Browse Articles
Discover research articles across all indexed journals
Reviewers for the <i>Journal</i> , January–June 2025
Enhanced activity localization and microscale dosimetry in alpha-emitter radiopharmaceutical therapy using integrated autoradiography and histological imaging
Abstract Alpha-emitter radiopharmaceutical therapy delivers highly localized radiation, offering potent therapeutic effects. However, microscale heterogeneity remains poorly characterized in vivo and may affect efficacy. This underscores the critical need for sub-organ dosimetry to better understand αRPT radiobiology and guide treatment optimization. While autoradiography enables high-resolution activity mapping, conventional approaches lack anatomical context for accurate dose mapping. To address this, we propose a comprehensive workflow integrating quantitative autoradiography with histological imaging. Tissues from αRPT-treated mice bearing HER2 + breast tumors were snap-frozen, sectioned, and imaged using autoradiography. The same sections were histologically stained and used for precise autoradiography-histology integration. These anatomical contexts were then used to accurately stack multiple sections in a 3D volume, and were used for subsequent microscale dosimetry. Both tumor and kidney tissues were analyzed. Snap-freezing in isopentane preserved tissue morphology optimally. Our method enabled precise activity localization, revealing significant accumulation in the kidney cortex region close to glomeruli. Anatomical context improved 3D reconstructions needed for accurate dose estimations in tumor tissue. This methodology enhances αRPT dosimetry by precise spatial mapping of autoradiography unto the underlying tissue morphology. These advancements provide crucial insights into αRPT spatial radiobiology at the near-cellular level and will aid in optimizing radiopharmaceutical design and treatment planning.
The Resurgence of Private Law in American Health Care
Surface appearance of poly lactic acid due to variations in material extrusion processing parameters
Oral Semaglutide and Cardiovascular Outcomes
Assessing the potential for carbon storage enhancement in forests of Xinjiang Uygur autonomous region, China
Presymptomatic Treatment of a Genetic Disease with a Small-Molecule Drug
Intraspecific functional traits of an invasive alien plant, Hyptis suaveolens differ with respect to land use types
A Crossover Trial of Hospital-Wide Lactated Ringer’s Solution versus Normal Saline
Comparison of left ventricular hemodynamic forces measured by transthoracic echocardiography and cardiac magnetic resonance imaging in healthy adults
Case 23-2025: A 28-Year-Old Woman with Respiratory Failure and Abnormal Chest Imaging
Coherent control of anisotropic SPPs in a symmetric double-layer metal/uniaxial dielectric structure
Expanding the Treat-to-Target Toolbox for Obesity and Diabetes Care
Non-antibiotics disrupt colonization resistance against enteropathogens
Abstract Non-antibiotic drugs can alter the composition of the gut microbiome1, but they have largely unknown implications for human health2. Here we examined how non-antibiotics affect the ability of gut commensals to resist colonization by enteropathogens3. We also developed an in vitro assay to assess enteropathogen growth in drug-perturbed microbial communities. Pathogenic Gammaproteobacteria were more resistant to non-antibiotics than commensals and their post-treatment expansion was potentiated. For 28% of the 53 drugs tested, the growth of Salmonella enterica subsp. enterica serovar Typhimurium. (S. Tm) in synthetic and human stool-derived communities was increased, and similar effects were observed for other enteropathogens. Non-antibiotics promoted pathogen proliferation by inhibiting the growth of commensals, altering microbial interactions and enhancing the ability of S. Tm to exploit metabolic niches. Drugs that promoted pathogen expansion in vitro increased the intestinal S. Tm load in mice. For the antihistamine terfenadine, drug-induced disruption of colonization resistance accelerated disease onset and increased inflammation caused by S. Tm. Our findings identify non-antibiotics as previously overlooked risk factors that may contribute to the development of enteric infections.
Molecular characterization of Kawasaki disease subgroups using cell-free RNA profiling
Abstract Kawasaki disease is a pediatric vasculitis and the leading cause of acquired heart disease in children. The heterogeneous clinical presentation of Kawasaki disease complicates diagnosis and treatment, highlighting the need for molecular signatures to stratify patients into subgroups to better understand pathogenesis. We performed plasma cell-free RNA sequencing on samples from 98 patients diagnosed with Kawasaki disease, 86 febrile children (62 viral infection, 24 bacterial infection), and 5 healthy children. The Kawasaki disease patients were previously classified into one of four clinical subgroups using 14 clinical variables. Significant differences were observed in cell-free RNA transcript abundance, pathway enrichment scores, and cell type-of-origin fractions, including differences in hepatocyte injury, mitochondrial dysfunction, platelet activation, and developmental markers. This study demonstrates the utility of cell-free RNA to characterize Kawasaki disease subgroups at a molecular level. Cell-free RNA profiles may be used as biomarkers for Kawasaki disease stratification and offer new insight into the pathogenesis of specific KD phenotypes.