PubMed:20206324 JSONTXT

{"project":"GoldHamster","denotations":[{"id":"T1","span":{"begin":0,"end":8},"obj":"SO:0001027"},{"id":"T2","span":{"begin":34,"end":40},"obj":"UBERON:0000479"},{"id":"T3","span":{"begin":51,"end":67},"obj":"D053840"},{"id":"T4","span":{"begin":51,"end":67},"obj":"D053840"},{"id":"T5","span":{"begin":93,"end":99},"obj":"CHEBI:26708"},{"id":"T6","span":{"begin":104,"end":111},"obj":"1895"},{"id":"T7","span":{"begin":104,"end":111},"obj":"CHEBI:29320"},{"id":"T8","span":{"begin":104,"end":111},"obj":"CHEBI:22984"},{"id":"T9","span":{"begin":112,"end":127},"obj":"D053447"},{"id":"T10","span":{"begin":112,"end":127},"obj":"D053447"},{"id":"T12","span":{"begin":164,"end":178},"obj":"D015222"},{"id":"T13","span":{"begin":189,"end":196},"obj":"1895"},{"id":"T16","span":{"begin":189,"end":204},"obj":"D015220"},{"id":"T17","span":{"begin":243,"end":259},"obj":"D053840"},{"id":"T18","span":{"begin":243,"end":259},"obj":"D053840"},{"id":"T19","span":{"begin":300,"end":308},"obj":"SO:0001027"},{"id":"T20","span":{"begin":406,"end":425},"obj":"D045506"},{"id":"T21","span":{"begin":406,"end":425},"obj":"D045506"},{"id":"T23","span":{"begin":438,"end":452},"obj":"D015222"},{"id":"T24","span":{"begin":457,"end":464},"obj":"1895"},{"id":"T27","span":{"begin":457,"end":472},"obj":"D015220"},{"id":"T28","span":{"begin":589,"end":595},"obj":"UBERON:0003674"},{"id":"T30","span":{"begin":632,"end":646},"obj":"D015222"},{"id":"T32","span":{"begin":687,"end":699},"obj":"C042288"},{"id":"T33","span":{"begin":687,"end":699},"obj":"C042288"},{"id":"T34","span":{"begin":687,"end":699},"obj":"CHEBI:135127"},{"id":"T35","span":{"begin":704,"end":713},"obj":"D020110"},{"id":"T36","span":{"begin":704,"end":713},"obj":"CHEBI:34923"},{"id":"T37","span":{"begin":704,"end":713},"obj":"CHEBI:91706"},{"id":"T38","span":{"begin":704,"end":713},"obj":"D020110"},{"id":"T40","span":{"begin":722,"end":729},"obj":"1895"},{"id":"T43","span":{"begin":722,"end":737},"obj":"D015220"},{"id":"T45","span":{"begin":777,"end":786},"obj":"11170"},{"id":"T44","span":{"begin":777,"end":786},"obj":"CHEBI:77734"},{"id":"T46","span":{"begin":777,"end":786},"obj":"CHEBI:9948"},{"id":"T47","span":{"begin":777,"end":786},"obj":"D014700"},{"id":"T48","span":{"begin":777,"end":786},"obj":"D014700"},{"id":"T49","span":{"begin":777,"end":786},"obj":"CHEBI:77736"},{"id":"T50","span":{"begin":824,"end":827},"obj":"PR:P04802"},{"id":"T51","span":{"begin":824,"end":827},"obj":"PR:Q9JID9"},{"id":"T54","span":{"begin":824,"end":827},"obj":"PR:O14492"},{"id":"T55","span":{"begin":824,"end":827},"obj":"P22325"},{"id":"T56","span":{"begin":824,"end":827},"obj":"PR:000003015"},{"id":"T57","span":{"begin":824,"end":827},"obj":"PR:Q9Z200"},{"id":"T58","span":{"begin":824,"end":827},"obj":"PR:P07288"},{"id":"T59","span":{"begin":824,"end":827},"obj":"PR:000014810"},{"id":"T60","span":{"begin":824,"end":827},"obj":"PR:P55228"},{"id":"T52","span":{"begin":824,"end":827},"obj":"UBERON:0002919"},{"id":"T53","span":{"begin":824,"end":827},"obj":"CHEBI:17709"},{"id":"T61","span":{"begin":872,"end":875},"obj":"PR:P04802"},{"id":"T62","span":{"begin":872,"end":875},"obj":"PR:Q9JID9"},{"id":"T65","span":{"begin":872,"end":875},"obj":"PR:O14492"},{"id":"T66","span":{"begin":872,"end":875},"obj":"P22325"},{"id":"T67","span":{"begin":872,"end":875},"obj":"PR:000003015"},{"id":"T68","span":{"begin":872,"end":875},"obj":"PR:Q9Z200"},{"id":"T69","span":{"begin":872,"end":875},"obj":"PR:P07288"},{"id":"T70","span":{"begin":872,"end":875},"obj":"PR:000014810"},{"id":"T71","span":{"begin":872,"end":875},"obj":"PR:P55228"},{"id":"T63","span":{"begin":872,"end":875},"obj":"UBERON:0002919"},{"id":"T64","span":{"begin":872,"end":875},"obj":"CHEBI:17709"},{"id":"T72","span":{"begin":931,"end":934},"obj":"PR:000033489"},{"id":"T73","span":{"begin":931,"end":934},"obj":"Q9UJA2"},{"id":"T74","span":{"begin":931,"end":934},"obj":"Q8H8U0"},{"id":"T75","span":{"begin":931,"end":934},"obj":"PR:Q8MZC4"},{"id":"T77","span":{"begin":931,"end":934},"obj":"Q07560"},{"id":"T78","span":{"begin":931,"end":934},"obj":"Q80ZM8"},{"id":"T79","span":{"begin":931,"end":934},"obj":"Q5U2V5"},{"id":"T80","span":{"begin":931,"end":934},"obj":"Q8MZC4"},{"id":"T81","span":{"begin":931,"end":934},"obj":"Q93YW7"},{"id":"T82","span":{"begin":931,"end":934},"obj":"O01916"},{"id":"T83","span":{"begin":931,"end":934},"obj":"PR:Q93YW7"},{"id":"T84","span":{"begin":931,"end":934},"obj":"PR:P0A6H8"},{"id":"T85","span":{"begin":931,"end":934},"obj":"PR:000005888"},{"id":"T76","span":{"begin":931,"end":934},"obj":"D038921"},{"id":"T108","span":{"begin":1030,"end":1033},"obj":"CHEBI:70255"},{"id":"T109","span":{"begin":1055,"end":1058},"obj":"CVCL_E459"},{"id":"T110","span":{"begin":1067,"end":1077},"obj":"UBERON:0002425"},{"id":"T111","span":{"begin":1067,"end":1077},"obj":"UBERON:0002348"},{"id":"T112","span":{"begin":1090,"end":1101},"obj":"UBERON:0002165"},{"id":"T128","span":{"begin":1306,"end":1316},"obj":"192213"},{"id":"T129","span":{"begin":1348,"end":1352},"obj":"615513"},{"id":"T130","span":{"begin":1360,"end":1370},"obj":"UBERON:0002425"},{"id":"T131","span":{"begin":1360,"end":1370},"obj":"UBERON:0002348"},{"id":"T132","span":{"begin":1383,"end":1394},"obj":"UBERON:0002165"},{"id":"T133","span":{"begin":1462,"end":1466},"obj":"615513"},{"id":"T134","span":{"begin":1474,"end":1484},"obj":"UBERON:0002425"},{"id":"T135","span":{"begin":1474,"end":1484},"obj":"UBERON:0002348"},{"id":"T137","span":{"begin":1650,"end":1664},"obj":"D015222"},{"id":"T138","span":{"begin":1669,"end":1676},"obj":"1895"},{"id":"T141","span":{"begin":1669,"end":1684},"obj":"D015220"},{"id":"T142","span":{"begin":1754,"end":1761},"obj":"1895"},{"id":"T145","span":{"begin":1754,"end":1769},"obj":"D015220"},{"id":"T147","span":{"begin":1904,"end":1918},"obj":"D015222"}],"text":"Genotype-phenotype correlation in tissue models of Brugada syndrome simulating patients with sodium and calcium channelopathies.\nBACKGROUND: Genetic defects in the sodium channel or in the calcium channel have been identified in patients with Brugada syndrome (BS). However, the differences in their genotype-phenotype correlations are still unclear.\nOBJECTIVE: We evaluated the phenotypic differences and therapeutic effects between the sodium channel and calcium channel abnormalities in in vitro models of BS.\nMETHODS: We created two models of BS in 18 isolated and arterially perfused canine right ventricular preparations: (1) sodium channel dysfunction model (Na model, n = 11) by pilsicainide and pinacidil and (2) calcium channel dysfunction model (Ca model, n = 7) by verapamil; optically mapped action potentials (APs) on their transmural surface; and evaluated APs and electrocardiograms (ECGs) at pacing cycle lengths (CLs) of 2,000 and 1,000 ms.\nRESULTS: CL = 1,000 ms: Both models had coved-type ST elevation in the ECG, longer AP duration (APD) in the epicardium than in the endocardium, and a similar incidence of spontaneous ventricular arrhythmias. However, the Ca model had a higher incidence of T wave alternans (TWA) than the Na-model. CL = 2,000 ms: ECGs of the Ca model converted to saddleback-type ST elevation with shorter APDs in the epicardium than in the endocardium, whereas the Na model still had coved-type ST elevation and longer APDs in the epicardium. None of the Ca model preparations had ventricular arrhythmias or TWA, although the Na model had frequent ventricular arrhythmias and TWA.\nCONCLUSION: Although both sodium channel and calcium channel dysfunction produced similar BS ECGs and arrhythmogenesis at 60 bpm, calcium channel dysfunction was associated with a higher incidence of TWA at 60 bpm, less ST elevation, and fewer arrhythmias at 30 bpm compared with sodium channel dysfunction."}

