• Publications
  • Influence
Dysfunction of endothelial protein C activation in severe meningococcal sepsis.
TLDR
In severe meningococcal sepsis, protein C activation is impaired, a finding consistent with down-regulation of the endothelial thrombomodulin-endothelial protein C receptor pathway. Expand
Disruption of sulphated glycosaminoglycans in intestinal inflammation
TLDR
It is suggested that inflammatory disruption of vascular and connective tissue GAGs may be an important pathogenetic mechanism, contributing to the leakage of protein and fluid, thrombosis, and tissue remodelling seen in inflammatory bowel disease. Expand
Postinfectious purpura fulminans caused by an autoantibody directed against protein S.
TLDR
Autoimmune protein S deficiency may be a common mechanism causing postinfectious idiopathic purpura fulminans, and recognition of the pathophysiologic mechanism may provide a rational basis for treatment. Expand
Alteration in glycosaminoglycan metabolism and surface charge on human umbilical vein endothelial cells induced by cytokines, endotoxin and neutrophils.
TLDR
Investigation of the GAG metabolism of cultured human umbilical vein endothelial cells in response to a range of inflammatory stimuli suggests changes in endothelial cell G AG metabolism during inflammation may contribute to the disturbance of vascular endothelial homeostasis associated with infectious and inflammatory states. Expand
Analysis of Pathogen-Host Cell Interactions in Purpura Fulminans: Expression of Capsule, Type IV Pili, and PorA by Neisseria meningitidis In Vivo
TLDR
Immunohistochemistry was used to determine the expression of capsule, type IV pili, and PorA by meningococci residing in the skin lesions of children with purpura fulminans, suggesting phase variation. Expand
Coagulation in severe sepsis: A central role for thrombomodulin and activated protein C
TLDR
The plasma components of the protein C pathway are down-regulated in sepsis, and decreased thrombomodulin expression may cause defective function of the endothelial component of this pathway in septic patients. Expand
Whole blood model of meningococcal bacteraemia--a method for exploring host-bacterial interactions.
TLDR
An ex vivo whole blood model of meningococcal bacteraemia was developed and secreted levels of tumour necrosis factor and neutrophil elastase secreted during whole blood assays did not correlate with bacterial growth or viability indicating a lack of relationship between killing and activation of phagocytes. Expand
Platelet immune complex interaction in pathogenesis of Kawasaki disease and childhood polyarteritis.
TLDR
Findings imply that different mechanisms have a role in distinct phases of Kawasaki disease, which is probably followed by an immune complex vasculitis that occurs when antibodies to the initiating agent appear in the circulation. Expand
The influence of capsulation and lipooligosaccharide structure on neutrophil adhesion molecule expression and endothelial injury by Neisseria meningitidis.
TLDR
Bacterial capsulation and LOS structure can influence neutrophil activation and endothelial injury and, as such, may be important in the pathogenesis of meningococcal sepsis. Expand
Neutrophil response to Neisseria meningitidis: inhibition of adhesion molecule expression and phagocytosis by recombinant bactericidal/permeability-increasing protein (rBPI21).
TLDR
It is proposed that PMNL priming by N. meningitidis results in an exaggerated activation and phagocytosis response to the organism. Expand
...
1
2
3
4
...