“
“Cortical spreading depression (CSD) has been shown to cause secondary cell loss in experimental models of brain injury and in patients, and blocking of CSD is a potential neuroprotective strategy.

Here we tested the hypothesis that gap junctions affect CSD under physiological conditions as well as infarct development in a rat two-vein occlusion model suited to study pathophysiology of the penumbra (n=71). We applied the gap junction blocker carbenoxolone (CBX) or saline intra-ventricularly. Interestingly, CBX temporarily increased systemic blood pressure and cortical blood flow (41% and 53%, 15 min after 250 CBX). We induced CSD with cortical microinjection of potassium chloride (KCl), counted how check details many spontaneous CSDs after CSD induction were elicited and measured the propagation velocity. After 250 mu g CBX administration, significant 37.5 +/- 6.5 additional CSDs were seen. CSD velocity increased significantly after 50 mu g and 250 mu g CBX. Occlusion of two adjacent cortical veins using Rose Bengal dye and fiberoptic illumination followed by 250 mu g CBX or saline showed a significant more than doubling of infarct volumes 7 days after CBX. The current experiments provide MK-0518 concentration evidence that CBX can accelerate the initiation and propagation of CSD suggesting opening of gap junctions is not required for CSD propagation. Blocking gap junctions worsens outcome from focal

cerebral ischemia. Hence, measures intended to improve spatial buffering via astroglial gap junctions could AG 14699 have therapeutic potential in disease processes involving CSD. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Purpose: We investigated the rate of diagnosis and treatment trends of hypospadias in Taiwan within the first 3 years of life.

Materials and Methods: We used a subset of the Taiwan National Health Insurance Research Database, which contains data on all inpatient and outpatient medical benefit claims, for the period 1997 through 2008 for a sample of 1 million individuals randomly drawn from

the population of 25.68 million who held membership in the National Health Insurance program during any part of the calendar year 2005. We analyzed claims data for all subjects who were diagnosed with hypospadias through age 3 years.

Results: Among 52,705 newborns (individuals whose claims included live birth) 178 were diagnosed with hypospadias within 3 years of birth. Thus, mean incidence was 33.8 per 10,000 live male births. The hypospadias repair rate was 14.3 per 10,000 live male births. There was no significant tendency toward increase or decrease in rates of diagnoses or repairs, or proportion of severe hypospadias. There were significant associations between rates of hypospadias diagnoses and urbanization level of the community where the diagnosis was made.