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Biomedical subjects

A J Rees

Publications and source records attributed to A J Rees.

133 records · Page 8Linked to original sources
PubMed1975

Use of charcoal haemoperfusion in the management of severely poisoned patients.

The clinical use of uncoated charcoal haemoperfusion systems, despite their efficacy, has hitherto been prevented by the occurrence of a number of adverse effects including charcoal embolism and marked thrombocytopenia. Charcoal coated with a synthetic hydrogel overcomes many of the disadvantages associated with the use of uncoated material in that there is a much reduced thrombocytopenia and no evidence of charcoal embolism. Six patients, severely poisoned as a result of overdoses of either a barbiturate or glutethimide, were haemoperfused using such a system. Four made complete recoveries, and the two patients who died had both suffered cardiorespiratory arrests before perfusion. In contrast to haemodialysis charcoal haemoperfusion is simple to initiate, less expensive in terms of manpower and equipment, and gives superior clearance data for all barbiturates and glutethimide. We believe that this technique may have a significant role to play in the management of the severely poisoned patient.

Adult↗
PubMedDate not supplied

New approaches to modify glomerular inflammation.

Glomerulonephritis remains the leading cause of end-stage renal failure and treatments for these conditions remain non-specific and with significant side effects. The cellular and molecular basis of acute and chronic inflammation is increasingly understood and the work in a number of animal models of nephritis demonstrates the potential of specific molecular interventions. These include preventing the migration of inflammatory cells by inhibiting the effects of chemokines or blocking endothelial/leucocyte adhesion interactions. Within damaged tissue it is possible to decrease the activity of pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumour necrosis factor (TNF) by using their natural antagonists, namely interleukin-1 receptor antagonist (IL-1ra) and soluble TNF receptors. In addition the behaviour of macrophages can be altered by the effects of anti-inflammatory cytokines including interleukin-4 (IL-4), interleukin-13 (IL-13), interleukin-10 (IL-10), interleukin-6 (IL-6) and transforming growth factor-beta (TGF-beta). By deactivating the inflammatory response of macrophages these cytokines can favour resolution of disease. The ability to use these approaches in clinical practice remains elusive, however the prospect of using gene transfer technology to deliver anti-inflammatory factors directly to the site of inflammation and our increasing understanding of the complexity of the control of inflammation bring such therapies closer.

Animals↗
PubMedDate not supplied

Rapidly progressive glomerulonephritis.

The management of rapidly progressive glomerulonephritis has been transformed over the past thirty years. It has become one of the few forms of glomerulonephritis that can be effectively treated, and today overall renal survival is as high as 70%. Effective management of patients with RPGN requires prompt and accurate diagnosis so that patients are appropriately treated, and long term follow up to minimise the risk of relapse in patients with some types of those disease.

Animals↗
PubMedDate not supplied

Rat mesangial cells have a selective role in macrophage recruitment and activation.

In proliferative glomerulonephritis glomeruli are the target of an inflammatory reaction involving macrophage recruitment and activation. We examined the role of mesangial cells in this process. Supernatants from basal, IL-1, IFN-tau or LPS-stimulated rat mesangial cells (MCS) were tested for chemotactic, colony-stimulating and activation effects on macrophages in vitro. IL-1-stimulated MCS produced a macrophage chemoattractant (p = 0.007 compared with basal MCS) and MCP-1 mRNA was detected in IL-1-stimulated mesangial cells. LPS or IL-1-stimulated MCS produced colony-stimulating activity (LPS p < 0.05, IL-1 p < 0.01, compared with basal MCS or control supernatant, CS). Macrophage activation, assessed by nitric oxide generation, was suppressed. This evidence from functional bioassays supports a selective role for mesangial cells in the control of macrophage-induced glomerular injury, whereby activated mesangial cells participate in the recruitment and proliferation of infiltrating macrophages, and suppresses at least one field of macrophage activation, namely nitric oxide generation.

Animals↗