T2 Relaxation Time and Apparent Diffusion Coefficient for Noninvasive Assessment of Renal Pathology After Acute Kidney Injury in Mice

2013 ◽  
Vol 48 (12) ◽  
pp. 834-842 ◽  
Author(s):  
Katja Hueper ◽  
Song Rong ◽  
Marcel Gutberlet ◽  
Dagmar Hartung ◽  
Michael Mengel ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Apparent Diffusion Coefficient ◽  
Kidney Injury ◽  
Renal Pathology ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Apparent Diffusion ◽  
Noninvasive Assessment

Changes in the apparent diffusion coefficient of water and T2 relaxation time in gerbil hippocampus after mild ischemia

Neuroreport ◽  
2000 ◽  
Vol 11 (15) ◽  
pp. 3333-3336 ◽  
Author(s):  
Lidong Zhu ◽  
Nobuhito Saito ◽  
Osamu Abe ◽  
Toshiyuki Okubo ◽  
Haruyasu Yamada ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Apparent Diffusion Coefficient ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Apparent Diffusion

Apparent Diffusion Coefficient, Fractional Anisotropy and T2 Relaxation Time Measurement

2007 ◽  
Vol 17 (4) ◽  
pp. 230-238 ◽  
Author(s):  
Xiao-Qi Ding ◽  
Jürgen Finsterbusch ◽  
Oliver Wittkugel ◽  
Christian Saager ◽  
Einar Goebell ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Apparent Diffusion Coefficient ◽  
Fractional Anisotropy ◽  
Time Measurement ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Relaxation Time Measurement ◽  
Apparent Diffusion

scholarly journals Secondary Reduction in the Apparent Diffusion Coefficient of Water, Increase in Cerebral Blood Volume, and Delayed Neuronal Death after Middle Cerebral Artery Occlusion and Early Reperfusion in the Rat

1999 ◽  
Vol 19 (12) ◽  
pp. 1354-1364 ◽  
Author(s):  
Menno van Lookeren Campagne ◽  
G. Roger Thomas ◽  
Harold Thibodeaux ◽  
James T. Palmer ◽  
Simon P. Williams ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Cerebral Blood Volume ◽  
Vascular Occlusion ◽  
T2 Relaxation Time ◽  
T2 Relaxation ◽  
Early Reperfusion ◽  
Occlusion Time ◽  
Contrast Enhanced ◽  
Apparent Diffusion

It has been reported recently that very delayed damage can occur as a result of focal cerebral ischemia induced by vascular occlusion of short duration. With use of diffusion-, T2-, and contrast-enhanced dynamic magnetic resonance imaging (MRI) techniques, the occlusion time dependence together with the temporal profile for this delayed response in a rat model of transient focal cortical ischemia have been established. The distal branch of the middle cerebral artery was occluded for 20, 30, 45, or 90 minutes. Twenty minutes of vascular occlusion with reperfusion exhibited no significant mean change in either the apparent diffusion coefficient of water (ADC) or the T2 relaxation time at 6, 24, 48, or 72 hours after reperfusion ( P = 0.97 and 0.70, respectively). Ninety minutes of ischemia caused dramatic tissue injury at 6 hours, as indicated by an increase in T2 relaxation times to 135% of the contralateral values ( P < 0.01). However, at intermediate periods of ischemia (30 to 45 minutes), complete reversal of the ADC was seen at 6 hours after reperfusion but was followed by a secondary decline over time, such that a 25% reduction in tissue ADC was seen at 24 as compared with 6 hours ( P < 0.02). This secondary response was accompanied by an increase in cerebral blood volume (CBV), as shown by contrast-enhanced dynamic MRI (120% of contralateral values; P < 0.001), an increase in T2 relaxation time (132%; P < 0.01), together with clear morphological signs of cell death. By day 18, the mean volume of missing cortical tissue measured with high-resolution MRI in animals occluded for 30 and 45 minutes was 50% smaller than that in 90-minute occluded animals ( P < 0.005). These data show that ultimate infarct size is reduced after early reperfusion and is occlusion time dependent. The early tissue recovery that is seen with intermediate occlusion times can be followed by cell death, which has a delayed onset and is accompanied by an increase in CBV.

scholarly journals Quantifying T 2 relaxation time changes within lesions defined by apparent diffusion coefficient in grey and white matter in acute stroke patients

2019 ◽  
Vol 64 (9) ◽  
pp. 095016 ◽  
Author(s):  
Robin A Damion ◽  
Michael J Knight ◽  
Bryony L McGarry ◽  
Rose Bosnell ◽  
Peter Jezzard ◽  
...  
Keyword(s):  
Diffusion Coefficient ◽  
Relaxation Time ◽  
White Matter ◽  
Apparent Diffusion Coefficient ◽  
Acute Stroke ◽  
Stroke Patients ◽  
Apparent Diffusion ◽  
Time Changes

scholarly journals A spatiotemporal theory for MRI T2 relaxation time and apparent diffusion coefficient in the brain during acute ischaemia: Application and validation in a rat acute stroke model

2015 ◽  
Vol 36 (7) ◽  
pp. 1232-1243 ◽  
Author(s):  
Michael J Knight ◽  
Bryony L McGarry ◽  
Harriet J Rogers ◽  
Kimmo T Jokivarsi ◽  
Olli HJ Gröhn ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Diffusion Coefficient ◽  
Relaxation Time ◽  
Apparent Diffusion Coefficient ◽  
Cerebral Ischaemia ◽  
Future Application ◽  
Acute Ischaemia ◽  
Cellular Environment ◽  
Apparent Diffusion ◽  
Cytotoxic Oedema

The objective of this study is to present a mathematical model which can describe the spatiotemporal progression of cerebral ischaemia and predict magnetic resonance observables including the apparent diffusion coefficient (ADC) of water and transverse relaxation time T2. This is motivated by the sensitivity of the ADC to the location of cerebral ischaemia and T2 to its time-course, and that it has thus far proven challenging to relate observations of changes in these MR parameters to stroke timing, which is of considerable importance in making treatment choices in clinics. Our mathematical model, called the cytotoxic oedema/dissociation (CED) model, is based on the transit of water from the extra- to the intra-cellular environment (cytotoxic oedema) and concomitant degradation of supramacromolecular and macromolecular structures (such as microtubules and the cytoskeleton). It explains experimental observations of ADC and T2, as well as identifying the rate of spread of effects of ischaemia through a tissue as a dominant system parameter. The model brings the direct extraction of the timing of ischaemic stroke from quantitative MRI closer to reality, as well as providing insight on ischaemia pathology by imaging in general. We anticipate that this may improve patient access to thrombolytic treatment as a future application.

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