The observations confirm the impaired kaliuretic potency of sgk1(

The observations confirm the impaired kaliuretic potency of sgk1(-/-) mice and point to a role of SGK1 in renal Na(+) reabsorption by mechanisms other than ENaC. Copyright (c) 2009 Epigenetics inhibitor S. Karger AG, Basel”
“Deferoxamine (DFO) and erythropoietin (EPO) have each been shown to provide neuroprotection in neonatal rodent models of brain injury. In view of the described anti-oxidative actions

of DFO and the antiapoptotic and anti-inflammatory effects of EPO, we hypothesized that the combination of DFO and EPO would increase neuroprotection after neonatal hypoxic-ischemic brain injury as compared to single DFO or EPO treatment. At postnatal day 7 rats underwent right common carotid artery occlusion followed by a 90-min exposure to 8% oxygen. Rats were treated intraperitoneally with DFO (200 mg/kg), recombinant human EPO (I kU/kg), a combination of DFO-EPO or vehicle at 0, 24 and 48 h after hypoxia-ischemia (HI) and were sacrificed at 72 h. DFO-EPO administration reduced the number of cleaved caspase 3-positive cells in the ipsilateral cerebral cortex. Early neuronal damage was assessed by staining for

microtubuli-associated protein (MAP)-2. In our model 63 +/- 9% loss of ipsilateral MAP-2 was observed after HI, indicating extensive brain injury. DFO, EPO or DFO-EPO treatment PD0332991 mouse did not improve neuronal integrity as defined by MAP-2. Cerebral white matter tracts were stained for myelin basic protein (MBP), a constituent of myelin. Hypoxia-ischemia strongly reduced MBP staining which suggests white matter damage. However, DFO, EPO and DFO-EPO treatment had no effect on the loss of MBP staining. Finally, HI-induced loss of striatal tyrosine hydroxylase staining was not attenuated by DFO, EPO or DFO-EPO. Although DFO-EPO treatment reduced the number of cleaved caspase 3(+) cells, treatment with DFO, EPO, or with the

combination of DFO and EPO did not protect against Acetophenone gray or white matter damage in the experimental setting applied. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“A thymidine-to-cytosine substitution in the -344 promoter region of the aldosterone synthase gene (CYP11B2) has been associated with essential hypertension in some but not all studies conducted in Chinese. We performed a meta-analysis to evaluate the association of the -344C/T polymorphism with essential hypertension in Chinese. A total of 7,472 individuals (4,259 unselected hypertensive patients and 3,213 normotensive controls) from 9 case-control studies were included in the present investigation. Significant associations between the risk of hypertension and the CC genotype and C allele frequencies were found in a total of 19 studies. Our findings support the notion that the CYP11B2-344C/T polymorphism is associated with essential hypertension.

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