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IFN-gamma plays a critical down-regulatory role in the induction and effector phase of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis.
TLDR
The results indicate that IFN-gamma is not essential for the generation or function of anti-MOG35-55 effector cells but does play an important role in down-regulating EAE at both the effector and induction phase of disease. Expand
Identification of sulfated oligosaccharide-based inhibitors of tumor growth and metastasis using novel in vitro assays for angiogenesis and heparanase activity.
TLDR
Sulfated oligosaccharides, which are structural mimics of heparan sulfate, were investigated as drug candidates and PI-88 was shown to inhibit the primary tumor growth of the highly invasive rat mammary adenocarcinoma 13762 MAT, and reduce the vascularity of tumors by approximately 30%, all of these effects being highly significant. Expand
Human malarial disease: a consequence of inflammatory cytokine release
TLDR
The evidence is considered that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. Expand
The pathophysiology of falciparum malaria.
TLDR
It is plausible that this will be demonstrable in severe falciparum malaria, and it is argued that it can best be understood in terms of excessive stimulation of normally useful pathways mediated by inflammatory cytokines, the prototype being tumor necrosis factor (TNF). Expand
Elevated secretion of reactive nitrogen and oxygen intermediates by inflammatory leukocytes in hyperacute experimental autoimmune encephalomyelitis: enhancement by the soluble products of
TLDR
A putative neuropathological role for ROI and RNI in HEAE is suggested, which may be mediated via cytokines emanating from autoreactive T lymphocytes, which could be largely attributed to heat-labile, soluble products released by these T cell lines. Expand
IFN-gamma is critical to the control of murine autoimmune encephalomyelitis and regulates both in the periphery and in the target tissue: a possible role for nitric oxide.
TLDR
The data suggest that IFN-gamma down-regulates EAE by inducing inducible NO synthase and subsequently NO production, both by macrophages in the periphery and, by inference, microglia and astrocytes in the target tissue. Expand
Pathogenesis of Malaria and Clinically Similar Conditions
TLDR
The pathogenesis of the disease caused by falciparum malaria is considered in the light of what has been learned about the roles of these mediators in these other diseases, as well as in malaria itself. Expand
Breakdown of the blood-brain barrier in murine cerebral malaria.
TLDR
The density of brain tissue, measured by a Percoll gradient technique, was significantly reduced in mice exhibiting cerebral symptoms, suggesting the occurrence of cerebral oedema. Expand
Killing of Plasmodium falciparum in vitro by nitric oxide derivatives
TLDR
In vitro susceptibility of the human malaria parasite Plasmodium falciparum to killing by nitric oxide and related molecules is investigated and nitrosothiol derivatives of cysteine and glutathione were found to be about a thousand times more active than nitrite. Expand
Proposed link between cytokines, nitric oxide and human cerebral malaria.
TLDR
It is proposed that when vascular generation of NO is particularly high this mediator could diffuse to nearby neurons, be misinterpreted as being of synaptic origin and thus interfere with orderly neuro-transmission. Expand
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