{"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T1","span":{"begin":141,"end":350},"obj":"BACKGROUND"},{"id":"T2","span":{"begin":362,"end":512},"obj":"OBJECTIVE"},{"id":"T3","span":{"begin":522,"end":958},"obj":"METHODS"},{"id":"T4","span":{"begin":968,"end":1623},"obj":"RESULTS"},{"id":"T5","span":{"begin":1636,"end":1931},"obj":"CONCLUSIONS"}],"text":"Genotype-phenotype correlation in tissue models of Brugada syndrome simulating patients with sodium and calcium channelopathies.\nBACKGROUND: Genetic defects in the sodium channel or in the calcium channel have been identified in patients with Brugada syndrome (BS). However, the differences in their genotype-phenotype correlations are still unclear.\nOBJECTIVE: We evaluated the phenotypic differences and therapeutic effects between the sodium channel and calcium channel abnormalities in in vitro models of BS.\nMETHODS: We created two models of BS in 18 isolated and arterially perfused canine right ventricular preparations: (1) sodium channel dysfunction model (Na model, n = 11) by pilsicainide and pinacidil and (2) calcium channel dysfunction model (Ca model, n = 7) by verapamil; optically mapped action potentials (APs) on their transmural surface; and evaluated APs and electrocardiograms (ECGs) at pacing cycle lengths (CLs) of 2,000 and 1,000 ms.\nRESULTS: CL = 1,000 ms: Both models had coved-type ST elevation in the ECG, longer AP duration (APD) in the epicardium than in the endocardium, and a similar incidence of spontaneous ventricular arrhythmias. However, the Ca model had a higher incidence of T wave alternans (TWA) than the Na-model. CL = 2,000 ms: ECGs of the Ca model converted to saddleback-type ST elevation with shorter APDs in the epicardium than in the endocardium, whereas the Na model still had coved-type ST elevation and longer APDs in the epicardium. None of the Ca model preparations had ventricular arrhythmias or TWA, although the Na model had frequent ventricular arrhythmias and TWA.\nCONCLUSION: Although both sodium channel and calcium channel dysfunction produced similar BS ECGs and arrhythmogenesis at 60 bpm, calcium channel dysfunction was associated with a higher incidence of TWA at 60 bpm, less ST elevation, and fewer arrhythmias at 30 bpm compared with sodium channel dysfunction."}

{"project":"Goldhamster2_Cellosaurus","denotations":[{"id":"T1","span":{"begin":261,"end":263},"obj":"CVCL_QW64|Transformed_cell_line|Homo sapiens"},{"id":"T2","span":{"begin":362,"end":364},"obj":"CVCL_5M23|Cancer_cell_line|Mesocricetus auratus"},{"id":"T3","span":{"begin":509,"end":511},"obj":"CVCL_QW64|Transformed_cell_line|Homo sapiens"},{"id":"T4","span":{"begin":522,"end":524},"obj":"CVCL_5M23|Cancer_cell_line|Mesocricetus auratus"},{"id":"T5","span":{"begin":547,"end":549},"obj":"CVCL_QW64|Transformed_cell_line|Homo sapiens"},{"id":"T6","span":{"begin":553,"end":555},"obj":"CVCL_T367|Transformed_cell_line|Chlorocebus aethiops"},{"id":"T7","span":{"begin":666,"end":668},"obj":"CVCL_7082|Cancer_cell_line|Homo sapiens"},{"id":"T8","span":{"begin":676,"end":682},"obj":"CVCL_D426|Transformed_cell_line|Mus musculus"},{"id":"T9","span":{"begin":680,"end":682},"obj":"CVCL_5986|Cancer_cell_line|Homo sapiens"},{"id":"T10","span":{"begin":714,"end":721},"obj":"CVCL_B527|Embryonic_stem_cell|Homo sapiens"},{"id":"T11","span":{"begin":757,"end":759},"obj":"CVCL_Z839|Spontaneously_immortalized_cell_line|Drosophila melanogaster"},{"id":"T12","span":{"begin":767,"end":772},"obj":"CVCL_D462|Transformed_cell_line|Mus