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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Medicine 20 (1969), S. 201-206 
    ISSN: 0066-4219
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 9 (2000), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The etiology and pathogenesis of psoriasis – one of the most common chronic, inflammatory, hyperproliferative skin disorders of man – have long fascinated dermatologists, pathologists and biologists alike. Here, we have a model disease that offers to study neuroectodermal-mesenchymal interactions in the widest sense possible. Epithelial, endothelial, and hematopoietic cells as well as neurons projecting into the skin apparently all interact with each other to generate the characteristic psoriatic lesion. For decades, the ongoing controversy on the molecular nature, choreography and hierarchy of these complex interactions e.g. between epidermal keratinocytes, T cells, neurotrophils, endothelial cells and sensory nerves has served as a driving force propelling investigative dermatology to ever new horizons. This debate has not only been at the heart of our quest to develop more effective forms of therapy for this socially crippling disease, but it also has profoundly influenced how we view the skin as a whole: the numerous competing theories on the pathogenesis of psoriasis published so far also are reflections on the evolution of mainstream thought in skin biology over the last decades. These days, conventional wisdom – infatuated with a T-cell-centered approach to inflammatory skin diseases – portrays psoriasis as an autoimmune disease, where misguided T lymphocyte activities cause secondary epithelial abnormalities. And yet, as this CONTROVERSIES feature reminds us, some authoritative “pockets of academic resistance” are still quite alive, and interpret psoriasis e.g. as a genetically determined, abnormal epithelial response pattern to infectious and/or physicochemical skin insults. Weighing the corresponding lines of argumentation is not only an intriguing, clinically relevant intellectual exercise, but also serves as a wonderful instrument for questioning our own views of the skin universe and its patterns of deviation from a state of homeostasis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A chronic delayed hypersensitivity reaction was produced in the pig stomach. In skin-sensitized animals 2–4 dinitrochlorobenzene (DNCB) in adhesive paste produced mucosal ulceration with intestinalization, edema, and marked round-cell infiltration of the submucosa, vascular congestion, perivascular cuffing, and fibrinoid arteriolar changes. When pigs that were not skin-sensitized were given DNCB in adhesive paste, no mucosal ulceration was seen. A similar but less intense cellular infiltrate and vascular change was present. Circulating antibodies to DNCB showed no relationship to the morphological lesion, while parietal cell antibody immunofluorescent titers parallel the intensity of the tissue response. Under the conditions of this experiment, parietal cell antibodies are not involved in the pathogenesis of the mucosal lesion.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-0832
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Activation of C3 and factor B in normal human serum by P. ovale was demonstrated using a standard unidirectional immunoelectrophoresis technique. Activation of complement by the alternative (properdin) pathway is a possible mechanism by which P. ovale may mediate an inflammatory response.
    Type of Medium: Electronic Resource
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