Perivascular Adipose Tissue Diminishes Nitric Oxide Bioavailability in Metabolic Syndrome

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Exercise Improves Vascular Dilator Reactivity in Chronically Stressed Rats with Pre-existing Metabolic Syndrome

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Exercise as a Treatment for Peripheral Vascular Dysfunction Caused by Metabolic Syndrome and Depression

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Correlation of Pain Scores, Analgesic Use, and Beck Anxiety Inventory Scores During Hospitalization in Lower Extremity Amputees

Post amputation pain can be debilitating for patients and families. Chronic pain is a common phenomenon after lower extremity amputation, occurring in up to 80% of this population. The purpose of this pilot study was to correlate post amputation pain scores to opioid analgesic consumption and Beck Anxiety Inventory (BAI) scores. Twenty-three patients with lower extremity amputation at an 827-bed acute care inner-city hospital were surveyed pre-operatively and post-operatively to determine if there was a significant correlation between anxiety and pain. A numeric scale was utilized by patients to rate their pain level, while the BAI was utilized to measure their anxiety levels

Aortic dysfunction in metabolic syndrome mediated by perivascular adipose tissue TNFα- and NOX2-dependent pathway

Aims—Perivascular adipose tissue (PVAT) is recognized for its vaso-active effects, however it’s unclear how Metabolic Syndrome impact thoracic-aorta (t)PVAT and the subsequent effect on functional and structural aortic stiffness. Methods & Results—Thoracic aorta and tPVAT were removed from 16–17 week old lean (LZR, n=16) and obese Zucker (OZR, n=16) rats. OZR presented with aortic endothelial dysfunction, assessed by wire-myography, and increased aortic stiffness, assessed by elastic modulus. OZR-tPVAT exudate further exacerbated the endothelial dysfunction reducing nitric oxide and endothelial dependent relaxation (p \u3c0.05). Additionally, OZR-tPVAT exudate had increased MMP9 activity (p\u3c0.05) and further increased elastic modulus of the aorta following 72- hours of coculture (p\u3c0.05). We found the observed aortic dysfunction caused by OZR-tPVAT was mediated through increased production and release of TNFα (p\u3c0.01), which was dependent on tPVAT NADPH-oxidase 2 (NOX2) activity. OZR-tPVAT ROS and subsequent aortic dysfunction was inhibited by TNFα neutralization and/ or inhibition of NOX2. Additionally, we found OZRtPVAT had reduced activity of the 20S proteasome’s active sites (p\u3c0.05) and reduced superoxide dismutase activity (p\u3c0.01). Conclusion—Metabolic syndrome causes tPVAT dysfunction through interplay between TNFα and NOX2 leading to tPVAT mediated aortic stiffness by activation of aortic ROS and increased MMP9 activity

Chronic exposure to electronic cigarettes results in impaired cardiovascular function in mice

Proponents for electronic cigarettes (E-cigs) claim that they are a safe alternative to tobacco-based cigarettes; however, little is known about the long-term effects of exposure to E-cig vapor on vascular function. The purpose of this study was to determine the cardiovascular consequences of chronic E-cig exposure. Female mice (C57BL/6 background strain) were randomly assigned to chronic daily exposure to E-cig vapor, standard (3R4F reference) cigarette smoke, or filtered air (n = 15/group). Respective whole body exposures consisted of four 1-h-exposure time blocks, separated by 30-min intervals of fresh air breaks, resulting in intermittent daily exposure for a total of 4 h/day, 5 days/wk for 8 mo. Noninvasive ultrasonography was used to assess cardiac function and aortic arterial stiffness (AS), measured as pulse wave velocity, at three times points (before, during, and after chronic exposure). Upon completion of the 8-mo exposure, ex vivo wire tension myography and force transduction were used to measure changes in thoracic aortic tension in response to vasoactive-inducing compounds. AS increased 2.5- and 2.8-fold in E-cig- and 3R4F-exposed mice, respectively, compared with air-exposed control mice (P \u3c 0.05). The maximal aortic relaxation to methacholine was 24% and 33% lower in E-cig- and 3R4F-exposed mice, respectively, than in controls (P \u3c 0.05). No differences were noted in sodium nitroprusside dilation between the groups. 3R4F exposure altered cardiac function by reducing fractional shortening and ejection fraction after 8 mo (P \u3c 0.05). A similar, although not statistically significant, tendency was also observed with E-cig exposure (P \u3c 0.10). Histological and respiratory function data support emphysema-associated changes in 3R4F-exposed, but not E-cig-exposed, mice. Chronic exposure to E-cig vapor accelerates AS, significantly impairs aortic endothelial function, and may lead to impaired cardiac function. The clinical implication from this study is that chronic use of E-cigs, even at relatively low exposure levels, induces cardiovascular dysfunction. NEW & NOTEWORTHY Electronic cigarettes (E-cigs) are marketed as safe, but there has been insufficient long-term exposure to humans to justify these claims. This is the first study to report the long-term in vivo vascular consequences of 8 mo of exposure to E-cig vapor in mice (equivalent to ~25 yr of exposure in humans). We report that E-cig exposure increases arterial stiffness and impairs normal vascular reactivity responses, similar to other risk factors, including cigarette smoking, which contribute to the development of cardiovascular disease

A Dual-Use Unmanned Aerial System for Precision Agriculture and Search and Rescue Applications

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140562/1/6.2016-0743.pd

Late-Emigrating Trunk Neural Crest Cells In Turtle Embryos Generate An Osteogenic Ectomesenchyme In The Plastron

Background: The turtle plastron is composed of a keratinized epidermis overlying nine dermal bones. Its developmental origin has been controversial; recent evidence suggests that the plastral bones derive from trunk neural crest cells (NCCs). Results: This study extends the observations that there is a turtle-specific, second wave of trunk NCC delamination and migration, after the original NCCs have reached their destination and differentiated. This second wave was confirmed by immunohistochemistry in whole-mounts and serial sections, by injecting DiI (1,1, di-octadecyl-3,3,3,3,-tetramethylindo-carbocyanine perchlorate) into the lumen of the neural tube and tracing labeled cells into the plastron, and by isolating neural tubes from older turtle embryos and observing delaminating NCCs. This later migration gives rise to a plastral ectomesenchyme that expresses NCC markers and can be induced to initiate bone formation. Conclusions: The NCCs of this second migration have properties similar to those of the earlier NCCs, but also express markers characteristic of cranial NCCs. The majority of the cells of the plastron mesenchyme express neural crest markers, and have osteogenic differentiation capabilities that are similar or identical to craniofacial ectomesenchyme. Our evidence supports the contention that turtle plastron bones are derived from a late emigrating population of cells derived from the trunk neural crest. Developmental Dynamics 242:1223-1235, 2013. (c) 2013 Wiley Periodicals, Inc