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Risk assessment and response is important for understanding human behavior. The divisive context surrounding the coronavirus pandemic inspires our exploration of risk perceptions and the polarization of mitigation practices (i.e., the degree to which the behaviors of people on the political "Left" diverge from those on the "Right"). Specifically, we investigate the extent to which the political polarization of willingness to comply with mitigation behaviors changes with risk perceptions.Analyses use data from two sources: an original dataset of Twitter posts and a nationally-representative survey. In the Twitter data, negative binomial regression models are used to predict mitigation intent measured using tweet counts. In the survey data, logit models predict self-reported mitigation behavior (vaccination, masking, and social distancing).Findings converged across both datasets, supporting the idea that the links between political orientation and willingness to follow mitigation guidelines depend on perceived risk. People on the Left are more inclined than their Right-oriented colleagues to follow guidelines, but this polarization tends to decrease as the perceived risk of COVID-19 intensifies. Additionally, we find evidence that exposure to COVID-19 infections sends ambiguous signals about the risk of the virus while COVID-19 related deaths have a more consistent impact on mitigation behaviors.Pandemic-related risks can create opportunities for perceived "common ground," between the political "Right" and "Left." Risk perceptions and politics interact in their links to intended COVID-19 mitigation behavior (as measured both on Twitter and in a national survey). Our results invite a more complex interpretation of political polarization than those stemming from simplistic analyses of partisanship and ideology.

Vitamin D is produced in the skin following exposure to sunlight. Ultraviolet (UV) B (UVB, 280–310 nm) results in isomerization of 7-dehydrocholesterol to previtamin D that spontaneously isomerizes to vitamin D. This pool of skin-derived vitamin D is the major source of vitamin D for animals. However, the mechanisms by which it becomes available remain undefined. It has been assumed that cutaneous vitamin D is transported into the circulation by vitamin D binding protein (DBP), but experimental evidence is lacking. To determine whether cutaneous vitamin D is transported by DBP, we utilized DBP(−/−) mice that were made vitamin D-deficient. These animals lack measurable 25(OH)D in blood and are hypocalcemic. As controls, DBP(+/+) animals were vitamin D depleted and made equally hypocalcemic. UV irradiation of DBP(+/+) animals restored serum calcium and serum 25(OH)D while the same treatment of DBP(−/−) animals failed to show either a serum calcium or 25(OH)D response despite having normal vitamin D production in skin. Intravenous injection of small amounts of recombinant DBP to the vitamin D-deficient DBP(−/−) mice restored the response to UV light. These results demonstrate a requirement for DBP to utilize cutaneously produced vitamin D.

Methods for generating differentially-private (DP) synthetic data have received recent attention as large government agencies such as the U.S. Census have decided to release DP synthetic data for public usage. In the synthetic data generation process, it is common to post-process the privatized results so that the final synthetic data agrees with what the data curator considers public information. Our contributions are three fold: 1) we show empirically that using post-processing to incorporate public information in contingency tables can lead to sub-optimal inference, 2) we propose an alternative Bayesian sampling framework that directly incorporates both noise due to DP and public information constraints, leading to improved inference, and 3) we demonstrate the proposed methodology on a study of the relationship between mortality rate and race in small areas given priviatized data from the CDC and U.S. Census.

Vitamin D and sunlight have each been reported to protect against the development of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). To date, the contribution of each has been unclear as ultra violet (UV) exposure also causes the generation of vitamin D in the skin. To examine whether the UV based suppression of EAE results, at least, in part from the production of vitamin D, we studied the effect of UV light on EAE in mice unable to produce 7-dehydroxycholesterol (7-DHC), the required precursor of vitamin D. Furthermore, we examined UV suppression of EAE in mice devoid of the vitamin D receptor (VDR). Our results demonstrate that UV light suppression of EAE occurs in the absence of vitamin D production and in the absence of VDR. Future investigations will focus on identifying the pathway responsible for the protective action of UV in EAE and presumably human MS.

Although ex vivo research suggests that vitamin D may play a role in innate and adaptive immunity, clear in vivo evidence is lacking. We have tested whether severe vitamin D deficiency alters the ability of mice to resist infection by Listeria. Our results show that vitamin D deficiency does not affect the LD50 of naïve mice in response to Listeria. To study the adaptive immune response, the LD50 for Listeria‐immunized mice was determined for vitamin D‐deficient and vitamin D‐sufficient mice. Although the LD50 clearly increased by immunization with inactivated Listeria, there was no effect of vitamin D deficiency on survival of mice infected with wild‐type Listeria. Thus, in this model of adaptive immunity, we could find no evidence of a role for vitamin D.

Many applications of High Altitude Ballooning (HAB) require maintaining a bearing in a non-inertial frame of reference, for example keeping a camera continuously pointed at the sun from a HAB payload in motion. Maintaining a consistent bearing is especially difficult on a HAB flight because it is hard to accurately measure and compensate the relative motion of the payload. In addition, friction, conservation of angular momentum, and errors in relative bearing measurement complicate the solution. This project aims to solve these issues using a combination of accelerometer data, gyro data, and a motor-driven platform. It was launched as part of the Far Horizons project at the Adler Planetarium, whose mission is bringing real space exploration down to Earth and into the hands of students, volunteers, and the public. The initial design was built for use in the 2017 Eclipse mission, but will also be used in missions such as mapping light pollution from a HAB platform. The system expands the capabilities of general HAB missions and can be open-sourced to provide the HAB community with a solution to a unique problem in High Altitude Ballooning.

Idiopathic pulmonary fibrosis (IPF) is a progressive and incurable fibroproliferative disorder characterized by unrelenting proliferation of fibroblasts and their deposition of collagen within alveoli, resulting in permanently scarred, nonfunctional airspaces. Normally, polymerized collagen suppresses fibroblast proliferation and serves as a physiological restraint to limit fibroproliferation after tissue injury. The IPF fibroblast, however, is a pathologically altered cell that has acquired the capacity to elude the proliferation-suppressive effects of polymerized collagen. The mechanism for this phenomenon remains incompletely understood. Here, we demonstrate that expression of α(2)β(1) integrin, a major collagen receptor, is pathologically low in IPF fibroblasts interacting with polymerized collagen. Low integrin expression in IPF fibroblasts is associated with a failure to induce PP2A phosphatase activity, resulting in abnormally high levels of phosphorylated (inactive) GSK-3β and high levels of active β-catenin in the nucleus. Knockdown of β-catenin in IPF fibroblasts inhibits their ability to proliferate on collagen. Interdiction of α(2)β(1) integrin in control fibroblasts reproduces the IPF phenotype and leads to the inability of these cells to activate PP2A, resulting in high levels of phosphorylated GSK-3β and active β-catenin and in enhanced proliferation on collagen. Our findings indicate that the IPF fibroblast phenotype is characterized by low α(2)β(1) integrin expression, resulting in a failure of integrin to activate PP2A phosphatase, which permits inappropriate activation of the β-catenin pathway.