Jin Zhang1 and Sungheon Gene Kim1
1Radiology, New York University School of Medicine, New York, NY, United States
Synopsis
In vivo measurement of cellular-interstitial
water exchange rate remains non-trivial. Its development is also hampered by
the lack of a gold standard method for validation. In this study, we have used
two complementary diffusion MRI methods to measure the water exchange rates.
Time-dependent diffusional kurtosis imaging was used to measure the water
exchange rate ($$$\tau_{ex}$$$) between
the intra- and extra-cellular spaces, while a constant gradient diffusion MRI
experiment was used to measure the intracellular water lifetime ($$$\tau_i$$$). These two measurements were conducted using GL261, a mouse glioma
tumor model.
Introduction
In vivo measurement of cellular-interstitial water exchange
rate remains non-trivial. Its development is also hampered by the lack of a
gold standard method for validation. Diffusion MRI (dMRI) is a unique in vivo imaging technique sensitive to cellular microstructure
at the scale of water diffusion length on the order of a few microns, such as
cell size, cell density, composition of the extracellular matrix, compartmental
diffusivities as well as water exchange between compartments.1,2 Diffusivity D, as well as higher-order dMRI
metrics including diffusional kurtosis K,
can reflect these tissue properties when measured with multiple diffusion
times. The purpose of this
study is to use two complementary dMRI methods to measure cellular-interstitial
water exchange rates and compare them for cross-validation. Using GL261, a
mouse glioma model, we measured the cellular-interstitial water exchange time ($$$\tau_{ex}$$$) in tumor tissue using time-dependent diffusion
kurtosis imaging (tDKI), and compared
that with the intracellular water lifetime ($$$\tau_i$$$) measured in the same tumors using constant gradient diffusion weighted
imaging (CG-DWI) experiments.3Methods
Six-to-eight week old C57BL6 mice with GL261
glioma tumor model (n = 6) were
included in this study performed using a Bruker 7T micro-MRI system with a
four-channel phased array cryogenically-cooled receive-only coil with a volume-transmit
coil. The animal body temperature was maintained at 36 ± 1 ºC during the scan. General
anesthesia was induced by 1.5% isoflurane in air.
$$$\tau_{ex}$$$ from tDKI: dMRI measurement was conducted with multiple
diffusion times between 20 and 800 ms while keeping the same b-values (b = 200, 500, 1000, 1500, 2000, 3000 s/mm2) by adjusting
the diffusion gradient strength. tDKI
data were acquired using a diffusion-weighted STEAM pulse sequence for tumor
center slice (1 mm thickness) in sagittal direction with EPI readout (TR/TE
= 8 s/30 ms, FOV = 20x20 mm, image matrix = 80x80, resolution = 0.25×0.25mm). tDKI data at each diffusion time t was
used to estimate D(t) and K(t) using a weighted linear
least-squares fit method. In the Kärger model (KM),4,5 the overall D=(1-ve)De+veDi=const,
while K(t) depends on t $$K(t)=K_0\frac{2\tau_{ex}}{t}\left[1-\frac{\tau_{ex}}{t}\left(1-e^{-\frac{t}{\tau_{ex}}}\right)\right]+K_\infty\hspace{3em}[1]$$ with the exchange time $$$\tau_{ex}$$$=ve$$$\tau_i$$$=(1-ve)$$$\tau_e$$$,
and K0 = 3$$$\frac{var\left(D\right)}{D^2}$$$,
where $$$var$$$(D)=ve(1-ve)(Di-De)2. ve is interstitial volume
fraction with $$$\tau_e$$$ denoting interstitial water lifetime. De and Di are extra- and
intracellular diffusivities. The KM was applied for the data with long enough
diffusion times where D(t) has
already become constant, while K(t) is still decreasing solely because of
the exchange, with a rate $$$1/\tau_{ex}$$$, Eq.[1].5 K$$$\infty$$$ accounts for tissue heterogeneity effects unrelated
to exchange.
$$$\tau_i$$$ from CG-DWI: The same tumor center slice in the sagittal direction was
also used for CG-DWI experiments with a STEAM-DWI sequence with TR/TE
= 5 s/30 ms, diffusion gradient duration δ = 7 ms,
and diffusion weighting gradient G = 150
mT/m. The sequence was run multiple times with a series of diffusion times; t = 20, 75, 100, 125, 150, 200 and 300 ms.
Assuming extracellular signal contributions were dephased completely with the
large q value when t is long enough, the intracellular
water lifetime $$$\tau_i$$$, was determined by the
monoexponential decay in long diffusion times.3 In order to avoid
the need to select the lower bound of diffusion time for this analysis, a
biexponential model was fit to the whole data set and the slow decay component
was used to estimate $$$\tau_i$$$.
Results
Figure 1 shows an example of D(t)
and K(t) data acquired from a mouse with GL261 tumor. When t
> 150 ms, D(t) does not show a noticeable change, while K(t) keeps decreasing monotonically.
This is where the above condition to extend the KM to tissue microstructure becomes
valid, such that Eq.[1] can be used to estimate $$$\tau_{ex}$$$. The fit shown in Figure 1d suggests that the
water exchange time $$$\tau_{ex}$$$ = 111 ms, which is in the range expected for cancer cells.6 Figure 2 shows an example of the
CG-DWI measurement for the same mouse shown in Figure 1. The slow component of
a biexponential fit to the whole data points (Figure 2d) corresponded to the
intracellular water lifetime of $$$\tau_i$$$ = 102 ms. Both $$$\tau_{ex}$$$ and $$$\tau_i$$$ measured in all six tumors, including multiple
scans for two tumors, were in a similar range as shown in Figure 3. Discussion and Conclusion
The preliminary results from this study suggest
that either of dMRI methods can be used to investigate the cellular-interstitial
water exchange and its potential as a biomarker for tumor aggressiveness and
treatment response. The CG-DWI method does not rely on a theoretical model, but
requires using stronger diffusion weightings than the tDKI methods, which leads to lower signal-to-noise ratio in the
data. It is expected that the tDKI method could be more easily applied in
clinical applications.Acknowledgements
NIH R01CA160620, NIH R01CA219964, P41EB017183, NIH/NCI
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