id
stringlengths 15
19
| document_id
stringlengths 15
19
| passages
list | entities
list | events
list | coreferences
list | relations
list |
---|---|---|---|---|---|---|
split_0_train_4500
|
split_0_train_4500
|
[
{
"id": "split_0_train_4500_passage",
"type": "progene_text",
"text": [
"In addition , small amino acid residues ( G and A ) were enriched at P7 and G at P8 ."
],
"offsets": [
[
0,
85
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4501
|
split_0_train_4501
|
[
{
"id": "split_0_train_4501_passage",
"type": "progene_text",
"text": [
"The primary anchors at P6 and P9 defining the phage - derived motif were present in most high - affinity I-Ag7 - binding peptides from IDDM candidate antigens but only in < or = 25 % of peptides that were low - affinity binders or failed to bind to I - Ag7 ."
],
"offsets": [
[
0,
258
]
]
}
] |
[
{
"id": "split_0_train_7090_entity",
"type": "progene_text",
"text": [
"I-Ag7"
],
"offsets": [
[
105,
110
]
],
"normalized": []
},
{
"id": "split_0_train_7091_entity",
"type": "progene_text",
"text": [
"I - Ag7"
],
"offsets": [
[
249,
256
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4502
|
split_0_train_4502
|
[
{
"id": "split_0_train_4502_passage",
"type": "progene_text",
"text": [
"A comparison of these results with the proposed motifs for peptide binding to I-Ag7 validates the one we have previously described ."
],
"offsets": [
[
0,
132
]
]
}
] |
[
{
"id": "split_0_train_7092_entity",
"type": "progene_text",
"text": [
"I-Ag7"
],
"offsets": [
[
78,
83
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4503
|
split_0_train_4503
|
[
{
"id": "split_0_train_4503_passage",
"type": "progene_text",
"text": [
"A role for focal adhesion kinase in phenylephrine - induced hypertrophy of rat ventricular cardiomyocytes ."
],
"offsets": [
[
0,
107
]
]
}
] |
[
{
"id": "split_0_train_7093_entity",
"type": "progene_text",
"text": [
"focal adhesion kinase"
],
"offsets": [
[
11,
32
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4504
|
split_0_train_4504
|
[
{
"id": "split_0_train_4504_passage",
"type": "progene_text",
"text": [
"A variety of agonists including phenylephrine ( PE ) induce hypertrophy in neonatal ventricular cardiomyocytes ."
],
"offsets": [
[
0,
112
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4505
|
split_0_train_4505
|
[
{
"id": "split_0_train_4505_passage",
"type": "progene_text",
"text": [
"Here we report that signals provided by extracellular matrix proteins ( ECM ) augment the PE - induced hypertrophic response of cardiomyocytes and provide evidence that ECM - dependent signaling is mediated in part by the protein tyrosine kinase , focal adhesion kinase ( FAK ) ."
],
"offsets": [
[
0,
279
]
]
}
] |
[
{
"id": "split_0_train_7094_entity",
"type": "progene_text",
"text": [
"protein tyrosine kinase"
],
"offsets": [
[
222,
245
]
],
"normalized": []
},
{
"id": "split_0_train_7095_entity",
"type": "progene_text",
"text": [
"focal adhesion kinase"
],
"offsets": [
[
248,
269
]
],
"normalized": []
},
{
"id": "split_0_train_7096_entity",
"type": "progene_text",
"text": [
"FAK"
],
"offsets": [
[
272,
275
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4506
|
split_0_train_4506
|
[
{
"id": "split_0_train_4506_passage",
"type": "progene_text",
"text": [
"Addition of PE to cultured neonatal cardiomyocytes stimulated sarcomeric organization , increased cell size , and induced atrial natriuretic factor in cardiomyocytes plated on the ECM protein laminin or fibronectin ."
