11,749 research outputs found

    TSE pathogenesis in cattle and sheep

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    Many studies have been undertaken in rodents to study the pathogenesis of transmissible spongiform encephalopathies (TSE). Only a few studies have focused on the pathogenesis of bovine spongiform encephalopathy (BSE) and scrapie in their natural hosts. In this review, we summarize the most recent insights into the pathogenesis of BSE and scrapie starting from the initial uptake of TSE agents and crossing of the gut epithelium. Following replication in the gut-associated lymphoid tissues (GALT), TSE agents spread to the enteric nervous system (ENS) of the gut. Infection is then carried through the efferent fibers of the post-ganglionic neurons of the parasympathetic and sympathetic nervous system to the pre-ganglionic neurons in the medulla oblongata of the brain and the thoracic segments of the spinal cord. The differences between the pathogenesis of BSE in cattle and scrapie in sheep are discussed as well as the possible existence of additional pathogenetic routes

    Fables de la Chine Antique, Tome II

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    This book is half of the larger-format canvas-bound predecessor of the identically named paperback book I have listed under 1980/84. The first text here is on 79 there. The order of texts changes slightly from time to time. The illustrations are the same. The cover picture here is the mirror-opposite of the cover picture there: a man sits before a fire over which a spitted turtle is roasting. There is a curious difference in names, whether of people or places. Thus L'Homme Qui Avait Peur des esprits (3) starts there Au sud de Xiashu vivait un homme nommé Juan Shuliang. The author is listed as Xunsi. Here, some twenty years earlier, the sentence reads Au sud de Sciacheou vivait un homme nommé Kiuan Siun-liang. The author is listed as Siun Tse. Here the title is pasted onto the gray paper cover in a lovely vertical red stripe. See my comments there and in the paperback Spanish and English versions of the book.This is a hardbound book (hard cover)Language note: FrenchRetold and Illustrated by Alice Shirle

    Ativismo no judiciário eleitoral: análise crítica dos julgamentos e das resoluções expedidas pelo TSE

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    TCC(graduação) - Universidade Federal de Santa Catarina. Centro de Ciências Jurídicas. Direito.A monografia objetiva estudar o Ativismo na Justiça Eleitoral em relação ao poder normativo que lhe compete. O objetivo principal da pesquisa, coincidente ao problema, reside em avaliar se as resoluções expedidas com base nesse poder do Judiciário Eleitoral que criam direitos, penalidades, inelegibilidades, obrigações, competências são consideradas inconstitucionais por violarem os princípios da separação de poderes, da legalidade, da segurança jurídica, as normas de organização judiciária e demais dispositivos legais. A hipótese é de que sim, tais instruções vão de encontro à Constituição Federal. Ademais, os objetivos secundários perpassam a exacerbação do Judiciário frente aos demais poderes estatais, apontando-se o ativismo judicial e suas causas, consequências e distinções. O trabalho averigua, também, os limites à regulamentação do Tribunal Superior Eleitoral – fonte considerável de posturas ativistas – e critica a desarmonia instalada no sistema constitucional de freios e contrapesos quando da usurpação da competência do Congresso Nacional pelos magistrados. Quanto à atualidade da pesquisa, é perceptível a tentativa contínua e recente do Judiciário em deixar sua passividade e atuar no intuito de moralizar a política brasileira por meio de normas gerais, abstratas e prospectivas, impedindo candidatos de concorrerem às eleições e também alterando o resultado do pleito. Concluiu-se que as resoluções analisadas, as quais instituíram a perda do mandato eletivo por infidelidade partidária e o requisito de aprovação das contas para se obter a certidão negativa eleitoral (Resolução TSE nº. 22.610/2007 e nº. 23.376/2012, respectivamente), devem ser expurgadas do ordenamento por serem inconstitucionais

    Two Genetically Defined Tram-Acting Loci Coordinately Regulate Overlapping Sets of Liver-Specific Genes

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    Mice homozygous for deletions around the albino locus fail to activate expression of a set of neonatal liver functions and die shortly after birth. This phenotype is thought to result from the loss of a positive trans-acting factor, denoted alf, in deletion homozygotes. Using differential cDNA screening, we isolated and characterized genes whose cell type-specific transcription is affected by alf and found as a common feature that expression of these genes is induced by glucocorticoids and cAMP. Surprisingly, a subset of these alf-responsive genes is negatively controlled by the tissue-specific extinguisher locus Tse-1. Administration of glucocorticoids and cAMP leads to reversal of Tse-1—mediated extinction of these genes. These results show that two trans-acting factors coordinately regulate expression of overlapping sets of liver-specific genes. We suggest that both the lethal phenotype and the extinguished state result from interference with hormone signal transduction

