57 research outputs found
Onboard Science Instrument Autonomy for the Detection of Microscopy Biosignatures on the Ocean Worlds Life Surveyor
The quest to find extraterrestrial life is a critical scientific endeavor
with civilization-level implications. Icy moons in our solar system are
promising targets for exploration because their liquid oceans make them
potential habitats for microscopic life. However, the lack of a precise
definition of life poses a fundamental challenge to formulating detection
strategies. To increase the chances of unambiguous detection, a suite of
complementary instruments must sample multiple independent biosignatures (e.g.,
composition, motility/behavior, and visible structure). Such an instrument
suite could generate 10,000x more raw data than is possible to transmit from
distant ocean worlds like Enceladus or Europa. To address this bandwidth
limitation, Onboard Science Instrument Autonomy (OSIA) is an emerging
discipline of flight systems capable of evaluating, summarizing, and
prioritizing observational instrument data to maximize science return. We
describe two OSIA implementations developed as part of the Ocean Worlds Life
Surveyor (OWLS) prototype instrument suite at the Jet Propulsion Laboratory.
The first identifies life-like motion in digital holographic microscopy videos,
and the second identifies cellular structure and composition via innate and
dye-induced fluorescence. Flight-like requirements and computational
constraints were used to lower barriers to infusion, similar to those available
on the Mars helicopter, "Ingenuity." We evaluated the OSIA's performance using
simulated and laboratory data and conducted a live field test at the
hypersaline Mono Lake planetary analog site. Our study demonstrates the
potential of OSIA for enabling biosignature detection and provides insights and
lessons learned for future mission concepts aimed at exploring the outer solar
system.Comment: 49 pages, 18 figures, submitted to The Planetary Science Journal on
2023-04-2
Asthma Discordance in Twins Is Linked to Epigenetic Modifications of T Cells
T cells mediate the inflammatory responses observed in asthma among genetically susceptible individuals and have been suspected to be prone to epigenetic regulation. However, these relationships are not well established from past clinical studies that have had limited capacity to control for the effects of variable genetic predisposition and early environmental exposures. Relying on a cohort of monozygotic twins discordant for asthma we sought to determine if epigenetic modifications in T cells were associated with current asthma and explored whether such modifications were associated with second hand smoke exposures. Our study was conducted in a monozygotic twin cohort of adult twin pairs (n = 21) all discordant for asthma. Regulatory T cell (Treg) and effector T cell (Teff) subsets were assessed for levels of cellular function, protein expression, gene expression and CpG methylation within Forkhead box P3 (FOXP3) and interferon gamma-γ (IFNγ) loci. Comparisons by asthma and current report of exposure to second hand smoke were made. Treg from asthmatic discordant twins demonstrated decreased FOXP3 protein expression and impaired Treg function that was associated with increased levels of CpG methylation within the FOXP3 locus when compared to their non-asthmatic twin partner. In parallel, Teff from discordant asthmatic twins demonstrated increased methylation of the IFNγ locus, decreased IFNγ expression and reduced Teff function when compared to Teff from the non-asthmatic twin. Finally, report of current exposure to second hand smoke was associated with modifications in both Treg and Teff at the transcriptional level among asthmatics. The results of the current study provide evidence for differential function of T cell subsets in monozygotic twins discordant for asthma that are regulated by changes in DNA methylation. Our preliminary data suggest exposure to second hand smoke may augment the modified T cell responses associated with asthma
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Payment instruments, finance and development
This paper studies the effects of a payment technology innovation (mobile money) on entrepreneurship and economic development in a quantitative dynamic general equilibrium model. In the model mobile money dominates fiat money as a medium of exchange, since it avoids the risk of theft, but comes with electronic transaction costs. We show that entrepreneurs with higher productivity and access to trade credit are more likely to adopt mobile money as a payment instrument vis-a-vis suppliers. Calibrating the stationary equilibrium of the model to match firm-level data from Kenya, we show significant quantitative implications of mobile money for entrepreneurial growth and macroeconomic development
Toll-like receptor signaling adapter proteins govern spread of neuropathic pain and recovery following nerve injury in male mice.
BackgroundSpinal Toll-like receptors (TLRs) and signaling intermediaries have been implicated in persistent pain states. We examined the roles of two major TLR signaling pathways and selected TLRs in a mononeuropathic allodynia.MethodsL5 spinal nerve ligation (SNL) was performed in wild type (WT, C57BL/6) male and female mice and in male Tlr2-/-Tlr3-/-, Tlr4-/-, Tlr5-/-, Myd88-/-, Triflps2, Myd88/Triflps2, Tnf-/-, and Ifnar1-/- mice. We also examined L5 ligation in Tlr4-/- female mice. We examined tactile allodynia using von Frey hairs. Iba-1 (microglia) and GFAP (astrocytes) were assessed in spinal cords by immunostaining. Tactile thresholds were analyzed by 1- and 2-way ANOVA and the Bonferroni post hoc test was used.ResultsIn WT male and female mice, SNL lesions resulted in a persistent and robust ipsilateral, tactile allodynia. In males with TLR2, 3, 4, or 5 deficiencies, tactile allodynia was significantly, but incompletely, reversed (approximately 50%) as compared to WT. This effect was not seen in female Tlr4-/- mice. Increases in ipsilateral lumbar Iba-1 and GFAP were seen in mutant and WT mice. Mice deficient in MyD88, or MyD88 and TRIF, showed an approximately 50% reduction in withdrawal thresholds and reduced ipsilateral Iba-1. In contrast, TRIF and interferon receptor null mice developed a profound ipsilateral and contralateral tactile allodynia. In lumbar sections of the spinal cords, we observed a greater increase in Iba-1 immunoreactivity in the TRIF-signaling deficient mice as compared to WT, but no significant increase in GFAP. Removing MyD88 abrogated the contralateral allodynia in the TRIF signaling-deficient mice. Conversely, IFNβ, released downstream to TRIF signaling, administered intrathecally, temporarily reversed the tactile allodynia.ConclusionsThese observations suggest a critical role for the MyD88 pathway in initiating neuropathic pain, but a distinct role for the TRIF pathway and interferon in regulating neuropathic pain phenotypes in male mice
1959: Abilene Christian College Bible Lectures - Full Text
UNTO ALL THE WORLD”
Being the Abilene Christian College Annual Bible Lectures 1959
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Visitor Cell Phone Application: An Innovative Design to Monitor Visitor Mobility in Acadia National Park
The goal of this project was to demonstrate the feasibility of using a mobile application to collect data about vehicle position and movement in Acadia National Park. This was done to show a proof of concept for a more effective way to collect data on vehicular traffic throughout the park. The data that was collected and stored by our application contained GPS location, time, and a user ID. Our project also determined the willingness of volunteers to download a mobile application for park research. The feasibility of the application was determined and suggestions were made regarding its future implementation. The application was distributed to visitors in the park in order to demonstrate the efficacy of the data collected. ArcGIS and Google Maps were used to display and analyze data
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