],
"offsets": [
[
0,
216
]
]
}
] |
[
{
"id": "split_0_train_7097_entity",
"type": "progene_text",
"text": [
"atrial natriuretic factor"
],
"offsets": [
[
122,
147
]
],
"normalized": []
},
{
"id": "split_0_train_7098_entity",
"type": "progene_text",
"text": [
"laminin"
],
"offsets": [
[
192,
199
]
],
"normalized": []
},
{
"id": "split_0_train_7099_entity",
"type": "progene_text",
"text": [
"fibronectin"
],
"offsets": [
[
203,
214
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4507
|
split_0_train_4507
|
[
{
"id": "split_0_train_4507_passage",
"type": "progene_text",
"text": [
"In contrast , cardiomyocytes plated on the non - adhesive substrate gelatin exhibited a reduced capacity to undergo these PE - stimulated hypertrophic changes ."
],
"offsets": [
[
0,
160
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4508
|
split_0_train_4508
|
[
{
"id": "split_0_train_4508_passage",
"type": "progene_text",
"text": [
"In cardiomyocytes cultured on ECM , PE stimulated a rapid increase in tyrosine phosphorylation of focal adhesion proteins including FAK , paxillin , and p130 Crk - associated substrate and subsequent formation of peripheral focal complexes ."
],
"offsets": [
[
0,
241
]
]
}
] |
[
{
"id": "split_0_train_7100_entity",
"type": "progene_text",
"text": [
"FAK"
],
"offsets": [
[
132,
135
]
],
"normalized": []
},
{
"id": "split_0_train_7101_entity",
"type": "progene_text",
"text": [
"paxillin"
],
"offsets": [
[
138,
146
]
],
"normalized": []
},
{
"id": "split_0_train_7102_entity",
"type": "progene_text",
"text": [
"p130 Crk - associated substrate"
],
"offsets": [
[
153,
184
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4509
|
split_0_train_4509
|
[
{
"id": "split_0_train_4509_passage",
"type": "progene_text",
"text": [
"Inhibition of the PE - induced hypertrophic response by genistein and herbimycin-A indicated a requirement for protein tyrosine kinases in PE signaling ."
],
"offsets": [
[
0,
153
]
]
}
] |
[
{
"id": "split_0_train_7103_entity",
"type": "progene_text",
"text": [
"protein tyrosine kinases"
],
"offsets": [
[
111,
135
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4510
|
split_0_train_4510
|
[
{
"id": "split_0_train_4510_passage",
"type": "progene_text",
"text": [
"To determine whether activation of FAK is required for PE - induced hypertrophy , a dominant - interfering mutant form of FAK , termed FRNK ( FAK - related non - kinase ) , was ectopically expressed in cardiomyocytes using a replication - defective adenovirus expression system ."
],
"offsets": [
[
0,
279
]
]
}
] |
[
{
"id": "split_0_train_7104_entity",
"type": "progene_text",
"text": [
"FAK"
],
"offsets": [
[
35,
38
]
],
"normalized": []
},
{
"id": "split_0_train_7105_entity",
"type": "progene_text",
"text": [
"FAK"
],
"offsets": [
[
122,
125
]
],
"normalized": []
},
{
"id": "split_0_train_7106_entity",
"type": "progene_text",
"text": [
"FRNK"
],
"offsets": [
[
135,
139
]
],
"normalized": []
},
{
"id": "split_0_train_7107_entity",
"type": "progene_text",
"text": [
"FAK - related non - kinase"
],
"offsets": [
[
142,
168
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4511
|
split_0_train_4511
|
[
{
"id": "split_0_train_4511_passage",
"type": "progene_text",
"text": [
"FRNK expression attenuated PE - stimulated hypertrophy as assessed by cell size , sarcomeric organization , and induction of atrial natriuretic factor ."
],
"offsets": [
[
0,
152
]
]
}
] |
[
{
"id": "split_0_train_7108_entity",
"type": "progene_text",
"text": [
"FRNK"
],
"offsets": [
[
0,
4
]
],
"normalized": []
},
{
"id": "split_0_train_7109_entity",
"type": "progene_text",
"text": [
"atrial natriuretic factor"
],
"offsets": [
[
125,
150
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4512
|
split_0_train_4512
|
[
{
"id": "split_0_train_4512_passage",
"type": "progene_text",
"text": [
"These data indicate that the signal transduction pathways leading to cardiomyocyte hypertrophy are strongly influenced by and/or dependent upon an integrin - mediated signaling process requiring FAK ."
