Our study shows that GADD45 gamma is quickly upregulated in the kidney with an obstructed ureter, enhancing the production of factors regulating the pathogenesis of kidney disease.”
“Obstructive sleep apnea (OSA) patients show compromised emotional and cognitive functions, including anterograde memory deficits. While some memory inadequacies in OSA may result from earlier-described structural deficits in the hippocampus, mammillary body injury also could contribute, since these structures receive projections from the hippocampus via the fornix, project heavily to the anterior thalamus, and have been implicated in other conditions with memory deficiencies, such as Korsakoff’s
syndrome. However, volume loss in mammillary selleck inhibitor bodies has not been reported in OSA, likely a consequence of logistic difficulties in size assessment. We TSA HDAC evaluated mammillary body volumes in 43 OSA (mean age +/- S.D., 46.9 +/- 9.2 years; mean apnea-hypopnea-index +/- S.D., 31.2 +/- 19.9 events/h) and 66 control subjects (age, 47.3 +/- 8.9 years). Two high-resolution T1-weighted image volumes were collected on a 3.0 T magnetic resonance scanner, averaged to improve signal-to-noise, and reoriented (without warping) into a common space. Brain sections containing both mammillary bodies were oversampled, and the bodies were manually traced and volumes calculated. OSA patients
showed significantly reduced left, right, and combined mammillary body volumes compared with control subjects, after partitioning for age, gender, and head size (multivariate linear model, p < 0.05). Left-side mammillary bodies showed greater volume reduction than the right side. Diminished mammillary body volume in OSA patients may be associated with memory and spatial orientation deficits found in the syndrome. The mechanisms contributing
to the volume loss are unclear, but may relate to hypoxic/ischemic processes, possibly assisted PD-1 inhibiton by nutritional deficiencies in the syndrome. (c) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Sepsis remains a serious problem in critically ill patients with the mortality increasing to over half when there is attendant acute kidney injury. alpha-Melanocyte-stimulating hormone is a potent anti-inflammatory cytokine that inhibits many forms of inflammation including that with acute kidney injury. We tested whether a new alpha-melanocyte-stimulating hormone analogue (AP214), which has increased binding affinity to melanocortin receptors, improves sepsis-induced kidney injury and mortality using a cecal ligation and puncture mouse model. In the lethal cecal ligation-puncture model of sepsis, severe hypotension and bradycardia resulted and AP214 attenuated acute kidney injury of the lethal model with a bell-shaped dose-response curve.