James W. Ji
Johns Hopkins University School of Medicine
7 Papers
71 Citations
James W. Ji is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Vascular endothelial growth factor & Angiogenesis. The author has an hindex of 6, co-authored 7 publications. Previous affiliations of James W. Ji include Johns Hopkins University.
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Papers
VEGF gradients, receptor activation, and sprout guidance in resting and exercising skeletal muscle
TL;DR: A three-dimensional computational model of skeletal muscle fibers, blood vessels, and interstitial space is applied to rat extensor digitorum longus and predicts that the high spatial heterogeneity of muscle fiber VEGF secretion in hypoxic tissue leads to significant gradients of V EGF concentration and VEGf receptor activation.
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Computational model of vascular endothelial growth factor spatial distribution in muscle and pro-angiogenic cell therapy.
TL;DR: A biophysically and molecularly detailed computational model is constructed to study microenvironmental transport of two isoforms of VEGF in rat extensor digitorum longus skeletal muscle under in vivo conditions and results in a platform for the design and evaluation of therapeutic approaches.
Skeletal muscle VEGF gradients in peripheral arterial disease: simulations of rest and exercise.
TL;DR: This study predicts that angiogenic therapy for PAD may be achieved not only through VEGF upregulation but also through modulation of VEGFRs and NRP1.
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A computational model of oxygen transport in skeletal muscle for sprouting and splitting modes of angiogenesis.
TL;DR: This study shows that under the steady-state conditions the effect of myoglobin (Mb) on oxygen transport was small, and this study also shows that when total blood flow in all three networks was made equal, the sprouting network had the lowest volume of hypoxic tissue of the three networks.
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Multi-scale Computational Models of Pro-angiogenic Treatments in Peripheral Arterial Disease
TL;DR: Exercise training, which results in increased V EGF secretion in hypoxic tissue and increased VEGF receptor expression, exhibits increases in both VEGFs concentration and VEGf gradients, and is predicted to be more effective than the other, VEG F-only treatments.