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Stiles, J.

Publications and source records attributed to Stiles, J..

2 recordsLinked to original sources

Movement abilities and brain development in preschoolers born very preterm

AimTo examine how healthy preschoolers born very preterm (VPT) with and without significant movement impairments differ from full term (FT) controls in subcortical brain volume measures and white matter diffusion properties.\n\nMethodA case-control, observational study of fifty-four VPT-born and 32 FT-born children were administered the Movement Assessment Battery for Children - Second Edition (MABC-2) and underwent MRI within 6-months of starting kindergarten. Selected subcortical structural volumes, fractional anisotropy (FA), and mean diffusivity (MD) of selected white matter tracts were compared across VPT children with movement impairments (VPT-abnormal), and VPT and FT children without movement impairments.\n\nResultsThe VPT-abnormal group had higher MD in the corpus callosum and inferior frontal-occipital fasciculus and lower FA in the anterior thalamic radiations, corpus callosum, and cingulum than the FT group. The forceps major was particularly affected in the VPT-abnormal group compared with the VPT and FT groups without movement impairments. Both VPT groups had reduced brainstem and cerebellar white matter volumes and larger lateral ventricles compared to the FT group.\n\nInterpretationMovement impairments in healthy VPT preschoolers were associated with more abnormalities in white matter integrity and reduced subcortical brain volumes most likely reflecting a greater extent of white matter damage associated with their very preterm birth.

neuroscience

Capillary morphogenesis gene 2 mediates multiple pathways of growth factor-induced angiogenesis by regulating endothelial cell chemotaxis

Pathological angiogenesis contributes to diseases as varied as cancer and corneal neovascularization. The vascular endothelial growth factor (VEGF) - VEGF receptor 2 (KDR/VEGFR2) axis has been the major target for treating pathological angiogenesis. However, VEGF-targeted therapies exhibit reduced efficacy over time, indicating that new therapeutic strategies are needed. Therefore, identifying new targets that mediate angiogenesis is of great importance. Here, we report that one of the anthrax toxin receptors, capillary morphogenesis gene 2 (ANTXR2/CMG2), plays an important role in mediating angiogenesis induced by both bFGF and VEGF. Inhibiting physiological ligand binding to CMG2 results in significant reduction of corneal neovascularization, endothelial tube formation and cell migration. We also report the novel finding that CMG2 mediates angiogenesis by regulating the direction of endothelial chemotactic migration without affecting overall cell motility.

biochemistry