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Biomedical subjects

P Boakye

Publications and source records attributed to P Boakye.

4 recordsLinked to original sources

HIV, sexual risk, and ethnicity among men in England who have sex with men.

OBJECTIVES: To examine ethnic group differences in HIV testing history and sexual HIV risk behaviours that may account for such differences, among men in England who have sex with men (MSM), in order to inform HIV prevention planning priorities. METHODS: A self completion survey in the summer of 2001 was carried out in collaboration with community based health promoters. Three recruitment methods were used: "gay pride" festivals, health promoter distributed leaflets, internet version advertised with gay service providers. The leaflet was produced with an alternative cover for targeted recruitment of black men. RESULTS: In a sample of 13,369 MSM living in England, 17.0% were from minority ethnic groups and 5.4% had tested HIV positive. Compared to the white British majority, Asian men were 0.32 times as likely to be living with diagnosed HIV infection, while black men were 2.06 times as likely to be doing so. Among men who had not tested HIV positive, Asian men were less likely to have sex with a known HIV positive partner, while black men were more likely to have insertive unprotected anal intercourse both with a partner they knew to be HIV positive and with a partner whose HIV status they did not know. CONCLUSIONS: Among MSM in England, HIV prevalence is higher among black men and lower among Asian men compared with the white British majority. Increased sexual HIV risk behaviour, especially exposure during insertive anal intercourse, accounts for some of this difference. HIV prevention programmes for MSM and African people should both prioritise black MSM.

Adolescent↗

Effects of 1-methyl-4-phenylpyridinium on isolated rat brain mitochondria: evidence for a primary involvement of energy depletion.

The effects of 1-methyl-4-phenylpyridinium (MPP+) on the oxygen consumption, ATP production, H2O2 production, and mitochondrial NADH-CoQ1 reductase (complex I) activity of isolated rat brain mitochondria were investigated. Using glutamate and malate as substrates, concentrations of 10-100 microM MPP+ had no effect on state 4 (-ADP) respiration but decreased state 3 (+ADP) respiration and ATP production. Incubating mitochondria with ADP for 30 min after loading with varying concentrations of MPP+ produced a concentration-dependent decrease in H2O2 production. Incubation of mitochondria with ADP for 60 min after loading with 100 microM MPP+ caused no loss of complex I activity after washing of MPP+ from the mitochondrial membranes. These data are consistent with MPP+ initially binding specifically to complex I and inhibiting both the flow of reducing equivalents and the production of H2O2 by the mitochondrial respiratory chain, without irreversibly damaging complex I. However, mitochondria incubated with H2O2 in the presence of Cu2+ ions showed decreased complex I activity. This study provides additional evidence that cellular damage initiated by MPP+ is due primarily to energy depletion caused by specific binding to complex I, any increased damage due to free radical production by mitochondria being a secondary effect.

1-Methyl-4-phenylpyridinium↗

Protection of ischaemic synaptosomes from calcium overload by addition of exogenous lactate.

In depolarised anoxic synaptosomes, in which lactate production was significantly raised compared with normoxic conditions, calcium uptake, net acetylcholine release, and the intrasynaptosomal calcium concentration were all significantly lowered. In contrast, lactate production in synaptosomes incubated under aglycaemic- and ischaemic-type conditions was significantly lower and basal calcium uptake, acetylcholine release, and intrasynaptosomal calcium concentration were elevated compared with normoxia. In addition, the increase in intrasynaptosomal calcium concentration under the ischaemic-type condition appeared to be greater than could be accounted for by the rise in calcium uptake alone. Intrasynaptosomal pH reflected the lactate production under each condition investigated. Addition of exogenous lactate to normoxic synaptosomes mimicked the effects observed in anoxia, suggesting that lactate itself may have blocked the calcium uptake, inhibiting the rise in intrasynaptosomal calcium and acetylcholine release occurring in depolarised anoxic synaptosomes. When lactate was added to ischaemic synaptosomes, the large rise in intrasynaptosomal calcium concentration, calcium uptake, and acetylcholine release were decreased, suggesting that lactate may have a protective role in preventing cell death by calcium overload under ischaemic-type conditions. Evidence is presented to suggest that the effect of L-lactate was due to the lactate moiety itself rather than the associated acidosis.

Acetylcholine↗