The Experts below are selected from a list of 282 Experts worldwide ranked by ideXlab platform
Eelco F M Wijdicks - One of the best experts on this subject based on the ideXlab platform.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2012Co-Authors: Jennifer E Fugate, Grant W. Mallory, Eelco F M WijdicksAbstract:Background Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, Parenchymal hematoma, or seizures. Methods Case report. Results A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem Parenchyma and ventricles. Conclusions Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem Parenchyma rather than oculomotor nerve injury from compression or stretch.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2011Co-Authors: Jennifer E Fugate, Grant W. Mallory, Eelco F M WijdicksAbstract:Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, Parenchymal hematoma, or seizures. Case report. A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem Parenchyma and ventricles. Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem Parenchyma rather than oculomotor nerve injury from compression or stretch.
Jason H. T. Bates - One of the best experts on this subject based on the ideXlab platform.
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airway Parenchymal interdependence in the lung slice
Respiratory Physiology & Neurobiology, 2013Co-Authors: Michael J Sanderson, Jason H. T. BatesAbstract:The explanted lung slice has become a popular in vitro system for studying how airways contract. Because the forces of airway-Parenchymal interdependence are such important modulators of airway narrowing, it is of significant interest to understand how the Parenchyma around a constricting airway in a lung slice behaves. We have previously shown that the predictions of the 2-dimensional distortion field around a constricting airway are substantially different depending on whether the Parenchyma is modeled as an elastic continuum versus a network of hexagonally arranged springs, which raises the question as to which model best explains the lung slice. We treated lung slices with methacholine and then followed the movement of a set of Parenchymal landmarks around the airway as it narrowed. The resulting Parenchymal displacement field was compared to the displacement fields predicted by the continuum and hexagonal spring network models. The predictions of the continuum model were much closer to the measured data than were those of the hexagonal spring network model, suggesting that the Parenchyma in the lung slice behaves like an elastic continuum rather than a network of discrete springs. This may be because the alveoli of the lung slice are filled with agarose in order to provide structural stability, causing the Parenchyma in the slice to act like a true mechanical continuum. How the air-filled Parenchyma in the intact lung behave in vivo remains an open question.
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influence of airway wall stiffness and Parenchymal tethering on the dynamics of bronchoconstriction
American Journal of Physiology-lung Cellular and Molecular Physiology, 2010Co-Authors: Mohammad A Khan, Michael J Sanderson, Jason H. T. Bates, Russ Ellis, Mark D Inman, Luke J JanssenAbstract:Understanding how tissue remodeling affects airway responsiveness is of key importance, but experimental data bearing on this issue remain scant. We used lung explants to investigate the effects of enzymatic digestion on the rate and magnitude of airway narrowing induced by acetylcholine. To link the observed changes in narrowing dynamics to the degree of alteration in tissue mechanics, we compared our experimental results with predictions made by a computational model of a dynamically contracting elastic airway embedded in elastic Parenchyma. We found that treatment of explanted airways with two different proteases (elastase and collagenase) resulted in differential effects on the dynamics of airway narrowing following application of ACh. Histological corroboration of these different effects is manifest in different patterns of elimination of collagen and elastin from within the airway wall and the surrounding Parenchyma. Simulations with a computational model of a dynamically contracting airway embedded in elastic Parenchyma suggest that elastase exerts its functional effects predominately through a reduction in Parenchymal tethering, while the effects of collagenase are more related to a reduction in airway wall stiffness. We conclude that airway and Parenchymal remodeling as a result of protease activity can have varied effects on the loads opposing ASM shortening, with corresponding consequences for airway responsiveness.
