3,518 research outputs found

    Habitable Zone Lifetime of Exoplanets around Main Sequence Stars

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    Funding: Dean's Scholarship at the University of East Anglia.The potential habitability of newly discovered exoplanets is initially assessed by determining whether their orbits fall within the circumstellar habitable zone of their star. However, the habitable zone (HZ) is not static in time or space, and its boundaries migrate outward at a rate proportional to the increase in luminosity of a star undergoing stellar evolution, possibly including or excluding planets over the course of the star’s main sequence lifetime. We describe the time that a planet spends within the HZ as its ‘‘habitable zone lifetime.’’ The HZ lifetime of a planet has strong astrobiological implications and is especially important when considering the evolution of complex life, which is likely to require a longer residence time within the HZ. Here, we present results from a simple model built to investigate the evolution of the ‘‘classic’’ HZ over time, while also providing estimates for the evolution of stellar luminosity over time in order to develop a ‘‘hybrid’’ HZ model. These models return estimates for the HZ lifetimes of Earth and 7 confirmed HZ exoplanets and 27 unconfirmed Kepler candidates. The HZ lifetime for Earth ranges between 6.29 and 7.79 · 109 years (Gyr). The 7 exoplanets fall in a range between ∼1 and 54.72 Gyr, while the 27 Kepler candidate planets’ HZ lifetimes range between 0.43 and 18.8 Gyr. Our results show that exoplanet HD 85512b is no longer within the HZ, assuming it has an Earth analog atmosphere. The HZ lifetime should be considered in future models of planetary habitability as setting an upper limit on the lifetime of any potential exoplanetary biosphere, and also for identifying planets of high astrobiological potential for continued observational or modeling campaigns.Publisher PDFPeer reviewe

    Roles of Na,K-ATPase in early development and trophectoderm differentiation.

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    Before implantation into the uterine wall, the mammalian embryo undergoes a period of cell division, cell shape change, and cell differentiation leading to the formation of an outer epithelium, the trophectoderm. The trophectoderm is the part of the embryo that initiates uterine contact and, after transformation to become the trophoblast, uterine invasion. Similar to the kidney nephron, the trophectoderm is a transporting epithelium with distinct apical and basolateral membrane domains; its function is to facilitate transepithelial Na+ and fluid transport for blastocoel formation. That transport is driven by Na,K-adenosine triphosphatase (ATPase) localized in basolateral membranes of the trophectoderm. Preimplantation embryos express multiple alpha and beta subunit isoforms of Na,K-ATPase, potentially constituting multiple isozymes, but the basolaterally located alpha1beta1 isozyme appears to function uniquely to drive fluid transport. Embryos unable to express alpha1 subunits because of targeted deletion of the gene are able to form a blastocoel, but they fail to maintain their integrity and expire during the peri-implantation period. Preimplantation embryos also express the gamma subunit, a modulator of Na,K-ATPase activity, but targeted deletion of that gene did not reveal an essential developmental role. The preimplantation embryo offers a unique model for understanding the roles of Na,K-ATPase subunit isoforms in epithelial development and transepithelial transport

    p38 mitogen-activated protein kinase (MAPK) first regulates filamentous actin at the 8-16-cell stage during preimplantation development.

