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Titlebook: Host-Parasite Cellular and Molecular Interactions in Protozoal Infections; K.-P. Chang,David Snary Conference proceedings 1987 Springer-Ve

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书目名称Host-Parasite Cellular and Molecular Interactions in Protozoal Infections
编辑K.-P. Chang,David Snary
视频video
丛书名称Nato ASI Subseries H:
图书封面Titlebook: Host-Parasite Cellular and Molecular Interactions in Protozoal Infections;  K.-P. Chang,David Snary Conference proceedings 1987 Springer-Ve
描述Tropical diseases such as leishmaniasis, malaria. trypanosomiasis, toxoplasmosis and amebiasis continue to plague the world, resulting in considerable morbidity and mortality, especially in the third world countries. These diseases are caused by a group of protozoa which have, over the years, undergone evolutionary adaptation to live often intracellularly in a parasitic way of life. So well-adapted have they become that they recognize the right hosts or cells to parasitize, yet at the same time they escape recognition and destruction by the host immune system. The mechanisms of such recognition and the escape of recognition are governed largely by host-parasite surface membrane interactions at the cellular and molecular level. Unique molecules produced by unusual pathways of these parasites have also been discovered and found to play important roles in their survival in the host. Understanding these mechanisms and pathways is essential not only to formulate a rational strategy for chemo- and immuno-prophylaxis and -therapy but also to unravel the mystery of biological evolution in symbiosis and parasitism. In the advent of our knowledge on the molecular biology and biochemistry of
出版日期Conference proceedings 1987
关键词Leishmania; Malaria; antibody; biochemistry; cell; defense mechanism; gene; glycoprotein; infection; interfer
版次1
doihttps://doi.org/10.1007/978-3-642-72840-2
isbn_softcover978-3-642-72842-6
isbn_ebook978-3-642-72840-2Series ISSN 1010-8793
issn_series 1010-8793
copyrightSpringer-Verlag Berlin Heidelberg 1987
The information of publication is updating

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1010-8793 nsiderable morbidity and mortality, especially in the third world countries. These diseases are caused by a group of protozoa which have, over the years, undergone evolutionary adaptation to live often intracellularly in a parasitic way of life. So well-adapted have they become that they recognize t
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Evolution of Antigenic Variation in African Trypanosomes the parasites while in the bloodstream of the host. On any one trypanosome, at any one time, this coat is essentially homogeneous, being comprised of a single glycoprotein species, known as the variant surface glycoprotein or VSG (Cross, 1975; Vickerman and Luckins, 1969).
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Metabolism of Trypanothione and Glutathionylspermidine in Trypanosomatidsein synthesis and regulation of enzyme activity C3]. The intracellular ratio of reduced to oxidized glutathione (GSH : GSSG) is kept high (GSSG < 1% of the total) due to the presence of the NADPH-dependent enzyme, glutathione reductase [E.C. 1.6.4.2].
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The Promastigote Surface Protease of Leishmania three strains of Leishmania previously shown by surface radioiodination, peptide mapping and antigenic crossreactivity to express gp63: L. major LRC-L137, L. donovani infantum LEM 75, and L. tropica LRC-L32 (Etges et al. 1985).
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A Specific Inhibitor of Trypanosoma Cruzi Neuraminidase Found in Human Plasmablished between 1903 and 1935 he described the disease, its etiology, its vectors and its reservoirs. Chagas’ disease predominantly striking the rural population, still represents an exciting challenge to the scientific community because the molecular mechanisms of its pathogenicity have yet to be unravelled.
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