Purpose: To develop and validate a framework for rapid, accurate, and repeatable whole-brain, multi-pool chemical exchange saturation transfer (CEST) imaging at 3 T, addressing challenges of long acquisition times and confounding factors.
Methods: A single-shot 3D true fast imaging with steady-state precession (True FISP) sequence was optimized for whole-brain multi-pool CEST. Rapid B0, B1, and T1 mapping was performed using a dual-echo modified four-angle method. A feed-forward neural network was developed for rapid B1 correction, trained against the conventional multi-power method. The apparent exchange-dependent relaxation (AREX) metric was used to correct for T1 and magnetization transfer (MT) effects. The framework was validated in phantoms and 50 healthy subjects, including a different-day test-retest repeatability assessment.
Results: The True FISP sequence yielded high-quality, whole-brain images with minimal artifacts and distortion in a clinically feasible scan time (~9 min). Phantom studies confirmed the effectiveness of B1 correction (coefficient of variation [CV] for the magnetization transfer ratio based on Lorentzian difference (MTRLD) of the MT pool decreased from 22.49% to 4.61%) and AREX-based confounder correction (CV for APT_AREX reduced from 33.6% to 6.9%). The neural network B1 correction showed excellent agreement with the conventional multi-power method in vivo (ICC > 0.95). High different-day test-retest repeatability was demonstrated across 96 brain regions, with the average CV for APT_AREX under 10% for 95 of 96 analyzed regions.
Conclusion: A rapid and robust framework for whole-brain quantitative multi-pool CEST imaging was successfully developed and validated. By integrating an efficient acquisition sequence with a streamlined correction pipeline, this approach overcomes key barriers to clinical translation, enabling reliable metabolic imaging for widespread brain pathologies.
Background: The rostral ventromedial medulla (RVM) is a brainstem structure that integrates descending modulatory signaling and contains neurons highly responsive to opioid receptor activation. Despite the well-established effects of opioids in the RVM, the neurochemical adaptations following sustained morphine exposure remain poorly understood. In particular, the contribution of G-protein-coupled inwardly rectifying potassium type 2 (GIRK2) channels, key mediators of opioid receptor-dependent antinociception has not been fully characterized. We hypothesized that GIRK2 channels are essential for morphine-induced metabolic alterations in the RVM.
Methods: In vivo proton nuclear magnetic resonance spectroscopy (1H NMR) was used to examine metabolite responses to prolonged morphine exposure. Metabolite profiles were compared between wild-type and GIRK2 heterozygous mutant (GIRK2+/-) mice before and after four days of subcutaneous implantation with placebo or morphine pellets.
Results: In wild-type mice, morphine exposure significantly increased levels of phosphocreatine, total creatine, glutamine, glutathione, taurine, and glycerophosphocholine plus phosphocholine (GPC + PCh), while decreasing N-acetylaspartate (NAA). These changes suggest enhanced energy storage, activation of antioxidant pathways, increased membrane turnover, and alterations in neuronal integrity and excitatory neurotransmission. In contrast, GIRK2+/- mice exhibited attenuated or opposite responses to morphine, characterized by elevated glutamate and reductions in glutamine, GPC + PCh, and total creatine, with no change in NAA. These differential responses indicate that GIRK2 channels influence neurochemical adaptations to morphine in the RVM.
Conclusion: These findings identify the GIRK2 channel as an important modulator of morphine-induced metabolic changes in the RVM. The observed neurochemical alterations likely reflect adaptive responses to sustained opioid exposure.
Purpose: To investigate the diagnostic value of the 3D multi-echo Dixon (ME-DIXON) and High-Speed T2-Corrected Multiecho Acquisition proton magnetic resonance spectroscopy (1H MRS, HISTO) sequences in MRI for lumbar spine osteoporosis.
Methods: This study enrolled 138 eligible participants (aged 41-70 years), all of whom underwent both lumbar spine MRI and quantitative computed tomography (QCT). Demographic data, proton density fat fraction (PDFF) values from L1 to L4 vertebrae, and QCT-derived bone mineral density (BMD) were systematically collected. Participants were stratified into three groups based on BMD: osteoporosis, osteopenia, and normal. Differences in vertebral PDFF parameters among these three BMD cohorts were compared using one-way analysis of variance (ANOVA). Receiver operating characteristic (ROC) analysis and correlation analysis were performed to evaluate diagnostic performance and assess the correlation between PDFF and BMD, respectively.
Results: The mean lumbar ME-DIXON-PDFF and HISTO-PDFF values showed negative correlations with BMD (r = -0.68, r = -0.56), age-adjusted(rp = -0.51, rp = -0.33) (all p < 0.05); Both ME-DIXON-PDFF (AUC = 0.833) and HISTO-PDFF (AUC = 0.819) demonstrated good diagnostic performance for osteoporosis. Performance improved after age adjustment (AUC = 0.868 for both models), with no significant difference between the two sequences (all p > 0.05).
Conclusion: This study confirms a strong inverse correlation between MRI-derived PDFF and QCT-based BMD, and demonstrates diagnostic equivalence between the fully automated HISTO sequence and the established ME-DIXON sequence for osteoporosis identification. These findings support PDFF as a promising imaging biomarker for bone density assessment and validate the technical feasibility of automated spinal fat quantification.

