73 papers
This study identifies myeloid HIF-1α as a critical driver of pulmonary fibrosis that sustains hypoxic fibrotic fronts by promoting macrophage persistence and fibroblast activation, demonstrating that targeting this pathway via lung-directed therapies effectively attenuates disease progression.
This study reveals that four-week exposure to 3.2 GHz pulsed electromagnetic radiation induces sex-specific pathological pathways in mice, causing severe reproductive impairment in males and neurobehavioral deficits in females, supported by distinct circulating protein biomarkers for each sex.
This study employs comparative genomics and functional network analysis to identify and characterize *Colletotrichum sublineola* effectors lacking conserved domains, mapping their interactions within key plant immune subsystems to elucidate the mechanisms of sorghum anthracnose pathogenicity.
This study reveals that platelets exacerbate acute liver injury by delivering extracellular vesicle-mediated aldolase A to Kupffer cells, triggering a metabolic reprogramming that drives pro-inflammatory activation and identifying ALDOA as a promising therapeutic target and biomarker.
This study identifies the 129Sv mouse strain as a novel model of hypertensive emergency that exhibits multi-organ microvascular injury independent of blood pressure levels, driven by a dysregulated VEGFA/sFlt-1 balance that can be partially reversed by PlGF-2 supplementation.
This study integrates pathology expertise with deep learning to address the diagnostic challenges of distinguishing drug-induced liver injury from autoimmune hepatitis using histopathological images, achieving a classification accuracy of 74% and an AUC of 0.81 while outlining future directions for improvement.
This study demonstrates that Genomic Informational Field Theory (GIFT), by preserving the fine-grained informational structure of phenotypic data, successfully recapitulates established Alzheimer's disease genetic associations while uncovering novel loci related to neuropathology and aging that traditional average-based GWAS approaches failed to detect.
This study utilizes AI-driven single-cell spatial mapping to define a novel tissue-state biomarker, the MDS Microarchitectural Perturbation Score (MDS-MAPS), which quantifies previously unrecognized bone marrow microarchitectural changes in myelodysplastic neoplasms that correlate strongly with specific genetic mutations and track disease activity and therapeutic response.
This case report integrates AI-assisted digital pathology with spatial proteomics to characterize the architectural evolution, immune evasion mechanisms, and signaling pathway reprogramming driving therapy resistance in metastatic mucinous colorectal carcinoma, ultimately proposing a personalized therapeutic framework targeting mucin-associated barriers.
This study confirms that cellular senescence drives extracellular matrix dysregulation in the peripheral lung tissue of COPD patients, particularly those with severe early-onset disease, by establishing strong in vivo correlations between senescence markers and altered expression of key ECM components like collagens, elastogenesis genes, and proteases.
This study utilizes a multiscale correlative approach combining in-vivo 4D phase-contrast microCT and ex-vivo AFM to demonstrate that extracellular matrix remodeling in fibrotic lungs alters their mechanical response to injurious ventilation, resulting in attenuated airspace enlargement compared to healthy lungs.
This study demonstrates that human brain tissue archived for up to 78 years, whether as paraffin-embedded blocks or in long-term fixative, remains suitable for robust immunohistochemical detection of key Alzheimer's and Lewy Body Disease pathologies, including α-synuclein, tau, and β-amyloid.
This study introduces PlacentaVision, an AI-based model that automates placental morphology measurements from digital photographs with high accuracy and standardization compared to human assessments, while highlighting that discrepancies are more pronounced in irregularly shaped or preterm placentas.
This study demonstrates that bradykinin-mediated vasogenic edema, driven by the kallikrein-kinin system, significantly contributes to the pathogenesis of cerebral malaria in both human patients and murine models, suggesting that inhibiting this pathway can protect against neurologic deterioration and improve survival.
This study demonstrates that glutathione plays a dual and critical role in chytridiomycosis by being essential for *Batrachochytrium dendrobatidis* survival and virulence while simultaneously mediating amphibian host resistance specifically during the initial invasion phase, suggesting that glutathione-targeted interventions could alter disease dynamics.
The study introduces HCCExplorer, a deep learning framework that converts routine H&E slides into virtual multiplex immunofluorescence to decode spatial immune interactions in hepatocellular carcinoma, achieving superior prognostic stratification and identifying novel protective immune niches that outperform existing clinical and computational models.
This study demonstrates that pharmacologic inhibition of the RNA-binding protein HuR using the inhibitor KH3 attenuates hypertension, inflammation, oxidative stress, and fibrosis in a mouse model of chronic kidney disease by disrupting a novel HuR-SGLT2 signaling axis, thereby identifying HuR as a promising therapeutic target for hypertensive CKD.
This study demonstrates that open-source large language models can accurately transform narrative kidney biopsy reports into structured, machine-readable data, significantly reducing manual effort for research while highlighting the continued need for human supervision when extracting interpretation-dependent elements.
This study reveals that hyperactivated glycolysis drives the early, spatially-patterned depletion of Kupffer cells during MASLD progression, establishing a causal link between enhanced glucose utilization and cell death that highlights metabolic pathways as potential therapeutic targets.
This study demonstrates that in equine endometrosis, increased TGFB1 transcription and reduced MKI67 expression are associated with early fibrotic lesions and epithelial damage, respectively, while IGF1 expression inversely correlates with the severity of histopathological changes and inflammatory infiltration.