Rapid B1-Insensitive MR Fingerprinting for Quantitative Kidney Imaging.

Background MR fingerprinting (MRF) provides rapid and simultaneous quantification of multiple tissue parameters in a single scan. Purpose To evaluate a rapid kidney MRF technique at 3.0 T in phantoms, healthy volunteers, and patients. Materials and Methods A 15-second kidney MRF acquisition was designed with 12 acquisition segments, a range of low flip angles (5°-12°), multiple magnetization preparation schema (T1, T2, and fat suppression), and an undersampled spiral trajectory. This technique was first validated in vitro using standardized T1 and T2 phantoms. Kidney T1 and T2 maps were then obtained for 10 healthy adult volunteers (mean age ± standard deviation, 35 years ± 13; six men) and three pediatric patients with autosomal recessive polycystic kidney disease (ARPKD) (mean age, 10 years ± 3; two boys) between August 2019 and October 2020 to evaluate the method in vivo. Results Results in nine phantoms showed good agreement with spin-echo-based T1 and T2 values (R2 > 0.99). In vivo MRF kidney T1 and T2 assessments in healthy adult volunteers (cortex: T1, 1362 msec ± 5; T2, 64 msec ± 5; medulla: T1, 1827 msec ± 94; T2, 69 msec ± 3) were consistent with values in the literature but with improved precision in comparison with prior MRF implementations. In vivo MRF-based kidney T1 and T2 values with and without B1 correction were in good agreement (R2 > 0.96, P < .001), demonstrating limited sensitivity to B1 field inhomogeneities. Additional MRF reconstructions using the first nine segments of the MRF profiles (11-second acquisition time) were in good agreement with the reconstructions using 12 segments (15-second acquisition time) (R2 > 0.87, P < .001). Repeat kidney MRF scans for the three patients with ARPKD on successive days also demonstrated good reproducibility (T1 and T2: <3% difference). Conclusion A kidney MR fingerprinting method provided in vivo kidney T1 and T2 maps at 3.0 T in a single breath hold with improved precision and no need for B1 correction. © RSNA, 2021 Online supplemental material is available for this article. See also the editorial by Laustsen in this issue.

Astrocyte Activation via Stat3 Signaling Determines the Balance of Oligodendrocyte versus Schwann Cell Remyelination.

Remyelination within the central nervous system (CNS) most often is the result of oligodendrocyte progenitor cells differentiating into myelin-forming oligodendrocytes. In some cases, however, Schwann cells, the peripheral nervous system myelinating glia, are found remyelinating demyelinated regions of the CNS. The reason for this peripheral type of remyelination in the CNS and what governs it is unknown. Here, we used a conditional astrocytic phosphorylated signal transducer and activator of transcription 3 knockout mouse model to investigate the effect of abrogating astrocyte activation on remyelination after lysolecithin-induced demyelination of spinal cord white matter. We show that oligodendrocyte-mediated remyelination decreases and Schwann cell remyelination increases in lesioned knockout mice in comparison with lesioned controls. Our study shows that astrocyte activation plays a crucial role in the balance between Schwann cell and oligodendrocyte remyelination in the CNS, and provides further insight into remyelination of CNS axons by Schwann cells.