L Gore, Flagstaff, Ariz) (1). Mean preoperative AAA size was 6.4 cm in group 1. All but 1 patient had an endoleak at the time of rupture. Of 14 patients with CT follow-up, only 3 patients had a known

increase in size (>= 5 mm) and only 3 were known to have an endoleak. Fifteen selleck kinase inhibitor patients were treated by a single intervention, whereas 3 patients underwent multiple procedures. In group 2, open repair was performed in 218 patients and EVAR in 15. Morbidity (66.7% vs 56.7%) and in-hospital mortality (38.9% vs 36.9%) were nearly identical between groups. One-year survival rates (27.8% vs 48.2%; P = .15) were also similar. The mortality rates for EVAR for primary rAAA was 20% as compared to 38.1% for open repair for rAAAs (P = .27).

Conclusion: rAAA remains a lethal problem in patients with and without prior EVAR alike. An existing endograft provides neither acute nor 1-year survival benefits after rAAA repairs. Prediction of patients at Pritelivir mouse risk for rupture post-EVAR is difficult, as only a minority of

patients had a known prior endoleak or sac enlargement. (J Vase Surg 2010;52:1127-34.)”
“Stroke is the third most common cause of death worldwide. Recent findings showed that the severity of cerebrovascular diseases including ischemic stroke correlates with inflammation mediated responses in the neural cells. During ischemia, inflammatory mediators including

tumor necrosis factor-alpha (TNF-alpha) and nitric oxide are produced by microglia, Oxygenase which play a central role in the pathogenesis of the disease. Ligusticum chuanxiong (LCX) is a commonly used traditional Chinese medicine (TCM) for empiric treatment of cerebrovascular and cardiovascular diseases for many centuries. By applying a bioactivity-guided fractionation scheme, two compounds with inhibition on neuroinflammation were isolated from LCX. Using chromatographic and spectrometric methods, they were identified to be senkyunolide A and Z-ligustilide. They could inhibit the production of proinflammatory mediators in lipopolysaccharide (LPS)-stimulated murine BV-2 microglial cells and human peripheral blood monocyte derived macrophages. In addition, both compounds protected Neuro-2a cells from neuroinflammatory toxicity induced by the conditioned culture media produced by LPS-stimulated BV-2 cells. The underlying mechanisms of action of senkyunolide A were further delineated. Its inhibitory effects were shown to be independent of the phosphorylation of mitogen-activated protein kinases (MAPK) and translocation of nuclear factor kappa B (NF-kappa B). However, senkyunolide A could increase the degradation of TNF-a mRNA and reduce its half life by 43%. In conclusion, bioactivity-guided fractionation is an effective way of isolating bioactive compounds from medicinal herbs.