musculus"},{"id":"T13","span":{"begin":1010,"end":1012},"obj":"CVCL_7025|Cancer_cell_line|Homo sapiens"},{"id":"T14","span":{"begin":1042,"end":1044},"obj":"CVCL_E457|Transformed_cell_line|Homo sapiens"},{"id":"T15","span":{"begin":1055,"end":1058},"obj":"CVCL_E459|Transformed_cell_line|Homo sapiens"},{"id":"T16","span":{"begin":1107,"end":1108},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T17","span":{"begin":1180,"end":1182},"obj":"CVCL_Z839|Spontaneously_immortalized_cell_line|Drosophila melanogaster"},{"id":"T18","span":{"begin":1193,"end":1194},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T19","span":{"begin":1247,"end":1249},"obj":"CVCL_7082|Cancer_cell_line|Homo sapiens"},{"id":"T20","span":{"begin":1284,"end":1286},"obj":"CVCL_Z839|Spontaneously_immortalized_cell_line|Drosophila melanogaster"},{"id":"T21","span":{"begin":1322,"end":1324},"obj":"CVCL_7025|Cancer_cell_line|Homo sapiens"},{"id":"T22","span":{"begin":1348,"end":1352},"obj":"CVCL_E459|Transformed_cell_line|Homo sapiens"},{"id":"T23","span":{"begin":1408,"end":1410},"obj":"CVCL_7082|Cancer_cell_line|Homo sapiens"},{"id":"T24","span":{"begin":1438,"end":1440},"obj":"CVCL_7025|Cancer_cell_line|Homo sapiens"},{"id":"T25","span":{"begin":1462,"end":1466},"obj":"CVCL_E459|Transformed_cell_line|Homo sapiens"},{"id":"T26","span":{"begin":1498,"end":1500},"obj":"CVCL_Z839|Spontaneously_immortalized_cell_line|Drosophila melanogaster"},{"id":"T27","span":{"begin":1569,"end":1571},"obj":"CVCL_7082|Cancer_cell_line|Homo sapiens"},{"id":"T28","span":{"begin":1714,"end":1716},"obj":"CVCL_QW64|Transformed_cell_line|Homo sapiens"},{"id":"T29","span":{"begin":1746,"end":1748},"obj":"CVCL_C917|Induced_pluripotent_stem_cell|Homo sapiens"},{"id":"T30","span":{"begin":1802,"end":1803},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T31","span":{"begin":1831,"end":1833},"obj":"CVCL_C917|Induced_pluripotent_stem_cell|Homo sapiens"},{"id":"T32","span":{"begin":1844,"end":1846},"obj":"CVCL_7025|Cancer_cell_line|Homo sapiens"},{"id":"T33","span":{"begin":1883,"end":1885},"obj":"CVCL_J925|Hybridoma|Mus musculus"}],"text":"Genotype-phenotype correlation in tissue models of Brugada syndrome simulating patients with sodium and calcium channelopathies.\nBACKGROUND: Genetic defects in the sodium channel or in the calcium channel have been identified in patients with Brugada syndrome (BS). However, the differences in their genotype-phenotype correlations are still unclear.\nOBJECTIVE: We evaluated the phenotypic differences and therapeutic effects between the sodium channel and calcium channel abnormalities in in vitro models of BS.\nMETHODS: We created two models of BS in 18 isolated and arterially perfused canine right ventricular preparations: (1) sodium channel dysfunction model (Na model, n = 11) by pilsicainide and pinacidil and (2) calcium channel dysfunction model (Ca model, n = 7) by verapamil; optically mapped action potentials (APs) on their transmural surface; and evaluated APs and electrocardiograms (ECGs) at pacing cycle lengths (CLs) of 2,000 and 1,000 ms.\nRESULTS: CL = 1,000 ms: Both models had coved-type ST elevation in the ECG, longer AP duration (APD) in the epicardium than in the endocardium, and a similar incidence of spontaneous ventricular arrhythmias. However, the Ca model had a higher incidence of T wave alternans (TWA) than the Na-model. CL = 2,000 ms: ECGs of the Ca model converted to saddleback-type ST elevation with shorter APDs in the epicardium than in the endocardium, whereas the Na model still had coved-type ST elevation and longer APDs in the epicardium. None of the Ca model preparations had ventricular arrhythmias or TWA, although the Na model had frequent ventricular arrhythmias and TWA.\nCONCLUSION: Although both sodium channel and calcium channel dysfunction produced similar BS ECGs and arrhythmogenesis at 60 bpm, calcium channel dysfunction was associated with a higher incidence of TWA at 60 bpm, less ST elevation, and fewer arrhythmias at 30 bpm compared with sodium channel dysfunction."}