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    BACKGROUND INFORMATION: The MAPK (mitogen-activated protein kinase) superfamily of proteins consists of four separate signalling cascades: the c-Jun N-terminal kinase or stress-activated protein kinases (JNK/SAPK); the ERKs (extracellular-signal-regulated kinases); the ERK5 or big MAPK1; and the p38 MAPK group of protein kinases, all of which are highly conserved. To date, our studies have focused on defining the role of the p38 MAPK pathway during preimplantation development. p38 MAPK regulates actin filament formation through the downstream kinases MAPKAPK2/3 (MAPK-activated protein kinase 2/3) or MAPKAPK5 [PRAK (p38 regulated/activated kinase)] and subsequently through HSP25/27 (heat-shock protein 25/27). We recently reported that 2-cell-stage murine embryos treated with cytokine-suppressive anti-inflammatory drugs (CSAIDtrade mark; SB203580 and SB220025) display a reversible blockade of development at the 8-16-cell stage, indicating that p38 (MAPK) activity is required to complete murine preimplantation development. In the present study, we have investigated the stage-specific action and role of p38 MAPK in regulating filamentous actin during murine preimplantation development. RESULTS: Treatment of 8-cell-stage embryos with SB203580 and SB220025 (CSAIDtrade mark) resulted in a blockade of preimplantation development, loss of rhodamine phalloidin fluorescence, MK-p (phosphorylated MAPKAPK2/3), HSP-p (phosphorylated HSP25/27) and a redistribution of alpha-catenin immunofluorescence by 12 h of treatment. In contrast, treatment of 2- and 4-cell-stage embryos with CSAIDtrade mark drugs resulted in a loss of MK-p and HSP-p, but did not result in a loss of rhodamine phalloidin fluorescence. All these effects of p38 MAPK inhibition were reversed upon removal of the inhibitor, and development resumed in a delayed but normal manner to the blastocyst stage. Treatment of 8-cell embryos with PD098059 (ERK pathway inhibitor) did not affect development or fluorescence of MK-p, HSP-p or rhodamine phalloidin. CONCLUSION: Murine preimplantation development becomes dependent on p38 MAPK at the 8-16-cell stage, which corresponds to the stage when p38 MAPK first regulates filamentous actin during early development

    Grey and white matter differences in Chronic Fatigue Syndrome : A voxel-based morphometry study

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    Conflicts of interest and source of funding The authors declare no conflicts of interest. This research was funded by the Medical Research Council (MR/J002712/1). AF is supported by Research Capability Funding from the Newcastle upon Tyne Hospitals NHS Foundation Trust and the Northumberland, Tyne and Wear NHS Foundation Trust.Peer reviewedPublisher PD

    Mitogen-activated protein kinase (MAPK) pathways mediate embryonic responses to culture medium osmolarity by regulating Aquaporin 3 and 9 expression and localization, as well as embryonic apoptosis.

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    BACKGROUND: In order to advance the development of culture conditions and increase the potential for supporting normal preimplantation embryo development in vitro, it is critical to define the mechanisms that early embryos utilize to survive in culture. We investigated the mechanisms that embryos employ in response to culture medium osmolarity. We hypothesized that mitogen-activated protein kinase (MAPK) pathways mediate responses to hyperosmotic stress by regulating Aquaporin (AQP) 3 and 9 expression as well as embryonic apoptosis. METHODS: Real-time reverse transcription and polymerase chain reaction and whole-mount immunofluorescence were used to determine the relative mRNA levels and protein localization patterns of AQP 3 and 9 after hyperosmotic medium treatment. RESULTS: At 6 and 24 h, a significant increase in Aqp 3 and 9 mRNA was observed in the sucrose hyperosmotic treatment compared with standard medium and glycerol controls. Blockade of MAPK14/11 negated the increase in Aqp 3 and 9 mRNA levels, whereas culture in a MAPK8 blocker did not. Hyperosmotic sucrose treatment significantly increased embryonic apoptosis which was negated in the presence of MAPK8 blocker, but not MAPK14/11 blocker. CONCLUSIONS: MAPK14/11 activation is a component of the rapid adaptive stress response mechanism that includes the effects of AQP mRNA expression and protein localization, whereas the MAPK8 pathway is a regulator of apoptosis

