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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0018792,
umls-concept:C0018801,
umls-concept:C0031809,
umls-concept:C0034787,
umls-concept:C0035696,
umls-concept:C0086418,
umls-concept:C0205088,
umls-concept:C0205314,
umls-concept:C0332307,
umls-concept:C0392756,
umls-concept:C0392762,
umls-concept:C0449851,
umls-concept:C0456205,
umls-concept:C0679622,
umls-concept:C1550605
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pubmed:issue |
8
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pubmed:dateCreated |
1997-1-2
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pubmed:databankReference | |
pubmed:abstractText |
The number of atrial angiotensin II binding sites is reduced in end-stage human heart failure. The goals of our study were the development of a quantitative polymerase chain reaction for angiotensin II receptor type 1 mRNA to determine the angiotensin receptor type 1 (AT1) mRNA content in the atria of patients with end-stage heart failure. We established a quantitative PCR based on coamplification of AT1 wild-type and an internal standard in the same PCR, followed by liquid-phase hybridization of PCR products in microtiter plates and quantitation by ELISA. Glyceraldehyde phosphate dehydrogenase mRNA in the same samples was used to relate the AT1 mRNA content to a stably expressed reference gene. Atrial samples from 11 patients with end-stage heart failure obtained at cardiac transplantation were compared with atrial samples from 11 patients with normal cardiac function undergoing routine cardiac surgery. A PCR/ELISA system with a variance of about 6% after reverse transcription and a linear measuring range was established. In the samples from 11 patients with end-stage heart failure a 58% decrease in AT1 mRNA content was found in comparison with 11 controls (heart failure: 185,680 +/- 196,912 AT1 mRNA copies/microgram RNA, controls: 440,555 +/- 268,456, P < 0.02). When AT1 mRNA content was related to glyceraldehyde phosphate dehydrogenase mRNA, a 65% decrease was detected (AT1/glyceraldehyde phosphate dehydrogenase: heart failure: 4.84 +/- 5.18; controls: 13.74 +/- 7.77; P < 0.005). Standardization of PCR resulting in a low coefficient of variance, high reproducibility, and large sample capacity is possible using optimal internal standardization and the liquid-phase hybridization/ELISA system for detection. The optimized PCR procedure indicated downregulation of atrial AT1 in end-stage human heart failure, suggesting a reduced capacity of the atria to respond to angiotensin II stimulation in end-stage heart failure.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Glyceraldehyde-3-Phosphate...,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0946-2716
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
74
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
447-54
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pubmed:dateRevised |
2011-7-8
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pubmed:meshHeading |
pubmed-meshheading:8872858-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:8872858-DNA Primers,
pubmed-meshheading:8872858-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:8872858-Female,
pubmed-meshheading:8872858-Gene Expression,
pubmed-meshheading:8872858-Glyceraldehyde-3-Phosphate Dehydrogenases,
pubmed-meshheading:8872858-Heart Failure,
pubmed-meshheading:8872858-Humans,
pubmed-meshheading:8872858-Male,
pubmed-meshheading:8872858-Middle Aged,
pubmed-meshheading:8872858-Molecular Sequence Data,
pubmed-meshheading:8872858-Myocardium,
pubmed-meshheading:8872858-Polymerase Chain Reaction,
pubmed-meshheading:8872858-RNA, Messenger,
pubmed-meshheading:8872858-Receptors, Angiotensin
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pubmed:year |
1996
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pubmed:articleTitle |
Reduced atrial angiotensin receptor type 1 mRNA content in end-stage human heart failure: assessment by a novel quantitative PCR-ELISA technique.
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pubmed:affiliation |
Innere Medizin/Kardiologie, Virchow Klinikum, Humboldt Universität, Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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