Parallel Paradigm for Ultraparallel Multi-Scale Brain Blood Flow Simulations

Author(s):  
L. Grinberg ◽  
G.E. Karniadakis
2019 ◽  
Vol 191 ◽  
pp. 104254 ◽  
Author(s):  
Minh Tuan Nguyen ◽  
Byoung Jin Jeon ◽  
Hyuk-Jae Chang ◽  
Sang-Wook Lee

2000 ◽  
Vol 39 (02) ◽  
pp. 37-42 ◽  
Author(s):  
P. Hartikainen ◽  
J. T. Kuikka

Summary Aim: We demonstrate the heterogeneity of regional cerebral blood flow using a fractal approach and singlephoton emission computed tomography (SPECT). Method: Tc-99m-labelled ethylcysteine dimer was injected intravenously in 10 healthy controls and in 10 patients with dementia of frontal lobe type. The head was imaged with a gamma camera and transaxial, sagittal and coronal slices were reconstructed. Two hundred fifty-six symmetrical regions of interest (ROIs) were drawn onto each hemisphere of functioning brain matter. Fractal analysis was used to examine the spatial heterogeneity of blood flow as a function of the number of ROIs. Results: Relative dispersion (= coefficient of variation of the regional flows) was fractal-like in healthy subjects and could be characterized by a fractal dimension of 1.17 ± 0.05 (mean ± SD) for the left hemisphere and 1.15 ± 0.04 for the right hemisphere, respectively. The fractal dimension of 1.0 reflects completely homogeneous blood flow and 1.5 indicates a random blood flow distribution. Patients with dementia of frontal lobe type had a significantly lower fractal dimension of 1.04 ± 0.03 than in healthy controls. Conclusion: Within the limits of spatial resolution of SPECT, the heterogeneity of brain blood flow is well characterized by a fractal dimension. Fractal analysis may help brain scientists to assess age-, sex- and laterality-related anatomic and physiological changes of brain blood flow and possibly to improve precision of diagnostic information available for patient care.


Fluids ◽  
2020 ◽  
Vol 6 (1) ◽  
pp. 11
Author(s):  
Magnus Andersson ◽  
Matts Karlsson

Model verification, validation, and uncertainty quantification are essential procedures to estimate errors within cardiovascular flow modeling, where acceptable confidence levels are needed for clinical reliability. While more turbulent-like studies are frequently observed within the biofluid community, practical modeling guidelines are scarce. Verification procedures determine the agreement between the conceptual model and its numerical solution by comparing for example, discretization and phase-averaging-related errors of specific output parameters. This computational fluid dynamics (CFD) study presents a comprehensive and practical verification approach for pulsatile turbulent-like blood flow predictions by considering the amplitude and shape of the turbulence-related tensor field using anisotropic invariant mapping. These procedures were demonstrated by investigating the Reynolds stress tensor characteristics in a patient-specific aortic coarctation model, focusing on modeling-related errors associated with the spatiotemporal resolution and phase-averaging sampling size. Findings in this work suggest that attention should also be put on reducing phase-averaging related errors, as these could easily outweigh the errors associated with the spatiotemporal resolution when including too few cardiac cycles. Also, substantially more cycles are likely needed than typically reported for these flow regimes to sufficiently converge the phase-instant tensor characteristics. Here, higher degrees of active fluctuating directions, especially of lower amplitudes, appeared to be the most sensitive turbulence characteristics.


2007 ◽  
Vol 22 (3) ◽  
pp. 135-148 ◽  
Author(s):  
Daniel S. O'Leary ◽  
Robert I. Block ◽  
Julie A. Koeppel ◽  
Susan K. Schultz ◽  
Vincent A. Magnotta ◽  
...  

Author(s):  
Stanley M. Yamashiro ◽  
Takahide Kato

A minimal model of cerebral blood flow and respiratory control was developed to describe hypocapnic and hypercapnic responses. Important non-linear properties such as cerebral blood flow changes with arterial partial pressure of carbon dioxide (PaCO2) and associated time dependent circulatory time delays were included. It was also necessary to vary cerebral metabolic rate as a function of PaCO2. The cerebral blood flow model was added to a previously developed respiratory control model to simulate central and peripheral controller dynamics for humans. Model validation was based on previously collected data. The variable time delay due to brain blood flow changes in hypercapnia was an important determinant of predicted instability due to non-linear interaction in addition to linear loop gain considerations. Peripheral chemoreceptor gains above a critical level, but within normal limits, was necessary to produce instability. Instability was observed in recovery from hypercapnia and hypocapnia. The 20 sec breath-hold test appears to be a simple test of brain blood flow mediated instability in hypercapnia. Brain blood flow was predicted to play an important role with non-linear properties. There is an important interaction predicted by the current model between central and peripheral control mechanisms related to instability in hypercapnia recovery. Post hyperventilation breathing pattern can also reveal instability tied to brain blood flow. Previous data collected in patients with chronic obstructive lung disease was closely fitted with the current model and instability predicted. Brain vascular volume was proposed as a potential cause of instability despite cerebral autoregulation promoting constant brain flow.


1961 ◽  
Vol 16 (1) ◽  
pp. 1-7 ◽  
Author(s):  
John R. Marshall ◽  
Christian J. Lambertsen

In 379 mice subjected to from 1 to 11 atm. of pO2 and 0 to 304 mm Hg of pCO2 for 90 minutes, oxygen was convulsigenic at pressures greater than 3 atm. and lethal at greater than 4 atm. Carbon dioxide in 1 atm. of O2 was not convulsigenic but was lethal at very high tensions. In the presence of O2 at high pressure (OHP) small elevations of CO2 tension shortened the preconvulsive latent period, whereas CO2 tensions greater than 120 mm Hg inhibited convulsions. Survival time in OHP was shortened by the addition of CO2. An interaction between OHP and CO2 effects is suggested by both the preconvulsive latent period and survival time data. The effects of CO2 on OHP and electroshock convulsions are compared and possible reasons for differences are discussed in light of the previously demonstrated general cortical depression and inhibition of convulsions by CO2. The potentiation of OHP convulsions by low CO2 tensions is probably due to effects on brain blood flow. Although death can occur without convulsions there is a tendency for animals susceptible to convulsions to be also susceptible to the lethal properties of OHP with CO2. Submitted on July 28, 1960


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