PubMed:27103577 / 559-854 JSONTXT

{"project":"LitCoin-sentences","denotations":[{"id":"T5","span":{"begin":0,"end":295},"obj":"Sentence"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-entities-OrganismTaxon-PD","denotations":[{"id":"T3","span":{"begin":43,"end":48},"obj":"OrganismTaxon"}],"attributes":[{"id":"A3","pred":"db_id","subj":"T3","obj":"NCBItxid:10090"},{"id":"A4","pred":"db_id","subj":"T3","obj":"NCBItxid:10088"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-entities","denotations":[{"id":"11256","span":{"begin":43,"end":48},"obj":"OrganismTaxon"},{"id":"11257","span":{"begin":56,"end":63},"obj":"DiseaseOrPhenotypicFeature"},{"id":"11258","span":{"begin":74,"end":79},"obj":"GeneOrGeneProduct"},{"id":"11259","span":{"begin":92,"end":102},"obj":"ChemicalEntity"},{"id":"11260","span":{"begin":118,"end":152},"obj":"GeneOrGeneProduct"},{"id":"11261","span":{"begin":154,"end":158},"obj":"GeneOrGeneProduct"},{"id":"11262","span":{"begin":236,"end":239},"obj":"ChemicalEntity"},{"id":"11263","span":{"begin":257,"end":260},"obj":"ChemicalEntity"}],"attributes":[{"id":"A11","pred":"db_id","subj":"11256","obj":"NCBITaxon:10090"},{"id":"A12","pred":"db_id","subj":"11257","obj":"MESH:D000860"},{"id":"A13","pred":"db_id","subj":"11258","obj":"NCBIGene:19013"},{"id":"A14","pred":"db_id","subj":"11259","obj":"MESH:D005227"},{"id":"A15","pred":"db_id","subj":"11260","obj":"NCBIGene:22229"},{"id":"A16","pred":"db_id","subj":"11261","obj":"NCBIGene:22229"},{"id":"A17","pred":"db_id","subj":"11262","obj":"MESH:D000255"},{"id":"A18","pred":"db_id","subj":"11263","obj":"MESH:D000255"}],"namespaces":[{"prefix":"_base","uri":"https://w3id.org/biolink/vocab/"},{"prefix":"MESH","uri":"http://id.nlm.nih.gov/mesh/"},{"prefix":"NCBITaxon","uri":"https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id="},{"prefix":"NCBIGene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"OMIM","uri":"https://www.omim.org/entry/"},{"prefix":"DBSNP","uri":"https://www.ncbi.nlm.nih.gov/snp/"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-GeneOrGeneProduct-v0","denotations":[{"id":"T12","span":{"begin":26,"end":30},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":49,"end":54},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":74,"end":78},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":92,"end":97},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":98,"end":102},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":118,"end":152},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":154,"end":158},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":197,"end":200},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":210,"end":216},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":236,"end":239},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":257,"end":260},"obj":"GeneOrGeneProduct"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-GeneOrGeneProduct-v2","denotations":[{"id":"T6","span":{"begin":49,"end":54},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":74,"end":78},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":98,"end":102},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":118,"end":152},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":154,"end":158},"obj":"GeneOrGeneProduct"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T6","span":{"begin":56,"end":63},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A6","pred":"originalLabel","subj":"T6","obj":"D000860"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T4","span":{"begin":74,"end":78},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":118,"end":152},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":154,"end":158},"obj":"GeneOrGeneProduct"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T3","span":{"begin":31,"end":34},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0007620"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T6","span":{"begin":56,"end":63},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A6","pred":"ID:","subj":"T6","obj":"D000860"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T5","span":{"begin":56,"end":63},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A5","pred":"#label","subj":"T5","obj":"D000860"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-Chemical-MeSH-CHEBI","denotations":[{"id":"T3","span":{"begin":236,"end":239},"obj":"ChemicalEntity"},{"id":"T5","span":{"begin":257,"end":260},"obj":"ChemicalEntity"}],"attributes":[{"id":"A3","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_30616"},{"id":"A4","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_15422"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_30616"},{"id":"A6","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_15422"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T2","span":{"begin":43,"end":48},"obj":"OrganismTaxon"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}

{"project":"LitCoin-training-merged","denotations":[{"id":"T5","span":{"begin":257,"end":260},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":236,"end":239},"obj":"ChemicalEntity"},{"id":"T6","span":{"begin":154,"end":158},"obj":"GeneOrGeneProduct"},{"id":"T24133","span":{"begin":118,"end":152},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":74,"end":78},"obj":"GeneOrGeneProduct"},{"id":"T43559","span":{"begin":56,"end":63},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T66653","span":{"begin":43,"end":48},"obj":"OrganismTaxon"}],"attributes":[{"id":"A6","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_15422"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_30616"},{"id":"A4","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_15422"},{"id":"A3","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_30616"},{"id":"A17438","pred":"#label","subj":"T43559","obj":"D000860"}],"text":"Compared with a normoxic, chow-fed control mouse heart, hypoxia decreased PPARα expression, fatty acid oxidation, and mitochondrial uncoupling protein 3 (UCP3) levels, while increasing glycolysis, all of which served to maintain normal ATP concentrations ([ATP]) and thereby, ejection fractions."}