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Parenchymal tethering airway wall stiffness and the dynamics of bronchoconstriction
Journal of Applied Physiology, 2007Co-Authors: Jason H. T. Bates, Anne-marie LauzonAbstract:We do not yet have a good quantitative understanding of how the force-velocity properties of airway smooth muscle interact with the opposing loads of Parenchymal tethering and airway wall stiffness to produce the dynamics of bronchoconstriction. We therefore developed a two-dimensional computational model of a dynamically narrowing airway embedded in uniformly elastic lung Parenchyma and compared the predictions of the model to published measurements of airway resistance made in rats and rabbits during the development of bronchoconstriction following a bolus injection of methacholine. The model accurately reproduced the experimental time-courses of airway resistance as a function of both lung inflation pressure and tidal volume. The model also showed that the stiffness of the airway wall is similar in rats and rabbits, and significantly greater than that of the lung Parenchyma. Our results indicate that the main features of the dynamical nature of bronchoconstriction in vivo can be understood in terms of the classic Hill force-velocity relationship operating against elastic loads provided by the surrounding lung Parenchyma and an airway wall that is stiffer than the Parenchyma.
Kevin C Oconnor - One of the best experts on this subject based on the ideXlab platform.
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related b cell clones populate the meninges and Parenchyma of patients with multiple sclerosis
Brain, 2011Co-Authors: Laura Lovato, Simon N Willis, Scott J Rodig, Tyler Caron, Stefany Almendinger, Owain W Howell, Richard Reynolds, Kevin C OconnorAbstract:In the central nervous system of patients with multiple sclerosis, B cell aggregates populate the meninges, raising the central question as to whether these structures relate to the B cell infiltrates found in Parenchymal lesions or instead, represent a separate central nervous system immune compartment. We characterized the repertoires derived from meningeal B cell aggregates and the corresponding Parenchymal infiltrates from brain tissue derived primarily from patients with progressive multiple sclerosis. The majority of expanded antigen-experienced B cell clones derived from meningeal aggregates were also present in the Parenchyma. We extended this investigation to include 20 grey matter specimens containing meninges, 26 inflammatory plaques, 19 areas of normal appearing white matter and cerebral spinal fluid. Analysis of 1833 B cell receptor heavy chain variable region sequences demonstrated that antigen-experienced clones were consistently shared among these distinct compartments. This study establishes a relationship between extraParenchymal lymphoid tissue and Parenchymal infiltrates and defines the arrangement of B cell clones that populate the central nervous system of patients with multiple sclerosis.
Jennifer E Fugate - One of the best experts on this subject based on the ideXlab platform.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2012Co-Authors: Jennifer E Fugate, Grant W. Mallory, Eelco F M WijdicksAbstract:Background Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, Parenchymal hematoma, or seizures. Methods Case report. Results A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem Parenchyma and ventricles. Conclusions Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem Parenchyma rather than oculomotor nerve injury from compression or stretch.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2011Co-Authors: Jennifer E Fugate, Grant W. Mallory, Eelco F M WijdicksAbstract:Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, Parenchymal hematoma, or seizures. Case report. A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem Parenchyma and ventricles. Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem Parenchyma rather than oculomotor nerve injury from compression or stretch.
Anne-marie Lauzon - One of the best experts on this subject based on the ideXlab platform.
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Parenchymal tethering airway wall stiffness and the dynamics of bronchoconstriction
Journal of Applied Physiology, 2007Co-Authors: Jason H. T. Bates, Anne-marie LauzonAbstract:We do not yet have a good quantitative understanding of how the force-velocity properties of airway smooth muscle interact with the opposing loads of Parenchymal tethering and airway wall stiffness to produce the dynamics of bronchoconstriction. We therefore developed a two-dimensional computational model of a dynamically narrowing airway embedded in uniformly elastic lung Parenchyma and compared the predictions of the model to published measurements of airway resistance made in rats and rabbits during the development of bronchoconstriction following a bolus injection of methacholine. The model accurately reproduced the experimental time-courses of airway resistance as a function of both lung inflation pressure and tidal volume. The model also showed that the stiffness of the airway wall is similar in rats and rabbits, and significantly greater than that of the lung Parenchyma. Our results indicate that the main features of the dynamical nature of bronchoconstriction in vivo can be understood in terms of the classic Hill force-velocity relationship operating against elastic loads provided by the surrounding lung Parenchyma and an airway wall that is stiffer than the Parenchyma.