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Visualizing lipid nanoparticle trafficking for mRNA vaccine delivery in non-human primates.
Mol Ther
January 2025
Department of Biological Engineering, Massachusetts Institute of Technology; Cambridge, MA, USA, 02139; Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology; Cambridge, MA, USA, 02139; Department of Chemical Engineering, Massachusetts Institute of Technology; Cambridge, MA, USA, 02139; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard University; Cambridge, MA, USA, 02139; Howard Hughes Medical Institute; Chevy Chase, MD, USA, 20815; Department of Materials Science of Engineering; Massachusetts Institute of Technology; Cambridge, MA, USA, 02139. Electronic address:
mRNA delivered using lipid nanoparticles (LNPs) has become an important subunit vaccine modality, but mechanisms of action for mRNA vaccines remain incompletely understood. Here, we synthesized a metal chelator-lipid conjugate enabling positron emission tomography (PET) tracer labeling of LNP/mRNA vaccines for quantitative visualization of vaccine trafficking in live mice and non-human primates (NHPs). Following i.
View Article and Find Full Text PDFLens-Free On-Chip Quantitative Phase Microscopy for Large Phase Objects Based on a Biplane Phase Retrieval Method.
Sensors (Basel)
December 2024
Smart Computational Imaging Laboratory (SCILab), School of Electronic and Optical Engineering, Nanjing University of Science and Technology, Nanjing 210094, China.
Lens-free on-chip microscopy (LFOCM) is a powerful computational imaging technology that combines high-throughput capabilities with cost efficiency. However, in LFOCM, the phase recovered by iterative phase retrieval techniques is generally wrapped into the range of -π to π, necessitating phase unwrapping to recover absolute phase distributions. Moreover, this unwrapping process is prone to errors, particularly in areas with large phase gradients or low spatial sampling, due to the absence of reliable initial guesses.
View Article and Find Full Text PDFThe Vimentin-Targeting Drug ALD-R491 Partially Reverts the Epithelial-to-Mesenchymal Transition and Vimentin Interactome of Lung Cancer Cells.
Cancers (Basel)
December 2024
Department of Oncology-Pathology, Karolinska Institutet, 171 64 Solna, Sweden.
The epithelial-to-mesenchymal transition (EMT) is a common feature in early cancer invasion. Increased vimentin is a canonical marker of the EMT; however, the role of vimentin in EMT remains unknown. To clarify this, we induced EMT in lung cancer cells with TGF-β1, followed by treatment with the vimentin-targeting drug ALD-R491, live-cell imaging, and quantitative proteomics.
View Article and Find Full Text PDFAttributable Risk and Consequences of Bone Mineral Density Deficits in Childhood Cancer Survivors.
JAMA Netw Open
January 2025
Division of Endocrinology, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
Importance: Data characterizing the severity and changing prevalence of bone mineral density (BMD) deficits and associated nonfracture consequences among childhood cancer survivors decades after treatment are lacking.
Objective: To evaluate risk for moderate and severe BMD deficits in survivors and to identify long-term consequences of BMD deficits.
Design, Setting, And Participants: This cohort study used cross-sectional and longitudinal data from the St Jude Lifetime (SJLIFE) cohort, a retrospectively constructed cohort with prospective follow-up.
Mustard Gas Induced Corneal Injury Involves Ferroptosis and p38 MAPK Signaling.
Invest Ophthalmol Vis Sci
January 2025
Harry S. Truman Memorial Veterans' Hospital, Columbia, Missouri, United States.
Purpose: Sulfur mustard gas (SM) exposure to eyes causes multiple corneal injuries including stromal cell loss in vivo. However, mechanisms mediating stromal cell loss/death remains elusive. This study sought to test the novel hypothesis that SM-induced toxicity to human corneal stromal fibroblasts involves ferroptosis mechanism via p38 MAPK signaling.
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