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Aims: To measure the therapeutic effect of an anti‐oxidant, edaravone (EDV), or neurotrophic treatment with nerve growth factor (NGF) as an add‐on treatment for alcohol‐related brain damage (ARBD). Design: Multi‐centre, randomised, single‐blinded, comparative clinical trial. Setting and participants: One hundred and twenty‐two inpatients recruited from seven hospitals in different regions of China, all diagnosed with ARBD and aged 18 to 65 years old; among them, only two were female. Intervention and comparator: Patients were randomly assigned to receive one of three treatments for 2 weeks: 40 patients, treatment as usual (TAU: a combination of intramuscular injections of thiamine, intravenous infusions of other B vitamins with vitamin C and oral medication with vitamin E per day); 40, EDV add‐on treatment to TAU (intravenous infusion with 30 mg of EDV twice per day); and 42, NGF add‐on treatment to TAU (intramuscular injection of 20 μg of NGF per day). The patients underwent follow‐up for 24 weeks. Measurements: The primary outcome was the composite score of executive cognitive function in the 2nd week after treatment, which was measured as the mean of the Z scores of the assessments, including the digit symbol substitute test (DSST), digit span memory test‐forward (DST‐F), digit span memory test‐reverse (DST‐R) and space span memory test (SSMT). The secondary outcomes were the composite scores at later follow‐ups, the score for each component of cognitive function, global cognitive function measured by the Montreal Cognitive Assessment (MoCA), craving for alcohol and the safety of the therapies. Findings EDV add‐on treatment improved the composite score of executive cognitive function better than TAU in the 2nd week (adjusted mean difference: 0.24, 95% confidence interval 0.06 to 0.41; P = 0.008), but NGF add‐on treatment did not (adjusted mean difference: 0.07, 95% confidence interval −0.09 to 0.24; P = 0.502). During the follow‐up to 24 weeks, EDV add‐on treatment improved the composite score of executive cognitive function and DST‐R score better than TAU (both P < 0.01). Craving for alcohol was relieved in all three groups. No severe adverse events were observed. Conclusion: The short‐term addition of edaravone to supplementary therapy treatment for alcohol‐related brain damage (ARBD) improved executive cognitive function in patients with ARBD. [ABSTRACT FROM AUTHOR]

ABSTRACT A novel chemiluminescence (CL) method was developed for the determination of 10-hydroxycamptothecin(HCPT) based on the CL reaction between [Ag(HIO6)2]5− and luminol in alkaline solution. CL emission of Ag(III) complex-luminol in alkaline medium was very different from that in acidic medium. A possible mechanism of enhanced CL emission was suggested. The enhanced effect of HCPT on CL emission of the [Ag(HIO6)2]5−-luminol system was found. The enhanced degree of CL emission was proportional to HCPT concentration. The effect of the reaction conditions on CL emission was examined. Under optimal conditions, the limit of detection was 6.5 × 10−9 g mL−1. The proposed method was applied for the determination of HCPT in real samples with the recoveries of 93.2-109% with the RSD of 1.7-3.3%. Copyright © 2010 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

A novel chemiluminescence (CL) method was developed for the determination of 10-hydroxycamptothecin(HCPT) based on the CL reaction between [Ag(HIO₆)₂]⁵⁻ and luminol in alkaline solution. CL emission of Ag(III) complex-luminol in alkaline medium was very different from that in acidic medium. A possible mechanism of enhanced CL emission was suggested. The enhanced effect of HCPT on CL emission of the [Ag(HIO₆)₂]⁵⁻-luminol system was found. The enhanced degree of CL emission was proportional to HCPT concentration. The effect of the reaction conditions on CL emission was examined. Under optimal conditions, the limit of detection was 6.5 × 10⁻⁹ g mL⁻¹. The proposed method was applied for the determination of HCPT in real samples with the recoveries of 93.2-109% with the RSD of 1.7-3.3%., (Copyright © 2010 John Wiley & Sons, Ltd.)