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Victoria Hildreth

Researcher at Newcastle University

Publications -  7
Citations -  772

Victoria Hildreth is an academic researcher from Newcastle University. The author has contributed to research in topics: Neural crest & Chromosome 21. The author has an hindex of 7, co-authored 7 publications receiving 719 citations. Previous affiliations of Victoria Hildreth include Centre for Life.

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An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes

TL;DR: A trans-species aneuploid mouse line that stably transmits a freely segregating, almost complete human chromosome 21 (Hsa21) is generated, which is a model of trisomy 21, which manifests as Down syndrome in humans and has phenotypic alterations in behavior, synaptic plasticity, cerebellar neuronal number, heart development, and mandible size that relate to human DS.
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Disruption of Planar Cell Polarity Signaling Results in Congenital Heart Defects and Cardiomyopathy Attributable to Early Cardiomyocyte Disorganization

TL;DR: It is proposed that heterozygosity for mutations in different genes in the planar cell polarity pathway may be an important mechanism for congenital heart defects and cardiomyopathy in humans.
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Autonomic innervation of the developing heart: origins and function.

TL;DR: This review discusses the timing of cardiac innervation in the chick and mouse, emphasizing the relationship of the cardiac neural networks to the anatomical structures within the heart, and summarizes the main neurotransmitters secreted by the developing sympathetic and parasympathetic autonomic divisions.
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Cells migrating from the neural crest contribute to the innervation of the venous pole of the heart.

TL;DR: It is confirmed that cells from the neural crest migrate to the venous pole of the heart, and that their major role is in the development of the parasympathetic innervation.
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Non-cell-autonomous roles for the planar cell polarity gene Vangl2 in development of the coronary circulation.

TL;DR: The data suggest that Vangl2 and Rho kinase act cell autonomously in the myocardium to regulate the organization of cardiomyocytes but also have non–cell-autonomous effects on the formation of the coronary vasculature.