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anaphylaxis/protease
Veza se sprema u međuspremnik
Page 1 od 211 rezultati
Plasma protease inhibitor and anaphylatoxin inactivator levels in chronic urticaria/angioedema and in patients experiencing anaphylactoid reactions to radiographic contrast media.
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Since a protease inhibitor or anaphylatoxin inactivator deficiency might explain why certain individuals are prone to develop chronic urticaria/angioedema or anaphylactoid reactions to radiographic contrast media, serum alpha 1-protease inhibitor, alpha 1-antichymotrypsin, alpha 2-macroglobulin,
Mast cell protease release and mucosal ultrastructure during intestinal anaphylaxis in the rat.
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Intestinal anaphylaxis is associated with disturbances in gut function that are antigen-specific and dependent on mast cell degranulation. Using an animal model of intestinal anaphylaxis, we have correlated alterations in water and electrolyte transport, associated with intraluminal challenge, with
Promoted expression of mast cell-specific proteases in IgE-dependent passive cutaneous anaphylaxis responses.
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BACKGROUND
Various factors can influence the protease expression phenotype of mast cells.
METHODS
In an effort to understand the potential role of the mast cell proteases in the IgE-dependent passive cutaneous anaphylaxis (PCA) responses of murine tissues, we studied the changes of proteases
Gut mucosal mast cells in Nippostrongylus-primed rats are the major source of secreted rat mast cell protease II following systemic anaphylaxis.
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The distribution of the predominant chymotrypsin-like enzyme of mucosal mast cells (rat mast cell protease II: RMCP II) was examined in naive and Nippostrongylus-primed rats both before and after the induction of systemic anaphylaxis. Anaphylactic secretion of RMCP II following i.v. challenge of
The effect of protein deficiency on systemic release of rat mucosal mast cell protease II during Nippostrongylus brasiliensis infection and following systemic anaphylaxis.
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Serum rat mucosal mast cell protease II (RMCPII) was measured in protein-deficient rats to assess mucosal mast cell (MMC) activation during primary infection with the nematode, Nippostrongylus brasiliensis, and during systemic anaphylaxis produced by Nippostrongylus antigen in immune animals. In the
Depletion of mucosal mast cell protease by corticosteroids: effect on intestinal anaphylaxis in the rat.
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Rats primed by infection with the intestinal nematode Nippostrongylus brasiliensis and challenged intravenously with soluble whole-worm antigen undergo systemic anaphylactic shock. The primary lesions are in the gut and include increased permeability of the mucosa together with release, into enteric
The presence in blood of both glycosaminoglycan and mucosal mast cell protease following systemic anaphylaxis in the rat.
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The appearance in blood of rat mast cell protease II (RMCPII) and glycosaminoglycan (GAG) was examined in normal and Nippostrongylus brasiliensis-primed rats challenged intravenously with worm antigen. Systemic release of these two products occurred only in immune recipients of antigen; substantial
Release of the mucosal mast cell granule chymase, rat mast cell protease-II, during anaphylaxis is associated with the rapid development of paracellular permeability to macromolecules in rat jejunum.
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The soluble granule chymase, rat mast cell protease-II (RMCP-II), is abundantly expressed in intestinal mucosal mast cells (MMC) but its function is not known. One hypothesis is that RMCP-II degrades the epithelial basement membrane and promotes the loss of enterocytes typically associated with type
Studies on tissue protease. V. Protease activity of tissues under anaphylactic shock state.
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[Anaphylactic shock and proteases. Absence of anti-anaphylactic activity in synthetic antifibrinolytic agents in the rabbit].
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Mechanism of anaphylaxis in the rabbit; further evidence against plasma protease mechanism.
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Anaphylactoid reaction induced by a protease inhibitor, nafamostat mesilate, following nine administrations in a hemodialysis patient.
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Role of complement in a murine model of peanut-induced anaphylaxis.
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Peanut allergy is severe and persisting from childhood to adulthood. However, there is no effective prophylaxis or treatment for peanut allergy. Little is known to about the molecular process in the pathogenesis of peanuts allergy, especially in innate immunity. Thus we investigated the role of
The tryptase, mouse mast cell protease 7, exhibits anticoagulant activity in vivo and in vitro due to its ability to degrade fibrinogen in the presence of the diverse array of protease inhibitors in plasma.
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Mouse mast cell protease (mMCP) 7 is a tryptase of unknown function expressed by a subpopulation of mast cells that reside in numerous connective tissue sites. Because enzymatically active mMCP-7 is selectively released into the plasma of V3 mastocytosis mice undergoing passive systemic anaphylaxis,
Chronic atherosclerotic mesenteric ischemia that started to develop symptoms just after anaphylaxis.
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An 83-year-old woman was referred to our emergency department with acute urticaria and sudden shortness of breath approximately 30 min after taking rectal diclofenac potassium for lumbago. After treatment with adrenaline and corticosteroids, the patient became hemodynamically stable and left the
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