Studies were not utilized in the calculations unless their qualit

Studies were not utilized in the calculations unless their quality score (utilizing both raters) was greater than 60%. For each of the above groupings, an average quality score was calculated and a calculation performed as to the percentage of studies that supported the hypothesis that pain is etiologically related to the above DSM-IV category of sleep disorders. Finally, the strength

and consistency of the evidence for this hypothesis was rated according to the AHCPR guidelines.

Results. Of the 41 reports, all had quality scores greater than 60%. In all the above groupings except for multivariate analysis, 100% of the studies supported this hypothesis. In the multivariate analysis grouping, 77.2% of the studies supported this hypothesis. The strength and consistency of this selleck compound evidence was rated at A (highest possible) for all study groupings except multivariate (B rating) and path analysis where there were too few studies to generate a conclusion. For all the studies combined, 89.7% of the studies supported this hypothesis. This evidence was rated as A:

consistent, multiple studies.

Conclusions. The results of this evidence-based structured review indicate that for the pain-sleep studies defined by the DSM-IV category of sleep disorder due to a general medical condition,chronic pain may be etiologically related to that sleep CX-5461 research buy problem. However, these results do not preclude this relationship from being bidirectional.”
“Objectives: Statins have been reported to suppress the progression of abdominal aortic aneurysm (AAA). However, the effects of statins on inflammatory processes and free radicals generation are poorly understood.

Methods: Wall samples from 51 patients (simvastatin patients, n = 34; non-statin patients, n = 17; matched by sex, age and aneurysm size) subjected to elective open AAA repair were analysed. We examined the effects of simvastatin this website on lipid peroxidation (4-hydroxy-trans-2-nonenal (4-HNE)), hydrogen peroxide (H2O2), tumour necrosis factor alpha (TNF-alpha) concentration,

superoxide dismutase (SOD) and catalase (CAT) activity as well as nuclear factor kappa B (NF-kappa B) pathway activation in human AAA wall samples.

Results: Treatment with simvastatin resulted in a decrease in 4-HNE and TNF-alpha concentration (median 4.18 mu g/mg protein vs. 4.75, p = 0.012; median 10.33 pg/ml vs. 11.81, p = 0.026, respectively). CAT activity was higher in the simvastatin group (median 3.98 U ml vs. 3.19, p = 0.023). NF-kappa B expression was lower (p = 0.018) in the simvastatin group. However, simvastatin had little effect on H2O2 concentration (p = 0.832) and SOD activity (p = 0.401).

Conclusion: Simvastatin inhibits free radials and TNF-alpha generation and improves antioxidant capacity of human AAA wall tissue, possibly through the suppression of NF-kappa B activity.

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