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Pulsatile Fluid Flow (pulsatile + fluid_flow)

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Medical Sciences100%

Selected Abstracts

Tumor necrosis factor , and interleukin-1, modulate calcium and nitric oxide signaling in mechanically stimulated osteocytes

ARTHRITIS & RHEUMATISM, Issue 11 2009
A. D. Bakker
Objective Inflammatory diseases often coincide with reduced bone mass. Mechanoresponsive osteocytes regulate bone mass by maintaining the balance between bone formation and resorption. Despite its biologic significance, the effect of inflammation on osteocyte mechanoresponsiveness is not understood. To fill this gap, we investigated whether the inflammatory cytokines tumor necrosis factor , (TNF,) and interleukin-1, (IL-1,) modulate the osteocyte response to mechanical loading. Methods MLO-Y4 osteocytes were incubated with TNF, (0.5,30 ng/ml) or IL-1, (0.1,10 ng/ml) for 30 minutes or 24 hours, or with calcium inhibitors for 30 minutes. Cells were subjected to mechanical loading by pulsatile fluid flow (mean ± amplitude 0.7 ± 0.3 Pa, 5 Hz), and the response was quantified by measuring nitric oxide (NO) production using Griess reagent and by measuring intracellular calcium concentration ([Ca2+]i) using Fluo-4/AM. Focal adhesions and filamentous actin (F-actin) were visualized by immunostaining, and apoptosis was quantified by measuring caspase 3/7 activity. Cell-generated tractions were quantified using traction force microscopy, and cytoskeletal stiffness was quantified using optical magnetic twisting cytometry. Results Pulsatile fluid flow increased [Ca2+]i within seconds (in 13% of cells) and NO production within 5 minutes (4.7-fold). TNF, and IL-1, inhibited these responses. Calcium inhibitors decreased pulsatile fluid flow,induced NO production. TNF, and IL-1, affected cytoskeletal stiffness, likely because 24 hours of incubation with TNF, and IL-1, decreased the amount of F-actin. Incubation with IL-1, for 24 hours stimulated osteocyte apoptosis. Conclusion Our results suggest that TNF, and IL-1, inhibit mechanical loading,induced NO production by osteocytes via abrogation of pulsatile fluid flow,stimulated [Ca2+]i, and that IL-1, stimulates osteocyte apoptosis. Since both NO and osteocyte apoptosis affect osteoclasts, these findings provide a mechanism by which inflammatory cytokines might contribute to bone loss and consequently affect bone mass in rheumatoid arthritis. [source]

Feasibility of k-t BLAST technique for measuring "seven-dimensional" fluid flow

JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2006
Ian Marshall PhD
Abstract Purpose To investigate the feasibility of rapid MR measurement of "seven-dimensional" (three velocity components, three dimensions, and time) fluid flow using the k-t Broad-use Linear Acquisition Speed-Up Technique (BLAST). Materials and Methods Complete k -space data were acquired for pulsatile fluid flow in a model of a stenosed carotid bifurcation. The data was subsampled to simulate "training" and "accelerated acquisition" data for reconstruction using k-t BLAST. Results Flow waveforms estimated from k-t BLAST reconstructions were in good agreement with those measured from the full data set for overall speedup factors up to approximately four times when slice-by-slice undersampling in ky was used. Accuracy was better than 25 mm/second or 7% (root-mean-square error) for individual time frames under these conditions. Flow patterns in the plane of symmetry, near the bifurcation, and in the stenosis were also in good agreement with those reconstructed from the full data set. Improved performance was obtained from undersampling in both ky and kz, when acceleration factors up to 12 times gave acceptable results. Conclusion The k-t BLAST technique can be applied to flow quantification, and may make feasible the acquisition of time-resolved blood flow from extended arterial regions within acceptable examination times. J. Magn. Reson. Imaging 2006. © 2006 Wiley-Liss, Inc. [source]

MRI measurement of time-resolved wall shear stress vectors in a carotid bifurcation model, and comparison with CFD predictions

JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2003
Panorea Papathanasopoulou MSc
Abstract Purpose To study pulsatile fluid flow in a physiologically realistic model of the human carotid bifurcation, and to derive wall shear stress (WSS) vectors. Materials and Methods WSS vectors were calculated from time-resolved 3D phase-contrast (PC) MRI measurements of the velocity field. The technique was first validated with sinusoidal flow in a straight tube, and then used in a model of a healthy human carotid bifurcation. Velocity measurements in the inflow and outflow regions were also used as boundary conditions for computational fluid dynamics (CFD) calculations of WSS, which were compared with those derived from MRI alone. Results The straight tube measurements gave WSS results that were within 15% of the theoretical value. WSS results for the phantom showed the main features expected from fluid dynamics, notably the low values in the bulb region of the internal carotid artery, with a return to ordered flow further downstream. MRI was not able to detect the high WSS values along the divider wall that were predicted by the CFD model. Otherwise, there was good general agreement between MRI and CFD. Conclusion This is the first report of time-resolved WSS vectors estimated from 3D-MRI data. The technique worked well except in regions of disturbed flow, where the combination with CFD modeling is clearly advantageous. J. Magn. Reson. Imaging 2003;17:153,162. © 2003 Wiley-Liss, Inc. [source]

Tumor necrosis factor , and interleukin-1, modulate calcium and nitric oxide signaling in mechanically stimulated osteocytes

ARTHRITIS & RHEUMATISM, Issue 11 2009
A. D. Bakker
Objective Inflammatory diseases often coincide with reduced bone mass. Mechanoresponsive osteocytes regulate bone mass by maintaining the balance between bone formation and resorption. Despite its biologic significance, the effect of inflammation on osteocyte mechanoresponsiveness is not understood. To fill this gap, we investigated whether the inflammatory cytokines tumor necrosis factor , (TNF,) and interleukin-1, (IL-1,) modulate the osteocyte response to mechanical loading. Methods MLO-Y4 osteocytes were incubated with TNF, (0.5,30 ng/ml) or IL-1, (0.1,10 ng/ml) for 30 minutes or 24 hours, or with calcium inhibitors for 30 minutes. Cells were subjected to mechanical loading by pulsatile fluid flow (mean ± amplitude 0.7 ± 0.3 Pa, 5 Hz), and the response was quantified by measuring nitric oxide (NO) production using Griess reagent and by measuring intracellular calcium concentration ([Ca2+]i) using Fluo-4/AM. Focal adhesions and filamentous actin (F-actin) were visualized by immunostaining, and apoptosis was quantified by measuring caspase 3/7 activity. Cell-generated tractions were quantified using traction force microscopy, and cytoskeletal stiffness was quantified using optical magnetic twisting cytometry. Results Pulsatile fluid flow increased [Ca2+]i within seconds (in 13% of cells) and NO production within 5 minutes (4.7-fold). TNF, and IL-1, inhibited these responses. Calcium inhibitors decreased pulsatile fluid flow,induced NO production. TNF, and IL-1, affected cytoskeletal stiffness, likely because 24 hours of incubation with TNF, and IL-1, decreased the amount of F-actin. Incubation with IL-1, for 24 hours stimulated osteocyte apoptosis. Conclusion Our results suggest that TNF, and IL-1, inhibit mechanical loading,induced NO production by osteocytes via abrogation of pulsatile fluid flow,stimulated [Ca2+]i, and that IL-1, stimulates osteocyte apoptosis. Since both NO and osteocyte apoptosis affect osteoclasts, these findings provide a mechanism by which inflammatory cytokines might contribute to bone loss and consequently affect bone mass in rheumatoid arthritis. [source]