Inflammation. 2: Its role in the healing of chronic wounds.
暂无分享,去创建一个
[1] S. Miller,et al. Bacteriology of chronic leg ulcers. , 1978, Archives of dermatology.
[2] A. Vaheri,et al. Proteolytic activity in leg ulcer exudate , 1993, Experimental dermatology.
[3] A. Bailey,et al. Prognostic value of markers of collagen remodeling in venous ulcers , 1999, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[4] J. Kere,et al. Patterns of matrix metalloproteinase and TIMP‐1 expression in chronic and normally healing human cutaneous wounds , 1996, The British journal of dermatology.
[5] C. Winterbourn,et al. Human neutrophil collagenase cleaves alpha 1-antitrypsin. , 1990, The Biochemical journal.
[6] W. Parks,et al. Collagenase-1 complexes with alpha2-macroglobulin in the acute and chronic wound environments. , 1998, The Journal of investigative dermatology.
[7] F. Komada,et al. Improvement in wound healing by epidermal growth factor (EGF) ointment. II. Effect of protease inhibitor, nafamostat, on stabilization and efficacy of EGF in burn. , 1991, Journal of pharmacobio-dynamics.
[8] R. Clark,et al. Fibronectin and fibrin provide a provisional matrix for epidermal cell migration during wound reepithelialization. , 1982, The Journal of investigative dermatology.
[9] T. Roth,et al. IL-10 and GM-CSF expression and the presence of antigen-presenting cells in chronic venous ulcers. , 1998, The Journal of surgical research.
[10] C. McCollum,et al. Up-regulation of elastase in acute wounds of healthy aged humans and chronic venous leg ulcers are associated with matrix degradation. , 1997, Laboratory investigation; a journal of technical methods and pathology.
[11] F. Grinnell,et al. Wound fluid from chronic leg ulcers contains elevated levels of metalloproteinases MMP-2 and MMP-9. , 1993, The Journal of investigative dermatology.
[12] C. N. Rao,et al. Alpha 1-antitrypsin is degraded and non-functional in chronic wounds but intact and functional in acute wounds: the inhibitor protects fibronectin from degradation by chronic wound fluid enzymes. , 1995, The Journal of investigative dermatology.
[13] M. Horan,et al. Aging alters the inflammatory and endothelial cell adhesion molecule profiles during human cutaneous wound healing. , 1998, Laboratory investigation; a journal of technical methods and pathology.
[14] M. Bonnefoy,et al. Implication of cytokines in the aggravation of malnutrition and hypercatabolism in elderly patients with severe pressure sores. , 1995, Age and ageing.
[15] R. Diegelmann,et al. Ability of chronic wound fluids to degrade peptide growth factors is associated with increased levels of elastase activity and diminished levels of proteinase inhibitors , 1997, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[16] K. Burnand,et al. Tissue and urokinase plasminogen activators in the environs of venous and ischaemic leg ulcers , 1993, The British journal of surgery.
[17] T. Krieg,et al. Expression and proteolysis of vascular endothelial growth factor is increased in chronic wounds. , 2000, The Journal of investigative dermatology.
[18] F. Grinnell. Fibronectin and wound healing , 1984, Journal of cellular biochemistry.
[19] G. Schultz,et al. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors , 1999, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[20] I. K. Cohen,et al. Modified cotton gauze dressings that selectively absorb neutrophil elastase activity in solution , 2001, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[21] M. Hallett,et al. Inappropriate neutrophil activation in venous disease , 1994, The British journal of surgery.
[22] M. Longaker,et al. Tissue inhibitor of metalloproteinases-1 is decreased and activated gelatinases are increased in chronic wounds. , 1995, The Journal of investigative dermatology.
[23] F. Grinnell,et al. Degradation of Fibronectin and Vitronectin and Vitronectin in Chronic Wound Fluid: Analysis by Cell Blotting, Immunoblotting, and Cell Adhesion Assays , 1992 .
[24] Y. Itoh,et al. Preferential Inactivation of Tissue Inhibitor of Metalloproteinases-1 That Is Bound to the Precursor of Matrix Metalloproteinase 9 (Progelatinase B) by Human Neutrophil Elastase (*) , 1995, The Journal of Biological Chemistry.
[25] I. K. Cohen,et al. MMP-8 is the predominant collagenase in healing wounds and nonhealing ulcers. , 1999, The Journal of surgical research.
[26] I. K. Cohen,et al. Interleukin-1alpha and collagenase activity are elevated in chronic wounds. , 1998, Plastic and reconstructive surgery.
[27] T. Tuan,et al. Temporal expression of urokinase plasminogen activator, plasminogen activator inhibitor and gelatinase‐B in chronic wound fluid switches from a chronic to acute wound profile with progression to healing , 1999, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[28] F. Arnold,et al. Postural vasoregulation and mediators of reperfusion injury in venous ulceration. , 1997, Journal of vascular surgery.
[29] M. Stacey,et al. Levels of Tumor Necrosis Factor-α (TNF-α) and Soluble TNF Receptors in Chronic Venous Leg Ulcers – Correlations to Healing Status , 1998 .
[30] F. Grinnell,et al. Fibronectin Degradation in Chronic Wounds Depends on the Relative Levels of Elastase, α1-Proteinase Inhibitor, and α2-Macroglobulin , 1996 .
[31] L. Norgren,et al. A randomized trial comparing cadexomer iodine and standard treatment in the out‐patient management of chronic venous ulcers , 1983, The British journal of dermatology.
[32] I. K. Cohen,et al. Wound fluids from human pressure ulcers contain elevated matrix metalloproteinase levels and activity compared to surgical wound fluids. , 1996, The Journal of investigative dermatology.
[33] H. Dvorak,et al. Role of the clotting system in cell-mediated hypersensitivity. II. Kinetics of fibrinogen/fibrin accumulation and vascular permeability changes in tuberculin and cutaneous basophil hypersensitivity reactions. , 1975, Journal of immunology.
[34] F. Grinnell,et al. Fibronectin profiles in normal and chronic wound fluid. , 1990, Laboratory investigation; a journal of technical methods and pathology.
[35] A. Rogers,et al. Involvement of proteolytic enzymes—plasminogen activators and matrix metalloproteinases—in the pathophysiology of pressure ulcers , 1995, Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society.
[36] T. Fitzgerald,et al. Fibronectin involvement in granulation tissue and wound healing in rabbits. , 1982, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.
[37] J. Raffetto,et al. The proliferative capacity of neonatal skin fibroblasts is reduced after exposure to venous ulcer wound fluid: A potential mechanism for senescence in venous ulcers. , 1999, Journal of vascular surgery.
[38] A. Vaheri,et al. Matrix metalloproteinases, gelatinase and collagenase, in chronic leg ulcers. , 1996, The Journal of investigative dermatology.
[39] C. Bunker,et al. Leukocytes: their role in the etiopathogenesis of skin damage in venous disease. , 1993, Journal of vascular surgery.