Publications by authors named "Joshua J Avila"

Purpose: Delayed fracture healing is a common consequence of polytrauma (PT) occurring in patients with multiple injuries. We believe that when early release of high mobility group box 1 (HMGB1) molecules from necrotic tissues exceed their normal levels in blood, they dysregulate immune responses associated with normal healing. This study investigates the detrimental effect of such dysregulate immune responses by targeting HMGB1 in a PT rat model with debilitating injuries.

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The purpose of this study was to characterize the genetic contribution to endothelial adaptation to exercise training. Vasoreactivity was assessed in aortas from four inbred mouse strains (129S1, B6, NON, and SJL) after 4 weeks of moderate intensity continuous exercise training (MOD), high intensity interval training (HIT) or in sedentary controls (SED). Intrinsic variations in endothelium-dependent vasorelaxation (EDR) to acetylcholine (ACh) as well as vasocontractile responses were observed across SED groups.

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Quantitative trait loci for exercise capacity and training-induced changes in exercise capacity were identified previously on mouse Chromosome 14. The aim of this study was to further investigate the role of Chromosome 14 in exercise capacity and responses to training in mice. Exercise phenotypes were measured in chromosome substitution strain mice carrying Chromosome 14 from the PWD/PhJ donor strain on the genetic background of a host C57BL/6J (B6) strain (B6.

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Background: Singular traumatic insults, such as bone fracture, typically initiate an appropriate immune response necessary to restore the host to pre-insult homeostasis with limited damage to self. However, multiple concurrent insults, such as a combination of fracture, blunt force trauma, and burns (polytrauma), are clinically perceived to result in abnormal immune response leading to inadequate healing and resolution. To investigate this phenomenon, we created a model rat model of polytrauma.

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Changes in cardiorespiratory fitness in response to a standardized exercise training protocol differ substantially between individuals. Results from cross-sectional, twin, and family studies indicate genetics contribute to individual differences in both baseline exercise capacity and the response to training. Exercise capacity and responses to training also vary between inbred strains of mice.

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Understanding the genetic influence on vascular reactivity is important for identifying genes underlying impaired vascular function. The purpose of this study was to characterize the genetic contribution to intrinsic vascular function and to identify loci associated with phenotypic variation in vascular reactivity in mice. Concentration response curves to phenylephrine (PE), potassium chloride (KCl), acetylcholine (ACh), and sodium nitroprusside (SNP) were generated in aortic rings from male mice (12 wk old) from 27 inbred mouse strains.

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Genetic factors determining exercise capacity and the magnitude of the response to exercise training are poorly understood. The aim of this study was to identify quantitative trait loci (QTL) associated with exercise training in mice. Based on marked differences in training responses in inbred NZW (-0.

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Objectives: The aim of the study was to examine the additive effect of resistance training (RT) to a dietary education (DE) intervention on emerging coronary heart disease (CHD) risk factors, concentration of apolipoproteins B (apoB) and A-I (apoA-I), and Dietary Approaches to Stop Hypertension (DASH) Diet Index scores in overweight and obese older adults.

Patients And Methods: This was an ancillary study of a randomized clinical trial held in the Fall of 2008 at the University of Rhode Island. Participants were overweight or obese subjects (mean body mass index [BMI] of 31.

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The impact of resistance training has not been thoroughly examined in overweight older adults undergoing weight loss. Subjects (n = 27) were overweight and obese (BMI 31.7 +/- 3.

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