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Audrey H. Poon

Researcher at McGill University Health Centre

Publications -  25
Citations -  6366

Audrey H. Poon is an academic researcher from McGill University Health Centre. The author has contributed to research in topics: Asthma & Population. The author has an hindex of 17, co-authored 25 publications receiving 5814 citations. Previous affiliations of Audrey H. Poon include Université du Québec à Chicoutimi & McGill University.

Papers
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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Association of vitamin D receptor genetic variants with susceptibility to asthma and atopy.

TL;DR: VDR genetic variants are identified as genetic risk factors for asthma/atopy and implicate a non-human leukocyte antigen immunoregulatory molecule in the pathogenesis of asthma and atopy.
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Alleles of the NRAMP1 gene are risk factors for pediatric tuberculosis disease

TL;DR: In this paper, a family-based control design was used to study the host genetic component of pediatric tuberculosis susceptibility, and the association of NRAMP1 with pediatric tuberculosis disease was significantly heterogeneous between simplex and multiplex families.
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Pathogenesis of severe asthma

TL;DR: Recent development in different cytokine signalling pathways, their interactions and steroid resistance, in the context of severe asthma pathogenesis are discussed.
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Genetic and histologic evidence for autophagy in asthma pathogenesis

TL;DR: A genetic association study to investigate whether single nucleotide polymorphisms (SNPs) in genes of the autophagy pathway are associated with asthma found that the association is likely due to the linkage disequilibrium between SNP rs12212740 and the causative variant of ATG5.