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Ann B. Millar

Researcher at University of Bristol

Publications -  89
Citations -  4471

Ann B. Millar is an academic researcher from University of Bristol. The author has contributed to research in topics: Vascular endothelial growth factor & Lung. The author has an hindex of 34, co-authored 89 publications receiving 3881 citations. Previous affiliations of Ann B. Millar include University of Bath & Southmead Hospital.

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Production of Interleukin 13 by Alveolar Macrophages from Normal and Fibrotic Lung

TL;DR: Findings show that IL-13 mRNA is not only a product of T cells, but is also expressed in both normal AMs and those from subjects with pulmonary fibrosis, and that at least some of the IL- 13 mRNA is translated into protein and secreted in subjects withmonary fibrosis.
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Expression of Functional Toll-Like Receptor-2 and -4 on Alveolar Epithelial Cells

TL;DR: It is shown that human primary ATII cells express mRNA and protein for both TLR-2 andTLR-4, which can be modulated by incubation with LPS and tumor necrosis factor, which suggests that ATII have the potential to contribute significantly to the host defense of the human alveolus against bacteria.
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Vascular endothelial growth factor may contribute to increased vascular permeability in acute respiratory distress syndrome.

TL;DR: It is concluded that VEGF makes a significant contribution to the endothelial cell permeability-inducing activity in plasma from patients with ARDS, and may play an important role in the development of noncardiogenic pulmonary edema in ARDS.
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Genetic variants associated with susceptibility to idiopathic pulmonary fibrosis in people of European ancestry: a genome-wide association study

TL;DR: The identification of AKAP13 as a susceptibility gene for IPF increases the prospect of successfully targeting RhoA pathway inhibitors in patients with IPF.
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Genome-Wide Association Study of Susceptibility to Idiopathic Pulmonary Fibrosis.

Richard J. Allen, +77 more
TL;DR: The observation that decreased DEPTOR expression associates with increased susceptibility to IPF supports recent studies demonstrating the importance of mTOR signaling in lung fibrosis, and new signals of association implicating KIF15 and MAD1L1 suggest a possible role of mitotic spindle-assembly genes in IPF susceptibility.