Compensation for Spherical Geometric and Absorption Effects on Lower Thermospheric Emission Intensities Derived from High Earth Orbit Images

Remote sensing of the atmosphere from high earth orbit is very attractive due to the large field of view obtained and a true global perspective. This viewpoint is complicated by earth curvature effects so that slant path enhancement and absorption effects, small from low earth orbit, become dominant even at small nadir view angles. The effect is further complicated by the large range of local times and solar zenith angles in a single image leading to a modulation of the image intensity by a significant portion of the diurnal height variation of the absorbing layer. The latter effect is significant in particular for mesospheric, stratospheric and auroral emissions due to their depth in the atmosphere. As a particular case, the emissions from atomic oxygen (130.4 and 135.6 nm) and molecular nitrogen (two LBH bands, LBHS from 140 to 160 nm and LBHL from 160 to 180 nm) as viewed from the Ultraviolet Imager (UVI) are examined. The LBH emissions are of particular interest since LBHS has significant 02 absorption while LBHL does not, In the case of auroral emissions this differential absorption, well examined in the nadir, gives information about the height of the emission and therefore the energy of the precipitating particles. Using simulations of the viewing geometry and images from the UVI we examine these effects and obtain correction factors to adjust to the nadir case with a significant improvement of the derived characteristic energy. There is a surprisingly large effect on the images from the 02 diurnal layer height changes. An empirical compensation to the nadir case is explored based on the local nadir and local zenith angles for each portion of the image. These compensations are demonstrated as applied to the above emissions in both auroral and dayglow images and compared to models. The extension of these findings to other instruments, emissions and spectral regions is examined

Processing and Transmission of Information

Contains research objectives and reports on three research projects.National Science Foundation (Grant GP-2495)National Institutes of Health (Grant MH-04737-04)National Aeronautics and Space Administration (Grant NsG-334)National Aeronautics and Space Administration (Grant NsG-496

High performance electromagnetic railgun launcher

A railgun operates at high pressure (up to 350 MPa) without structural damage and is readily disassembled for inspection, maintenance and component testing. A rail assembly is pressed into a hoop-wound epoxy fiberglass containment tube and clamped within a steel compression frame. The geometry of the rail assembly permits rail movement without insulator intrusion and achieves bore sealing during rail movement at maximum pressure. The rail assembly also has replaceable insulator inserts which are isolated from rail re-bound shock. Fused quartz insulator inserts provide the best results. A flash tube is provided at the gun muzzle to suppress precursor discharge and commutate precursor current back to the armature. To realize increased velocity without sacrificing in-bore projectile stability, a cut-corner projectile is used having a L/D ratio as small as 0.65 which reduces the mass by about 11%.Board of Regents, University of Texas Syste

Alternative models for academic family practices

BACKGROUND: The Future of Family Medicine Report calls for a fundamental redesign of the American family physician workplace. At the same time, academic family practices are under economic pressure. Most family medicine departments do not have self-supporting practices, but seek support from specialty colleagues or hospital practice plans. Alternative models for academic family practices that are economically viable and consistent with the principles of family medicine are needed. This article presents several "experiments" to address these challenges. METHODS: The basis of comparison is a traditional academic family medicine center. Apart of the faculty practice plan, our center consistently operated at a deficit despite high productivity. A number of different practice types and alternative models of service delivery were therefore developed and tested. They ranged from a multi-specialty office arrangement, to a community clinic operated as part of a federally-qualified health center, to a team of providers based in and providing care for residents of an elderly public housing project. Financial comparisons using consistent accounting across models are provided. RESULTS: Academic family practices can, at least in some settings, operate without subsidy while providing continuity of care to a broad segment of the community. The prerequisites are that the clinicians must see patients efficiently, and be able to bill appropriately for their payer mix. CONCLUSION: Experimenting within academic practice structure and organization is worthwhile, and can result in economically viable alternatives to traditional models

1972: Abilene Christian College Bible Lectures - Full Text

THE CHURCH AND THE FUTURE Being the Abilene Christian College Annual Bible Lectures 1972 Published by ABILENE CHRISTIAN COLLEGE BOOK STORE ACC Station Abilene, Texas 7960

