These findings would have important implications in both clinical and research-related activities aimed at the management of nocturia in older adults.”
“Developmental white matter damage is a brain pathology associated with several selleck kinase inhibitor long-term neurological disorders. An inflammatory insult has been suggested as the major instigating

event. This study investigated the relative influence of inflammation, blood-brain barrier permeability and glial ontogeny in white matter damage. Systemic inflammation was induced in Monodelphis domestica (opossum) by serial intraperitoneal injections of lipopolysaccharide at different stages of brain development. Volume of white matter was estimated for the external capsule. Blood-brain barrier permeability was assessed immunocytochemically. Bleomycin supplier Quantitative RT-PCR was used to measure relative levels of mRNA for IL-1 beta, IL-6 and COX-2. Developmental changes in numbers and appearance of microglia and

astrocytes were estimated. Results showed that in response to systemic inflammation, white matter was reduced in the external capsule during a circumscribed period only. At the same developmental stage blood-brain barrier permeability was altered, cerebral inflammatory response was present and numbers of microglia increased. However, the periods of altered blood-brain barrier permeability and the cerebral inflammatory response were longer than the period of the external capsule’s susceptibility to white matter damage, which coincided with the developmental increase in the number of astrocytes in this tract. Thus, the mechanism of white matter damage following systemic inflammation is multifactorial, including cerebral inflammation and breakdown of

brain barriers occurring simultaneously at specific stages of glial cell development. Crown Copyright (C) 2009 Published by Elsevier Ireland Ltd. All rights reserved.”
“Bcl-2 homology domain 3 (BH3)-only pro-apoptotic proteins may play an important role in upstream cell death signaling pathways underlying ischemic brain injury. Puma is a potent BH3-only protein that can be induced via p53, FoxO3a and endoplasmic reticulum stress pathways and is Selleckchem Mocetinostat upregulated by global cerebral ischemia. To more completely define the contribution of Puma to ischemic brain injury we measured the expressional response of Puma to transient focal cerebral ischemia in mice and also compared infarct volumes in puma-deficient versus puma-expressing mice. Real-time quantitative PCR determined puma mRNA levels were significantly increased 8 h after 90 min middle cerebral artery (MCA) occlusion in the ipsilateral cortex, while expression remained unchanged contralaterally. Puma protein levels were also increased in the ischemic cortex over the same period, However, cortical and striatal infarct volumes were not significantly different between puma-deficient and puma-expressing mice at 24 h, and no differences between genotypes were found for post-ischemic neurological deficit scores.