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* * * * Figure 2-27 Maturation of mononuclear phagocytes. (From Abbas AK, et al: Cellular and Molecular Immunology, 5th ed. Philadelphia, Saunders, 2003.) * ESR: A test that measures the rate at which red blood cells settle through a column of liquid. A non-specific index of inflammation * * * Figure 2-22 : (1) return to normal vascular permeability; (2) drainage of edema fluid and proteins into lymphatics or (3) by pinocytosis into macrophages; (4) phagocytosis of apoptotic neutrophils and (5) phagocytosis of necrotic debris; and (6) disposal of macrophages. Macrophages also produce growth factors that initiate the subsequent process of repair. Note the central role of macrophages in resolution. (Modified from Haslett C, Henson PM: In Clark R, Henson PM (eds): The Molecular and Cellular Biology of Wound Repair. New York, Plenum Press, 1996.) * * * * * * * Patient with a Methicillin-resistant Staphylococcus aureus wound infection, and classic signs of inflammation. * * * * * * * * * Figure 2-15 Interrelationships between the four plasma mediator systems triggered by activation of factor XII (Hageman factor). Note that thrombin induces inflammation by binding to protease-activated receptors (principally PAR-1) on platelets, endothelium, smooth muscle cells, and other cells. * * Figure 2-14 The activation and functions of the complement system. Activation of complement by different pathways leads to cleavage of C3. The functions of the complement system are mediated by breakdown products of C3 and other complement proteins, and by the membrane attack complex (MAC). The steps in the activation and regulation of complement are described in Box 2-2. * * Figure 2-16 Generation of arachidonic acid metabolites and their roles in inflammation. The molecular targets of action of some anti-inflammatory drugs are indicated by a red X. COX, cyclooxygenase; HETE, hydroxyeicosatetraenoic acid; HPETE, hydroperoxyeicosatetraenoic acid. * Figure 2-17 Biosynthesis of leukotriene
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