{"project":"Allie","denotations":[{"id":"SS1_20206324_2_0","span":{"begin":243,"end":259},"obj":"expanded"},{"id":"SS2_20206324_2_0","span":{"begin":261,"end":263},"obj":"abbr"},{"id":"SS1_20206324_7_0","span":{"begin":805,"end":822},"obj":"expanded"},{"id":"SS2_20206324_7_0","span":{"begin":824,"end":827},"obj":"abbr"},{"id":"SS1_20206324_7_1","span":{"begin":880,"end":898},"obj":"expanded"},{"id":"SS2_20206324_7_1","span":{"begin":900,"end":904},"obj":"abbr"},{"id":"SS1_20206324_7_2","span":{"begin":916,"end":929},"obj":"expanded"},{"id":"SS2_20206324_7_2","span":{"begin":931,"end":934},"obj":"abbr"},{"id":"SS1_20206324_9_0","span":{"begin":1042,"end":1053},"obj":"expanded"},{"id":"SS2_20206324_9_0","span":{"begin":1055,"end":1058},"obj":"abbr"},{"id":"SS1_20206324_10_0","span":{"begin":1215,"end":1231},"obj":"expanded"},{"id":"SS2_20206324_10_0","span":{"begin":1233,"end":1236},"obj":"abbr"}],"relations":[{"id":"AE1_20206324_2_0","pred":"abbreviatedTo","subj":"SS1_20206324_2_0","obj":"SS2_20206324_2_0"},{"id":"AE1_20206324_7_0","pred":"abbreviatedTo","subj":"SS1_20206324_7_0","obj":"SS2_20206324_7_0"},{"id":"AE1_20206324_7_1","pred":"abbreviatedTo","subj":"SS1_20206324_7_1","obj":"SS2_20206324_7_1"},{"id":"AE1_20206324_7_2","pred":"abbreviatedTo","subj":"SS1_20206324_7_2","obj":"SS2_20206324_7_2"},{"id":"AE1_20206324_9_0","pred":"abbreviatedTo","subj":"SS1_20206324_9_0","obj":"SS2_20206324_9_0"},{"id":"AE1_20206324_10_0","pred":"abbreviatedTo","subj":"SS1_20206324_10_0","obj":"SS2_20206324_10_0"}],"text":"Genotype-phenotype correlation in tissue models of Brugada syndrome simulating patients with sodium and calcium channelopathies.\nBACKGROUND: Genetic defects in the sodium channel or in the calcium channel have been identified in patients with Brugada syndrome (BS). However, the differences in their genotype-phenotype correlations are still unclear.\nOBJECTIVE: We evaluated the phenotypic differences and therapeutic effects between the sodium channel and calcium channel abnormalities in in vitro models of BS.\nMETHODS: We created two models of BS in 18 isolated and arterially perfused canine right ventricular preparations: (1) sodium channel dysfunction model (Na model, n = 11) by pilsicainide and pinacidil and (2) calcium channel dysfunction model (Ca model, n = 7) by verapamil; optically mapped action potentials (APs) on their transmural surface; and evaluated APs and electrocardiograms (ECGs) at pacing cycle lengths (CLs) of 2,000 and 1,000 ms.\nRESULTS: CL = 1,000 ms: Both models had coved-type ST elevation in the ECG, longer AP duration (APD) in the epicardium than in the endocardium, and a similar incidence of spontaneous ventricular arrhythmias. However, the Ca model had a higher incidence of T wave alternans (TWA) than the Na-model. CL = 2,000 ms: ECGs of the Ca model converted to saddleback-type ST elevation with shorter APDs in the epicardium than in the endocardium, whereas the Na model still had coved-type ST elevation and longer APDs in the epicardium. None of the Ca model preparations had ventricular arrhythmias or TWA, although the Na model had frequent ventricular arrhythmias and TWA.\nCONCLUSION: Although both sodium channel and calcium channel dysfunction produced similar BS ECGs and arrhythmogenesis at 60 bpm, calcium channel dysfunction was associated with a higher incidence of TWA at 60 bpm, less ST elevation, and fewer arrhythmias at 30 bpm compared with sodium channel dysfunction."}