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Titlebook: Biological Amplification Systems in Immunology; Noorbibi K. Day,Robert A. Good Book 1977 Plenum Publishing Corporation 1977 antibody.antig

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發(fā)表于 2025-3-21 18:29:20 | 只看該作者 |倒序瀏覽 |閱讀模式
期刊全稱Biological Amplification Systems in Immunology
影響因子2023Noorbibi K. Day,Robert A. Good
視頻videohttp://file.papertrans.cn/188/187298/187298.mp4
學科分類Comprehensive Immunology
圖書封面Titlebook: Biological Amplification Systems in Immunology;  Noorbibi K. Day,Robert A. Good Book 1977 Plenum Publishing Corporation 1977 antibody.antig
影響因子Interest in complement developed at the end of the nineteenth century from observations on cellular and humoral defense mechanisms against bacteria. It was recognized at that time that there were factors in body fluids of animals and man that were capable of killing and lysing bacteria in the absence of cellular factors. Due to the efforts of two of the founders of immunology, Bordet and Ehrlich, and their colleagues, by 1912 the multicomponent nature of complement action was well recognized, the sequence of reaction of the components in the lysis of erythrocytes was defined, complement fixation as a major tool for studying antibody-antigen interaction was well established, and studies on the physicochemical properties of the components had been started. Yet, with a few notable exceptions, research on complement was largely abandoned by most "mainstream" immunologists for the following two or three decades. When one looks at the contents of the present volume, it is hard to imagine that as recently as 20 years ago, there were probably fewer than ten major laboratories where complement research was the primary theme. The contents attest to the fact that there are today dozens of lab
Pindex Book 1977
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https://doi.org/10.1007/978-3-662-28565-7oduction of chemotactic gradients as well as the ability of wandering cells to respond normally to such gradients appears to be critical for immunologically mediated host defense. Dysfunctions of leukocyte chemotaxis may render an individual more susceptible to infectious, inflammatory, and perhaps
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Kinderkultur , der Versuch einer Ann?herungtic leukemia and dermatitis herpetiformis; C3 with increased frequency of infections, in particular, of the pulmonary apparatus; C4 with lupus erythematosus; C5 deficiency with membranous glomerulonephritis, vasculitis, arthritis, and propensity to bacterial infections; C5 abnormality with Leiner’s
地板
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https://doi.org/10.1007/978-3-531-92776-3pecific inhibitor. Irrespective of which mechanism(s) mentioned is the basis for each specific deficiency, we shall denote genes resulting in deficient C components as C° genes; e.g., C2° is a C2-deficient gene.
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https://doi.org/10.1007/978-3-531-92776-3 done in a recent review by Nishioka (1976), who reiterates the need to take an overview of the entire immune system and the interplay of its component parts in the tumor-host relationship. Nishioka divides the immunological surveillance system into four segments: (1) the classical pathway of the co
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Book 1977wo or three decades. When one looks at the contents of the present volume, it is hard to imagine that as recently as 20 years ago, there were probably fewer than ten major laboratories where complement research was the primary theme. The contents attest to the fact that there are today dozens of lab
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ollowing two or three decades. When one looks at the contents of the present volume, it is hard to imagine that as recently as 20 years ago, there were probably fewer than ten major laboratories where complement research was the primary theme. The contents attest to the fact that there are today dozens of lab978-1-4684-2546-8978-1-4684-2544-4
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Complement Synthesis,have raised important general questions about the control of plasma protein metabolism, which can be approached with current methods. One purpose of this chapter is to emphasize these actual and potential applications of studies of complement biosynthesis.
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Biologic Aspects of Leukocyte Chemotaxis,oduction of chemotactic gradients as well as the ability of wandering cells to respond normally to such gradients appears to be critical for immunologically mediated host defense. Dysfunctions of leukocyte chemotaxis may render an individual more susceptible to infectious, inflammatory, and perhaps
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