    Endogenous Viral Etiology of Prion Diseases

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    Transmissible spongiform encephalopathies (TSEs), or prion diseases, are a group of incurable neurodegenerative disorders, including Kuru and Creutzfeldt-Jakob disease in humans, “mad cow” disease in cattle, and scrapie in sheep. This paper presents structural, genetic, and evolutionary evidence supporting an endogenous TSE virus model that integrates the three major traditional views on the nature of TSE pathogens, the conventional virus view, the prion hypothesis, and the virino concept, into a novel conceptual and evolutionary framework. According to this model, the TSE pathogens are symbiotic endogenous viruses that inadvertently produce transmissible viral particles that lack the viral genome and are composed primarily of the viral prion protein (PrP). Production of defective viral particles that contain a partial genome or lack the viral genome entirely is a relatively common event in the life cycle of many viruses. Similar to the normal viral particles, which contain a genome, these defective viral particles can be transmitted to new host cells. Obviously, in the absence of viral genome, these protein-only viral particles cannot establish a productive infection. However, if these viral particles enter a host cell that carries the parental or a related virus and induce the production of similar protein-only particles, then they would appear as self-replicating, protein-only infectious pathogens if mistakenly taken out from the context of the viral life cycle. This misconception, which is rooted into the current dogma of viruses as viral particles, led to the development of the prion theory. The endogenous TSE virus model is consistent with the TSE data and offers solutions to many enigmatic features associated with TSE, including the function of PrP that, despite more than two decades of TSE research conducted primarily within the framework of the prion hypothesis, is still not known. According to the TSE endogenous virus model, PrP is the protein of an endogenous virus that has co-evolved with their vertebrate hosts by providing a protective function against pathogenic viruses. The evidence for the endogenous TSE virus model and for the antiviral protective function of PrP is strong, and they are fully open to additional experimental testing. The endogenous virus model opens the TSE research field to new interpretations and directions, both in basic research and in associated biomedical and public health fields, and could lead to development of new diagnostic and therapeutic approaches

    Scoping Software Engineering for AI:The TSE Perspective

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    IEEE TSE would like to take a more nuanced approach with respect to reviewing these “SE for AI” papers. Specifically, we observe that submitted manuscripts frequently go into the depths of core AI techniques to improve them in various ways. The question that editors, reviewers, and authors themselves therefore often ask is whether some of the submitted manuscripts are a good fit for SE venues such as IEEE TSE, or would be a better fit for more AI- or ML-specialized venues instead

    TSEi – TSE Infectivity Model

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    <p>The TSE Infectivity Model (TSEi), developed for EFSA by a contractor, allows: i) the comparison of the level of transmissible spongiform encephalopathies (TSE) infectivity in animal tissues; ii) the estimation of the impact of risk management options (removal of specified risk material) at single animal level and at animal population (country) level; and iii) the estimation of the impact of processing on the TSE infectivity level.</p> <p>TSEi was developed in Microsoft Excel with the use of the stochastic add-in Palisade @Risk version 6.2.1., and is supported by a user-friendly interface that allows for the input of the various data and parameters needed. Two interfaces are provided: BSE in cattle (validated) and scrapie in sheep (not validated, provided for demonstration purposes). TSEi has been applied within an assessment of the bovine spongiform encephalopathy (BSE) risk in bovine intestines and mesentery, in particular to estimate the BSE infectious load in tissues from infected animals at different ages and the total yearly infectious load that could enter the food and feed chain in 27 European Union Member States (Adkin et al., 2014; EFSA BIOHAZ Panel, 2014).</p> <p>TSEi includes BSE data for two example countries (country MM, representing a medium-sized country with TSE testing started in 2003 and some BSE positive findings; country LL, representing a large-sized country with TSE testing started in 2002 and a high number of BSE positive findings). TSEi can be run with those fictitious data, or after inclusion of real data for any country of interest by the user.</p> <p> </p>Microsoft Excel and @Ris

    Book Review: Leave No Nurse Behind: Nurses Working with disAbilities

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    Author: Donna Maheady Reviewer: Alice Tse, PhD, APRN, RN Publisher: iUniverse, 2006 Paper, ISBN: 0-595-39649-6, 146 pages Cost: $14.9

    Prions and Transmissible Spongiform Encephalopathy (TSE) Chemotherapeutics: A Common Mechanism for Anti-TSE Compounds?

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    No validated treatments exist for transmissible spongiform encephalopathies (TSEs or prion diseases) in humans or livestock. The search for TSE therapeutics is complicated by persistent uncertainties about the nature of mammalian prions and their pathogenic mechanisms. In pursuit of anti-TSE drugs, we and others have focused primarily on blocking conversion of normal prion protein, PrP^C, to the TSE-associated isoform, PrP^Sc. Recently developed high-throughput screens have hastened the identification of new inhibitors with strong in vivo anti-TSE activities such as porphyrins, phthalocyanines, and phosphorthioated oligonucleotides. New routes of administration have enhanced beneficial effects against established brain infections. Several different classes of TSE inhibitors share structural similarities, compete for the same site(s) on PrP^C, and induce the clustering and internalization of PrP^C from the cell surface. These activities may represent a common mechanism of action for these anti-TSE compounds

    Schram (Stuart R.) - The political thought of Mao Tse-tung. Schram (Stuart R.) ed. - Mao Tsé-toung. Textes traduits et présentés par Stuart Schram

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    Cadart Claude. Schram (Stuart R.) - The political thought of Mao Tse-tung. Schram (Stuart R.) ed. - Mao Tsé-toung. Textes traduits et présentés par Stuart Schram. In: Revue française de science politique, 14ᵉ année, n°3, 1964. pp. 575-577
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