1,084 research outputs found

    Paper Session I-B - The Great Observatories Program

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    Although astronomy has been practiced since ancient times, the universe remains veiled in mystery. Limited for centuries to observations in the visible band of the electromagnetic spectrum, the ability to place instruments in space above the filtering atmosphere has given scientists access to the Universe at virtually all wavelengths revealing intriguing objects and events. Over the past two decades, NASA has introduced increasingly sensitive telescopes into space to make observations across the electromagnetic spectrum. Each successive telescope has exploited newly developed technologies to extend the limits of sensitivity and provide greater insight into the structure of stars, galaxies, and the cosmos. A new generation of space observatories now offers significant new gains in sensitivity through the use of state-of-the-art technologies. These observatories include: the Gamma Ray Observatory which will explore the most energetic part of the spectrum across a much greater wavelength range than its predecessors; the Advanced X-Ray Astrophysics Facility that will cover the X-ray portion of the spectrum with a hundred-fold improvement in sensitivity; the Hubble Space Telescope which will penetrate deep into the Universe in visible and ultraviolet light, observing objects with at least ten times more clarity than is now possible with ground-based optical telescope; and the Space Infrared Telescope Facility which will span the infrared part of the spectrum with a thousand-fold increase in sensitivity. These new observatories, along with supporting facilities on the ground and in space, will open the Universe to greatly increased scrutiny. While the introduction of new technologies, particularly over the last decade, has led to a dramatic increase in astronomical discoveries, the discoveries to date constitute only a fraction of the total to be made

    Electron Spin Resonance In Argon-ion-implanted Silicon

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    A new paramagnetic center with g = 2.0029 is observed, in both n- and p-type silicon after they are heavily implanted (higher than 1017 ions/cm2) with 150-keV argon ions. © 1973 American Institute of Physics

    A Gene for Autosomal Recessive Limb-Girdle Muscular Dystrophy in Manitoba Hutterites Maps to Chromosome Region 9q31-q33: Evidence for Another Limb-Girdle Muscular Dystrophy Locus

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    SummaryCharacterized by proximal muscle weakness and wasting, limb-girdle muscular dystrophies (LGMDs) are a heterogeneous group of clinical disorders. Previous reports have documented either autosomal dominant or autosomal recessive modes of inheritance, with genetic linkage studies providing evidence for the existence of at least 12 distinct loci. Gene products have been identified for five genes responsible for autosomal recessive forms of the disorder. We performed a genome scan using pooled DNA from a large Hutterite kindred in which the affected members display a mild form of autosomal recessive LGMD. A total of 200 markers were used to screen pools of DNA from patients and their siblings. Linkage between the LGMD locus and D9S302 (maximum LOD score 5.99 at recombination fraction .03) was established. Since this marker resides within the chromosomal region known to harbor the gene causing Fukuyama congenital muscular dystrophy (FCMD), we expanded our investigations, to include additional markers in chromosome region 9q31-q34.1. Haplotype analysis revealed five recombinations that place the LGMD locus distal to the FCMD locus. The LGMD locus maps close to D9S934 (maximum multipoint LOD score 7.61) in a region that is estimated to be ∼4.4 Mb (Genetic Location Database composite map). On the basis of an inferred ancestral recombination, the gene may lie in a 300-kb region between D9S302 and D9S934. Our results provide compelling evidence that yet another gene is involved in LGMD; we suggest that it be named “LGMD2H.

    Space based astronomy: Teacher's guide with activities

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    This curriculum guide uses hands-on activities to help students and teachers understand the significance of space-based astronomy - astronomical observations made from outer space. The guide contains few of the traditional activities found in many astronomy guides such as constellation studies, lunar phases, and planetary orbits. Instead, it tells the story of why it is important to observe celestial objects from outer space and how to study the entire electromagnetic spectrum. The guide begins with a survey of astronomy related NASA spacecraft. This is followed by a collection of activities in four units: (1) the atmospheric filter; (2) the electromagnetic spectrum; (3) collecting electromagnetic radiation; and (4) down to Earth. A curriculum index identifies the curriculum areas each activity addresses. The guide concludes with a glossary, reference list, a NASA Resources list, and an evaluation card. It is designed for students in grades 5 through 8

    The Role of Ejecta in the Small Crater Populations on the Mid-Sized Saturnian Satellites

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    We find evidence that crater ejecta play an important role in the small crater populations on the Saturnian satellites, and more broadly, on cratered surfaces throughout the Solar System. We measure crater populations in Cassini images of Enceladus, Rhea, and Mimas, focusing on image data with scales less than 500 m/pixel. We use recent updates to crater scaling laws and their constants to estimate the amount of mass ejected in three different velocity ranges: (i) greater than escape velocity, (ii) less than escape velocity and faster than the minimum velocity required to make a secondary crater (v_min), and (iii) velocities less than v_min. Although the vast majority of mass on each satellite is ejected at speeds less than v_min, our calculations demonstrate that the differences in mass available in the other two categories should lead to observable differences in the small crater populations; the predictions are borne out by the measurements we have made to date. Rhea, Tethys, and Dione have sufficient surface gravities to retain ejecta moving fast enough to make secondary crater populations. The smaller satellites, such as Enceladus but especially Mimas, are expected to have little or no traditional secondary populations because their escape velocities are near the threshold velocity necessary to make a secondary crater. Our work clarifies why the Galilean satellites have extensive secondary crater populations relative to the Saturnian satellites. The presence, extent, and sizes of sesquinary craters (craters formed by ejecta that escape into temporary orbits around Saturn before re-impacting the surface) is not yet well understood. Finally, our work provides further evidence for a "shallow" size-frequency distribution (slope index of ~2 for a differential power-law) for comets a few km diameter and smaller. [slightly abbreviated]Comment: Submitted to Icarus. 77 double-spaced pages, including 25 figures and 5 table

