Citations

PurposeIn 2D SENSE‐accelerated 3D Cartesian acquisition, the net acceleration factor R is the product of the two individual accelerations, R = RY × RZ. Acceleration Apportionment tailors acceleration parameters (RY, RZ) to improve parallel imaging performance on a patient‐ and coil‐specific basis and is demonstrated in contrast‐enhanced MR angiography.MethodsA performance metric is defined based on coil sensitivity information which identifies the (RY, RZ) pair that optimally trades off image quality with scan time reduction on a patient‐specific basis. Acceleration Apportionment is evaluated using retrospective analysis of contrast‐enhanced MR angiography studies, and prospective studies in which optimally apportioned parameters are compared with standard acceleration parameters.ResultsThe retrospective studies show strong variability in optimal acceleration parameters between anatomic regions and between patients. Prospective application of apportionment to foot contrast‐enhanced MR angiography with an 8‐channel receiver array provides a 20% increase in net acceleration with improved contrast‐to‐noise ratio. Application to 16‐channel contrast‐enhanced MR angiography of the feet and calves suggests 10% acceleration increase to R > 13 and no contrast‐to‐noise ratio loss. The specific implementation allows the optimum (RY, RZ) pair to be determined within one minute.ConclusionOptimum 2D SENSE acceleration parameters can be automatically chosen on a per‐exam basis to allow improved performance without disrupting the clinical workflow. Magn Reson Med 71:672–680, 2014. © 2013 Wiley Periodicals, Inc.

ObjectiveChildren with childhood‐onset rheumatoid arthritis (RA) include those with rheumatoid factor or anti–citrullinated protein antibody–positive juvenile idiopathic arthritis. To test the hypothesis that adult‐onset RA–associated variants are also associated with childhood‐onset RA, we investigated RA‐associated variants at 5 loci in a cohort of patients with childhood‐onset RA. We also assessed the cumulative association of these variants in susceptibility to childhood‐onset RA using a weighted genetic risk score (wGRS).MethodsA total of 155 children with childhood‐onset RA and 684 healthy controls were genotyped for 5 variants in the PTPN22, TRAF1/C5, STAT4, and TNFAIP3 loci. High‐resolution HLA–DRB1 genotypes were available for 149 cases and 373 controls. We tested each locus for association with childhood‐onset RA via logistic regression. We also computed a wGRS for each subject, with weights based on the natural log of the published odds ratios (ORs) for the alleles investigated, and used logistic regression to test the wGRS for association with childhood‐onset RA.ResultsChildhood‐onset RA was associated with TNFAIP3 rs10499194 (OR 0.60 [95% confidence interval 0.44–0.83]), PTPN22 rs2476601 (OR 1.61 [95% confidence interval 1.11–2.31]), and STAT4 rs7574865 (OR 1.41 [95% confidence interval 1.06–1.87]) variants. The wGRS was significantly different between cases and controls (P < 2 × 10−16). Individuals in the third to fifth quintiles of wGRS had a significantly increased disease risk compared to baseline (individuals in the first quintile). Higher wGRS was associated with increased risk of childhood‐onset RA, especially among males.ConclusionThe magnitude and direction of the association between TNFAIP3, STAT4, and PTPN22 variants and childhood‐onset RA are similar to those observed in RA, suggesting that adult‐onset RA and childhood‐onset RA share common genetic risk factors. Using a wGRS, we have demonstrated the cumulative association of RA‐associated variants with susceptibility to childhood‐onset RA.

SummaryOxidative stress is a determining factor of cellular senescence and aging and a potent inducer of the tumour‐suppressor p53. Resistance to oxidative stress correlates with delayed aging in mammals, in the absence of accelerated tumorigenesis, suggesting inactivation of selected p53‐downstream pathways. We investigated p53 regulation in mice carrying deletion of p66, a mutation that retards aging and confers cellular resistance and systemic resistance to oxidative stress. We identified a transcriptional network of ~200 genes that are repressed by p53 and encode for determinants of progression through mitosis or suppression of senescence. They are selectively down‐regulated in cultured fibroblasts after oxidative stress, and, in vivo, in proliferating tissues and during physiological aging. Selectivity is imposed by p66 expression and activation of p44/p53 (also named Delta40p53), a p53 isoform that accelerates aging and prevents mitosis after protein damage. p66 deletion retards aging and increases longevity of p44/p53 transgenic mice. Thus, oxidative stress activates a specific p53 transcriptional response, mediated by p44/p53 and p66, which regulates cellular senescence and aging.

Background and Purpose— Endovascular therapy has increasingly become the most common treatment for unruptured cerebral aneurysms in the United States. We evaluated a national, multi-hospital database to examine recent utilization trends and compare periprocedural outcomes between clipping and coiling treatments of unruptured aneurysms. Methods— The Premier Perspective database was used to identify patients hospitalized between 2006 to 2011 for unruptured cerebral aneurysm who underwent clipping or coiling therapy. A logistic propensity score was generated for each patient using relevant patient, procedure, and hospital variables, representing the probability of receiving clipping. Covariate balance was assessed using conditional logistic regression. Following propensity score adjustment using 1:1 matching methods, the risk of in-hospital mortality and morbidity was compared between clipping and coiling cohorts. Results— A total of 4899 unruptured aneurysm patients (1388 clipping, 3551 coiling) treated at 120 hospitals were identified. Following propensity score adjustment, clipping patients had a similar likelihood of in-hospital mortality (odds ratio [OR], 1.43; 95% confidence interval [CI], 0.49–4.44; P =0.47) but a significantly higher likelihood of unfavorable outcomes, including discharge to long-term care (OR, 4.78; 95% CI, 3.51–6.58; P <0.0001), ischemic complications (OR, 3.42; 95% CI, 2.39–4.99; P <0.0001), hemorrhagic complications (OR, 2.16; 95% CI, 1.33–3.57; P <0.0001), postoperative neurological complications (OR, 3.39; 95% CI, 2.25–5.22; P <0.0001), and ventriculostomy (OR, 2.10; 95% CI, 1.01–4.61; P =0.0320) compared with coiling patients. Conclusions— Among patients treated for unruptured intracranial aneurysms in a large sample of hospitals in the United States, clipping was associated with similar mortality risk but significantly higher periprocedural morbidity risk compared with coiling.