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Conventional PET/CT scanners with standard axial field-ofview (SAFOV) usually cover around 23-26 cm [1,2]. Over the last decade, however, there has been tremendous effort in the development of long axial field-of-view (LAFOV) PET/ CT scanners, and several of them have entered the clinical arena [3][4][5]. It is well recognized that, with LAFOV PET/ CT scanners, one could image better (e.g. reconstruct at higher resolution and detect smaller lesions), image faster, image longer after tracer injection, and image gently (e.g., at a much lower radiopharmaceutical dose than usual, which will enable more PET scans in the children population, as well as more repeated scans in the adult population) [1].In the July issue of European Journal of Nuclear Medicine and Molecular Imaging, a superbly designed and executed study on the first clinical implementation of a LAFOV PET/CT scanner was reported by Dr. Rominger and colleagues from Bern University Hospital, University of Bern, Switzerland [5]. This is a prospective, nonrandomized, dual-arm crossover, comparative imaging study with a clearly stated hypothesis and inclusion/exclusion criteria. The number of patients needed for the study (> 40) was calculated to provide robust statistical analysis. In addition, three PET tracers ( 18 F-FDG, 18 F-PSMA-1007, and 68 Ga-DOTA-TOC) and 2 PET isotopes ( 18 F and 68 Ga)This article is part of the Topical Collection on Technology.

ischemia can cause an ischemic core and salvageable surrounding tissue (termed as penumbra). The penumbra has been regarded as a pharmacological target for ischemic stroke treatment. [2] Restoring cerebral blood flow is currently the most effective approach for reducing the number of damaged neuron in the ischemic penumbra. [3] Although intravenous thrombolysis can effectively restore blood supply in the penumbra, its use is limited by a short time window during which it can be safely and effectively performed. [4] Additionally, restoring blood flow can arouse a cerebral ischemicreperfusion (I-R) injury, which results in the amplification of the inflammatory response and the aggravation of secondary damage. The infiltration of peripheral monocytes/macrophages (M o /M ϕ ) is a crucial inflammatory injury mechanism, which induces neuronal apoptosis and nervous system dysfunction. In addition, a recent study has also highlighted the pivotal role of M o /M ϕ in the repair process, indicating that regulation of the balance of M o /M ϕ can be an effective method for the treatment of cerebral I-R injury. [5] The spleen is an immediate reservoir of M o /M ϕ , which has more M o /M ϕ than the entire circulatory system. [6] The spleen is also the primary source of inflammatory cells, which can infiltrate the ischemic penumbra during the early phase of an ischemic stroke. [7] In the ischemic penumbra, M o /M ϕ can be classically activated to the M1 phenotype of macrophages (M1-macrophage), secrete pro-inflammatory cytokines, and release oxygen free radicals. [8] Due to their heterogeneity and high versatility, M o /M ϕ can also be polarized into M2-macrophages, which are involved in anti-inflammatory and repair processes through their capability to secrete anti-inflammatory cytokines. [9] Therefore, reducing the number of splenic M1-macrophages and increasing the number of splenic M2-macrophages can effectively protect neurons from the damaged microenvironment in the penumbra.Glabridin (Gla) possesses multiple pharmacological activities, including antioxidant, anti-inflammatory, and neuroprotective. [10] As a peroxisome proliferator-activated receptor-γ (PPARγ) specific antagonist, Gla is also involved in cell proliferation and differentiation. [11] Previous studies demonstrated that PPAR-γ activation could result in the M2 polarization of During cerebral ischemia-reperfusion (I-R) injury, the infiltration of monocyte/ macrophages (M o /M ϕ ) into the ischemic penumbra causes inflammatory damage but also regulates tissue repair in the penumbra. The regulation and balance of M o /M ϕ polarization is considered as a potential therapeutic target for treating cerebral I-R injury. Herein, these findings demonstrate that glabridin (Gla)-loaded nanoparticles (i.e., NP Gla -5k) can effectively inhibit M1-polarization and enhance M2-polarization of M o /M ϕ . Positron emission tomography (PET) imaging shows that NP Gla -5k can selectively accumulate in the spleen following intravenous injection. Spleen-targeted Cy5-NP Gla -5k can...

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