Brief executive-function assessment tool: A new cognitive impairment screening tool for alcohol and other drug services.

Accurate screening for cognitive impairment in alcohol and other drug (AOD) services would help to identify individuals who may need supports to obtain the greatest benefit from substance use disorder (SUD) treatment. At present there is no screening measure that has been developed specifically to detect cognitive impairment in a SUD population. This study examines the psychometric properties of the Brief Executive-function Assessment Tool (BEAT), which was specifically designed for this purpose. This study involving 501 individuals with SUD and 145 normal control participants established internal consistency (n = 646; 0.734), interrater (n = 60; 0.994), and test-retest reliability (n = 177; 0.845), and construct (all correlations p ≤ 0.05), and criterion (n = 467; ANCOVA p < 0.001) validity. Test operating characteristics (n = 500; 87% sensitivity, 71% specificity, 21% PPP, and 99% NPP) were also established relative to an independent criterion variable made up of three established performance-based neuropsychological tests. Findings support the reliability and validity of the BEAT as a screening measure of executive function impairment with high sensitivity and a low rate of false negatives.

Randomised controlled trial of hydroquinine in muscle cramps.

BACKGROUND: Although quinine and hydroquinine are commonly prescribed for muscle cramps, controlled clinical trials of these drugs have reported mixed findings about efficacy. We investigated hydroquinine therapy in otherwise healthy adults who had frequent, ordinary muscle cramps. METHODS: This randomised, double-blind, placebo-controlled, parallel-group trial consisted of three consecutive 2-week periods: qualification, treatment, and washout, 68 women and 44 men who had at least three muscle cramps per week were enrolled. During the treatment period, participants were randomly assigned 300 mg daily dose of hydroquinine hydrobromide dihydrate (54 participants) or placebo (58). The frequency, severity (1-10), duration, and location of muscle cramps, as well as any side-effects, were recorded by participant in daily diaries. The primary outcome measures were the number of muscle cramps and the number of days during which the participants had muscle cramps (cramp-days). FINDINGS: We excluded five participants from both groups from the analysis. Thus, data from 49 hydroquinine-group participants and 53 placebo-group participants were analysed. In both groups the total number of muscle cramps and the number of cramp-days decreased during the treatment period compared with the qualification period. However, these improvements were greater in the hydroquinine group than in the placebo group. The hydroquinine-group participants reported a median of 8 (95% CI 7-12) fewer cramps and median of 3 (1-4) fewer cramp-days, whereas those on placebo reported only 3 (0-5) fewer cramps and 1 (0-5) fewer cramp-days. 32 (65%) of participants in the hydroquinine group had a 50% or greater reduction in the number of muscle cramps. After the onset of cramps, hydroquinine did not reduce the severity or duration of cramps. We also found a sustained effect after treatment had stopped. Hydroquinine was well tolerated, and resulted in only mild side-effects. INTERPRETATION: In our study, 300 mg hydroquinine was safe to take in the short-term and significantly more effective than placebo in the prevention of frequent, ordinary muscle cramps. This therapeutic effect outlasted the duration of treatment.

Cross-pathway regulation: histidine-mediated control of histidine, tryptophan, and arginine biosynthetic enzymes in Neurospora crassa.

In Neurospora crassa, histidine starvation of histidine mutants resulted in derepression of histidine, tryptophan, and arginine biosynthetic enzymes. The same tripartite derepression occurred in wild-type strain 74A when it was grown in medium supplemented with 3-amino-1,2,4-triazole, an inhibitor of histidine biosynthesis. Histidine-mediated derepression of tryptophan and arginine biosynthetic enzymes was not due to a lowered intracellular concentration of tryptophan or arginine, respectively. A discussion of possible mechanisms and of similar studies in prokaryotic and eukaryotic organisms is presented.