177 research outputs found

    Blended Spaces: Reimagining Civic Education in a Digital Era

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    While traditional civic education in the United States is inextricably linked to notions of a public sphere, this paper argues that the digital era requires a reimagining of this premise. The opaque nature of digital spaces makes it difficult for young people to understand how large of an audience they are interacting with and to what extent a conversation that may feel private is rebounding across public contexts. In this conceptual paper, we (1) use semiotic squares to present publicly private and privately public as two ways to reinterpret traditional presumptions about the role of ā€œthe publicā€ in civic education and (2) present the implications of these blended spaces for civic education and civic learning. The paper asks, what does it mean to prepare young people for interaction in the ā€œpublicā€ sphere within our classrooms today? By drawing on a vignette of teacher practice, we articulate what civic education could be for students around the world in the 21st century

    Educating for Equitable Voting

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    Voting instruction typically provided to students is focused on educating for informed voting, but we believe it is essential that schools educate for informed and equitable voting. Indeed, in a well-functioning democratic society, participants need to be prepared to engage in critical, but civil, discourse with and about people who look and think differently from themselves, which necessitates learning about issues of equity. Drawing on the efforts of 20 in-service educators to promote equitable voting ahead of the 2020 election, this study examines the ways in which participants incorporated issues of equity into their instruction and the conditions that supported or limited these efforts. We also discuss our concerns with how voting was taught by participants and provide recommendations for what educating for equitable voting might look like, a goal that has taken on added importance given recent challenges to how Kā€“12 teachers can talk about issues of equity in the classroom

    An Investigation into Glomeruli Detection in Kidney H&E and PAS Images using YOLO

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    Context: Analyzing digital pathology images is necessary to draw diagnostic conclusions by investigating tissue patterns and cellular morphology. However, manual evaluation can be time-consuming, expensive, and prone to inter- and intra-observer variability. Objective: To assist pathologists using computerized solutions, automated tissue structure detection and segmentation must be proposed. Furthermore, generating pixel-level object annotations for histopathology images is expensive and time-consuming. As a result, detection models with bounding box labels may be a feasible solution. Design: This paper studies. YOLO-v4 (You-Only-Look-Once), a real-time object detector for microscopic images. YOLO uses a single neural network to predict several bounding boxes and class probabilities for objects of interest. YOLO can enhance detection performance by training on whole slide images. YOLO-v4 has been used in this paper. for glomeruli detection in human kidney images. Multiple experiments have been designed and conducted based on different training data of two public datasets and a private dataset from the University of Michigan for fine-tuning the model. The model was tested on the private dataset from the University of Michigan, serving as an external validation of two different stains, namely hematoxylin and eosin (H&E) and periodic acid-Schiff (PAS). Results: Average specificity and sensitivity for all experiments, and comparison of existing segmentation methods on the same datasets are discussed. Conclusions: Automated glomeruli detection in human kidney images is possible using modern AI models. The design and validation for different stains still depends on variability of public multi-stain datasets

    Variation in a Darwin Wasp (Hymenoptera: Ichneumonidae) Community along an Elevation Gradient in a Tropical Biodiversity Hotspot: Implications for Ecology and Conservation

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    Understanding how biodiversity varies from place to place is a fundamental goal of ecology and an important tool for halting biodiversity loss. Parasitic wasps (Hymenoptera) are a diverse and functionally important animal group, but spatial variation in their diversity is poorly understood. We survey a community of parasitic wasps (Ichneumonidae: Pimplinae) using Malaise traps up a mountain in the Brazilian Atlantic Rainforest, and relate the catch to biotic and abiotic habitat characteristics. We find high species richness compared with previous similar studies, with abundance, richness, and diversity peaking at low to intermediate elevation. There is a marked change in community composition with elevation. Habitat factors strongly correlated with elevation also strongly predict changes in the pimpline community, including temperature as well as the density of bamboo, lianas, epiphytes, small trees, and herbs. These results identify several possible surrogates of pimpline communities in tropical forests, which could be used as a tool in conservation. They also contribute to the growing evidence for a typical latitudinal gradient in ichneumonid species richness, and suggest that low to medium elevations in tropical regions will sometimes conserve the greatest number of species locally, but to conserve maximal biodiversity, a wider range of elevations should also be targeted

    Estrogen inhibits the vascular injury response in estrogen receptor beta -deficient female mice

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    The protective effects of estrogen in the cardiovascular system result from both systemic effects and direct actions of the hormone on the vasculature. Two estrogen receptors have been identified, ERĪ± and ERĪ². We demonstrated previously that estrogen inhibits the response to vascular injury in both wild-type and ERĪ±-deficient mice, and that ERĪ² is expressed in the blood vessels of each, suggesting a role for ERĪ² in the vascular protective effects of estrogen. In the present study, we examined the effect of estrogen administration on mouse carotid arterial injury in ERĪ²-deficient mice. Surprisingly, in ovariectomized female wild-type and ERĪ² knockout mice, 17Ī²-estradiol markedly and equally inhibited the increase in vascular medial area and the proliferation of vascular smooth muscle cells after vascular injury. These data demonstrate that ERĪ² is not required for estrogen-mediated inhibition of the response to vascular injury, and suggest that either of the two known estrogen receptors is sufficient to protect against vascular injury, or that another unidentified estrogen receptor mediates the vascular protective effects of estrogen

