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Walker, E. C.

Publications and source records attributed to Walker, E. C..

2 recordsLinked to original sources

Biologically-Inspired Digital Histology for Deep Phenotyping of Placental Composition Changes Across Major Lesion Types

Placenta pathology provides diagnostic insights for understanding pregnancy complications and guides maternal and perinatal care. While placental abnormalities reflect both acute and chronic maternal-fetal health states, the organs spatial and temporal heterogeneity poses significant challenges for systematic histological analysis. To date, there has been no analysis of cell populations and their relationship to placental lesions due to the scale of annotations required by expert pathologists. The Histology Analysis Pipeline.PY (HAPPY), previously published by our group, is a hierarchical deep learning approach for quantitative single-cell resolution analysis of H&E slides. Here we apply HAPPY to analyse 130 slides from 62 live full-term pregnancies across healthy controls and four common placental lesion types (infarction, perivillous fibrin, avascular villi, and intervillous thrombosis). We computed cell-type and tissue-structure compositions, established the expected range of healthy variation, and quantified slide-level deviation from this reference using compositional data analysis. Our results reveal significant cellular composition differences between histologically normal and lesioned placentas, including increased extra-villous trophoblasts and leukocytes, coupled with decreases in Hofbauer cells. These changes accompanied distinctive tissue microstructural alterations, particularly increased fibrin deposition and changes to the villous structures. The magnitude of compositional deviation increased with infarction size but not with intervillous thrombosis. Importantly, many differences extend beyond visibly affected areas, indicating organ-wide adaptive responses rather than purely discrete focal pathologies. This quantitative characterisation provides insights into relationships between specific pathologies and placental structure, demonstrating the potential of AI-based methods to enhance conventional histopathological assessment for research and clinical practice.

pathology↗

The effect of carbamazepine on bone structure and strength in control and Osteogenesis Imperfecta (Col1a2 +/p.G610C) mice

The inherited brittle bone disease osteogenesis imperfecta (OI) is commonly caused by COL1A1 and COL1A2 mutations that disrupt the collagen I triple helix. This causes intracellular endoplasmic reticulum (ER) retention of the misfolded collagen and can result in a pathological ER stress response. A therapeutic approach to reduce this toxic mutant load could be to stimulate mutant collagen degradation by manipulating autophagy and/or ER-associated degradation. Since carbamazepine (CBZ) both stimulates autophagy of misfolded collagen X and improves skeletal pathology in a metaphyseal chondrodysplasia model, we tested the effect of CBZ on bone structure and strength in 3 week-old male OI Col1a2 +/p.G610C and control mice. Treatment for 3 or 6 weeks with CBZ, at the dose effective in metaphyseal chondrodysplasia, provided no therapeutic benefit to Col1a2 +/p.G610C mouse bone structure, strength, or composition, measured by micro-computed tomography, three point bending tests and Fourier-transform infrared microspectroscopy. In control mice however, CBZ treatment for 6 weeks impaired femur growth and led to lower femoral cortical and trabecular bone mass. These data, showing the negative impact of CBZ treatment on the developing mouse bones, raise important issues which must be considered in any human clinical applications of CBZ in growing individuals.

pathology↗