    The Lectin-like Domain of Thrombomodulin Confers Protection from Neutrophil-mediated Tissue Damage by Suppressing Adhesion Molecule Expression via Nuclear Factor κB and Mitogen-activated Protein Kinase Pathways

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    Thrombomodulin (TM) is a vascular endothelial cell (EC) receptor that is a cofactor for thrombin-mediated activation of the anticoagulant protein C. The extracellular NH2-terminal domain of TM has homology to C-type lectins that are involved in immune regulation. Using transgenic mice that lack this structure (TMLeD/LeD), we show that the lectin-like domain of TM interferes with polymorphonuclear leukocyte (PMN) adhesion to ECs by intercellular adhesion molecule 1–dependent and –independent pathways through the suppression of extracellular signal–regulated kinase (ERK)1/2 activation. TMLeD/LeD mice have reduced survival after endotoxin exposure, accumulate more PMNs in their lungs, and develop larger infarcts after myocardial ischemia/reperfusion. The recombinant lectin-like domain of TM suppresses PMN adhesion to ECs, diminishes cytokine-induced increase in nuclear factor κB and activation of ERK1/2, and rescues ECs from serum starvation, findings that may explain why plasma levels of soluble TM are inversely correlated with cardiovascular disease. These data suggest that TM has antiinflammatory properties in addition to its role in coagulation and fibrinolysis

    MutPred Splice: machine learning-based prediction of exonic variants that disrupt splicing

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    We have developed a novel machine-learning approach, MutPred Splice, for the identification of coding region substitutions that disrupt pre-mRNA splicing. Applying MutPred Splice to human disease-causing exonic mutations suggests that 16% of mutations causing inherited disease and 10 to 14% of somatic mutations in cancer may disrupt pre-mRNA splicing. For inherited disease, the main mechanism responsible for the splicing defect is splice site loss, whereas for cancer the predominant mechanism of splicing disruption is predicted to be exon skipping via loss of exonic splicing enhancers or gain of exonic splicing silencer elements. MutPred Splice is available at http://mutdb.org/mutpredsplice

    Exploration an the Search for Origins: A Vision for Ultraviolet-Optical-Infrared Space Astronomy

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    Public support and enthusiasm for astronomy have been strong in the final decades of the twentieth century. Nowhere is this better demonstrated than with the Hubble Space Telescope (HCT), a grand endeavor, which is enabling astronomers to make giant strides in understanding our universe, our place in it, and our relation to it. The NASAs first infrared observatory, the Space Infrared Telescope Facility (SIRTF), promises to take the crucial next steps towards understanding the formation of stars and galaxies. Toward their completion, the HST and Beyond Committee identifies major goals, whose accomplishment will justify a commitment well into the next century: (1) the detailed study of the birth and evolution of normal galaxies such as the Milky Way; (2) the detection of Earth-like planets around other stars and the search for evidence of life on them; (3) NASA should develop a space observatory of aperture 4m or larger, optimized for imaging and spectroscopy over the wavelength range 1-5 microns; and (4) NASA should develop the capability for space interferometry

    Acute Lead Exposure Increases Arterial Pressure: Role of the Renin-Angiotensin System

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    Background: Chronic lead exposure causes hypertension and cardiovascular disease. Our purpose was to evaluate the effects of acute exposure to lead on arterial pressure and elucidate the early mechanisms involved in the development of lead-induced hypertension. Methodology/Principal Findings: Wistar rats were treated with lead acetate (i.v. bolus dose of 320 μg/Kg), and systolic arterial pressure, diastolic arterial pressure and heart rate were measured during 120 min. An increase in arterial pressure was found, and potential roles of the renin-angiotensin system, Na+,K+-ATPase and the autonomic reflexes in this change in the increase of arterial pressure found were evaluated. In anesthetized rats, lead exposure: 1) produced blood lead levels of 37±1.7 μg/dL, which is below the reference blood concentration (60 μg/dL); 2) increased systolic arterial pressure (Ct: 109±3 mmHg vs Pb: 120±4 mmHg); 3) increased ACE activity (27% compared to Ct) and Na+,K+-ATPase activity (125% compared to Ct); and 4) did not change the protein expression of the α1-subunit of Na+,K+-ATPase, AT1 and AT2. Pre-treatment with an AT1 receptor blocker (losartan, 10 mg/Kg) or an ACE inhibitor (enalapril, 5 mg/Kg) blocked the lead-induced increase of arterial pressure. However, a ganglionic blockade (hexamethonium, 20 mg/Kg) did not prevent lead's hypertensive effect. Conclusion: Acute exposure to lead below the reference blood concentration increases systolic arterial pressure by increasing angiotensin II levels due to ACE activation. These findings offer further evidence that acute exposure to lead can trigger early mechanisms of hypertension development and might be an environmental risk factor for cardiovascular diseaseThis study was supported by grants from CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior) and CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico)/FAPES (Fundação de Amparo à Pesquisa do Espírito Santo)/FUNCITEC (Fundação de Ciência e Tecnologia)(39767531/07), Brazil and from MCINN (Ministerio de Ciencia e Innovación) (SAF 2009- 07201) and ISCIII (Instituto de Salud Carlos III) (Red RECAVA- Red Temática de Investigación en Enfermedades Cardiovasculares del Instituto de Salud Carlos III, RD06/0014/0011), Spai
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