Simultaneous multislice triple-echo steady-state (SMS-TESS) T1, T2, PD, and off-resonance mapping in the human brain

2018 ◽  
Vol 80 (3) ◽  
pp. 1088-1100 ◽  
Author(s):  
Rahel Heule ◽  
Zarko Celicanin ◽  
Sebastian Kozerke ◽  
Oliver Bieri
Keyword(s):  
Steady State ◽  
Human Brain ◽  
Simultaneous Multislice

Sequential dynamic susceptibility contrast MR experiments in human brain: Residual contrast agent effect, steady state, and hemodynamic perturbation

1995 ◽  
Vol 34 (5) ◽  
pp. 655-663 ◽  
Author(s):  
Jonathan M. Levin ◽  
Marc J. Kaufman ◽  
Marjorie H. Ross ◽  
Jack H. Mendelson ◽  
Luis C. Maas ◽  
...  
Keyword(s):  
Steady State ◽  
Human Brain ◽  
Contrast Agent ◽  
Dynamic Susceptibility ◽  
Dynamic Susceptibility Contrast ◽  
Susceptibility Contrast

scholarly journals Differentiation of Glucose Transport in Human Brain Gray and White Matter

2001 ◽  
Vol 21 (5) ◽  
pp. 483-492 ◽  
Author(s):  
Robin A. de Graaf ◽  
Jullie W. Pan ◽  
Frank Telang ◽  
Jing-Huei Lee ◽  
Peter Brown ◽  
...  
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Steady State ◽  
White Matter ◽  
Magnetic Resonance ◽  
Human Brain ◽  
Glucose Transport ◽  
Gray Matter ◽  
Transport Model ◽  
Transport Activity ◽  
Brain Glucose

Localized 1H nuclear magnetic resonance spectroscopy has been applied to determine human brain gray matter and white matter glucose transport kinetics by measuring the steady-state glucose concentration under normoglycemia and two levels of hyperglycemia. Nuclear magnetic resonance spectroscopic measurements were simultaneously performed on three 12-mL volumes, containing predominantly gray or white matter. The exact volume compositions were determined from quantitative T1 relaxation magnetic resonance images. The absolute brain glucose concentration as a function of the plasma glucose level was fitted with two kinetic transport models, based on standard (irreversible) or reversible Michaelis-Menten kinetics. The steady-state brain glucose levels were similar for cerebral gray and white matter, although the white matter levels were consistently 15% to 20% higher. The ratio of the maximum glucose transport rate, Vmax, to the cerebral metabolic utilization rate of glucose, CMRGlc, was 3.2 ± 0.10 and 3.9 ± 0.15 for gray matter and white matter using the standard transport model and 1.8 ± 0.10 and 2.2 ± 0.12 for gray matter and white matter using the reversible transport model. The Michaelis-Menten constant Km was 6.2 ± 0.85 and 7.3 ± 1.1 mmol/L for gray matter and white matter in the standard model and 1.1 ± 0.66 and 1.7 ± 0.88 mmol/L in the reversible model. Taking into account the threefold lower rate of CMRGlc in white matter, this finding suggests that blood–brain barrier glucose transport activity is lower by a similar amount in white matter. The regulation of glucose transport activity at the blood–brain barrier may be an important mechanism for maintaining glucose homeostasis throughout the cerebral cortex.

scholarly journals Simultaneous measurement of glucose transport and utilization in the human brain

2011 ◽  
Vol 301 (5) ◽  
pp. E1040-E1049 ◽  
Author(s):  
Alexander A. Shestov ◽  
Uzay E. Emir ◽  
Anjali Kumar ◽  
Pierre-Gilles Henry ◽  
Elizabeth R. Seaquist ◽  
...  
Keyword(s):  
Steady State ◽  
Human Brain ◽  
Kinetic Parameters ◽  
Glucose Transport ◽  
Plasma Glucose ◽  
Data Extraction ◽  
Glucose Levels ◽  
H Nmr ◽  
Time Courses ◽  
State Models

Glucose is the primary fuel for brain function, and determining the kinetics of cerebral glucose transport and utilization is critical for quantifying cerebral energy metabolism. The kinetic parameters of cerebral glucose transport, K M t and Vmax t, in humans have so far been obtained by measuring steady-state brain glucose levels by proton (1H) NMR as a function of plasma glucose levels and fitting steady-state models to these data. Extraction of the kinetic parameters for cerebral glucose transport necessitated assuming a constant cerebral metabolic rate of glucose ( CMR glc) obtained from other tracer studies, such as 13C NMR. Here we present new methodology to simultaneously obtain kinetic parameters for glucose transport and utilization in the human brain by fitting both dynamic and steady-state 1H NMR data with a reversible, non-steady-state Michaelis-Menten model. Dynamic data were obtained by measuring brain and plasma glucose time courses during glucose infusions to raise and maintain plasma concentration at ∼17 mmol/l for ∼2 h in five healthy volunteers. Steady-state brain vs. plasma glucose concentrations were taken from literature and the steady-state portions of data from the five volunteers. In addition to providing simultaneous measurements of glucose transport and utilization and obviating assumptions for constant CMR glc, this methodology does not necessitate infusions of expensive or radioactive tracers. Using this new methodology, we found that the maximum transport capacity for glucose through the blood-brain barrier was nearly twofold higher than maximum cerebral glucose utilization. The glucose transport and utilization parameters were consistent with previously published values for human brain.

Transient and steady-state visual activity in the human brain

NeuroImage ◽  
2000 ◽  
Vol 11 (5) ◽  
pp. S704
Author(s):  
R.R. Ramírez ◽  
C. Horenstein ◽  
J. Schulman ◽  
R. Jagow ◽  
P. Mitra ◽  
...  
Keyword(s):  
Steady State ◽  
Human Brain ◽  
Visual Activity ◽  
Transient And Steady State

scholarly journals Synaptic vesicle pools are a major hidden resting metabolic burden of nerve terminals

2020 ◽  
Author(s):  
Camila Pulido ◽  
Timothy Aidan Ryan
Keyword(s):  
Cognitive Impairment ◽  
Steady State ◽  
Energy Consumption ◽  
Human Brain ◽  
Synaptic Vesicle ◽  
Atp Synthesis ◽  
Nerve Terminals ◽  
Metabolic Rates ◽  
On Demand ◽  
Vesicle Pools

The human brain is a uniquely vulnerable organ as interruption in fuel supply leads to acute cognitive impairment on rapid time scales. The reasons for this vulnerability are not well understood, but nerve terminals are likely loci of this vulnerability as they do not store sufficient ATP molecules and must synthesize them on-demand during activity or suffer acute degradation in performance. The requirements for on-demand ATP synthesis however depends in part on the magnitude of resting metabolic rates. We show here that, at rest, synaptic vesicle (SV) pools are a major source of presynaptic basal energy consumption. This basal metabolism arises from SV-resident V-ATPases compensating for a hidden resting H+ efflux from the SV lumen. We show that this steady-state H+ efflux is 1) mediated by vesicular neurotransmitter transporters, 2) independent of the SV cycle, 3) accounts for ~half of the resting synaptic energy consumption and 4) contributes to nerve terminal intolerance of fuel deprivation.

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