73 papers
This study demonstrates that angiotensin II infusion, but not norepinephrine-induced hypertension, exacerbates aortic pathology and induces lethal dissections and branch aneurysms in Fbn1C1041G/+ mice, indicating that angiotensin II drives disease progression through mechanisms beyond simple blood pressure elevation.
This study identifies that extracellular DNASE1L3 dysfunction leads to the accumulation of inflammatory self-DNA, thereby driving obesity-associated metabolic complications, and demonstrates that restoring DNASE1L3 activity can prevent these metabolic diseases.
This study demonstrates that spinal muscular atrophy involves significant cardiac pathology characterized by structural abnormalities and cardiomyocyte-intrinsic metabolic shifts driven by SMN deficiency-induced upregulation of PTEN signaling.
This study of 2,800 respiratory specimens in Quzhou, China, from late 2023 to mid-2024 reveals that influenza virus, *Streptococcus pneumoniae*, and adenovirus are the dominant pathogens causing acute respiratory infections, with infection rates varying significantly by age, season, and region, thereby highlighting the need for continuous multi-pathogen surveillance and integrated prevention strategies in the post-pandemic era.
This study demonstrates that chemotherapy-treated Wilms tumours retain distinct spatial gradients of progenitor and cancer stem cell-associated markers within viable blastemal foci, suggesting the persistence of a therapy-resistant stem cell niche that may drive tumour relapse.
A 2022/23 retrospective study of English NHS trusts reveals that poor compliance with the recommended four-hour pre-analytical delay for blood cultures is significantly linked to laboratory centralization, highlighting an urgent need for investment to improve sepsis management and antimicrobial stewardship.
This study identifies survivin as a key mechanosensitive regulator in glioblastoma that links extracellular matrix stiffness to tumor proliferation and extracellular matrix remodeling, suggesting its potential as a therapeutic target to disrupt this stiffness-driven growth cycle.
This study functionally characterizes 43 HCN1 variants to establish a genotype-phenotype framework demonstrating that loss-of-function mutations are associated with non-epileptic or milder neurodevelopmental disorders, whereas gain-of-function and mixed variants drive severe epilepsy, while also identifying allosteric modulators capable of normalizing mutant channel function.
Chronic metabolic endotoxemia induces sex-specific temporomandibular joint osteoarthritis in female rats, but not males, by triggering adipose tissue dysfunction and amplifying local leptin-mediated inflammatory signaling within the joint.
This study reveals that Fraser's Dolphins, despite being tight-skinned mammals, uniquely regenerate complex rete ridge architecture with minimal scarring following large full-thickness wounds, challenging the conventional view that high-tension environments inevitably lead to fibrotic repair.
This study demonstrates that cross-modal training using Xenium spatial transcriptomics data enables a DINO-DETR deep learning model to accurately detect and quantify vascular niches in routine H&E whole-slide images, revealing that high AI-derived vascular cell proportions serve as an independent prognostic indicator for worse survival in astrocytoma patients.
This study demonstrates that pharmacologic inhibition of the integrated stress response and RIPK3-mediated necroptosis, particularly through the repurposing of cancer drugs pazopanib and ponatinib, restores epithelial barrier function and homeostasis in Crohn's disease by reversing a reversible, epithelial-intrinsic barrier defect.
This study demonstrates that PAD4-dependent macrophage extracellular traps (METs) drive maladaptive cardiac remodeling and heart failure by promoting fibroblast activation, with clinical data showing that elevated MET levels correlate with worse cardiac function and survival in patients.
In experimental cardiometabolic HFpEF, CD4 T cell-derived IFNγ drives pathological extracellular matrix stiffening and diastolic dysfunction by inducing LOXL3-mediated collagen crosslinking in cardiac fibroblasts via the HIF1 signaling pathway, a mechanism that can be therapeutically targeted to improve cardiac function.
This study demonstrates that a U-Net ensemble with pixel- and tile-level uncertainty estimation can robustly quantify liver fibrosis across heterogeneous multi-centre cohorts by identifying artefacts and unreliable predictions, thereby enhancing the reliability of digital pathology workflows without relying solely on stain standardization.
The MOSAIC framework is an explainable AI system that decomposes breast cancer histologic grading into its constituent components to significantly reduce inter-observer variability and improve prognostic stratification compared to traditional manual assessment.
Hepatocyte-specific deletion of the PRC2 component Eed eliminates H3K27me3, leading to liver injury and fibrosis while paradoxically accelerating liver mass recovery in surviving mice, thereby demonstrating that precise PRC2-mediated epigenetic repression is essential for maintaining liver homeostasis and regulating regenerative outcomes.
This longitudinal study characterizes the progressive liver disease in the PEX1-G844Asp mouse model of mild Zellweger Spectrum Disorder, revealing that global peroxisome dysfunction drives hepatopathy through PPAR-mediated hyperplasia and steatosis, as well as systemic lipid deficiency caused by hypoglycemia and reduced lipogenesis, thereby identifying novel therapeutic targets.
This study presents a multi-component functionalized *Bifidobacterium longum* hydrogel (INPs@BL@Gel) that synergistically treats colitis-associated anxiety and depression by delivering targeted anti-inflammatory agents to the gut while simultaneously modulating the gut-brain axis through microbiota restoration and neuroactive metabolite production.
This study demonstrates that inducible activation of Protein Kinase A (PKA) in osteoblasts via deletion of the Prkar1a regulatory subunit triggers a severe high bone turnover phenotype characterized by cortical bone breakdown, impaired differentiation, and enhanced osteoclastogenesis, closely resembling several human bone diseases.