Randomisation was by remote computer allocation. Our primary endpoints, collected via postal questionnaires, were participants’ reports of urinary incontinence and incremental cost per quality-adjusted life year (QALY)

after 12 months. Group assignment was masked from outcome assessors, but this masking was not possible for participants or caregivers. We used intention-to-treat analyses to compare the primary outcome at 12 months. This study is registered, number ISRCTN87696430.

Findings In the intervention group in trial 1, the rate of urinary incontinence at 12 months (148 [76%] of 196) was not significantly different from the control group (151 [77%] of 195; absolute risk difference [RD] -1.9%, 95% CI -10 to 6). In trial 2, the difference in the rate of urinary incontinence at 12 months (126 [65%] of 194) from buy FK506 the control group was not significant (125 [62%] of 203; RD 3.4%, 95% CI 6 to 13). Adjusting for minimisation factors or doing treatment-received analyses did not change these results in either trial. No adverse effects were reported. In both MI-503 price trials,

the intervention resulted in higher mean costs per patient (180 pound and 209 pound respectively) but we did not identify evidence of an economically important difference in QALYs (0.002 [95% CI -0.027 to 0.023] and -0.00003 [-0.026 to 0.026]).

Interpretation In settings where information about pelvic-floor exercise is widely available, one-to-one conservative physical therapy for men who are incontinent after prostate surgery is unlikely to be effective or cost effective. The high rates of persisting incontinence after 12 months suggest a substantial unrecognised and unmet need for management in these men.”
“Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. The ‘amyloid cascade hypothesis’ assigns the amyloid-beta-peptide (A beta) a central role in the pathogenesis of AD. Although it is not yet established, whether

the resulting A beta aggregates are the causative agent or just a result of the disease progression, polymerization of A beta has been identified as a major feature during AD pathogenesis. Inhibition of the A beta polymer formation, thus, has emerged as Selinexor a potential therapeutic approach. In this context, we identified peptides consisting of D-enantiomeric amino acid peptides (D-peptides) that bind to A beta. D-peptides are known to be more protease resistant and less immunogenic than the respective L-enantiomers. Previously, we have shown that a 12mer D-peptide specifically binds to A beta amyloid plaques in brain tissue sections from former AD patients. In vitro obtained binding affinities to synthetic A beta revealed a K(d) value in the submicromolar range.