The Experts below are selected from a list of 14907 Experts worldwide ranked by ideXlab platform
Paul S Tofts - One of the best experts on this subject based on the ideXlab platform.
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improved accuracy of human cerebral blood perfusion measurements using arterial spin labeling accounting for Capillary water permeability
Magnetic Resonance in Medicine, 2002Co-Authors: Laura M Parkes, Paul S ToftsAbstract:A two-compartment exchange model for perfusion quantification using arterial spin labeling (ASL) is presented, which corrects for the assumption that the Capillary Wall has infinite permeability to water. The model incorporates an extravascular and a blood compartment with the permeability surface area product (PS) of the Capillary Wall characterizing the passage of water between the compartments. The new model predicts that labeled spins spend longer in the blood compartment before exchange. This makes an accurate blood T(1) measurement crucial for perfusion quantification; conversely, the tissue T(1) measurement is less important and may be unnecessary for pulsed ASL experiments. The model gives up to 62% reduction in perfusion estimate for human imaging at 1.5T compared to the single compartment model. For typical human perfusion rates at 1.5T it can be assumed that the venous outflow signal is negligible. This simplifies the solution, introducing only one more parameter than the single compartment model, PS/v(bw), where v(bw) is the fractional blood water volume per unit volume of tissue. The simplified model produces an improved fit to continuous ASL data collected at varying delay time. The fitting yields reasonable values for perfusion and PS/v(bw).
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improved accuracy of human cerebral blood perfusion measurements using arterial spin labeling accounting for Capillary water permeability
Magnetic Resonance in Medicine, 2002Co-Authors: Laura M Parkes, Paul S ToftsAbstract:A two-compartment exchange model for perfusion quantification using arterial spin labeling (ASL) is presented, which corrects for the assumption that the Capillary Wall has infinite permeability to water. The model incorporates an extravascular and a blood compartment with the permeability surface area product (PS) of the Capillary Wall characterizing the passage of water between the compartments. The new model predicts that labeled spins spend longer in the blood compartment before exchange. This makes an accurate blood T1 measurement crucial for perfusion quantification; conversely, the tissue T1 measurement is less important and may be unecessary for pulsed ASL experiments. The model gives up to 62% reduction in perfusion estimate for human imaging at 1.5T compared to the single compartment model. For typical human perfusion rates at 1.5T it can be assumed that the venous outflow signal is negligible. This simplifies the solution, introducing only one more parameter than the single compartment model, PS/vbw, where vbw is the fractional blood water volume per unit volume of tissue. The simplified model produces an improved fit to continuous ASL data collected at varying delay time. The fitting yields reasonable values for perfusion and PS/vbw. Magn Reson Med 48:27‐41, 2002. © 2002 Wiley-Liss, Inc.
Laura M Parkes - One of the best experts on this subject based on the ideXlab platform.
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improved accuracy of human cerebral blood perfusion measurements using arterial spin labeling accounting for Capillary water permeability
Magnetic Resonance in Medicine, 2002Co-Authors: Laura M Parkes, Paul S ToftsAbstract:A two-compartment exchange model for perfusion quantification using arterial spin labeling (ASL) is presented, which corrects for the assumption that the Capillary Wall has infinite permeability to water. The model incorporates an extravascular and a blood compartment with the permeability surface area product (PS) of the Capillary Wall characterizing the passage of water between the compartments. The new model predicts that labeled spins spend longer in the blood compartment before exchange. This makes an accurate blood T(1) measurement crucial for perfusion quantification; conversely, the tissue T(1) measurement is less important and may be unnecessary for pulsed ASL experiments. The model gives up to 62% reduction in perfusion estimate for human imaging at 1.5T compared to the single compartment model. For typical human perfusion rates at 1.5T it can be assumed that the venous outflow signal is negligible. This simplifies the solution, introducing only one more parameter than the single compartment model, PS/v(bw), where v(bw) is the fractional blood water volume per unit volume of tissue. The simplified model produces an improved fit to continuous ASL data collected at varying delay time. The fitting yields reasonable values for perfusion and PS/v(bw).
