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erysipelas/protease

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ArtiklarKliniska testerPatent
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[Changes in the kallikrein-kinin system of patients with erythematous and hemorrhagic forms of erysipelas].

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The state of the kallikrein-kinin system of the blood (KKS): kallikrein (KK), prekallikrein (PK), general arginine-esterase activity (GAEA), alpha 1 inhibitor of protease (IP) and alpha 2-macroglobulin (MG). The initial period of the disease was characterized by an increase of the level of KK, GAEA,

[The use of the kallikrein-kininogen system indices in the prognosis of the development of hemorrhagic erysipelas].

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A number of the kallikrein-kinin system parameters (kallikrein, prekallikrein, total arginine esterase activity, alpha 1 protease inhibitor, and alpha 2 macroglobulin) were measured in 59 patients with erythematous erysipelas and in 51 ones with hemorrhagic erysipelas over the course of the disease.
A recent study with isogenic strains constructed by recombinant DNA strategies unambiguously documented that a highly conserved extracellular cysteine protease expressed by Streptococcus pyogenes (group A Streptococcus [GAS]) is a critical virulence factor in a mouse model of invasive disease (S.

Antiprotease activity in urine of patients with inflammatory skin disorders.

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Polymorphonuclear leukocytes contain well-defined proteolytic enzymes in their azurophilic granules that can be released into tissues during inflammation, producing a localized excess of proteases that causes a protease-antiprotease imbalance with subsequent tissue destruction. The antiproteolytic

Human leukocyte elastase and cathepsin G are specific inhibitors of C5a-dependent neutrophil enzyme release and chemotaxis.

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Circulating human neutrophils from patients with severe inflammatory disorders such as erysipelas and sepsis are specifically desensitized to complement factor C5a stimulation but not to stimulation with other stimuli like N-formyl-methionyl-leucyl-phenylalanine (FMLP), interleukin-8 (IL-8),
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