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PubMed:7479827 JSONTXT 17 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-142 Sentence denotes Molecular basis of human mitochondrial very-long-chain acyl-CoA dehydrogenase deficiency causing cardiomyopathy and sudden death in childhood.
T1 0-142 Sentence denotes Molecular basis of human mitochondrial very-long-chain acyl-CoA dehydrogenase deficiency causing cardiomyopathy and sudden death in childhood.
TextSentencer_T2 143-233 Sentence denotes beta-Oxidation of long-chain fatty acids provides the major source of energy in the heart.
T2 143-233 Sentence denotes beta-Oxidation of long-chain fatty acids provides the major source of energy in the heart.
TextSentencer_T3 234-414 Sentence denotes Defects in enzymes of the beta-oxidation pathway cause sudden, unexplained death in childhood, acute hepatic encephalopathy or liver failure, skeletal myopathy, and cardiomyopathy.
T3 234-414 Sentence denotes Defects in enzymes of the beta-oxidation pathway cause sudden, unexplained death in childhood, acute hepatic encephalopathy or liver failure, skeletal myopathy, and cardiomyopathy.
TextSentencer_T4 415-575 Sentence denotes Very-long-chain acyl-CoA dehydrogenase [VLCAD; very-long-chain-acyl-CoA:(acceptor) 2,3-oxidoreductase, EC 1.3.99.13] catalyzes the first step in beta-oxidation.
T4 415-575 Sentence denotes Very-long-chain acyl-CoA dehydrogenase [VLCAD; very-long-chain-acyl-CoA:(acceptor) 2,3-oxidoreductase, EC 1.3.99.13] catalyzes the first step in beta-oxidation.
TextSentencer_T5 576-672 Sentence denotes We have isolated the human VLCAD cDNA and gene and determined the complete nucleotide sequences.
T5 576-672 Sentence denotes We have isolated the human VLCAD cDNA and gene and determined the complete nucleotide sequences.
TextSentencer_T6 673-878 Sentence denotes Polymerase chain reaction amplification of VLCAD mRNA and genomic exons defined the molecular defects in two patients with VLCAD deficiency who presented with unexplained cardiac arrest and cardiomyopathy.
T6 673-878 Sentence denotes Polymerase chain reaction amplification of VLCAD mRNA and genomic exons defined the molecular defects in two patients with VLCAD deficiency who presented with unexplained cardiac arrest and cardiomyopathy.
TextSentencer_T7 879-1041 Sentence denotes In one, a homozygous mutation in the consensus dinucleotide of the donor splice site (g+1-->a) was associated with universal skipping of the prior exon (exon 11).
T7 879-1041 Sentence denotes In one, a homozygous mutation in the consensus dinucleotide of the donor splice site (g+1-->a) was associated with universal skipping of the prior exon (exon 11).
TextSentencer_T8 1042-1272 Sentence denotes The second patient was a compound heterozygote, with a missense mutation, C1837-->T, changing the arginine at residue 613 to tryptophan on one allele and a single base deletion at the intron-exon 6 boundary as the second mutation.
T8 1042-1272 Sentence denotes The second patient was a compound heterozygote, with a missense mutation, C1837-->T, changing the arginine at residue 613 to tryptophan on one allele and a single base deletion at the intron-exon 6 boundary as the second mutation.
TextSentencer_T9 1273-1492 Sentence denotes This initial delineation of human mutations in VLCAD suggests that VLCAD deficiency reduces myocardial fatty acid beta-oxidation and energy production and is associated with cardiomyopathy and sudden death in childhood.
T9 1273-1492 Sentence denotes This initial delineation of human mutations in VLCAD suggests that VLCAD deficiency reduces myocardial fatty acid beta-oxidation and energy production and is associated with cardiomyopathy and sudden death in childhood.