Purpose: Although Ω-plot-driven quantification of in vivo amide exchange properties has been demonstrated, differences in scan parameters may complicate the fidelity of determination. This work systematically evaluated the use of quasi-steady-state (QUASS) Z-spectra reconstruction to standardize in vivo amide exchange quantification across acquisition conditions and further determined it in vivo.
Methods: Simulation and in vivo rodent brain chemical exchange saturation transfer (CEST) data at 4.
Purpose: CEST MRI detects complex tissue changes following acute stroke. Our study aimed to test if spinlock model-based fitting of the quasi-steady-state (QUASS)-reconstructed equilibrium CEST MRI improves the determination of multi-pool signal changes over the commonly-used model-free Lorentzian fitting in acute stroke.
Theory And Methods: Multiple three-pool CEST Z-spectra were simulated using Bloch-McConnell equations for a range of T , relaxation delay, and saturation times.
Purpose: Chemical exchange saturation transfer (CEST) MRI is promising for detecting dilute metabolites and microenvironment properties, which has been increasingly adopted in imaging disorders such as acute stroke and cancer. However, in vivo CEST MRI quantification remains challenging because routine asymmetry analysis (MTR ) or Lorentzian decoupling measures a combined effect of the labile proton concentration and its exchange rate. Therefore, our study aimed to quantify amide proton concentration and exchange rate independently in a cardiac arrest-induced global ischemia rat model.
View Article and Find Full Text PDFBrain pH is thought to be important in epilepsy. The regulation of brain pH is, however, still poorly understood in animal models of chronic seizures (SZ) as well as in patients with intractable epilepsy. We used chemical exchange saturation transfer (CEST) MRI to noninvasively determine if the pH is alkaline shifted in a rodent model of the mesial temporal lobe (MTL) epilepsy with chronic SZ.
View Article and Find Full Text PDFPurpose: To develop fast multi-slice apparent T (T ) mapping for accurate cerebral blood flow (CBF) quantification with arterial spin labeling (ASL) MRI.
Methods: Fast multi-slice T was measured using a modified inversion recovery echo planar imaging (EPI) sequence with simultaneous application of ASL tagging radiofrequency (RF) and gradient pulses. The fast multi-slice T measurement was compared with the single-slice T imaging approach, repeated per slice.
Purpose: Our study aimed to develop accelerated microscopic diffusional kurtosis imaging (μDKI) and preliminarily evaluated it in a rodent model of chronic epilepsy.
Methods: We investigated two μDKI acceleration schemes of reduced sampling density and angular range in a phantom and wild-type rats, and further tested μDKI method in pilocarpine-induced epilepsy rats using a 4.7 Tesla MRI.
Purpose: Diffusional kurtosis imaging (DKI) measures the deviation of the displacement probability from a normal distribution, complementing the data commonly acquired by diffusion MRI. It is important to elucidate the sources of kurtosis contrast, particularly in biological tissues where microscopic kurtosis (intrinsic kurtosis) and diffusional heterogeneity may co-exist.
Methods: We have developed a technique for microscopic kurtosis MRI, dubbed microscopic diffusional kurtosis imaging (µDKI), using a symmetrized double diffusion encoding (s-DDE) EPI sequence.
Purpose: Chemical exchange saturation transfer (CEST) MRI has been used for quantitative assessment of dilute metabolites and/or pH in disorders such as acute stroke and tumor. However, routine asymmetry analysis (MTR ) may be confounded by concomitant effects such as semisolid macromolecular magnetization transfer (MT) and nuclear Overhauser enhancement. Resolving multiple contributions is essential for elucidating the origins of in vivo CEST contrast.
View Article and Find Full Text PDFObjective: Diffusion kurtosis imaging (DKI) has emerged as a new acute stroke imaging approach, augmenting routine DWI. Although it has been shown that a diffusion lesion without kurtosis abnormality is more likely to recover after reperfusion, whereas a kurtosis lesion shows poor response, little is known about the underlying pathophysiologic profile of the kurtosis lesion versus the kurtosis lesion-diffusion lesion mismatch.
Materials And Methods: We performed multiparametric MRI, including arterial spin labeling, pH-sensitive amide proton transfer, and DKI, in a rodent model of acute stroke caused by embolic middle cerebral artery occlusion.
Purpose: Chemical exchange saturation transfer (CEST) MRI has shown promise in tissue characterization in diseases like stroke and tumor. However, in vivo CEST imaging such as amide proton transfer (APT) MRI is challenging because of concomitant factors such as direct water saturation, macromolecular magnetization transfer, and nuclear overhauser effect (NOE), which lead to a complex contrast in the commonly used asymmetry analysis (MTRasym). Here, we propose a direct saturation-corrected CEST (DISC-CEST) analysis for simplified decoupling and quantification of in vivo CEST effects.
View Article and Find Full Text PDFPurpose: To determine the origins of in vivo magnetization transfer asymmetry contrast during acute ischemic stroke, particularly in the diffusion lesion, perfusion lesion, and their mismatch using a middle cerebral artery occlusion rat model of acute stroke.
Methods: Adult male Wistar rats underwent multiparametric MRI of diffusion, perfusion, T , and amide proton transfer (APT) imaging at 4.7 T following a middle cerebral artery occlusion procedure.
Delayed ischemic postconditioning (Post C), which involves a brief ischemia followed by reperfusion 2 days after 8-10min global cerebral ischemia (GCI), has been shown to exert a remarkable protection of the vulnerable hippocampal CA1 region of the brain and attenuation of behavioral deficits, although the mechanisms remain poorly understood. The purpose of the current study was to explore the effect of Post C upon mitochondrial integrity, cytochrome c release and Bax translocation as a potential key mechanism for Post C protection of the critical hippocampal CA1 region neurons. The results of the study revealed that ischemic Post C (3min) administered 2 days after 8-min GCI exerted a robust preservation from GCI injury, as evidenced by the increase of NeuN-positive and the decrease of TUNEL-positive cells, as well as morphological features of mitochondrial integrity in the hippocampal CA1 region.
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