915 resultados para Spinal anesthesia
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We would like to thank the study participants and the clinical and research staff at the Queen Elizabeth National Spinal Injury Unit, as without them this study would not have been possible. We are grateful for the funding received from Glasgow Research Partnership in Engineering for the employment of SC during data collection for this study. We would like to thank the Royal Society of Edinburgh's Scottish Crucible scheme for providing the opportunity for this collaboration to occur. We are also indebted to Maria Dumitrascuta for her time and effort in producing inter-repeatability results for the shape models.
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We would like to thank the study participants and the clinical and research staff at the Queen Elizabeth National Spinal Injury Unit, as without them this study would not have been possible. We are grateful for the funding received from Glasgow Research Partnership in Engineering for the employment of SC during data collection for this study. We would like to thank the Royal Society of Edinburgh's Scottish Crucible scheme for providing the opportunity for this collaboration to occur. We are also indebted to Maria Dumitrascuta for her time and effort in producing inter-repeatability results for the shape models.
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© 2015 American Neurological Association. Funded by The Euan MacDonald Center for Motor Neurone Disease Research The SMA Trust Muscular Dystrophy UK The SMA Trust The SMA Trust Motor Neurone Disease Association National Institute for Health Research Great Ormond Street Hospital Biomedical Research Center Medical Research Council Great Ormond Street Hospital Charity
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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.
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Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.
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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.
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BACKGROUND: Preclinical studies have found differential effects of isoflurane and propofol on the Alzheimer's disease (AD)-associated markers tau, phosphorylated tau (p-tau) and amyloid-β (Aβ). OBJECTIVE: We asked whether isoflurane and propofol have differential effects on the tau/Aβ ratio (the primary outcome), and individual AD biomarkers. We also examined whether genetic/intraoperative factors influenced perioperative changes in AD biomarkers. METHODS: Patients undergoing neurosurgical/otolaryngology procedures requiring lumbar cerebrospinal fluid (CSF) drain placement were prospectively randomized to receive isoflurane (n = 21) or propofol (n = 18) for anesthetic maintenance. We measured perioperative CSF sample AD markers, performed genotyping assays, and examined intraoperative data from the electronic anesthesia record. A repeated measures ANOVA was used to examine changes in AD markers by anesthetic type over time. RESULTS: The CSF tau/Aβ ratio did not differ between isoflurane- versus propofol-treated patients (p = 1.000). CSF tau/Aβ ratio and tau levels increased 10 and 24 h after drain placement (p = 2.002×10-6 and p = 1.985×10-6, respectively), mean CSF p-tau levels decreased (p = 0.005), and Aβ levels did not change (p = 0.152). There was no interaction between anesthetic treatment and time for any of these biomarkers. None of the examined genetic polymorphisms, including ApoE4, were associated with tau increase (n = 9 polymorphisms, p > 0.05 for all associations). CONCLUSION: Neurosurgery/otolaryngology procedures are associated with an increase in the CSF tau/Aβ ratio, and this increase was not influenced by anesthetic type. The increased CSF tau/Aβ ratio was largely driven by increases in tau levels. Future work should determine the functional/prognostic significance of these perioperative CSF tau elevations.
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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.
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Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.
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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.
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Spinal cord injury (SCI) is a devastating neurological disorder that affects thousands of people each year. Although in recent decades significant progress has been made in relation to understanding the molecular and cellular events underlying the nervous damage, spinal cord injury is still a highly disabling condition for which there is no curative therapy. People affected by spinal cord injuries manifested dysfunction or loss, temporary or permanent, of motor, sensory and / or autonomic functions depending on the spinal lesion damaged. Currently, the incidence rate of this type of injury is approximately 15-40 cases per million people worldwide. At the origin of these lesions are: road accidents, falls, interpersonal violence and the practice of sports. In this work we placed the hypothesis that HA is one of the component of the scar tissue formed after a compressive SCI, that it is likely synthetised by the perilesional glial cells and that it might support the permeation of the glial scar during the late phase of SCI. Nowadays, much focus is drawn on the recovery of CNS function, made impossible after SCI due to the high content of sulfated proteoglycans in the extracellular matrix. Counterbalancing the ratio between these proteoglycans and hyaluronic acid could be one of the experimental therapy to re-permeate the glial scar tissue formed after SCI, making possible axonal regrowth and functional recovery. Therefore, we established a model of spinal cord compression in mice and studied the glial scar tissue, particularly through the characterization of the expression of enzymes related to the metabolism of HA and the subsequent concentration thereof at different distances of the lesion epicenter. Our results show that the lesion induced in mice shows results similar to those produced in human lesions, in terms of histologic similarities and behavioral results. but these animals demonstrate an impressive spontaneous reorganization mechanism of the spinal cord tissue that occurs after injury and allows for partial recovery of the functions of the CNS. As regards the study of the glial scar, changes were recorded at the level of mRNA expression of enzymes metabolizing HA i.e., after injury there was a decreased expression of HA synthases 1-2 (HAS 1-2) and an increase of the expression HAS3 synthase mRNA, as well as the enzymes responsible for the HA catabolism, HYAL 1-2. But the amount of HA measured through the ELISA test was found unchanged after injury, it is not possible to explain this fact only with the change of expression of enzymes. At two weeks and in response to SCI, we found synthesized HA by reactive astrocytes and probably by others like microglial cells as it was advanced by the HA/GFAP+ and HA/IBA1+ cells co-location.