Methods
We carried out an analysis of genomewide association data generated from four large cohorts composing the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium, including 19,602 white persons (mean [+/- SD] age, 63 +/- 8 years) in whom 1544 incident strokes (1164 ischemic strokes) developed over an average follow-up of 11
years. We tested the markers most strongly associated with stroke in a replication cohort of 2430 black persons with 215 incident strokes (191 ischemic strokes), another cohort of 574 black persons with 85 incident strokes (68 ischemic strokes), and 652 Dutch persons with ischemic stroke and 3613 unaffected persons.
Results
Two intergenic single-nucleotide polymorphisms on chromosome 12p13 and within 11 kb of the gene NINJ2 were associated with stroke (P<5×10(-8)). NINJ2 encodes an adhesion molecule expressed in glia and shows increased expression after nerve injury. Direct genotyping showed that rs12425791 was associated with an increased risk of total (i.e., all types) and ischemic stroke, with hazard ratios of 1.30 (95% confidence interval [CI], 1.19 to 1.42) and 1.33 (95% CI, 1.21 to 1.47), 1 respectively, yielding population attributable risks of 11% and 12% in the discovery cohorts. Corresponding hazard ratios
were 1.35 (95% CI, 1.01 to 1.79; P = 0.04) and 1.42 (95% CI, 1.06 to 1.91; P = 0.02) in the large cohort of black persons and 1.17 (95% CI, 1.01 to 1.37; P = 0.03) and 1.19 (95% CI, 1.01 to 1.41; P = 0.04) in the Dutch sample; the results of an underpowered analysis of the smaller black cohort were nonsignificant.
Conclusions
A genetic locus on chromosome 12p13 is associated with an increased risk of stroke.”
“Objective: Abdominal aortic aneurysm (AAA) rupture is believed to occur when the local mechanical stress
exceeds the local mechanical strength of the wall tissue. On the basis of this hypothesis, the knowledge of the stress acting on the wall of an unruptured aneurysm could be useful in determining the risk of rupture. The role of asymmetry has previously been identified in idealized AAA models and is now studied using realistic AAAs in the current work.
Methods. Fifteen patient-specific AAAs were studied to estimate the relationship between wall stress and geometrical parameters. Three-dimensional AAA models were reconstructed from computed tomography scan data. The stress distribution on the AAA wall was evaluated by the finite element method, and peak wall stress was compared with both diameter and centerline asymmetry. A simple method of determining asymmetry was adapted and developed. Statistical analyses were performed to deter-mine potential significance of results.
Results. Mean von Mises peak wall stress +/- standard deviation was 0.4505 +/- 0.1.4 MPa (range, 0.3157-0.9048 MPa). Posterior wall stress increases with anterior centerline asymmetry.