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Nick P. Talbot

Researcher at University of Oxford

Publications -  66
Citations -  2868

Nick P. Talbot is an academic researcher from University of Oxford. The author has contributed to research in topics: Hypoxia (medical) & Hypoxic pulmonary vasoconstriction. The author has an hindex of 22, co-authored 58 publications receiving 1871 citations. Previous affiliations of Nick P. Talbot include Saint Peter's University & Churchill Hospital.

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Medium-term effects of SARS-CoV-2 infection on multiple vital organs, exercise capacity, cognition, quality of life and mental health, post-hospital discharge

TL;DR: A significant proportion of COVID-19 patients discharged from hospital experience ongoing symptoms of breathlessness, fatigue, anxiety, depression and exercise limitation at 2-3 months from disease-onset.
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Physical, cognitive, and mental health impacts of COVID-19 after hospitalisation (PHOSP-COVID): a UK multicentre, prospective cohort study.

Rachael A. Evans, +780 more
TL;DR: In this paper, the effects of COVID-19-related hospitalisation on health and employment, to identify factors associated with recovery, and to describe recovery phenotypes were determined.
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Mutation of von Hippel-Lindau tumour suppressor and human cardiopulmonary physiology.

TL;DR: The phenotype associated with Chuvash polycythaemia demonstrates that VHL plays a major role in the underlying calibration and homeostasis of the respiratory and cardiovascular systems, most likely through its central role inThe regulation of HIF.
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Human pulmonary vascular response to 4 h of hypercapnia and hypocapnia measured using Doppler echocardiography

TL;DR: The human pulmonary circulatory response to changes in Pco(2) has a slower time course and greater sensitivity than is commonly assumed, and vascular tone in the normal pulmonary circulation is substantial.
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Effects of Iron Supplementation and Depletion on Hypoxic Pulmonary Hypertension: Two Randomized Controlled Trials

TL;DR: Hypoxic pulmonary hypertension may be attenuated by iron supplementation and exacerbated by iron depletion, as measured by the effect of varying iron availability on pulmonary artery systolic pressure (PASP).