Metabolic effects of intermittent hypoxia in mice: steady versus high-frequency applied hypoxia daily during the rest period.

Intermittent hypoxia (IH) is a frequent occurrence in sleep and respiratory disorders. Both human and murine studies show that IH may be implicated in metabolic dysfunction. Although the effects of nocturnal low-frequency intermittent hypoxia (IH(L)) have not been extensively examined, it would appear that IH(L) and high-frequency intermittent hypoxia (IH(H)) may elicit distinct metabolic adaptations.

Disrupted sleep without sleep curtailment induces sleepiness and cognitive dysfunction via the tumor necrosis factor-α pathway.

Background: Sleepiness and cognitive dysfunction are recognized as prominent consequences of sleep deprivation. Experimentally induced short-term sleep fragmentation, even in the absence of any reductions in total sleep duration, will lead to the emergence of excessive daytime sleepiness and cognitive impairments in humans. Tumor necrosis factor (TNF)-α has important regulatory effects on sleep, and seems to play a role in the occurrence of excessive daytime sleepiness in children who have disrupted sleep as a result of obstructive sleep apnea, a condition associated with prominent sleep fragmentation.

Conservative management of iatrogenic esophageal perforation in head and neck cancer patients with esophageal stricture.

Objective: Evaluate the efficacy of conservative management of iatrogenic esophageal perforation following dilatation of a stricture secondary to the treatment of head and neck cancer.

Study Design: Case series with chart review.

Subjects And Methods: Retrospective chart review of 24 patients with esophageal perforation treated at the Detroit Medical Center from 1999 to 2008.

Brain endothelial HSP-70 stress response coincides with endothelial and pericyte death after brain trauma.

Objectives: Our objective was to characterize the heat shock response (HSR) in a model of traumatic brain injury (TBI) and to determine the association of HSR to cell death.

Methods: We used immunofluorescent detection of HSP-70 to characterize HSR and TUNEL labeling to determine the pattern of cell death.

Results: HSP-70 immunofluorescence revealed a steady increase from 4 to 48 hours following TBI, culminating in a ubiquitous expression with the capillary bed 48 hours post-TBI.

Renal ischemia and reperfusion activates the eIF 2 alpha kinase PERK.

Inhibition of protein synthesis occurs in the post-ischemic reperfused kidney but the molecular mechanism of renal translation arrest is unknown. Several pathways have been identified whereby cell stress inhibits translation initiation via phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF 2 alpha, phospho-form eIF 2 alpha(P)]. Here, we report a 20-fold increase in eIF 2 alpha(P) in kidney homogenates following 10 min of cardiac arrest-induced ischemia and 10 min reperfusion.