(c) 2009 Elsevier Ltd. All rights reserved.”
“Accumulating evidence suggests that urokinase plasminogen activator (uPA) is involved in vascular remodeling and lumen stenosis after angioplasty and stenting. We have shown previously that increased uPA expression greatly promotes neointima formation

and inward arterial remodeling after balloon injury. To evaluate the role of inflammation in early mechanisms responsible for inward arterial remodeling induced by uPA and elucidate the mechanisms of remodeling, we characterized changes in the expression profiles of 8,799 genes in injured rat carotid arteries 1 and 4 days after recombinant https://www.selleckchem.com/products/jsh-23.html uPA treatment compared to vehicle. We used a standard model of the balloon catheter injury of the rat carotid followed by periadventitial application to the injured vessel of either uPA dissolved in Pluronic gel, or plain gel. Vessels were harvested and analyzed by immunohistochemistry, morphometry, microarray gene expression profiling and quantitative RT-PCR. Periadventitial

application of uPA significantly reduced lumen size and vessel area encompassed by the external elastic ARS-1620 lamina at both 1 and 4 days after treatment. Inflammatory cells accumulated in the arterial adventitia at both 1 and 4 days after uPA treatment. On the 4th day, increases in the areas and arterial cell numbers of all arterial layers were found. Among 79 differentially expressed known genes 1 day after uPA application, 12 proinflammatory genes, including TNF-alpha and TACE, and 15 genes related to mitochondrial metabolism and oxidative stress regulation were identified. Four days after injury in uPA-treated arteries, 3 proinflammatory and 2 oxidation-related genes were

differentially expressed. We conclude that uPA likely promotes inward arterial remodeling by regulating oxidative stress and inflammation after arterial injury. Copyright (c) 2008 S. Karger AG, Basel”
“Selective sparing of abstract relative to concrete words has been documented only exceptionally in aphasia, Etofibrate following bilateral temporal damage. In this paper we present a new case with sparing of abstract word processing and impairment of concrete words due to selective atrophy of the left anterior temporal regions.

In our subject, the reversal of the concreteness effect was restricted to nouns. Performance on nouns was not homogeneous. Proper names (people and landmarks) were very severely damaged. Among common names, living entities were selectively impaired in comparison to non-living entities. Category-specific damage for living beings resulted from widespread loss of conceptual information, and perceptual information was less impaired than associative knowledge. This observation challenges theories explaining the reversal of concreteness effect with a selective loss of perceptual information.