451 |
Examining the Regulation of Inflammation through CD200 and CD200R Following Spinal Cord InjuryBrautigam, Bryan A. January 2013 (has links)
No description available.
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452 |
SURFACE MODIFICATION OF TEXTILE FIBERS AND CORDS BY PLASMA POLYMERIZATION FOR IMPROVEMENT OF ADHESION TO POLYMERIC MATRICESLuo, Shijian 22 May 2002 (has links)
No description available.
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453 |
The effects of T-lymphocytes on secondary neurodegeneration and recovery of function after experimental spinal contusion injuryJones, T. Bucky 29 September 2004 (has links)
No description available.
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454 |
Re-educating the injured spinal cord by operant conditioning of a reflex pathwayChen, Yi 21 September 2006 (has links)
No description available.
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455 |
Role of the innate immune response and toll-like receptors following spinal cord injury in the mouseKigerl, Kristina Ann 28 November 2006 (has links)
No description available.
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456 |
Consequences of differential macrophage activation after spinal cord traumaLongbrake, Erin E. 17 May 2007 (has links)
No description available.
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457 |
Mechanisms of impaired humoral immunity after high thoracic spinal cord injuryLucin, Kurt M. 23 August 2007 (has links)
No description available.
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458 |
Mechanisms of Human CD34+ Stem Cell-Mediated Regulation of Osteoporosis in a Preclinical ModelAggarwal, Reeva 19 December 2012 (has links)
No description available.
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459 |
Adjustment to spinal cord injury : social support locus of control time since onset of injury /Smith, Patricia Ann January 1984 (has links)
No description available.
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460 |
Time and Frequency Domain Analysis of Physiological Features During Autonomic Dysreflexia After Spinal Cord InjuryAna K Kirby (13140681) 22 July 2022 (has links)
<p> </p>
<p>Persons with a spinal cord injury (SCI) often suffer from secondary complications including the dysfunction of the autonomic nervous system below the level of injury. For persons with a SCI at or above T6, autonomic dysreflexia (AD) may be triggered by noxious stimulation below the level of injury causing rapid sympathetic hyperactivation, leading to paroxysmal hypertension. If AD is not recognized and managed promptly, this increase in blood pressure can lead to stroke, organ damage, and/or death. Currently, AD is only detected in clinical settings through continuous blood pressure monitoring. Recent studies have revealed that rapid detection of AD is possible by using extracted features from electrocardiogram (ECG) data collected non-invasively and applying a five-layer neural network.</p>
<p>This project focuses on further characterization of physiological responses before and during AD to detect the overreaction of sympathetic nerve activity prior to the detrimental increase in hypertension. Using a rat model with implanted telemetry and noninvasive sensors, an acclimation protocol was developed to minimize noise and motion artifacts during data collection. We induced AD in a controlled manner using colorectal distention (CRD). We analyzed skin nerve activity (SKNA) and heart rate variability parameters in the time and frequency domain to improve the non-invasive detection of AD. A four-week acclimation protocol exposed a minimal increase in sympathetic activity during experimentation despite long periods of restraint. Results indicated an increase in SKNA features occurred about 18 seconds before the gold standard increase in blood pressure. Additionally, integrated SKNA features in the frequency domain quantified nerve activity and low frequency components were found to be dominant during AD, providing another parameter that could be included in an AD detection system to improve accuracy. In humans, SKNA may be used to alert patients of the onset of AD, allowing caretakers to respond quickly and make necessary changes to decrease the severe effects of AD.</p>
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