Journal: npj Imaging

Article Title: Development and validation of an activatable PET radiotracer reporting extracellular myeloperoxidase activity for the detection of unstable atherosclerotic plaque

doi: 10.1038/s44303-026-00156-9

Figure Lengend Snippet: a , b Blood kinetics of [ 68 Ga]Ga-IEMA up to 90 min after intravenous administration of the radiotracer (102.6 ± 1.5 µL, 8.2 ± 3.8 MBq) into Apoe –/– mice without (non-TS Apoe –/– , n = 6) and with Tandem Stenosis (TS) surgery (TS Apoe –/– , n = 8) as measured by in vivo positron emission tomography (PET) imaging of the left ventricle. Image analysis using an exponential two-phase decay model shows that [ 68 Ga]Ga-IEMA was eliminated from the blood in a biexponential manner typical of radiotracers with extracellular distribution and renal clearance, as indicated in ( b ). c Reversed-phase HPLC of urine directly after collection from non-TS Apoe –/– ( n = 3) and TS Apoe –/– ( n = 4) mice 90 min after administration of [ 68 Ga]Ga-IEMA (104.8 ± 3.8 µL, 11.4 ± 2.6 MBq) showing intact radiotracer at 10.8 min and the formation of a new compound eluting at 10.0 min. Representative chromatograms for urine obtained from non-TS Apoe –/– and TS Apoe –/– mice are shown. d Percentage of total signal (peaks at 10.8 and 10.0 min) present in the peak at 10.0 min. * P < 0.05 (Mann–Whitney test).

Article Snippet: Male apolipoprotein E gene-deficient ( Apoe –/– ) mice purchased originally from Charles Rivers Laboratories (Edinburgh, UK) were housed and bred in the Biological Service Facility at King’s College London.

Techniques: In Vivo, Positron Emission Tomography, Imaging, MANN-WHITNEY

Journal: npj Imaging

Article Title: Development and validation of an activatable PET radiotracer reporting extracellular myeloperoxidase activity for the detection of unstable atherosclerotic plaque

doi: 10.1038/s44303-026-00156-9

Figure Lengend Snippet: a Representative in situ images after dissection show (i) the presence of atherosclerotic lesions in the brachiocephalic artery (BCA) known to contain stable lesions in both Apoe –/– mice without (non-TS) and with Tandem Stenosis (TS); (ii) the selective presence of atherosclerotic lesions known to have characteristics of unstable plaque in Segment I (Seg I) of TS but not the corresponding lesion-free anatomical location in non-TS mice (white arrow); and (iii) the lesion-free left carotid artery (LCA) (scale bar = 0.5 mm). b Representative whole-body coronal images of in vivo PET imaging with [ 68 Ga]Ga-IEMA in non-TS ( n = 6) and TS Apoe –/– mice ( n = 8) 50–60 min after administration of the radiotracer (102.6 ± 1.5 µL, 8.2 ± 3.8 MBq). c Transverse images at the level of Seg I and contralateral LCA show increased retention of [ 68 Ga]Ga-IEMA in Seg I compared with the anatomical location corresponding to Seg I in control non-TS Apoe –/– mice, where plaque is absent (white arrow) (scale bar = 2 cm). d Zoomed images taken at the level of Seg I and the BCA from three different mice per group showing increased signal due to increased retention of [ 68 Ga]Ga-IEMA in Seg I (yellow box) compared with the BCA in TS Apoe –/– mice (green box). The images also confirm a lack of retention [ 68 Ga]Ga-IEMA in the site corresponding to Seg I in non-TS Apoe –/– mice (broken yellow box) (scale bar = 0.5 mm). e Maximum standardized uptake value (SUV max ) of Seg I and BCA obtained from in vivo PET images 50–60 min post-injection of [ 68 Ga]Ga-IEMA in non-TS Apoe –/– (open squares) and TS Apoe –/– mice (filled circles). * P < 0.05 (ANOVA with a Tukey post hoc test). T trachea.

Article Snippet: Male apolipoprotein E gene-deficient ( Apoe –/– ) mice purchased originally from Charles Rivers Laboratories (Edinburgh, UK) were housed and bred in the Biological Service Facility at King’s College London.

Techniques: In Situ, Dissection, In Vivo, Imaging, Control, Injection