],
"offsets": [
[
0,
200
]
]
}
] |
[
{
"id": "split_0_train_7110_entity",
"type": "progene_text",
"text": [
"integrin"
],
"offsets": [
[
147,
155
]
],
"normalized": []
},
{
"id": "split_0_train_7111_entity",
"type": "progene_text",
"text": [
"FAK"
],
"offsets": [
[
195,
198
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4513
|
split_0_train_4513
|
[
{
"id": "split_0_train_4513_passage",
"type": "progene_text",
"text": [
"Structural basis for the network of functional cooperativities in cytochrome c(3 ) from Desulfovibrio gigas : solution structures of the oxidised and reduced states ."
],
"offsets": [
[
0,
166
]
]
}
] |
[
{
"id": "split_0_train_7112_entity",
"type": "progene_text",
"text": [
"cytochrome c(3 )"
],
"offsets": [
[
66,
82
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4514
|
split_0_train_4514
|
[
{
"id": "split_0_train_4514_passage",
"type": "progene_text",
"text": [
"Cytochrome c(3) is a 14 kDa tetrahaem protein that plays a central role in the bioenergetic metabolism of Desulfovibrio spp. This involves an energy transduction mechanism made possible by a complex network of functional cooperativities between redox and redox / protolytic centres ( the redox - Bohr effect ) , which enables cytochrome c(3) to work as a proton activator ."
],
"offsets": [
[
0,
373
]
]
}
] |
[
{
"id": "split_0_train_7113_entity",
"type": "progene_text",
"text": [
"Cytochrome c(3)"
],
"offsets": [
[
0,
15
]
],
"normalized": []
},
{
"id": "split_0_train_7114_entity",
"type": "progene_text",
"text": [
"cytochrome c(3)"
],
"offsets": [
[
326,
341
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4515
|
split_0_train_4515
|
[
{
"id": "split_0_train_4515_passage",
"type": "progene_text",
"text": [
"The three - dimensional structures of the oxidised and reduced Desulfovibrio gigas cytochrome c(3) in solution were solved using 2D ( 1 ) H-NMR data ."
],
"offsets": [
[
0,
150
]
]
}
] |
[
{
"id": "split_0_train_7115_entity",
"type": "progene_text",
"text": [
"cytochrome c(3)"
],
"offsets": [
[
83,
98
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4516
|
split_0_train_4516
|
[
{
"id": "split_0_train_4516_passage",
"type": "progene_text",
"text": [
"The reduced protein structures were calculated using INDYANA , an extended version of DYANA that allows automatic calibration of NOE data ."
],
"offsets": [
[
0,
139
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4517
|
split_0_train_4517
|
[
{
"id": "split_0_train_4517_passage",
"type": "progene_text",
"text": [
"The oxidised protein structure , which includes four paramagnetic centres , was solved using the program PARADYANA , which also includes the structural paramagnetic parameters ."
],
"offsets": [
[
0,
177
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4518
|
split_0_train_4518
|
[
{
"id": "split_0_train_4518_passage",
"type": "progene_text",
"text": [
"In this case , initial structures were used to correct the upper and lower volume restraints for paramagnetic leakage , and angle restraints derived from ( 13 ) C Fermi contact shifts of haem moiety substituents were used for the axial histidine ligands ."
],
"offsets": [
[
0,
255
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4519
|
split_0_train_4519
|
[
{
"id": "split_0_train_4519_passage",
"type": "progene_text",
"text": [
"Despite the reduction of the NOE intensities by paramagnetic relaxation , the final family of structures is of similar precision and accuracy to that obtained for the reduced form ."
