Ketamine, both acutely (0 5-5 0 mg/kg i p ) and chronically (0 5-

Ketamine, both acutely (0.5-5.0 mg/kg i.p.) and chronically (0.5-2.5 mg/kg daily for 10 days) resulted in a dose-dependent and prolonged decrease in immobility in FST in WKY rats only, suggesting an antidepressant-like effect in this model. Chronic treatment with an effective dose of ketamine also

resulted in an increase in AMPA/NMDA receptor density ratio in the hippocampus of WKY rats. LMA was not affected by any ketamine treatment in either strain. These results indicate a rapid and lasting antidepressant-like effect www.selleckchem.com/products/Raltegravir-(MK-0518).html of a low ketamine dose in WKY rat model of depression. Moreover, the increase in AMPA/NMDA receptor density in the hippocampus could be a contributory factor to behavioral effects of ketamine. These findings suggest potential therapeutic benefit in simultaneous reduction of central NMDA and elevation of AMPA receptor function in treatment of depression. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Obsessive-compulsive disorder (OCD) affects approximately 2-3% of the population and is characterized by recurrent intrusive thoughts (obsessions) and repetitive behaviors or mental acts (compulsions), typically performed in response to obsessions or related anxiety. In the past few decades, the prevailing models of OCD pathophysiology

have focused on cortico-striatal circuitry. More recent neuroimaging evidence, however, points to critical involvement of the lateral PS-341 mouse and medial orbitofrontal cortices, YAP-TEAD Inhibitor 1 mw the dorsal anterior cingulate cortex and amygdalo-cortical circuitry, in addition to cortico-striatal circuitry, in the pathophysiology of the disorder. In this review, we elaborate proposed features of OCD pathophysiology beyond the classic parallel cortico-striatal pathways and argue that this evidence suggests that fear extinction, in addition to behavioral inhibition, is impaired in OCD.”
“Purpose: Congenital obstructive uropathy can lead to end stage renal disease. Progression to end stage renal disease in childhood is well described but long-term prognosis in adulthood has not been thoroughly investigated. In this study

we evaluated the risk of end stage renal disease in patients with posterior urethral valves.

Materials and Methods: During 1953 to 2003 a total of 200 male patients were treated for posterior urethral valves at our institution and of these 193 could be followed for renal outcome. Followup data on patients treated with dialysis or kidney transplantation were collected from patient records and the Finnish Kidney Transplantation Registry, and data on deceased patients were collected from hospital records and the Finnish Population Register Centre.

Results: Median patient age at evaluation was 31 years (range 6 to 69). Of the 193 patients followed 44 (22.8%) had progression to end stage renal disease. According to a Kaplan-Meier analysis the lifetime risk of end stage renal disease was 28.5% (SE 3.8%). No patient had end stage renal disease after the age of 34 years.

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