    Spatial search by quantum walk

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    Grover's quantum search algorithm provides a way to speed up combinatorial search, but is not directly applicable to searching a physical database. Nevertheless, Aaronson and Ambainis showed that a database of N items laid out in d spatial dimensions can be searched in time of order sqrt(N) for d>2, and in time of order sqrt(N) poly(log N) for d=2. We consider an alternative search algorithm based on a continuous time quantum walk on a graph. The case of the complete graph gives the continuous time search algorithm of Farhi and Gutmann, and other previously known results can be used to show that sqrt(N) speedup can also be achieved on the hypercube. We show that full sqrt(N) speedup can be achieved on a d-dimensional periodic lattice for d>4. In d=4, the quantum walk search algorithm takes time of order sqrt(N) poly(log N), and in d<4, the algorithm does not provide substantial speedup.Comment: v2: 12 pages, 4 figures; published version, with improved arguments for the cases where the algorithm fail

    Rapid assembly of highly-functionalised difluorinated cyclooctenones via ring-closing metathesis

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    Building block methodology from trifluoroethanol and ringclosing metathesis using a Fürstner modification of Grubbs’ conditions allows the rapid synthesis of novel difluorinated cyclooctenones

    Geology and Aquifer Sensitivity of Quaternary Glacial Deposits Overlying a Portion of the Mahomet Buried Bedrock Valley Aquifer System

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    To characterize the distribution of Holocene and Late Quaternary deposits and to assess the contamination potential of the Mahomet Aquifer, surficial geologic and aquifer sensitivity maps of the Gibson City East 7.5-Minute Quadrangle were created. Geologic data, extent, and thickness of the geologic materials were coupled with LiDAR topographic data and analyzed using ESRI’s ArcGIS 10.6.1. Aquifer sensitivity to contamination was calculated based on the depth to the first aquifer unit, aquifer thickness, and the lithology of the aquifer materials. The surficial geologic mapping identified five lithostratigraphic units: the Cahokia Formation, the Equality Formation, the Henry Formation, and the Yorkville and Batestown Members of the Lemont Formation. The southeast to northwest trending Illiana Morainic System is the most prominent feature in the study area and delineates the maximum extent of the glaciers during the Livingston Phase of glaciation. Postglacial deposits of the Cahokia Formation, alluvium, interfinger, and overlie with glacial outwash of the Henry Formation along channels and drainage ways downslope of the moraine. The areas of least sensitivity are located over the Illiana Morainic System, whereas the greatest potential to contamination occurs where the thickest deposits of the Henry Formation and Cahokia Formation lie at or just below the land surface

    Assessment of regional gray matter loss in dementia with Lewy bodies: a surface-based MRI analysis.

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    OBJECTIVE: To compare magnetic resonance imaging (MRI) patterns of cortical thinning in subjects with dementia with Lewy bodies (DLB), Alzheimer's disease (AD), and normal aging and investigate the relationship between cortical thickness and clinical measures. METHODS: Study participants (31 DLB, 30 AD, and 33 healthy comparison subjects) underwent 3-Tesla T1-weighted MRI and completed clinical and cognitive assessments. We used the FreeSurfer analysis package to measure cortical thickness and investigated the patterns of cortical thinning across groups. RESULTS: Cortical thinning in AD was found predominantly in the temporal and parietal areas extending into the frontal lobes (N = 63, df = 59, t >3.3, p 3.6, p 2.8, p <0.01 uncorrected). CONCLUSION: Cortical thickness may be a sensitive measure for characterising gray matter loss in DLB and highlights important structural imaging differences between the conditions.The study was funded by the Sir Jules Thorn Charitable Trust [grant ref: 05/JTA] and supported by the National Institute for Health Research (NIHR) Newcastle Biomedical Research Centre in Ageing and Chronic Disease and Biomedical Research Unit in Lewy Body Dementia based at Newcastle upon Tyne Hospitals NHS Foundation Trust and Newcastle University, and the Biomedical Research Centre and Unit in Dementia based at Cambridge University Hospitals NHS Foundation Trust.This is the accepted manuscript. The final version is available from Elsevier at http://www.sciencedirect.com/science/article/pii/S106474811400219X
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