Reduction of adhesion formation by intraperitoneal administration of Arg-Gly-Asp-containing peptides.

Objective: To evaluate the ability of a variety of peptides containing the Arg-Gly-Asp (RGD) sequence to reduce the formation of intraperitoneal adhesions in a rabbit model.

Design: Prospective, randomized, double-blinded study.

Setting: University-based laboratory.

Reduction of adhesion formation in rabbits by intraperitoneal administration of lazaroid formulations.

Adhesion formation is a major source of postoperative morbidity and mortality. In this study, the ability of a variety of lazaroid formulations [the antioxidant 21-aminosteroid PNU74006F (tirilazad) and the non-steroidal 2-methylaminochroman derivative PNU83,836E] to reduce i.p.

Effect of administration of malathion for 90 days on macrophage function and mast cell degranulation.

Previous studies have shown that acute, oral administration of malathion modulated the humoral immune response to T cell-dependent antigen, mitogenic responses, macrophage function and mast cell degranulation. In this report, the effects of malathion administration for 90 days on macrophage function, as measured by respiratory burst capacity, phagocytic capability and the production of cathepsin D, and mast cell integrity were assessed. A dose-dependent increase in respiratory burst activity was observed at all doses tested.

Effect of acute administration of malathion by oral and dermal routes on serum histamine levels.

Previous studies have shown that acute, oral administration of malathion increased the generation of a humoral immune response, stimulated macrophage function and caused mast cell degranulation and histamine release. In this study, the effect of acute administration of various doses of malathion via oral and dermal routes to mice and rats on serum levels of histamine was evaluated. Oral administration of malathion to mice led to an increase in the level of serum histamine 4 and 8 h after administration.

Effects of oral administration of malathion on the course of disease in MRL-lpr mice.

Malathion administration at non-cholinergical doses was shown to elevate macrophage, proliferative and humoral immune responses. This study examined the effects of malathion on autoimmunity, autoantibody formation, macrophage function and mitogenic responses in MRL-lpr mice (genetically predisposed to autoimmune disease) and MRL-+/+ mice. Malathion, 33-300mg/kg, was administered by gavage once per week, beginning at 6 weeks of age.

Effects of malathion metabolites on degranulation of and mediator release by human and rat basophilic cells.

In the present study, the effects of malathion and malathion derivatives on histamine and beta-hexosaminidase release by RBL-1 cells, rat peritoneal mast cells (RPMC), and human peripheral blood basophils (HPBB) and cutaneous mast calls were examined. One hour of incubation of RBL-1 cells with all organophosphate compounds tested, except for malathion and malathion monoacid, led to an increase in histamine release. beta-Hexosaminidase, an enzyme released by basophilic cells and a biochemical marker of degranulation, was not released from RBL-1 cells after 1 h of exposure to organophosphate compounds.

Contributions of inflammatory mast cell mediators to alterations in macrophage function after malathion administration.

Recent studies using mast cell-defined mice showed that the presence of mast cells was necessary for the increase in macrophage function observed after oral administration of malathion and reconstitution with bone marrow-derived mast cells restored the ability of malathion to increase macrophage function. In addition, the release of mast cell mediators (blocked by cromolyn) and histamine (action blocked by pyrilamine) was shown to be involved in the action of malathion on macrophage function. In the present study, the contribution of inflammatory mediators (i.

Immunotoxicity of medical devices. Symposium overview.

Determination of the ability of a medical device to interact with the immune system currently involves assessment of the immunogenic potential and biocompatibility of the device or an extract of the device. However, implants are often in the body for extended periods of time and/or are placed by a surgical procedure that in and of itself will generate an acute inflammatory response. This symposium discussed studies that have been performed to evaluate the immunogenicity of various devices consisting of several different compositions (i.

Reduction of adhesion formation by intraperitoneal administration of anti-inflammatory peptide 2.

Adhesion formation is a major source of postoperative morbidity and mortality. Therefore, the reduction of postoperative adhesion formation would be of clinical benefit. Various modalities have been shown to reduce adhesion formation, including fibrinolytic enzymes, nonsteroidal anti-inflammatory drugs, and barriers that reduce the apposition of sites of potential adhesion formation.

Reduction of adhesion formation by intraperitoneal administration of a recombinant Hirudin analog.

Adhesion formation is a major source of postoperative morbidity and mortality. Therefore, the reduction of postoperative adhesion formation would be of clinical benefit. Various modalities have been shown to reduce adhesion formation, including fibrinolytic enzymes, nonsteroidal anti-inflammatory drugs, and barriers that reduce the apposition of sites of potential adhesion formation.

Contribution of mast cell mediators to alterations in macrophage function after malathion administration.

Previous studies showed that acute administration of noncholinergic doses of malathion increased macrophage function and the generation of a primary humoral immune response to a T-dependent antigen and caused mast cell degranulation. Recent studies using mast cell-deficient mice showed that the presence of mast cells was necessary for the increase in macrophage function observed after oral administration of malathion, and reconstitution with bone marrow-derived mast cells restored the ability of malathion to increase macrophage function. In the present study, the contribution of mast cell mediators to alterations in macrophage function after oral administration of malathion was examined.

Effects of malathion on humoral immunity and macrophage function in mast cell-deficient mice.

Malathion, when administered at noncholinergic doses, was previously shown to enhance the humoral immune response to a T-dependent antigen, sheep red blood cells (SRBC), and macrophage function. In addition, malathion was shown to cause mast cell degranulation. The hypothesis that mast cells contribute to the observed alterations in humoral immunity and macrophage function was determined by examination of the effects of acute administration of malathion to mast cell-deficient mice on macrophage function and the generation of a humoral immune response to SRBC.

Mechanism of the modulation of murine peritoneal cell function and mast cell degranulation by low doses of malathion.

Malathion is a widely used organophosphate pesticide that modulates immune function at noncholinergic doses. Previous studies showed that this alteration in immune function was the result of enhanced macrophage function. In the present study, the effects of low doses of purified malathion (as low as 0.