In vivo electrophysiological recordings in rats exposed to chronic stress unveiled disturbance of correlated local field potential activity between the PFC and limbic structures as well as impairment of synaptic plasticity induction in the limbic-PFC pathways. However, these stress-induced alterations in limbic PFC interaction were distinct along with the dorsal-ventral

axis within the PFC, with greater stress vulnerability in the dorsal than the ventral PFC, such that alterations in the dorsal PFC became evident with much shorter duration of repeated stress exposure than those occurring in the ventral PFC. In agreement with the stress-induced alterations in limbic PFC interaction, spike firing patterns of neurons in the dorsal and ventral selleck products PFC were also differently modulated by chronic stress. These results suggest that chronic stress produces heterogeneous cellular and neural network adaptation and maladaptation within the PFC that affect limbic information integration mechanisms. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Background check details Low values of estimated glomerular filtration rate (eGFR) predispose to acute kidney injury, and proteinuria is a marker of kidney disease. We aimed to investigate how eGFR and proteinuria jointly modified the risks of acute kidney

injury and subsequent adverse clinical outcomes.

Methods We did

ARS-1620 a cohort study of 920 985 adults residing in Alberta, Canada, between 2002 and 2007. Participants not needing chronic dialysis at baseline and with at least one outpatient measurement of both serum creatinine concentration and proteinuria (urine dipstick or albumin-creatinine ratio) were included. We assessed hospital admission with acute kidney injury with validated administrative codes; other outcomes were all-cause mortality and a composite renal outcome of end-stage renal disease or doubling of serum creatinine concentration.

Findings During median follow-up of 35 months (range 0-59 months), 6520 (0.7%) participants were admitted with acute kidney injury. In those with eGFR 60 mL/min per 1.73 m(2) or greater, the adjusted risk of admission with this disorder was about 4 times higher in those with heavy proteinuria measured by dipstick (rate ratio 4.4 vs no proteinuria, 95% CI 3.7-5.2). The adjusted rates of admission with acute kidney injury and kidney injury needing dialysis remained high in participants with heavy dipstick proteinuria for all values of eGFR. The adjusted rates of death and the composite renal outcome were also high in participants admitted with acute kidney injury, although the rise associated with this injury was attenuated in those with low baseline eGFR and heavy proteinuria.