409 resultados para Marburg
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Signatur des Originals: S 36/F10751
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Master of the Saint. Elizabeth Panels; 4 ft. 2 13/64 in.x 3 ft. 7 7/64 in.; oil on panel
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Includes bibliographies.
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Mode of access: Internet.
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Cover title: Gutachten der Kurhessischen Juristen-Facultät zu Marburg, über die Ansprüche der israelitischen Gemeinde zu Frankfurt am Main.
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Ebola virus is a highly pathogenic filovirus causing severe hemorrhagic fever with high mortality rates. It assembles heterogenous, filamentous, enveloped virus particles containing a negative-sense, single-stranded RNA genome packaged within a helical nucleocapsid (NC). We have used cryo-electron microscopy and tomography to visualize Ebola virus particles, as well as Ebola virus-like particles, in three dimensions in a near-native state. The NC within the virion forms a left-handed helix with an inner nucleoprotein layer decorated with protruding arms composed of VP24 and VP35. A comparison with the closely related Marburg virus shows that the N-terminal region of nucleoprotein defines the inner diameter of the Ebola virus NC, whereas the RNA genome defines its length. Binding of the nucleoprotein to RNA can assemble a loosely coiled NC-like structure; the loose coil can be condensed by binding of the viral matrix protein VP40 to the C terminus of the nucleoprotein, and rigidified by binding of VP24 and VP35 to alternate copies of the nucleoprotein. Four proteins (NP, VP24, VP35, and VP40) are necessary and sufficient to mediate assembly of an NC with structure, symmetry, variability, and flexibility indistinguishable from that in Ebola virus particles released from infected cells. Together these data provide a structural and architectural description of Ebola virus and define the roles of viral proteins in its structure and assembly
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The filoviruses, Marburg and Ebola, are non-segmented negative-strand RNA viruses causing severe hemorrhagic fever with high mortality rates in humans and nonhuman primates. The sequence of events that leads to release of filovirus particles from cells is poorly understood. Two contrasting mechanisms have been proposed, one proceeding via a "submarine-like" budding with the helical nucleocapsid emerging parallel to the plasma membrane, and the other via perpendicular "rocketlike" protrusion. Here we have infected cells with Marburg virus under BSL-4 containment conditions, and reconstructed the sequence of steps in the budding process in three dimensions using electron tomography of plastic-embedded cells. We find that highly infectious filamentous particles are released at early stages in infection. Budding proceeds via lateral association of intracellular nucleocapsid along its whole length with the plasma membrane, followed by rapid envelopment initiated at one end of the nucleocapsid, leading to a protruding intermediate. Scission results in local membrane instability at the rear of the virus. After prolonged infection, increased vesiculation of the plasma membrane correlates with changes in shape and infectivity of released viruses. Our observations demonstrate a cellular determinant of virus shape. They reconcile the contrasting models of filovirus budding and allow us to describe the sequence of events taking place during budding and release of Marburg virus. We propose that this represents a general sequence of events also followed by other filamentous and rod-shaped viruses.
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Digital Image
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Digital Image
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This is the first of three books about the history of Geoffrey Lynfield's family. It is about four Lilienfeld brothers--Geoffrey Lynfield's grandfather and his brothers. They were born in the Jewish enclave of Marburg and ended up in South Africa when and where the first diamonds were discovered. The manuscript also includes photographs and documents.
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Childhood in traditional Jewish atmosphere; description of general and Jewish life in Frankfurt am Main; family life; education in Jewish school "Philantropin"; university education in Heidelberg, Leipzig, Munich, Berlin and Marburg; military service prior to World War I.
