abnormalities of connective tissue, including in the lungs, kidneys, and skin, consistent with systemic dysregulation of collagen homeostasis within the extracellular matrix. Both Crtap-/- lung and kidney glomeruli showed increased cellular proliferation. Histologically, the lungs showed increased alveolar spacing, while the kidneys showed evidence of segmental glomerulosclerosis, with abnormal collagen deposition. The Crtap-/- skin had decreased mechanical integrity. In addition to the expected loss of proline 986 3-hydroxylation in α1(I) and α1(II) chains, there was also loss of 3Hyp at proline 986 in α2(V) chains. In contrast, at two of the known 3Hyp sites in α1(IV) chains from Crtap-/- kidneys there were normal levels of 3-hydroxylation. On a cellular level, loss of CRTAP in human OI fibroblasts led to a secondary loss of P3H1, and vice versa. These data suggest that both CRTAP and P3H1 are required to maintain a stable complex that 3-hydroxylates canonical proline sites within clade A (types I, II, and V) collagen chains. Loss of this activity leads to a multi-systemic connective tissue disease that affects bone, cartilage, lung, kidney, and skin

The management of diabetic ketoacidosis in children

The object of this review is to provide the definitions, frequency, risk factors, pathophysiology, diagnostic considerations, and management recommendations for diabetic ketoacidosis (DKA) in children and adolescents, and to convey current knowledge of the causes of permanent disability or mortality from complications of DKA or its management, particularly the most common complication, cerebral edema (CE). DKA frequency at the time of diagnosis of pediatric diabetes is 10%–70%, varying with the availability of healthcare and the incidence of type 1 diabetes (T1D) in the community. Recurrent DKA rates are also dependent on medical services and socioeconomic circumstances. Management should be in centers with experience and where vital signs, neurologic status, and biochemistry can be monitored with sufficient frequency to prevent complications or, in the case of CE, to intervene rapidly with mannitol or hypertonic saline infusion. Fluid infusion should precede insulin administration (0.1 U/kg/h) by 1–2 hours; an initial bolus of 10–20 mL/kg 0.9% saline is followed by 0.45% saline calculated to supply maintenance and replace 5%–10% dehydration. Potassium (K) must be replaced early and sufficiently. Bicarbonate administration is contraindicated. The prevention of DKA at onset of diabetes requires an informed community and high index of suspicion; prevention of recurrent DKA, which is almost always due to insulin omission, necessitates a committed team effort