    Responsiveness of sphingosine phosphate lyase insufficiency syndrome to vitamin B6 cofactor supplementation

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    Sphingosine- 1- phosphate (S1P) lyase is a vitamin B6- dependent enzyme that degrades sphingosine- 1- phosphate in the final step of sphingolipid metabolism. In 2017, a new inherited disorder was described caused by mutations in SGPL1, which encodes sphingosine phosphate lyase (SPL). This condition is referred to as SPL insufficiency syndrome (SPLIS) or alternatively as nephrotic syndrome type 14 (NPHS14). Patients with SPLIS exhibit lymphopenia, nephrosis, adrenal insufficiency, and/or neurological defects. No targeted therapy for SPLIS has been reported. Vitamin B6 supplementation has therapeutic activity in some genetic diseases involving B6- dependent enzymes, a finding ascribed largely to the vitaminā€™s chaperone function. We investigated whether B6 supplementation might have activity in SPLIS patients. We retrospectively monitored responses of disease biomarkers in patients supplemented with B6 and measured SPL activity and sphingolipids in B6- treated patient- derived fibroblasts. In two patients, disease biomarkers responded to B6 supplementation. S1P abundance and activity levels increased and sphingolipids decreased in response to B6. One responsive patient is homozygous for an SPL R222Q variant present in almost 30% of SPLIS patients. Molecular modeling suggests the variant distorts the dimer interface which could be overcome by cofactor supplementation. We demonstrate the first potential targeted therapy for SPLIS and suggest that 30% of SPLIS patients might respond to cofactor supplementation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/162713/2/jimd12238.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/162713/1/jimd12238_am.pd

    17Ī²-Estradiol Prevents Early-Stage Atherosclerosis in Estrogen Receptor-Alpha Deficient Female Mice

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    Estrogen is atheroprotective and a high-affinity ligand for both known estrogen receptors, ERĪ± and ERĪ². However, the role of the ERĪ± in early-stage atherosclerosis has not been directly investigated and is incompletely understood. ERĪ±-deficient (ERĪ±āˆ’/āˆ’) and wild-type (ERĪ±+/+) female mice consuming an atherogenic diet were studied concurrent with estrogen replacement to distinguish the actions of 17Ī²-estradiol (E2) from those of ERĪ± on the development of early atherosclerotic lesions. Mice were ovariectomized and implanted with subcutaneous slow-release pellets designed to deliver 6 or 8ā€‰Ī¼g/day of exogenous 17Ī²-estradiol (E2) for a period of up to 4Ā months. Ovariectomized mice (OVX) with placebo pellets (E2-deficient controls) were compared to mice with endogenous E2 (intact ovaries) and exogenous E2. Aortas were analyzed for lesion area, number, and distribution. Lipid and hormone levels were also determined. Compared to OVX, early lesion development was significantly (pā€‰<ā€‰0.001) attenuated by E2 with 55ā€“64% reduction in lesion area by endogenous E2 and >90% reduction by exogenous E2. Compared to OVX, a decline in lesion number (2- to 4-fold) and lesser predilection (~4-fold) of lesion formation in the proximal aorta also occurred with E2. Lesion size, development, number, and distribution inversely correlated with circulating plasma E2 levels. However, atheroprotection was independent of ERĪ± status, and E2 athero-protection in both genotypes was not explained by changes in plasma lipid levels (total cholesterol, triglyceride, and high-density lipoprotein cholesterol). The ERĪ± is not essential for endogenous/exogenous E2-mediated protection against early-stage atherosclerosis. These observations have potentially significant implications for understanding the molecular and cellular mechanisms and timing of estrogen action in different estrogen receptor (ER) deletion murine models of atherosclerosis, as well as implications to human studies of ER polymorphisms and lipid metabolism. Our findings may contribute to future improved clinical decision-making concerning the use of hormone therapy

    Endogenous adenine mediates kidney injury in diabetic models and predicts diabetic kidney disease in patients

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    Diabetic kidney disease (DKD) can lead to end-stage kidney disease (ESKD) and mortality; however, few mechanistic biomarkers are available for high-risk patients, especially those without macroalbuminuria. Urine from participants with diabetes from the Chronic Renal Insufficiency Cohort (CRIC) study, the Singapore Study of Macro-angiopathy and Micro-vascular Reactivity in Type 2 Diabetes (SMART2D), and the American Indian Study determined whether urine adenine/creatinine ratio (UAdCR) could be a mechanistic biomarker for ESKD. ESKD and mortality were associated with the highest UAdCR tertile in the CRIC study and SMART2D. ESKD was associated with the highest UAdCR tertile in patients without macroalbuminuria in the CRIC study, SMART2D, and the American Indian study. Empagliflozin lowered UAdCR in nonmacroalbuminuric participants. Spatial metabolomics localized adenine to kidney pathology, and single-cell transcriptomics identified ribonucleoprotein biogenesis as a top pathway in proximal tubules of patients without macroalbuminuria, implicating mTOR. Adenine stimulated matrix in tubular cells via mTOR and stimulated mTOR in mouse kidneys. A specific inhibitor of adenine production was found to reduce kidney hypertrophy and kidney injury in diabetic mice. We propose that endogenous adenine may be a causative factor in DKD.</p
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