],
"offsets": [
[
0,
181
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4520
|
split_0_train_4520
|
[
{
"id": "split_0_train_4520_passage",
"type": "progene_text",
"text": [
"Comparison of the two structures shows that , although the global folds of the two families of structures are similar , significant localised differences occur upon change of redox state , some of which could not be detected by comparison with the X - ray structure of the oxidised state : ( 1 ) there is a redox - linked concerted rearrangement of Lys80 and Lys90 that results in the stabilisation of haem moieties II and III when both molecules are oxidised or both are reduced , in agreement with the previously measured positive redox cooperativity between these two haem moieties ."
],
"offsets": [
[
0,
586
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4521
|
split_0_train_4521
|
[
{
"id": "split_0_train_4521_passage",
"type": "progene_text",
"text": [
"This cooperativity regulates electron transfer , enabling a two - electron step adapted to the function of cytochromes c(3) as the coupling partner of hydrogenase ; and ( 2 ) the movement of haem I propionate 13 towards the interior of the protein upon reduction explains the positive redox - Bohr effect , establishing the structural basis for the redox - linked proton activation mechanism necessary for energy conservation , driving ATP synthesis ."
],
"offsets": [
[
0,
451
]
]
}
] |
[
{
"id": "split_0_train_7116_entity",
"type": "progene_text",
"text": [
"cytochromes c(3)"
],
"offsets": [
[
107,
123
]
],
"normalized": []
},
{
"id": "split_0_train_7117_entity",
"type": "progene_text",
"text": [
"hydrogenase"
],
"offsets": [
[
151,
162
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4522
|
split_0_train_4522
|
[
{
"id": "split_0_train_4522_passage",
"type": "progene_text",
"text": [
"The muscle mitogen - activated protein kinase is altered in sporadic inclusion body myositis ."
],
"offsets": [
[
0,
94
]
]
}
] |
[
{
"id": "split_0_train_7118_entity",
"type": "progene_text",
"text": [
"mitogen - activated protein kinase"
],
"offsets": [
[
11,
45
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4523
|
split_0_train_4523
|
[
{
"id": "split_0_train_4523_passage",
"type": "progene_text",
"text": [
"OBJECTIVE :"
],
"offsets": [
[
0,
11
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4524
|
split_0_train_4524
|
[
{
"id": "split_0_train_4524_passage",
"type": "progene_text",
"text": [
"To examine the origin of hyperphosphorylated proteins within the vacuolated myofibers in sporadic inclusion body myositis (s-IBM ) and search for dysregulated intracellular protein phosphorylation ."
],
"offsets": [
[
0,
198
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4525
|
split_0_train_4525
|
[
{
"id": "split_0_train_4525_passage",
"type": "progene_text",
"text": [
"BACKGROUND :"
],
"offsets": [
[
0,
12
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4526
|
split_0_train_4526
|
[
{
"id": "split_0_train_4526_passage",
"type": "progene_text",
"text": [
"s-IBM is morphologically characterized by primary endomysial inflammation and vacuolated myofibers containing tubulofilaments that originate from cytoskeletal proteins ."
],
"offsets": [
[
0,
169
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4527
|
split_0_train_4527
|
[
{
"id": "split_0_train_4527_passage",
"type": "progene_text",
"text": [
"Mitogen - activated protein kinases ( MAPKs ) play a role in regulating phosphorylation and maintaining the stability of the cytoskeletal architecture ."
],
"offsets": [
[
0,
152
]
]
}
] |
[
{
"id": "split_0_train_7119_entity",
"type": "progene_text",
"text": [
"Mitogen - activated protein kinases"
],
"offsets": [
[
0,
35
]
],
"normalized": []
},
{
"id": "split_0_train_7120_entity",
"type": "progene_text",
"text": [
"MAPKs"
],
"offsets": [
[
38,
43
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4528
|
split_0_train_4528
|
[
{
"id": "split_0_train_4528_passage",
"type": "progene_text",
"text": [
"METHODS :"
],
"offsets": [
[
0,
9
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4529
|
split_0_train_4529
|
[
{
"id": "split_0_train_4529_passage",
"type": "progene_text",
"text": [
"Muscle biopsies from seven patients with s-IBM and 15 controls were examined for the expression of the active components of the various MAPKs , including p44 / 42MAPK , p38MAPK , p46JNK1 , p54JNK2 , and p54JNK3 , using immunocytochemistry and Western blot analysis ."
