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Paul A.T. Kelly

Researcher at University of Edinburgh

Publications -  125
Citations -  4820

Paul A.T. Kelly is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Receptor & Cerebral blood flow. The author has an hindex of 39, co-authored 125 publications receiving 4659 citations. Previous affiliations of Paul A.T. Kelly include Western General Hospital.

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Memory reconsolidation: sensitivity of spatial memory to inhibition of protein synthesis in dorsal hippocampus during encoding and retrieval.

TL;DR: This study explored the idea that reconsolidation occurs in spatial memory when animals retrieve memory under circumstances in which new memory encoding is likely to occur and compared the impact of anisomycin in two conditions.
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Perivascular Microapplication of Endothelin-1: A New Model of Focal Cerebral Ischaemia in the Rat

TL;DR: It is suggested that perivascular microapplication of Et-1 may provide a useful model for the study of the functional disturbances associated with focal cerebral ischaemia in the conscious rat.
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Comparison of long and short forms of the prolactin receptor on prolactin-induced milk protein gene transcription

TL;DR: It is established that only the long form of the prolactin receptor is involved in milk protein gene transcription.
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Identification and sequence analysis of a second form of prolactin receptor by molecular cloning of complementary DNA from rabbit mammary gland.

TL;DR: Two lambda gt11 clones containing fragments of cDNA encoding the prolactin receptor from rabbit mammary gland were isolated using a rat liver prolactIn receptor cDNA probe to establish the sequence identity of this form of prolact in receptor with the growth hormone receptor.
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Programming of rat muscle and fat metabolism by in utero overexposure to glucocorticoids

TL;DR: The data suggest that hyperglycemia in 6-month-old rats exposed to dexamethasone in utero is not due to attenuated peripheral glucose disposal, however, increased GR and attenuated fatty acid uptake specifically in visceral adipose are consistent with insulin resistance in this crucial metabolic depot and could indirectly contribute to increased hepatic glucose output.