Isbn: 9781489997487 - immunogenetics of autoimmune disease (10 risultati)

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  • Lingua: Inglese

    Editore: Springer, 2014

    1489997482 / 9781489997487

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    Condizione: New. In English.

  • Lingua: Inglese

    Editore: Springer, 2014

    1489997482 / 9781489997487

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    Lingua: Inglese

    Editore: Springer US, 2014

    1489997482 / 9781489997487

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    Taschenbuch. Condizione: Neu. Immunogenetics of Autoimmune Disease | David Brassat (u. a.) | Taschenbuch | xi | Englisch | 2014 | Springer US | EAN 9781489997487 | Verantwortliche Person für die EU: Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg, juergen[dot]hartmann[at]springer[dot]com | Anbieter: preigu.

  • Lingua: Inglese

    Editore: Springer, 2014

    1489997482 / 9781489997487

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    Da: Brook Bookstore On Demand, Napoli, NA, ItaliaBrook Bookstore On Demand

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  • Lingua: Inglese

    Editore: Springer US Dez 2014, 2014

    1489997482 / 9781489997487

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    Da: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, GermaniaBuchWeltWeit Ludwig Meier e.K.

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    Taschenbuch. Condizione: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -utoimmunity is the downstream outcome of a rather extensive and coordinated series of events that include loss of self-tolerance, peripheral lymphocyte Aactivation, disruption of the blood-systems barriers, cellular infiltration into the target organs and local inflammation. Cytokines, adhesion molecules, growth factors, antibodies, and other molecules induce and regulate critical cell functions that perpetuate inflammation, leading to tissue injury and clinical phenotype. The nature and intensity of this response as well as the physiological ability to restore homeostasis are to a large extent conditioned by the unique amino acid sequences that define allelic variants on each of the numerous participating mol ecules. Therefore, the coding genes in their germline configuration play a primary role in determining who is at risk for developing such disorders, how the disease progresses, and how someone responds to therapy. Although genetic components in these diseases are clearly present, the lack of obvious and homogeneous modes of transmission has slowed progress by prevent ing the full exploitation of classical genetic epidemiologic techniques. Furthermore, autoimmune diseases are characterized by modest disease risk heritability and m- tifaceted interactions with environmental influences. Yet, several recent discoveries have dramatically changed our ability to examine genetic variation as it relates to human disease. In addition to the development of large-scale laboratory methods and tools to efficiently recognize and catalog DNA diversity, over the past few years there has been real progress in the application of new analytical and data-manage ment approaches. 172 pp. Englisch.

  • Lingua: Inglese

    Editore: Springer US, 2014

    1489997482 / 9781489997487

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    Da: moluna, Greven, Germaniamoluna

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    Condizione: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. All chapters written by experts in the fieldSummarizes latest advancements in the fieldEssential reading for both immunologists and neuroscientistsApplications for researchers as well as medical professionals working in the field of .

  • Lingua: Inglese

    Editore: Springer, 2014

    1489997482 / 9781489997487

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    Da: Majestic Books, Hounslow, Regno UnitoMajestic Books

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    Condizione: New. Print on Demand pp. 158.

  • Lingua: Inglese

    Editore: Springer US, Springer New York Dez 2014, 2014

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    Da: buchversandmimpf2000, Emtmannsberg, BAYE, Germaniabuchversandmimpf2000

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    Taschenbuch. Condizione: Neu. This item is printed on demand - Print on Demand Titel. Neuware -utoimmunity is the downstream outcome of a rather extensive and coordinated series of events that include loss of self-tolerance, peripheral lymphocyte Aactivation, disruption of the blood-systems barriers, cellular infiltration into the target organs and local inflammation. Cytokines, adhesion molecules, growth factors, antibodies, and other molecules induce and regulate critical cell functions that perpetuate inflammation, leading to tissue injury and clinical phenotype. The nature and intensity of this response as well as the physiological ability to restore homeostasis are to a large extent conditioned by the unique amino acid sequences that define allelic variants on each of the numerous participating mol ecules. Therefore, the coding genes in their germline configuration play a primary role in determining who is at risk for developing such disorders, how the disease progresses, and how someone responds to therapy. Although genetic components in these diseases are clearly present, the lack of obvious and homogeneous modes of transmission has slowed progress by prevent ing the full exploitation of classical genetic epidemiologic techniques. Furthermore, autoimmune diseases are characterized by modest disease risk heritability and m- tifaceted interactions with environmental influences. Yet, several recent discoveries have dramatically changed our ability to examine genetic variation as it relates to human disease. In addition to the development of large-scale laboratory methods and tools to efficiently recognize and catalog DNA diversity, over the past few years there has been real progress in the application of new analytical and data-manage ment approaches.Springer Verlag GmbH, Tiergartenstr. 17, 69121 Heidelberg 172 pp. Englisch.

  • Lingua: Inglese

    Editore: Springer, 2014

    1489997482 / 9781489997487

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    Da: Biblios, frankfurt am main, HESSE, GermaniaBiblios

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    Condizione: New. PRINT ON DEMAND pp. 158.

  • Lingua: Inglese

    Editore: Humana, 2014

    1489997482 / 9781489997487

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    Taschenbuch. Condizione: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - utoimmunity is the downstream outcome of a rather extensive and coordinated series of events that include loss of self-tolerance, peripheral lymphocyte Aactivation, disruption of the blood-systems barriers, cellular infiltration into the target organs and local inflammation. Cytokines, adhesion molecules, growth factors, antibodies, and other molecules induce and regulate critical cell functions that perpetuate inflammation, leading to tissue injury and clinical phenotype. The nature and intensity of this response as well as the physiological ability to restore homeostasis are to a large extent conditioned by the unique amino acid sequences that define allelic variants on each of the numerous participating mol ecules. Therefore, the coding genes in their germline configuration play a primary role in determining who is at risk for developing such disorders, how the disease progresses, and how someone responds to therapy. Although genetic components in these diseases are clearly present, the lack of obvious and homogeneous modes of transmission has slowed progress by prevent ing the full exploitation of classical genetic epidemiologic techniques. Furthermore, autoimmune diseases are characterized by modest disease risk heritability and m- tifaceted interactions with environmental influences. Yet, several recent discoveries have dramatically changed our ability to examine genetic variation as it relates to human disease. In addition to the development of large-scale laboratory methods and tools to efficiently recognize and catalog DNA diversity, over the past few years there has been real progress in the application of new analytical and data-manage ment approaches.