],
"offsets": [
[
0,
266
]
]
}
] |
[
{
"id": "split_0_train_7121_entity",
"type": "progene_text",
"text": [
"MAPKs"
],
"offsets": [
[
136,
141
]
],
"normalized": []
},
{
"id": "split_0_train_7122_entity",
"type": "progene_text",
"text": [
"p44 / 42MAPK"
],
"offsets": [
[
154,
166
]
],
"normalized": []
},
{
"id": "split_0_train_7123_entity",
"type": "progene_text",
"text": [
"p38MAPK"
],
"offsets": [
[
169,
176
]
],
"normalized": []
},
{
"id": "split_0_train_7124_entity",
"type": "progene_text",
"text": [
"p46JNK1"
],
"offsets": [
[
179,
186
]
],
"normalized": []
},
{
"id": "split_0_train_7125_entity",
"type": "progene_text",
"text": [
"p54JNK2"
],
"offsets": [
[
189,
196
]
],
"normalized": []
},
{
"id": "split_0_train_7126_entity",
"type": "progene_text",
"text": [
"p54JNK3"
],
"offsets": [
[
203,
210
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4530
|
split_0_train_4530
|
[
{
"id": "split_0_train_4530_passage",
"type": "progene_text",
"text": [
"The expression of selected phosphorylated components was also examined in the same specimens ."
],
"offsets": [
[
0,
94
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4531
|
split_0_train_4531
|
[
{
"id": "split_0_train_4531_passage",
"type": "progene_text",
"text": [
"RESULTS :"
],
"offsets": [
[
0,
9
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4532
|
split_0_train_4532
|
[
{
"id": "split_0_train_4532_passage",
"type": "progene_text",
"text": [
"In s-IBM , but not the disease controls , the vacuolated muscle fibers express active p42MAPK but not JNK or p38MAPK ."
],
"offsets": [
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"p38MAPK"
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109,
116
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] |
[] |
[] |
[] |
split_0_train_4533
|
split_0_train_4533
|
[
{
"id": "split_0_train_4533_passage",
"type": "progene_text",
"text": [
"Western blots of cell lysates confirmed the hyperexpression of p42MAPK and demonstrated a novel 35 kD phosphoprotein ."
],
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[
0,
118
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]
}
] |
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{
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"text": [
"p42MAPK"
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63,
70
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}
] |
[] |
[] |
[] |
split_0_train_4534
|
split_0_train_4534
|
[
{
"id": "split_0_train_4534_passage",
"type": "progene_text",
"text": [
"Antibodies against phosphoepitopes of the 35 kD protein preferentially immunostained antigens within the vacuolated muscle fibers of s-IBM but not disease controls ."
],
"offsets": [
[
0,
165
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4535
|
split_0_train_4535
|
[
{
"id": "split_0_train_4535_passage",
"type": "progene_text",
"text": [
"CONCLUSION :"
],
"offsets": [
[
0,
12
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4536
|
split_0_train_4536
|
[
{
"id": "split_0_train_4536_passage",
"type": "progene_text",
"text": [
"In s-IBM , there is increased p42MAPK activation and abnormal intracellular protein phosphorylation with selective accumulation of a 35 kD phosphoprotein within the vacuolated fibers ."
],
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[
0,
184
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]
}
] |
[
{
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"type": "progene_text",
"text": [
"p42MAPK"
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[
30,
37
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}
] |
[] |
[] |
[] |
split_0_train_4537
|
split_0_train_4537
|
[
{
"id": "split_0_train_4537_passage",
"type": "progene_text",
"text": [
"Although the hyperexpression of 35kD protein may represent cytoskeletal by - products due to heightened p42MAPK activation , its abundant expression only in s-IBM implies that hyperphosphorylated myofibrillar proteins may be involved in the primary disease process ."