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Viruses that originate in bats may be the most notorious emerging zoonoses that spill over from wildlife into domestic animals and humans. Understanding how these infections filter through ecological systems to cause disease in humans is of profound importance to public health. Transmission of viruses from bats to humans requires a hierarchy of enabling conditions that connect the distribution of reservoir hosts, viral infection within these hosts, and exposure and susceptibility of recipient hosts. For many emerging bat viruses, spillover also requires viral shedding from bats, and survival of the virus in the environment. Focusing on Hendra virus, but also addressing Nipah virus, Ebola virus, Marburg virus and coronaviruses, we delineate this cross-species spillover dynamic from the within-host processes that drive virus excretion to land-use changes that increase interaction among species. We describe how land-use changes may affect co-occurrence and contact between bats and recipient hosts. Two hypotheses may explain temporal and spatial pulses of virus shedding in bat populations: episodic shedding from persistently infected bats or transient epidemics that occur as virus is transmitted among bat populations. Management of livestock also may affect the probability of exposure and disease. Interventions to decrease the probability of virus spillover can be implemented at multiple levels from targeting the reservoir host to managing recipient host exposure and susceptibility.
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Viruses that originate in bats may be the most notorious emerging zoonoses that spill over from wildlife into domestic animals and humans. Understanding how these infections filter through ecological systems to cause disease in humans is of profound importance to public health. Transmission of viruses from bats to humans requires a hierarchy of enabling conditions that connect the distribution of reservoir hosts, viral infection within these hosts, and exposure and susceptibility of recipient hosts. For many emerging bat viruses, spillover also requires viral shedding from bats, and survival of the virus in the environment. Focusing on Hendra virus, but also addressing Nipah virus, Ebola virus, Marburg virus and coronaviruses, we delineate this cross-species spillover dynamic from the within-host processes that drive virus excretion to land-use changes that increase interaction among species. We describe how land-use changes may affect co-occurrence and contact between bats and recipient hosts. Two hypotheses may explain temporal and spatial pulses of virus shedding in bat populations: episodic shedding from persistently infected bats or transient epidemics that occur as virus is transmitted among bat populations. Management of livestock also may affect the probability of exposure and disease. Interventions to decrease the probability of virus spillover can be implemented at multiple levels from targeting the reservoir host to managing recipient host exposure and susceptibility.
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Lists of Jews in the "Breidenbach Land" from the 18th to the 20th century..
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Embora Hans Kelsen tenha desenvolvido suas ideias sobre a justiça em diversos artigos e capítulos de livros, o jusfilósofo nunca edificou uma obra mais profunda, monográfica ou sistemática sobre a questão do justo. Suas considerações, o mais das vezes proferidas incidentalmente quando da análise e crítica das teorias do direito natural, se encontram, a bem dizer, dispersas por diversas produções. A leitura integral e conjunta de seus estudos, entretanto, permite a identificação da mesma e coerente concepção de filosofia moral que perpassa todos os seus escritos, concepção esta que sugere a relatividade, subjetividade e irracionalidade da questão do justo. Sem o propósito de ser uma biografia intelectual ou uma psicanálise do conhecimento das conclusões kelsenianas sobre o problema da justiça, o objetivo da presente dissertação, além da tentativa de realizar uma exposição sistemática da própria teoria da justiça de Kelsen dispersa por uma multiplicidade de trabalhos, nem todos disponíveis ou publicados em língua portuguesa , consiste na análise dos pressupostos e justificativas teórico-filosóficos que, utilizados pelo jusfilósofo como embasamento de suas inferências sobre o tema, o conduzem a afirmar a incognoscibilidade de qualquer conceito absoluto, objetivo e universal de justiça, ou a viabilidade de uma razão prática. A meta maior desta dissertação, portanto, é o estabelecimento e elucidação das premissas extraídas por Kelsen do pensamento teórico-filosófico de Max Weber, Immanuel Kant (além dos neokantismos de Marburgo e Baden), Wittgenstein, e dos neopositivistas do Círculo de Viena, para rejeitar lógico-gnosiologicamente as concepções absolutistas do justo, bem como a possibilidade de discutir ou definir racionalmente a justiça e as normas morais dela decorrentes. A partir de elementos colhidos dessas diferentes correntes intelectuais, Kelsen desacredita, com base na distinção entre enunciados sobre fatos (racionais e verificáveis) e proposições relativas a valores (irracionais e não verificáveis), a capacidade humana de cognição dos valores em geral e, mais ainda, a existência e cognoscibilidade de valores absolutos em sua ótica, requisitos imprescindíveis para a exequibilidade de qualquer sistema objetivo de moralidade ou para especulações racionais sobre a justiça.