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

Journal: bioRxiv

Article Title: Molecular dynamics of Brodmann Area 22 in development and autism

doi: 10.64898/2026.03.31.715694

Figure Lengend Snippet: a , Differentially accessible regions (DARs) in NDD/ASD donors. Each point represents an ATAC-seq peak. Dark red and blue indicate FDR-significant (FDR < 0.05) increased and decreased accessibility in cases, respectively; lighter colors indicate nominal significance ( P < 0.05). b , Top 10 transcription factor motifs with recurrent differential accessibility across cell types (All comparison). Motifs and the number of cell types with FDR-significant differential accessibility are shown. c , Differentially accessible motifs (DAMs) across cell types. Each point represents a motif-cell type pair; green indicates RFX-family motifs in excitatory neurons. DAMs were identified using linear models implemented in limma (Methods). d , RFX3 differential motif accessibility (log 2 FC) across excitatory, inhibitory, and non-neuronal cell types for All, NDD/ASD, and ASD comparisons. e , Relationship between differential RFX3 motif accessibility and differential RFX3 expression in excitatory neurons (NDD/ASD). Points colored by nominal significance in accessibility and/or expression. X-axis is the log 2 FC from differential motif accessibility analysis and the y-axis is the log 2 FC for differential gene expression analysis. f , Enrichment of immediate early genes (IEGs) among DEGs in significant (FDR < 0.05) cell types (NDD/ASD). Odds ratios and 95% confidence intervals from Fisher’s exact test. g , Differential expression of IEGs in L4/5 IT1 neurons (NDD/ASD). Red and blue indicate FDR-significant (FDR < 0.05) increased and decreased expression in cases, respectively.

Article Snippet: The following steps were followed per the Multiome protocol using 10x Genomics’ Chromium Next GEM Single Cell Multiome ATAC + Gene Expression User Guide Rev E. The resulting Gene Expression and ATAC libraries underwent quality control and quantification using a High Sensitivity DNA Bioanalyzer 2100 (Agilent) to ensure adequate concentration and curve quality before sequencing.

Techniques: Comparison, Expressing, Gene Expression, Quantitative Proteomics

Journal: Science Advances

Article Title: Activation of the YAP1/pSTAT3/NRP1 axis in peritendinous sensory nerves promotes tendon healing

doi: 10.1126/sciadv.aec1272

Figure Lengend Snippet: ( A ) The total protein levels of YAP1, pSTAT3 Tyr 705 , and STAT3 with and without ES. β-actin was used as an internal control. n = 3. ( B ) The nuclear protein levels of YAP1 and pSTAT3 Tyr 705 with and without ES. Histone H3 was used as an internal control. n = 3. ( C ) Intersection of neurite outgrowth–related genes across multiple databases. ( D and E ) Enrichment pathways of neurite outgrowth–related genes transcribed via pSTAT3 Tyr 705 , as predicted by GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, respectively. ( F ) qRT-PCR results for the mRNA expression of neurite outgrowth–related genes transcribed via pSTAT3, including MAP3K13, NRP1, PTPRF, and GSK3B. n = 3. ( G ) Protein levels of NRP1 with and without ES. β-actin was used as an internal control. n = 3. ( H ) Predicted STAT3 binding motif sequence from the JASPAR database. ( I ) Dual-luciferase assays. n = 3. ( J ) Schematic representation of the NRP1 promoter region, highlighting the predicted STAT3 binding site (blue box) and the locations of forward (F) and reverse (R) primers used for ChIP-PCR. ( K ) ChIP-PCR analysis revealed that compared with the IgG control, the NRP1 promoter fragment was enriched in the chromatin precipitated by the anti-STAT3 antibody, confirming that STAT3 occupied the predicted site. n = 3. ( L ) Expression levels of CGRP in the supernatant of DRGn with and without ES. n = 8. n.s., not significant.

Article Snippet: Culture supernatants from treated DRGn were collected, and concentrations of CGRP (lot no. E-EL-R0135, Elabscience, China) were quantified using ELISA kits according to the manufacturer’s protocols.

Techniques: Control, Quantitative RT-PCR, Expressing, Binding Assay, Sequencing, Luciferase

Journal: Science Advances

Article Title: Activation of the YAP1/pSTAT3/NRP1 axis in peritendinous sensory nerves promotes tendon healing

doi: 10.1126/sciadv.aec1272

Figure Lengend Snippet: ( A ) Schematic diagram of DRGn treatment and detection. ( B and C ) Protein expression levels and quantitative results of pSTAT3 Tyr 705 and NRP1 in vitro in the absence or presence of shSTAT3 and ES. β-actin was used as an internal control. n = 3. ( D and E ) Protein expression levels and quantitative results of YAP1 and NRP1 in vitro in the absence or presence of shYAP1 and ES. β-actin was used as an internal control. n = 3. ( F to I ) Protein expression levels and quantitative results of pSTAT3 Tyr 705 , YAP1, and NRP1 in the absence or presence of shSTAT3, shYAP1, and ES. n = 3. ( J ) Schematic illustration of the cross-talk between DRGn and HUVECs. ( K and L ) Expression levels of CGRP in the supernatant of DRGn under different treatments. n = 8. ( M ) Wound scratch assay in HUVECs under different treatments. n = 3. Ctrl, control.

Article Snippet: Culture supernatants from treated DRGn were collected, and concentrations of CGRP (lot no. E-EL-R0135, Elabscience, China) were quantified using ELISA kits according to the manufacturer’s protocols.

Techniques: Expressing, In Vitro, Control, Wound Healing Assay