PubMed · 8810193
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1996. Malaria.. https://pubmed.ncbi.nlm.nih.gov/8810193/
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In March this year, Drug and Therapeutics Bulletin held its sixth annual symposium on 'Why Treatments Fail'. The subject was chosen in the belief that the more we understand treatment failure, the greater the chances of developing strategies that succeed. The symposium explored failure of medicines at a molecular level; failure of prescribers to put knowledge into practice; failure of prescribers to cope with changes in diagnostic criteria; problems around doctors' and patients' failure to communicate with each other; failures of the NHS to meet patients' expectations; computer programmes that help patients see the potential consequences of treatment failures; the cost of failure to the NHS. Here we summarise the talks, incorporating ideas that arose in discussion.
INTRODUCTION: We studied the hippocampal region using Fluid Attenuation Inversion Recovery (Turbo-FLAIR) sequences to detect signal intensity abnormalities, and volumetric sequences to detect cortical thickness changes, in patients with drug-resistant temporal epilepsy. MATERIALS AND METHODS: We examined 30 patients with drug-resistant temporal epilepsy with a 1.5 Tesla unit (NT 15 Philips Gyroscan). Conventional SE, Turbo SE, IR, Turbo-FLAIR, volumetric 3D sequences on coronal plane, PD, T2-weighted SE sequences on axial plane, T1-weighted SE on sagittal plane were performed. Signal intensity and volumetric computerized measurements were obtained using the SUN system. RESULTS: Differences in signal intensity values between the two hippocampal regions were found in 18 patients with Turbo-FLAIR sequences. In 6 of these patients no significant differences in computerized evaluation of signal intensity were detected with either conventional or Turbo-SE sequences. Volumetric analysis showed hippocampal cortex thinning in 9 of 18 patients with hippocampal signal intensity abnormalities. CONCLUSIONS: Turbo-FLAIR were the best sequences for the detection of signal intensity changes in the hippocampal region. Such changes are strongly suggestive of hippocampal sclerosis, especially when associated with cortical atrophy.
The effects of forty-one plant polyphenols on the activity of glutathione reductase (GSH-RD) were studied. These polyphenols showed varying degrees of concentration-dependent inhibition on the enzyme, with IC50 values that varied from approximately 40 microM to 1 mM. 4'-Hydroxychalcone and tannic acid were among the more potent inhibitors, with IC50 values of 47.3 and 50.4 microM, respectively. Different classes of polyphenols varied in potency in the following order: chalcones > tannic acid > flavonoids > coumarins > catechins. Analysis of structure-activity relationships showed certain chemical structures to be important for the inhibition of GSH-RD: (a) C-5 and C-7 hydroxylations in the A-ring, a carbonyl group at C-4, and the B-ring attached to C-2 in flavonoids; (b) C-2' and C-4' hydroxylations in chalcones; and (c) C-6 and C-7 hydroxylations in coumarins. The inhibition of GSH-RD by tannic acid and quercetin was time dependent and irreversible, whereas that by 4'-hydroxychalcone and esculin was reversible but not time dependent. Enhanced inhibition of GSH-RD by the four polyphenols 4'-hydroxychalcone, quercetin, butein, and acacetin was observed in the presence of NADPH. Kinetic studies showed that both tannic acid and 4'-hydroxychalcone exhibited non-competitive inhibition on GSH-RD towards glutathione disulfide.