About: Merry L. Lindsey

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

American cardiac physiologist

Attributes	Values
rdf:type	Item
description	forskare (sv) 연구원 (ko) গবেষক (bn) 研究者 (ja) araştırmacı (tr) эрдэмтэн (mn) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) onderzoeker (nl) hulumtuese (sq) American cardiac physiologist (en)
rdfs:label	Merry L. Lindsey (en) Merry L. Lindsey (es) Merry L. Lindsey (nl) Merry L. Lindsey (sl) Merry L. Lindsey (ast) ميري ليندسي (ar)
skos:prefLabel	Merry L. Lindsey (en) Merry L. Lindsey (es) Merry L. Lindsey (nl) Merry L. Lindsey (sl) Merry L. Lindsey (ast) ميري ليندسي (ar)
name	Merry L. Lindsey (en) Merry L. Lindsey (es) Merry L. Lindsey (nl) Merry L. Lindsey (sl) Merry L. Lindsey (ast) ميري ليندسي (ar)
Scopus author ID	wds:Q47610305-C53456BE-9FF3-46CC-9C40-ED72A16DA24B
Scopus author ID	56826281500
instance of	wds:Q47610305-41DA5591-B016-4C8A-8CD0-1513D8C97B34
instance of	Homo sapiens
Google Knowledge Graph ID	wds:Q47610305-B10B8C87-C9DF-4564-93E7-EB9A791989F5
Google Knowledge Graph ID	http://g.co/kg/g/11f0yrmvh6
Google Knowledge Graph ID	/g/11f0yrmvh6
skos:altLabel	Merry Lindsey (en)
occupation	wds:Q47610305-C5D6F982-9C30-4877-9EFD-00B914D819AD
employer	wds:Q47610305-10945AB9-5A2F-42F8-8282-1EA9EAE12933 wds:Q47610305-4CC8C65A-08D3-49D8-B1DA-1749DFF8D9DE
sex or gender	wds:Q47610305-81DC3B91-BB2A-425F-8563-21E44CACDD4C
ISNI	wds:q47610305-86b9dc4c-4ef0-9482-0418-3c3909df7aa7
VIAF ID	wds:Q47610305-59bb47a9-4911-440b-884c-7c977ab4c7d1
Library of Congress authority ID	wds:q47610305-e37d3222-437a-a601-e24c-5b1de6fdfcec
DBLP author ID	wds:Q47610305-E3A98931-C916-431A-9F35-3A5E4234C688
family name	wds:Q47610305-19FC88A2-06D7-4478-9CFA-E38D01E8E915
WorldCat Identities ID (superseded)	wds:q47610305-e505da45-4420-d838-5bed-a0bfc960df46
National Library of Israel J9U ID	wds:q47610305-6ed30464-49ed-4b88-f844-d01c1bcc267f
VIAF ID	http://viaf.org/viaf/7225148209316200460006
Library of Congress authority ID	http://id.loc.gov/authorities/names/n2016190496
DBLP author ID	https://dblp.org/pid/121/2721.rdf
occupation	researcher
employer	University of Nebraska Medical Center Meharry Medical College
sex or gender	female organism
ISNI	0000000496074978
VIAF ID	7225148209316200460006
Library of Congress authority ID	n2016190496
DBLP author ID	121/2721
family name	Lindsey
WorldCat Identities ID (superseded)	lccn-n2016190496
National Library of Israel J9U ID	987007386511905171
ORCID iD	wds:Q47610305-1EA472C1-AFDE-426D-90D1-E92D5507A42A
ORCID iD	https://orcid.org/0000-0002-4090-0391
ORCID iD	0000-0002-4090-0391
ResearcherID	wds:Q47610305-53DCFA2D-2E5C-40B9-B7CA-AD6208A76F6F
ResearcherID	B-2650-2012
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q47610305 Merry Lindsey https://ar.wikipedia.org/wiki/%D9%85%D9%8A%D8%B1%D9%8A_%D9%84%D9%8A%D9%86%D8%AF%D8%B3%D9%8A
is author of	Cardiac wound healing post-myocardial infarction: a novel method to target extracellular matrix remodeling in the left ventricle Transformative Impact of Proteomics on Cardiovascular Health and Disease: A Scientific Statement From the American Heart Association Using extracellular matrix proteomics to understand left ventricular remodeling Stability analysis of genetic regulatory network with additive noises. Combining experimental and mathematical modeling to reveal mechanisms of macrophage-dependent left ventricular remodeling Cardiac extracellular proteome profiling and membrane topology analysis using glycoproteomics. Integrative computational and experimental approaches to establish a post-myocardial infarction knowledge map. Using systems biology approaches to understand cardiac inflammation and extracellular matrix remodeling in the setting of myocardial infarction Proteomic analysis identifies in vivo candidate matrix metalloproteinase-9 substrates in the left ventricle post-myocardial infarction. Matrix metalloproteinase-9 gene deletion facilitates angiogenesis after myocardial infarction. Endothelial nitric oxide synthase limits left ventricular remodeling after myocardial infarction in mice. Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded hearts Negative elongation factor controls energy homeostasis in cardiomyocytes IL-10 is induced in the reperfused myocardium and may modulate the reaction to injury HDL-cholesterol levels and cardiovascular risk: acCETPing the context. Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction Matrix-dependent mechanism of neutrophil-mediated release and activation of matrix metalloproteinase 9 in myocardial ischemia/reperfusion Walking the oxidative stress tightrope: a perspective from the naked mole-rat, the longest-living rodent Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling Extracellular matrix turnover and signaling during cardiac remodeling following MI: causes and consequences. Temporal and spatial expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases following myocardial infarction. Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction. Induction of monocyte chemoattractant protein-1 in the small veins of the ischemic and reperfused canine myocardium. Resident cardiac mast cells degranulate and release preformed TNF-alpha, initiating the cytokine cascade in experimental canine myocardial ischemia/reperfusion Cytokines and the microcirculation in ischemia and reperfusion Matrix metalloproteinase-28 deletion amplifies inflammatory and extracellular matrix responses to cardiac aging CC chemokine receptor 5 deletion impairs macrophage activation and induces adverse remodeling following myocardial infarction. Extracellular matrix remodeling following myocardial injury.

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