We examined the prevalence and clinical significance of carotid s

We examined the prevalence and clinical significance of carotid stent fractures or deformations following CAS.

Methods: Two

hundred thirty-one CAS performed in 219 patients at one academic institution between August 2000 and March 2009 were reviewed. One hundred sixteen stents (57 closed cell, 59 open cell) were evaluated with multiplanar plain films of the neck to assess for stent fracture or deformation. Stent fracture was identified by wire strut disruption. Deformation was defined as an increase in Selleckchem WZB117 stent-cell area from stent strut distortion. Study endpoints included rate of stent fracture or deformation determined using Kaplan-Meier and life table analysis. Factors associated with stent fracture or deformation were identified by Cox regression. Effect of stent fracture or deformation on recurrent carotid artery stenosis >70% requiring reintervention and postoperative stroke was studied.

Results: There were five stent

fractures (4%) and 27 deformed stems (23%). Rate of stent fracture or deformation was 15% at 2 years and 50% at 4 years. Deformations were significantly more common in open cell stents than in closed cell stents (58% vs 5% at 4 years, P < .00005). Presence of calcified plaque on plain film was significantly associated with increased rate of stent fracture or deformation (P = .0006). At median follow-up of 25 months, restenosis requiring treatment occurred in four (5%) and late stroke in one (1%). Neither stent fracture nor deformation

was associated with late stroke or reintervention.

Conclusions: Stent fracture and deformation is not buy Citarinostat uncommon following CAS and is associated with the presence of heavy calcification. Whether a carotid stent fractures or deforms correlates with stent design. Larger studies are necessary to determine the possible clinical significance of carotid stent fracture and deformation. (J Vase Surg 2011;54:685-90.)”
“Caloric restriction (CR) without malnutrition slows the aging process and extends lifespan in diverse species by unknown mechanisms. The inverse linear relationship between calorie Mephenoxalone intake and lifespan suggests that regulators of energy metabolism are important in the actions of CR. Studies in several species reveal tissue-specific changes in energy metabolism with CR and suggest that metabolic reprogramming plays a critical role in its mechanism of aging retardation. We herein describe common signatures of CR and suggest how they can slow aging. We discuss recent advances in understanding the function of key metabolic regulators that probably coordinate the response to altered nutrient availability with CR and how the pathways they regulate can retard the aging process.”
“BACKGROUND: A significant number of medulloblastomas (MBs) originate from abnormal activation of the sonic hedgehog/patched (SHH/PTC) signaling pathway.

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