Results: Observation of video was the most costly data processing method with total cost of (sic) 30,630, and was 1.2-fold more costly than inclinometry ((sic) 26,255), and 2.5-fold more costly than self-reported data ((sic) 12,491). Simulated scenarios showed altering design strategy could substantially impact processing costs. This was shown for both fixed parameters,
such as software development and training costs, and variable parameters, such as the number of work-shift files processed, as well as the sampling frequency for video observation. When data collection and data processing Pfizer Licensed Compound Library costs were combined, the cost difference between video and inclinometer methods was reduced to 7%; simulated data showed this difference could be diminished and, even, reversed at larger study sample sizes. Self-report remained substantially less costly under all design strategies, but produced alternate exposure metrics.
Conclusions: These findings build on the previously published data collection phase cost model by reporting costs for post-collection data processing of the same
data set. Together, these models permit empirically based study planning and identification of cost-efficient study designs.”
“Background and objective: High-altitude pulmonary oedema (HAPE) is a non-cardiogenic hydrostatic oedema involving a genetic learn more component. Considering the low incidence of HAPE, sample sizes in current reports are relatively limited. We aimed to assess the association between Selleckchem Nutlin3a the angiotensin-converting enzyme (ACE) I/D polymorphism
and HAPE via a meta-analysis of published and unpublished data.
Materials and methods: We searched PubMed, CBM, CNKI, and Cochrane Library Database before 20 November 2010. A random-effects model was applied (STATA) and study quality was assessed in duplicate.
Results: A total of five studies including 305 cases and 662 controls were meta-analysed. The summary odds ratio (OR) indicated that no significant differences in risk of developing HAPE were found between carriers of ACE D and I alleles (OR = 1.20; 95% confidence interval (CI), 0.98-1.48; p = 0.084). Lack of association persisted for genotypes under the recessive mode. However, genotype association under the dominant mode showed D allele carriers significantly conferred a 1.55-fold increased HAPE risk compared with II genotype carriers (95% CI, 1.15-2.08; p = 0.004). Funnel plot and Egger’s test suggested no evidence of publication bias.
Conclusions: Our results supported the notion that ACE D allele carriers were at significant increased risk of developing HAPE.”
“Background: Treatment duration varies with the type of therapy and a patient’s recovery speed. Including such a variation in randomized controlled trials (RCTs) enables comparison of the actual therapeutic potential of different therapies in clinical care.