Followup included prostate specific antigen tests at I month and

Followup included prostate specific antigen tests at I month and then every 3 months after treatment, and a random prostate biopsy at 6 months. Failure was defined according to prostate specific antigen nadir, positive findings on followup biopsy and biochemical failure according to Phoenix criteria.

Results: Median patient age was 72 years old, median baseline prostate specific antigen was 7.3 ng/ml, and disease stage was T1 in 44.1%, T2 in 42.5% and T3a in 13.4% of patients. Median followup was 23.8 months. After high intensity focused ultrasound treatment prostate

specific antigen decreased to a median nadir of 0.15 ng/ml. Median prostate specific antigen at 3 and 6 months was 0.30 and 0.54 ng/ml, respectively. At 6 months the negative biopsy rate was 66.1%. There was no

biochemical evidence of DihydrotestosteroneDHT in vivo disease in 71.9% overall. On multivariate analysis prostate specific antigen nadir became the only independent predictor of no biochemical evidence of disease and positive biopsy at a cutoff of 0.40 ng/ml.

Conclusions: A favorable outcome of high intensity focused ultrasound is associated with lower baseline prostate specific antigen, lower prostate specific antigen nadir, lower Gleason score and lower tumor stage. As with any novel technology long-term data will be required before this technique gains widespread clinical acceptance.”
“Recently it has been shown that effects of aging and pathologically induced changes of basal ganglia structures may have quite similar AZD5582 mw effects on cognitive functions mediated by the medial prefrontal cortex. The question appears, if this pattern may be assignable to other cognitive

functions that 4-Hydroxytamoxifen mouse are mediated via the basal ganglia and medial prefrontal brain areas. Error processing is a component of executive functions that also depends on these areas and especially on the anterior cingulate cortex (ACC). Hence we ask, if error processing functions are differentially modulated by normal aging and basal ganglia diseases. Error processing mechanisms in these groups were investigated using a cognitive event-related potential (ERP), the error negativity. Enrolling an extended sample of young and elderly controls, as well as patients with Parkinson’s and Huntington’s disease, we show that modulations of error processing differ between aging, different basal ganglia diseases. Despite that the examined basal ganglia disorder groups (Parkinson’s and Huntington’s disease) differ in their age they show similar modulations in error processing, suggesting that aging effects are overridden by pathogenic effects. The study shows that it may be valuable to compare aging not only to different forms of basal ganglia disorders in order to gain knowledge about age- and disease-related mechanisms and the effects of these on cognitive functions. Diseases of the basal ganglia may impact error processing above and beyond the effects of normal aging.

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