Hospitals often promote healthy lifestyles, but little is known about nurses’ actual diet and physical activity. Greater understanding about these lifestyle choices for clinical nurses may improve existing hospital-based programs and/or create desirable services. This article discusses a study that considered diet and physical activity of clinical nurses, using elements of Pender’s self-care theory as a conceptual framework. Study methods included a cross-sectional, correlational design and a convenience sample of 278 nurses who worked on units with 24 hours/day and seven days-per-week responsibilities. Participants completed diet and exercise questionnaires about perceptions of attitudes and opinions, barriers, diet benefits/exercise motivators, self-efficacy, and locus of control, and personal and work characteristics. Diet and activity categories were created. Study results demonstrated that over 50% of nurses had moderately healthy diets but were insufficiently active. Healthy diet and physical activity levels were associated with higher self-efficacy, more diet benefits and physical activity motivators, fewer perceived barriers, and confidence in body image. The article discussion and conclusion sections note areas for future research and suggest that focused interventions that address benefits, motivators, and self-efficacy may increase participation in hospital-based programs and enhance healthy lifestyle for hospital-based clinical nurses.

Background/Objectives: Fluid dynamic models of the cerebral vasculature are being developed to evaluate intracranial vascular pathology. Fluid–structure interaction modeling provides an opportunity for more accurate simulation of vascular pathology by modelling the vessel wall itself in conjunction with the fluid forces. Accuracy of these models is heavily dependent on the parameters used. Of those studied, elastin has been considered a key component used in aortic and common carotid artery modeling. We studied elastin thickness to determine if there was significant variation between cerebral artery territories to suggest its importance in cerebral blood vessel biomechanical response and provide reference data for modeling intracranial elastin. Elastin thickness was compared to vessel location, thickness, diameter, and laterality within human intracranial arteries. Methods: Tissue was taken from five human cadaveric heads preserved in formaldehyde from each intracranial vessel distribution bilaterally and stained with Van Gieson stain for elastin. A total of 160 normal cerebral vascular artery specimens were obtained from 17 different cerebrovascular regions. Two reviewers measured elastin thickness for each sample at five different locations per sample using Aperio ImageScope (Leica Biosystems, Deer Park, IL, USA). Statistical analysis of the samples was performed using mixed-models repeated measures regression methods. Results: There was a significant difference between anterior circulation (6.01 µm) and posterior circulation (4.4 µm) vessel elastin thickness (p-value < 0.05). Additionally, two predictive models of elastin thickness were presented, utilizing a combination of anterior versus posterior circulation, vessel diameter, and vessel wall thickness, which demonstrated significance for prediction with anterior versus posterior combined with vessel diameter and wall thickness. Conclusions: Elastin thicknesses are significantly different between anterior and posterior circulation vessels, which may explain the differences seen in aneurysm rupture risk for anterior versus posterior circulation aneurysms. Additionally, we propose two potential models for predicting elastin thickness based on vessel location, vessel diameter, and vessel wall thickness, all of which can be obtained using preoperative imaging techniques. These findings suggest that elastin plays an important role in cerebral vascular wall integrity, and this data will further enable fluid–structure interaction modeling parameters to be more precise in an effort to provide predictive modeling for cerebrovascular pathology.

Barrett’s esophagus (BE), a consequence of gastroesophageal reflux disease (GERD), is a premalignant condition for esophageal adenocarcinoma. Impaired gastric emptying leads to increased gastric volume and therefore more severe reflux. We seek to investigate the association between gastroparesis and BE and the predictors of BE among patients with gastroparesis. This is a retrospective review of patients seen at Cleveland Clinic between 2011 and 2016 who had an upper endoscopy and a gastric emptying study. Demographics, symptoms, medications, endoscopic and histological findings, and therapeutic interventions were abstracted. Risk of BE among gastroparesis group and control group was assessed, and logistic regression analysis was performed to identify predictors of BE among gastroparesis patients. Of the 4,154 patients, 864 (20.8%) had gastroparesis and 3, 290 (79.2%) had normal gastric emptying. The mean age was 51.4 ± 16.4 years, 72% were women and 80% were Caucasians. Among the gastroparesis group, 18 (2.1%) patients had BE compared to 71 (2.2%) cases of BE in the control group, P = 0.89. There were no differences in gender, race, reflux symptoms, or esophageal findings between the two groups. Among gastroparesis group, predictors of developing BE were a history of alcohol use (odds ratio [OR] 6.76; 95% confidence intervals [CI]: 1.65–27.67, P = 0.008), history of pyloroplasty (OR: 8.228; CI: 2.114–32.016, P = 0.002), and hiatal hernia (OR: 8.014; CI: 2.053–31.277, P = 0.003). Though gastroparesis is a known contributing factor for GERD, there was no increased prevalence of BE in gastroparesis. Among patients with gastroparesis, predictors of BE are history of alcohol use, hiatal hernia, and pyloroplasty.