Bullous skin disorders following radiotherapy.
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Breast Neoplasms↗
Biomedical subjects
A Hartley
Publications and source records attributed to A Hartley.
Complex I inhibitors induce dose-dependent apoptosis in PC12 cells: relevance to Parkinson's disease.
The mode of cell death in Parkinson's disease (PD) substantia nigra is uncertain. However, evidence is accumulating that certain of the biochemical abnormalities present in PD nigra at the time of death may precipitate apoptosis. We have investigated the mode of death induced by complex I inhibition of dopaminergic cell cultures, and our results suggest that both 1-methyl-4-phenylpyridinium and rotenone cause apoptosis at low concentrations and necrosis at high concentrations. This dose-dependent shift in the mode of cell death induced by these mitochondrial toxins may have important implications for the mechanisms of neuronal cell death in PD.
1-Methyl-4-phenylpyridinium↗
Free radicals and mitochondrial dysfunction in Parkinson's disease.
The precise relationship of the complex I deficiency in PD to the dopaminergic cell death and aetiology of this disorder is as yet unknown. However, evidence is accruing that this mitochondrial defect may play a central role in the cascade of events that terminates in nigral neuronal loss. Further work needs to be carried out to determine the molecular mechanisms that underlie the complex I deficiency as these may provide important indicators to the ultimate cause of PD. This may involve a genetic abnormality of complex I that may convey a susceptibility to developing PD. Alternatively, exogenous or endogenous toxic agents may target nigral complex I along pathways similar to those recognized for MPTP. A combination of a genetic predisposition in addition to an environmental precipitant has gained substantial support as an explanation for the cause of PD.
Cell Death↗
The chelation of nonheme iron within sickle erythrocytes by the hydroxypyridinone chelator CP094.
Nonheme, nonferritin iron has been detected in membrane preparations from sickle erythrocytes and has been suggested to catalyze free radical reactions in these cells contributing to the development of membrane oxidation. In this study the hydroxypyridinone iron chelator, CP094, currently being evaluated as a potentially therapeutic chelator, and desferrioxamine have been studied for their abilities to chelate the nonheme iron within intact sickle erythrocytes under physiological conditions. The results suggest that CP094 can enter sickle erythrocytes, chelate nonheme iron and suppress membrane lipid peroxidation within a timescale in which desferrioxamine does not enter the cells. Suppression of lipid peroxidation showed no protective effect in an in vitro system inducing the formation of irreversibly sickled cells.
Anemia, Sickle Cell↗
Reducing the effects of adjacent distractors by narrowing attention.
Three experiments explored the gradual narrowing of visual attention to a letter target when other letters were positioned close by. The method by which attention was narrowed involved presenting a digit target immediately prior to the latter target and in the same location for progressively shorter durations and requiring the subject to identify both the digit target and the letter target before responding. The response time data from the first 2 experiments indicated that shorter durations of the digit reduced the amount of information processed from noise letters positioned on either side of the letter target. In the third experiment, in which separation of letters was increased slightly, the response times indicated that the information from flanking noise letters may have been virtually eliminated.
Adult↗
Desferrioxamine as a lipid chain-breaking antioxidant in sickle erythrocyte membranes.
The mechanism of action of desferrioxamine in the inhibition of the catalysis of iron-induced oxidative damage has been ascribed to its ability to chelate available ferric ion (Kb = 10(31)). However, recent work has proposed that the trihydroxamate moiety of desferrioxamine can also be involved in electron transfer reactions involving the superoxide radical, peroxidase/hydrogen peroxide mixtures and ferryl myoglobin radicals. In this study we report evidence for the ability of desferrioxamine to inhibit peroxidative damage to pathological membranes with which non-haem iron is associated through a mechanism of action as a lipid chain breaking antioxidant, independently of its iron chelating properties.
Anemia, Sickle Cell↗
Desferrioxamine and membrane oxidation: radical scavenger or iron chelator?
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Anemia, Sickle Cell↗