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Wound healing inflammation

Fibrinogen is a fibrous protein that was first classified with keratin, myosin, and epidermin based on its 5.1 A repeat in wide-angle X-ray diffraction patterns (Bailey et al., 1943), which was later discovered to be associated with the Q-helical coiled-coil structure. It is a glycoprotein normally present in human blood plasma at a concentration of about 2.5 g/L and is essential for hemostasis, wound healing, inflammation, angiogenesis, and other biological functions. It is a soluble macromolecule, but forms a clot or insoluble gel on conversion to fibrin by the action of the... [Pg.248]

Panthenol is frequently used in ointments and solutions for the treatment of burns, anal fissures, and inflammation of the conjunctiva. The vitamin has to be substituted in patients on total parenteral nutrition and in those who regularly undergo dialysis. Hypervitamin-osis has not been observed for doses up to 5 g/d (22). Furthermore, the administration of pantothenic acid leads to improved surgical wound healing due to its antiinflammatory properties. [Pg.933]

Key Words Fibrosis chemokines chemokine receptors inflammation wound healing Thl Th2. [Pg.295]

Recently, the notion that the chronicity of inflammation may not actually drive the fibrogenic process has been widely appreciated (Tables 1, 2, and 3). Some propose that it is indeed the alteration of the mesenchymal cell phenotypes that disrupts the balance between collagen synthesis and degradation in the wound-healing process, highlighted by clinical evidence that shows unsuccessful treatment of fibrosis with anti-inflammatory or immunosuppressive drugs (18,19). One scenario is that mesenchymal cells (myofibroblasts and fibroblasts) are phenotypically altered and thus do not undergo apoptosis after resolution. [Pg.297]

Chronic inflammation is a leading component and contributing event to the pathogenesis of fibrotic disease, where a normal inflammatory response to injury becomes a chronic, pathologic wound-healing response. [Pg.297]

Fibrosis is a dynamic progression of dysregulated wound healing that results from chronic inflammation. It is a common pathology regardless of the tissue involved, and therefore, the mechanisms that progress to fibrosis can be widely applied. The recruitment, activation, and proliferation of inflammatory cells and their cooperation with resident cells appears to rely on the action of chemokines and the differential expression of the chemokine receptors by these cells. Thus, chemokine receptors make particularly attractive therapeutic targets. [Pg.310]

Cytokines are produced mainly by the leukocytes (white blood cells). They are potent polypeptide molecules that regulate the immune and inflammation functions, as well as hematopoiesis (production of blood cells) and wound healing. There are two major classes of cytokines (1) lymphokines and monokines and (2) growth factors. [Pg.113]

Hemorrhagic disease with no connective tissue problems Gum hyperplasia, inflammation, loss of teeth Skeletal deformity in children foot wound healing Anemia... [Pg.150]

Neovascularization in artherosclerotic lesions may be regulated by VEGF, as this factor is over-expressed by different cells in the plaque tissue [40-42]. The increased serum levels of VEGF that correlate with disease activity in patients with Crohn s disease and ulcerative colitis, indicate a role for this cytokine in promoting inflammation. Most likely, increased vascn-lar permeability and/or wound healing via its pro-angiogenic activity are the basis for this effect [43]. [Pg.177]


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See also in sourсe #XX -- [ Pg.91 ]




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