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improved accuracy of human cerebral blood perfusion measurements using arterial spin labeling accounting for Capillary water permeability
Magnetic Resonance in Medicine, 2002Co-Authors: Laura M Parkes, Paul S ToftsAbstract:A two-compartment exchange model for perfusion quantification using arterial spin labeling (ASL) is presented, which corrects for the assumption that the Capillary Wall has infinite permeability to water. The model incorporates an extravascular and a blood compartment with the permeability surface area product (PS) of the Capillary Wall characterizing the passage of water between the compartments. The new model predicts that labeled spins spend longer in the blood compartment before exchange. This makes an accurate blood T1 measurement crucial for perfusion quantification; conversely, the tissue T1 measurement is less important and may be unecessary for pulsed ASL experiments. The model gives up to 62% reduction in perfusion estimate for human imaging at 1.5T compared to the single compartment model. For typical human perfusion rates at 1.5T it can be assumed that the venous outflow signal is negligible. This simplifies the solution, introducing only one more parameter than the single compartment model, PS/vbw, where vbw is the fractional blood water volume per unit volume of tissue. The simplified model produces an improved fit to continuous ASL data collected at varying delay time. The fitting yields reasonable values for perfusion and PS/vbw. Magn Reson Med 48:27‐41, 2002. © 2002 Wiley-Liss, Inc.
Jeffrey H Miner - One of the best experts on this subject based on the ideXlab platform.
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the amphibian kidney s filtration barrier where is the glomerular basement membrane
American Journal of Physiology-renal Physiology, 2009Co-Authors: Jeffrey H MinerAbstract:to the editor: Tanner and colleagues ([8][1]) combined the imaging sensitivity of in vivo two-photon microscopy with the distinctive architecture of the salamander Necturus ' glomerular Capillary Wall (GCW) to investigate several important issues regarding the mechanisms of glomerular filtration and
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update on the glomerular filtration barrier
Current Opinion in Nephrology and Hypertension, 2009Co-Authors: George Jarad, Jeffrey H MinerAbstract:Purpose of the review The nephrology community lacks a unified view of protein sieving through the glomerular Capillary Wall (GCW). The GCW consists of three distinct but closely interacting layers: the fenestrated endothelium, with its glycocalyx; the podocytes, with their interdigitated foot processes and slit diaphragms; and the intervening glomerular basement membrane (GBM). Proteinuria is associated with abnormalities in any one layer, suggesting that each contributes to the glomerular filtration barrier (GFB). Proteinuria can also be induced in the context of a normal GCW. Here we review some classic studies as well as some newer concepts and present competing hypotheses about the GFB.
John B West - One of the best experts on this subject based on the ideXlab platform.
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invited review pulmonary Capillary stress failure
Journal of Applied Physiology, 2000Co-Authors: John B WestAbstract:The pulmonary blood-gas barrier is an extraordinary bioengineering structure because of its vast area but extreme thinness. Despite this, almost no attention has been given to its mechanical properties. The remarkable area and thinness come about because gas exchange occurs by passive diffusion. However, the barrier also needs to be immensely strong to withstand the very high stresses in the Capillary Wall when Capillary pressure rises during exercise. The strength of the thin region of the barrier comes from type IV collagen in the basement membranes. When the stresses in the Capillary Walls rise to high levels, ultrastructural changes occur in the barrier, a condition known as stress failure. Physiological conditions that alter the properties of the barrier include severe exercise in elite human athletes. Animals that have been selectively bred for high aerobic activity, such as Thoroughbred racehorses, consistently break their pulmonary capillaries during galloping. Pathophysiological conditions causing stress failure include high-altitude pulmonary edema and overinflation of the lung, which frequently occurs with mechanical ventilation. Remodeling of the Capillary Wall occurs in response to increased Wall stress in diseases such as mitral stenosis. The barrier is able to maintain its extreme thickness with sufficient strength as a result of continual regulation of its Wall structure. How it does this is a central problem in lung biology.
