Treating AIDS: dilemmas of unequal access in Uganda.

The price of antiretroviral (ARV) medicines in Uganda has fallen dramatically in recent years and more people are under treatment. By mid-2003 it was estimated that 10 000 people were taking ARVs. Drawing on participant observation, qualitative interviews, work with key informants and document reviews, we seek to map out the channels through which ARVs are being made available to people and to describe and assess the social implications of the present system of distribution. Four channels of access to ARV medicines were common in mid-2003: (i) Medicines were provided free in structured research and treatment programmes funded by donors, but only to those who lived in a defined catchment area and met inclusion criteria. (ii) Gazetted treatment centres provided drugs on a fee-for-service basis; these urban-based institutions account for the largest number of drugs dispensed. (iii) Private practitioners, mainly based in Kampala, provided discrete treatment for those who could afford it. (iv) Finally, medicines were 'facilitated' along informal networks, supplying friends and relatives on a less regular basis, sometimes for free, sometimes for cash. However, access to ARVs remains highly uneven. We argue that cheaper drugs make possible different kinds of access, different qualities of care, and a growing awareness of inequity. Because the price of drugs has fallen drastically, middle-class families now have the possibility of buying them. But this requires tough prioritising and many cannot follow the regimen regularly. Health workers must consider whether patients will be able to purchase the drugs or not. In a kind of popular social pharmacy, people assess who can and should and does get access to ARVs. Further research should examine the whole range of ARV access channels in different countries and the associated patterns of social differentiation and exclusions.

Antiatherosclerotic effects of nicardipine and nifedipine in cholesterol-fed rabbits.

Dutch-belted rabbits fed a 2% cholesterol diet for 8 weeks developed atherosclerotic lesions that covered 37.2% +/- 3.5% of the aortic luminal surface. In samples of aortic arch, accumulation of cholesterol and triglyceride was also observed. Oral administration of nicardipine or nifedipine at dosages of 40 mg/kg twice daily for 8 weeks reduced plaque area by 49.2% and 58.7%, respectively. Nicardipine and nifedipine reduced cholesterol accumulation in the aortic arch by 74.5% and 69%, respectively. Triglyceride accumulation was totally abolished. Neither drug significantly altered cholesterol concentration of plasma low density lipoprotein or high density lipoprotein, although nicardipine produced a 42% reduction in cholesterol concentration of the d less than 1.006 g/ml fraction. The above results suggest potential therapeutic utility of nicardipine in atherosclerosis.

On the identification and biological properties of prostaglandin J2.

Prostaglandin D2 spontaneously decomposes at physiological pH and temperature to 9-deoxy-delta 9-PGD2 (designated PGJ2). We developed a TLC procedure for the isolation of PGJ2 which was identified by both proton-NMR and mass spectrometry. Freshly prepared PGJ2 was active in inhibiting aggregation induced by ADP in citrated human platelet rich plasma. As reported by Fukushima et al. (1). PGJ2 was less active (x 0.1-0.25) than PGD2 as an inhibitor. Concentrations of PGJ2 that markedly inhibited aggregation of human platelets were generally incapable of inhibiting aggregation of rat or guinea pig platelets. Using a heterologous system of human platelets mixed with guinea pig plasma samples (2), it was shown that the ability of PGJ2 to inhibit platelet aggregation was lost immediately following intravenous injection in anesthetized guinea pigs. This apparent rapid uptake and/or degradation of PGJ2 might also explain why PGJ2 had no effect on blood pressure of anesthetized guinea pigs. PGJ2 was potent in inhibiting proliferation of cultured vascular smooth muscle cells, mouse melanoma cells and mouse fibroblasts. Less potent anti-proliferative effects were seen with two other degradation products of PGD2, one of which was the delta 12 metabolite reported (3,4) to be formed from PGJ2 in a reaction catalyzed by serum albumin.