],
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[
0,
266
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]
}
] |
[
{
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"type": "progene_text",
"text": [
"p42MAPK"
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[
104,
111
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}
] |
[] |
[] |
[] |
split_0_train_4538
|
split_0_train_4538
|
[
{
"id": "split_0_train_4538_passage",
"type": "progene_text",
"text": [
"Mechanism of atherosclerotic calcification ."
],
"offsets": [
[
0,
44
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4539
|
split_0_train_4539
|
[
{
"id": "split_0_train_4539_passage",
"type": "progene_text",
"text": [
"Calcification is almost invariably associated with atherosclerotic plaque lesions ."
],
"offsets": [
[
0,
83
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4540
|
split_0_train_4540
|
[
{
"id": "split_0_train_4540_passage",
"type": "progene_text",
"text": [
"Recent data suggest that plaque calcification is an active , regulated process similar to osteogenesis ."
],
"offsets": [
[
0,
104
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4541
|
split_0_train_4541
|
[
{
"id": "split_0_train_4541_passage",
"type": "progene_text",
"text": [
"In order to clarify the mechanism of plaque calcification , we developed an in vitro model of vascular calcification by utilizing bovine vascular smooth muscle cells ( BVSMCs ) ."
],
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[
0,
178
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4542
|
split_0_train_4542
|
[
{
"id": "split_0_train_4542_passage",
"type": "progene_text",
"text": [
"This model is useful in that diffuse and massive calcification can be induced within 2 weeks and thereby biochemical analyses of vascular calcification can be performed ."
],
"offsets": [
[
0,
170
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4543
|
split_0_train_4543
|
[
{
"id": "split_0_train_4543_passage",
"type": "progene_text",
"text": [
"We have analyzed several aspects of vascular calcification by using this model and demonstrated as follows : 1 ) in vitro calcification of BVSMCs is regulated by calciotropic hormones and BVSMCs are equipped with a unique autocrine and/or paracrine system regulating calcium metabolism ."
],
"offsets": [
[
0,
287
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4544
|
split_0_train_4544
|
[
{
"id": "split_0_train_4544_passage",
"type": "progene_text",
"text": [
"2) Sodium - dependent phosphate cotransport plays a crucial role in BVSMC calcification as well as in mineralization of skeletal tissues ."
],
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[
0,
138
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4545
|
split_0_train_4545
|
[
{
"id": "split_0_train_4545_passage",
"type": "progene_text",
"text": [
"3) BVSMCs acquire osteoblastic phenotype under certain conditions ."
],
"offsets": [
[
0,
67
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4546
|
split_0_train_4546
|
[
{
"id": "split_0_train_4546_passage",
"type": "progene_text",
"text": [
"Finally , we discuss the roles of macrophages in the development of atherosclerotic calcification ."
],
"offsets": [
[
0,
99
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]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4547
|
split_0_train_4547
|
[
{
"id": "split_0_train_4547_passage",
"type": "progene_text",
"text": [
"Interferon - gamma ( IFN-gamma ) induces gene expression of 25-hydrovitamin D-1 alpha-hydroxylase ( 1 alpha OHase ) and its activity in macrophages ."
],
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[
0,
149
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]
}
] |
[
{
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0,
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21,
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60,
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"text": [
"1 alpha OHase"
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[
100,
113
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}
] |
[] |
[] |
[] |
split_0_train_4548
|
split_0_train_4548
|
[
{
"id": "split_0_train_4548_passage",
"type": "progene_text",
"text": [
"Since 1 alpha OHase can locally convert 25-hydroxyvitamin D into 1 alpha , 25-dihydroxyvitamin D ( 1,25(OH)2D ) , an active metabolite of vitamin D , it is suggested that local production of 1,25(OH)2D by macrophages may promote atherosclerotic calcification ."
],
"offsets": [
[
0,
260
]
]
}
] |
[
{
"id": "split_0_train_7137_entity",
"type": "progene_text",
"text": [
"1 alpha OHase"
],
"offsets": [
[
6,
19
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4549
|
split_0_train_4549
|
[
{
"id": "split_0_train_4549_passage",
"type": "progene_text",
"text": [
"Moreover , macrophages may be involved in the phenotypic changes of vascular smooth muscle cells ( VSMCs ) to acquire calcifying capacity ."