Targeting macrophage Histone deacetylase 3 stabilizes atherosclerotic lesions

Macrophages are key immune cells found in atherosclerotic plaques and critically shape atherosclerotic disease development. Targeting the functional repertoire of macrophages may hold novel approaches for future atherosclerosis management. Here, we describe a previously unrecognized role of the epigenomic enzyme Histone deacetylase 3 (Hdac3) in regulating the atherosclerotic phenotype of macrophages. Using conditional knockout mice, we found that myeloid Hdac3 deficiency promotes collagen deposition in atherosclerotic lesions and thus induces a stable plaque phenotype. Also, macrophages presented a switch to anti-inflammatory wound healing characteristics and showed improved lipid handling. The pro-fibrotic phenotype was directly linked to epigenetic regulation of the Tgfb1 locus upon Hdac3 deletion, driving smooth muscle cells to increased collagen production. Moreover, in humans, HDAC3 was the sole Hdac upregulated in ruptured atherosclerotic lesions, Hdac3 associated with inflammatory macrophages, and HDAC3 expression inversely correlated with pro-fibrotic TGFB1 expression. Collectively, we show that targeting the macrophage epigenome can improve atherosclerosis outcome and we identify Hdac3 as a potential novel therapeutic target in cardiovascular disease

Psychosocial risk factors for suicidality in children and adolescents

Suicidality in childhood and adolescence is of increasing concern. The aim of this paper was to review the published literature identifying key psychosocial risk factors for suicidality in the paediatric population. A systematic two-step search was carried out following the PRISMA statement guidelines, using the terms 'suicidality, suicide, and self-harm' combined with terms 'infant, child, adolescent' according to the US National Library of Medicine and the National Institutes of Health classification of ages. Forty-four studies were included in the qualitative synthesis. The review identified three main factors that appear to increase the risk of suicidality: psychological factors (depression, anxiety, previous suicide attempt, drug and alcohol use, and other comorbid psychiatric disorders); stressful life events (family problems and peer conflicts); and personality traits (such as neuroticism and impulsivity). The evidence highlights the complexity of suicidality and points towards an interaction of factors contributing to suicidal behaviour. More information is needed to understand the complex relationship between risk factors for suicidality. Prospective studies with adequate sample sizes are needed to investigate these multiple variables of risk concurrently and over time

Mechanisms Establishing TLR4-Responsive Activation States of Inflammatory Response Genes

Precise control of the innate immune response is required for resistance to microbial infections and maintenance of normal tissue homeostasis. Because this response involves coordinate regulation of hundreds of genes, it provides a powerful biological system to elucidate the molecular strategies that underlie signal- and time-dependent transitions of gene expression. Comprehensive genome-wide analysis of the epigenetic and transcription status of the TLR4-induced transcriptional program in macrophages suggests that Toll-like receptor 4 (TLR4)-dependent activation of nearly all immediate/early- (I/E) and late-response genes results from a sequential process in which signal-independent factors initially establish basal levels of gene expression that are then amplified by signal-dependent transcription factors. Promoters of I/E genes are distinguished from those of late genes by encoding a distinct set of signal-dependent transcription factor elements, including TATA boxes, which lead to preferential binding of TBP and basal enrichment for RNA polymerase II immediately downstream of transcriptional start sites. Global nuclear run-on (GRO) sequencing and total RNA sequencing further indicates that TLR4 signaling markedly increases the overall rates of both transcriptional initiation and the efficiency of transcriptional elongation of nearly all I/E genes, while RNA splicing is largely unaffected. Collectively, these findings reveal broadly utilized mechanisms underlying temporally distinct patterns of TLR4-dependent gene activation required for homeostasis and effective immune responses

From old organisms to new molecules: integrative biology and therapeutic targets in accelerated human ageing

Understanding the basic biology of human ageing is a key milestone in attempting to ameliorate the deleterious consequences of old age. This is an urgent research priority given the global demographic shift towards an ageing population. Although some molecular pathways that have been proposed to contribute to ageing have been discovered using classical biochemistry and genetics, the complex, polygenic and stochastic nature of ageing is such that the process as a whole is not immediately amenable to biochemical analysis. Thus, attempts have been made to elucidate the causes of monogenic progeroid disorders that recapitulate some, if not all, features of normal ageing in the hope that this may contribute to our understanding of normal human ageing. Two canonical progeroid disorders are Werner’s syndrome and Hutchinson-Gilford progeroid syndrome (also known as progeria). Because such disorders are essentially phenocopies of ageing, rather than ageing itself, advances made in understanding their pathogenesis must always be contextualised within theories proposed to help explain how the normal process operates. One such possible ageing mechanism is described by the cell senescence hypothesis of ageing. Here, we discuss this hypothesis and demonstrate that it provides a plausible explanation for many of the ageing phenotypes seen in Werner’s syndrome and Hutchinson-Gilford progeriod syndrome. The recent exciting advances made in potential therapies for these two syndromes are also reviewed