Introduction: The use of forced-swim, rat-validated cognition tests in mouse models of traumatic brain injury (TBI) raises methodological concerns; such models are vulnerable to a number of confounding factors including impaired motor function and stress-induced non-compliance (failure to swim). This study evaluated the ability of a Radial Water Tread (RWT) maze, designed specifically for mice, that requires no swimming to distinguish mice with controlled cortical impact (CCI) induced TBI and Sham controls. Methods: Ten-week-old, male C57BL6/J mice were randomly assigned to receive either Sham (n = 14) or CCI surgeries (n = 15). Mice were tested for sensorimotor deficits via Gridwalk test and Noldus CatWalk gait analysis at 1 and 32 days post-injury. Mice received RWT testing at either 11 days (early time point) or 35 days (late time point) post-injury. Results: Compared to Sham-treated animals, CCI-induced TBI resulted in significant impairment in RWT maze performance. Additionally, CCI injured mice displayed significant deficits on the Gridwalk test at both 1 day and 32 days post-injury, and impairment in the CatWalk task at 1 day, but not 32 days, compared to Shams. Conclusions: The Radial Water Tread maze capitalizes on the natural tendency of mice to avoid open areas in favor of hugging the edges of an apparatus (thigmotaxis), and replaces a forced-swim model with water shallow enough that the animal is not required to swim, but aversive enough to motivate escape. Our findings indicate the RWT task is a sensitive species-appropriate behavioral test for evaluating spatial memory impairment in a mouse model of TBI.

Objective: Natural history studies of type B aortic dissection (TBAD) commonly report all-cause mortality. Our aim was to determine cause-specific mortality in TBAD and to evaluate the clinical characteristics associated with aorta-related and nonaorta-related mortality.Methods: Clinical and administrative records were reviewed for patients with acute TBAD between 1995 and 2017. Demographics, comorbidities, presentation, and initial imaging findings were abstracted. Cause of death was ascertained through a multimodality approach using electronic health records, obituaries, social media, Social Security Death Index, and state mortality records. Causes of death were classified as aorta related, nonaorta related, or unknown. A Fine-Gray multivariate competing risk regression model for subdistribution hazard ratio was employed to analyze the association of clinical characteristics with aorta-related and nonaorta-related mortality.Results: A total of 275 individuals met inclusion criteria (61.1 6 13.7 years, 70.9% male, 68% white). Mean survival after discharge was 6.3 6 4.7 years. Completeness of follow-up Clark C index was 0.87. All-cause mortality was 50.2% (n ¼ 138; mean age, 70.1 6 14.6 years) including an in-hospital mortality of 8.4%. Cause-specific mortality was aorta related, nonaorta related, and unknown in 51%, 43%, and 6%, respectively. Compared with patients with nonaorta-related mortality, patients with aorta-related mortality were younger at acute TBAD (69.5 6 11.2 years vs 61.6 6 15.5 years; P ¼ .001), underwent more descending thoracic aortic repairs (19.4% vs 45.8%; P ¼ .002), and had a shorter survival duration (5.7 6 3.9 vs 3.4 6 4.5 years; P ¼ .002). There was clear variation in cause of death by each decade of life, with higher aortarelated mortality among those younger than 50 years and older than 70 years and a stepwise increase in nonaortarelated mortality with each increasing decade (P < .001). All-cause mortality at 1 year, 3 years, and 10 years was 15%, 24%, and 57%, respectively. After accounting for competing risks, the cumulative incidence of aorta-related mortality at 1 year, 3 years, and 10 years was 8.9%, 16.5%, and 27.2%, respectively, and that of nonaorta-related mortality was 2.7%, 7.2%, and 29%, respectively. A maximum descending thoracic aortic diameter >4 cm was associated with an increase in hazard of aorta-related mortality by 84% (subdistribution hazard ratio, 1.84; 95% confidence interval, 1.03-3.28) on multivariate competing risk regression analysis.Conclusions: TBAD is associated with high 10-year mortality. Those at risk for aorta-related mortality have a clinical phenotype different from that of individuals at risk for nonaorta-related mortality. This information is important for building risk prediction models that account for competing mortality risks and to direct optimal and individualized surgical and medical management of TBAD.

True radial artery aneurysm in a patient with somatic mosaicism for a mutation in a platelet-derived growth factor receptor β gene,

65 years old had a prevalence of 4.3%. Among smokers, increased risk of AAA was found in current smokers (OR, 2.95; 2.10-4.15) and hypertensives (OR, 1.53; 1.11-2.11). There were no additional significant risk factors for nonsmokers. Conclusions: This study shows that there remain high-risk groups outside the current guidelines who would likely benefit from AAA screening, specifically male smokers 45 to 65 years old. Risk factors for AAA include male sex, smoking, cardiac disease, family history of AAA, and age.