Our prospective pilot-phase trial demonstrates superior image quality and evaluation of skeletal disease extent with (18)F NaF PET/CT over (99m)Tc MDP scintigraphy and (18)F FDG PET/CT. At the same time, (18)F FDG PET detects extraskeletal disease that can significantly change disease management. As such, a combination of (18)F FDG PET/CT and (18)F NaF PET/CT may be necessary for cancer detection. Additional evaluation with larger cohorts is required to confirm these preliminary findings.

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# These authors contributed equally to this work. AbstractPurpose-2-Deoxy-2-[ 18 F]fluoro-D-glucose (FDG) is the most commonly used positron emission tomography (PET) tracer for oncological and neurological imaging, but it has limitations on detecting tumor or inflammation in brain gray matter. In this study, we describe the development of 2-deoxy-2-[ 18 F]fluorosorbitol ( 18 F-FDS) and its possible application in lesion detection around brain area.Procedures-18 F-FDS was obtained by reduction of FDG using NaBH 4 (81±4% yield in 30 min). Cell uptake/efflux experiments in cell culture and small animal PET imaging on tumor and inflammation models were performed.Results-Despite the low accumulation in cell culture, 18 F-FDS had good tumor uptake and contrast in the subcutaneous U87MG tumor model (4.54%ID/g at 30 min post-injection). Minimal uptake in the normal mouse brain facilitated good tumor contrast in both U87MG and GL-26 orthotopic tumor models. 18 F-FDS also had increased uptake in the inflamed foci of the TPAinduced acute inflammation model.Conclusions-Because of the ease of synthesis and favorable in vivo kinetics, 18 F-FDS may have potential applications in certain cases where FDG is inadequate (e.g., brain tumor).

Aberrant redox signaling underlies the pathophysiology of many chronic metabolic diseases, including type 2 diabetes (T2D). Methodologies aimed at rebalancing systemic redox homeostasis have had limited success. A noninvasive, sustained approach would enable the long-term control of redox signaling for the treatment of T2D. We report that static magnetic and electric fields (sBE) noninvasively modulate the systemic GSH-to-GSSG redox couple to promote a healthier systemic redox environment that is reducing. Strikingly, when applied to mouse models of T2D, sBE rapidly ameliorates insulin resistance and glucose intolerance in as few as three days with no observed adverse effects. Scavenging paramagnetic byproducts of oxygen metabolism with SOD2 in hepatic mitochondria fully abolishes these insulin sensitizing effects, demonstrating that mitochondrial superoxide mediates induction of these therapeutic changes. Our findings introduce a remarkable redox-modulating phenomenon that exploits endogenous electromagneto-receptive mechanisms for the noninvasive treatment of T2D, and potentially other redox-related diseases.

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