Databases searched included MEDLINE (R), CENTRAL and Embase (R). Data were tabulated from case series and from randomized controlled trials, and data were pooled where appropriate.
Results: Our literature search identified 432 titles and 23 full articles were included in the final
review. Three randomized placebo controlled trials addressing the use of botulinum toxin-A were identified (99 patients total). The pooled random effects estimate of effect across all 3 studies was 3.88 (95% CI -6.15, -1.62), meaning that patients treated with botulinum toxin-A had 3.88 fewer incontinence episodes per day. Urogenital Distress Inventory data revealed significant improvements in quality of life compared with placebo with a standardized www.selleckchem.com/products/LY294002.html mean difference of -0.62 (CI -1.04, -0.21). Data from case series demonstrated significant improvements in overactive bladder symptoms and quality of life, despite heterogeneity in methodology
find more and case mix. However, based on the randomized controlled trials there was a 9-fold increased odds of increased post-void residual after botulinum toxin-A compared with placebo (8.55; 95% CI 3.22, 22.71).
Conclusions: Intravesical injection of botulinum toxin resulted in improvement in medication refractory overactive bladder symptoms. However, the risk of increased post-void residual and symptomatic urinary retention was significant. Several questions remain concerning the optimal administration of botulinum toxin-A for the patient with overactive bladder.”
“Activation of astrocytes surrounding amyloid plaques is a hallmark of Alzheimer disease
(AD) with consequences yet poorly understood. Astrocytes are characterized by a high level of intercellular communication mediated by two gap-junction forming proteins, connexin-43 and connexin-30. As astroglial connexins (Cxs) are involved in neuronal dysfunctions and death, we have analyzed their expression pattern in two murine models of AD, that is two different beta-amyloid precursor protein (APP)/presenilin1(PS1) mice, using western blot and immunohistochemistry analyzed in confocal microscopy. In young mice at 2 months, before the emergence of beta-amyloid (A beta) deposits, the distribution of both Cxs was similar to that of control mice. In older animals >= 4 months, local modifications in Thalidomide connexin immunostaining pattern were observed in the microenvironment of dense core A beta plaques. In a majority of plaques, an elevated immunoreactivity was detected for both Cxs contributing to the overall increase in connexin expression detected in 18 month old APP/PS1 mice. Activated microglial cells did not contribute to the elevated connexin immunoreactivity that was concentrated in astroglial processes infiltrating the plaques. In a small proportion of plaques (<= 15%) a depletion of immunoreactive connexin puncta was also found.