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structure strength failure and remodeling of the pulmonary blood gas barrier
Annual Review of Physiology, 1999Co-Authors: John B West, Odile MathieucostelloAbstract:The pulmonary blood-gas barrier needs to satisfy two conflicting requirements. It must be extremely thin for efficient gas exchange, but also immensely strong to withstand the extremely high stresses in the Capillary Wall when Capillary pressure rises during exercise. The strength of the blood-gas barrier on the thin side is attributable to the type IV collagen in the basement membranes. However, when the Wall stresses rise to very high levels, ultrastructural changes in the barrier occur, a condition known as stress failure. Physiological conditions that alter the properties of the barrier include intense exercise in elite human athletes. Some animals, such as Thoroughbred racehorses, consistently break their alveolar capillaries during galloping, causing hemorrhage. Pathophysiological conditions causing stress failure include neurogenic pulmonary edema, high-altitude pulmonary edema, left heart failure, and overinflation of the lung. Remodeling of the Capillary Wall occurs in response to increased Wall stress, a good example being the thickening of the Capillary basement membrane in diseases such as mitral stenosis. The blood-gas barrier is able to maintain its extreme thinness with sufficient strength only through continual regulation of its Wall structure. Recent experimental work suggests that rapid changes in gene expression for extracellular matrix proteins and growth factors occur in response to increases in Capillary Wall stress. How the blood-gas barrier is regulated to be extremely thin but sufficiently strong is a central issue in lung biology.
Jose Maria Gutierrez - One of the best experts on this subject based on the ideXlab platform.
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hemorrhage caused by snake venom metalloproteinases a journey of discovery and understanding
Toxins, 2016Co-Authors: Jose Maria Gutierrez, Alexandra Rucavado, Teresa Escalante, Cristina HerreraAbstract:The historical development of discoveries and conceptual frames for understanding the hemorrhagic activity induced by viperid snake venoms and by hemorrhagic metalloproteinases (SVMPs) present in these venoms is reviewed. Histological and ultrastructural tools allowed the identification of the Capillary network as the main site of action of SVMPs. After years of debate, biochemical developments demonstrated that all hemorrhagic toxins in viperid venoms are zinc-dependent metalloproteinases. Hemorrhagic SVMPs act by initially hydrolyzing key substrates at the basement membrane (BM) of capillaries. This degradation results in the weakening of the mechanical stability of the Capillary Wall, which becomes distended owing of the action of the hemodynamic biophysical forces operating in the circulation. As a consequence, the Capillary Wall is disrupted and extravasation occurs. SVMPs do not induce rapid toxicity to endothelial cells, and the pathological effects described in these cells in vivo result from the mechanical action of these hemodynamic forces. Experimental evidence suggests that degradation of type IV collagen, and perhaps also perlecan, is the key event in the onset of microvessel damage. It is necessary to study this phenomenon from a holistic, systemic perspective in which the action of other venom components is also taken into consideration.
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hemorrhage induced by snake venom metalloproteinases biochemical and biophysical mechanisms involved in microvessel damage
Toxicon, 2005Co-Authors: Jose Maria Gutierrez, Alexandra Rucavado, Teresa Escalante, Cecilia DiazAbstract:Zinc-dependent metalloproteinases are responsible for the hemorrhagic activity characteristic of viperid snake venoms. Snake venom metalloproteinases (SVMPs) are classified in various groups (P-I-IV), according to their domain composition. P-III SVMPs, comprising metalloproteinase, disintegrin-like and cysteine-rich domains, exert more potent hemorrhagic activity than P-I SVMPs, which present only the metalloproteinase domain. SVMPs degrade various components of the basement membrane and are also able to hydrolyze endothelial cell membrane proteins, such as integrins and cadherins, involved in cell-matrix and cell-cell adhesion. In addition, disintegrin-like and cysteine-rich domains interact with endothelial cell integrins, interfering with their adhesion to extracellular matrix. Hemorrhage induced by SVMPs is an extremely rapid event in vivo, with Capillary endothelial cells showing drastic structural alterations within few minutes. In contrast, observations in cell culture conditions do not evidence such rapid endothelial cell damage. Instead, the main effect is detachment and rounding of these cells; it is only after several hours of incubation that cells show evidence of apoptotic damage. This apparent discrepancy between in vivo and in vitro observations can be explained if biophysical forces operating on microvessels in vivo are taken into consideration. It is proposed that SVMP-induced hemorrhage occurs in vivo by a 'two-step' mechanism. Initially, SVMPs degrade basement membrane and adhesion proteins, thus weakening the Capillary Wall and perturbing the interactions between endothelial cells and the basement membrane. Then, transmural pressure acting on the weakened Capillary Wall causes distention. As a consequence, endothelial cells become very thin, until the integrity of the Capillary Wall is lost at some points, where extravasation occurs. In addition, endothelial cells become more susceptible to blood flow-dependent shear stress, which further contributes to Capillary Wall disruption.
