From the pursuit of excellence to the quest for significance: Promotion of a Childsafe South Africa

Trauma represents a major burden of disease in South Africa. Children are disproportionately affected by trauma; rightly, childhood trauma can be referred to as ‘the neglected childhood killer disease’. Unlike the field of infectious diseases, where vaccinations and prevention are the norm, paediatric trauma is usually ignored and prevention strategies are scarce. In this article, we review paediatric trauma and its effect on our society in light of the development of more effective child safety promotion strategies

Normal left ventricular function does not protect against propafenone-induced incessant ventricular tachycardia

Propafenone is a class Ic anti-arrhythmic agent with mild B-blocking properties which has recently become available in South Africa. We have used the drug in 3 patients with sustained m.onomorphic ventricular tachycardia not due to ischaemic heart disease. All had norm.al left ventricular function; 1 had Wegener's granulom.atosis and 2 had arrhythmogenic right ventricular dysplasia. In the latter 2, propafenone provoked incessant monomorphic ventricular tachycardia which persisted for m.ore than 24 hours despite repeated efforts at term.ination. The morphology was similar to the patients' spontaneous ventricular tachycardia, but the rate was slower and the QRS complexes broader, consistent with propafenone's marked ability to slow intraventricular conduction. It is postulated that incessant tachycardia results from. perpetuation of re-entry due to marked conduction slowing produced by the drug. Previous reports have suggested that this is most likely to occur in patients with poor left ventricular function, but our experience indicates that those with normal left ventricular function are also at risk, particularly if the substrate for reentry is present. Propafenone, like all other powerful antiarrhythmic agents, may provoke life-threatening arrhythmias and should be used with great caution after due consideration of the indications, even in patients with norm.al left ventricular function

Reduced lethality in mice receiving a combined dose of cyclophosphamide and busulphan.

Animals treated with a sufficiently high dose of busulphan die about 14 days later from bone marrow failure. A single, appropriately timed injection of cyclophosphamide can save these mice. The nature of this protection is shown to be the cyclophosphamide induced elaboration of a humoral factor which stimulates haemopoietic recovery

Enhanced anti-tumour activity of carmustine (BCNU) with tumour necrosis factor in vitro and in vivo.

The effects on experimental melanoma of a combination of recombinant human tumour necrosis factor alpha (rhTNF alpha) and carmustine (BCNU) were studied in vitro and in vivo. In vitro, BCNU alone was cytotoxic to murine B16 melanoma cells, and at all concentrations of BCNU this toxicity was increased by the addition of TNF. In vivo, BCNU and TNF, when given separately, caused tumour growth delay of B16 melanoma and of human melanoma xenografts in immune-deprived mice. The combination of TNF at low dose 2.5 x 10(5) U kg-1 = 122 ng kg-1) with BCNU (35 mg kg-1) resulted in significant growth delay (compared with either drug alone) in B16 melanoma (P = 0.005). There was no significant increase in toxicity as assessed by weight loss and peripheral blood counts. Experiments with human melanoma xenografts yielded similar results (P = 0.001) but only at higher doses of TNF (1 x 10(6) U kg-1 = 489 ng kg-1). The enhancement of BCNU cytotoxicity by TNF may be important if it can be translated into patients with melanoma. A randomised study is now underway to investigate the clinical potential of this observation