],
"offsets": [
[
0,
139
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4550
|
split_0_train_4550
|
[
{
"id": "split_0_train_4550_passage",
"type": "progene_text",
"text": [
"Therefore , the phenotypic changes of VSMCs in atherosclerotic plaque may contribute to the development of atherosclerotic calcification ."
],
"offsets": [
[
0,
138
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4551
|
split_0_train_4551
|
[
{
"id": "split_0_train_4551_passage",
"type": "progene_text",
"text": [
"A mutation in the Corynebacterium glutamicum ltsA gene causes susceptibility to lysozyme , temperature - sensitive growth , and L-glutamate production ."
],
"offsets": [
[
0,
152
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]
}
] |
[
{
"id": "split_0_train_7138_entity",
"type": "progene_text",
"text": [
"ltsA"
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[
45,
49
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},
{
"id": "split_0_train_7139_entity",
"type": "progene_text",
"text": [
"lysozyme"
],
"offsets": [
[
80,
88
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4552
|
split_0_train_4552
|
[
{
"id": "split_0_train_4552_passage",
"type": "progene_text",
"text": [
"The Corynebacterium glutamicum mutant KY9714 , originally isolated as a lysozyme - sensitive mutant , does not grow at 37 degrees C ."
],
"offsets": [
[
0,
133
]
]
}
] |
[
{
"id": "split_0_train_7140_entity",
"type": "progene_text",
"text": [
"lysozyme"
],
"offsets": [
[
72,
80
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],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4553
|
split_0_train_4553
|
[
{
"id": "split_0_train_4553_passage",
"type": "progene_text",
"text": [
"Complementation tests and DNA sequencing analysis revealed that a mutation in a single gene of 1 , 920 bp , ltsA ( lysozyme and temperature sensitive ) , was responsible for its lysozyme sensitivity and temperature sensitivity ."
],
"offsets": [
[
0,
228
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]
}
] |
[
{
"id": "split_0_train_7141_entity",
"type": "progene_text",
"text": [
"ltsA"
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108,
112
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{
"id": "split_0_train_7142_entity",
"type": "progene_text",
"text": [
"lysozyme and temperature sensitive"
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115,
149
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{
"id": "split_0_train_7143_entity",
"type": "progene_text",
"text": [
"lysozyme"
],
"offsets": [
[
178,
186
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4554
|
split_0_train_4554
|
[
{
"id": "split_0_train_4554_passage",
"type": "progene_text",
"text": [
"The ltsA gene encodes a protein homologous to the glutamine - dependent asparagine synthetases of various organisms , but it could not rescue the asparagine auxotrophy of an Escherichia coli asnA asnB double mutant ."
],
"offsets": [
[
0,
216
]
]
}
] |
[
{
"id": "split_0_train_7144_entity",
"type": "progene_text",
"text": [
"ltsA"
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"offsets": [
[
4,
8
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"normalized": []
},
{
"id": "split_0_train_7145_entity",
"type": "progene_text",
"text": [
"glutamine - dependent asparagine synthetases"
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"offsets": [
[
50,
94
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],
"normalized": []
},
{
"id": "split_0_train_7146_entity",
"type": "progene_text",
"text": [
"asnA"
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"offsets": [
[
191,
195
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],
"normalized": []
},
{
"id": "split_0_train_7147_entity",
"type": "progene_text",
"text": [
"asnB"
],
"offsets": [
[
196,
200
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4555
|
split_0_train_4555
|
[
{
"id": "split_0_train_4555_passage",
"type": "progene_text",
"text": [
"Replacement of the N-terminal Cys residue ( which is conserved in glutamine - dependent amidotransferases and is essential for enzyme activity ) by an Ala residue resulted in the loss of complementation in C. glutamicum ."
],
"offsets": [
[
0,
221
]
]
}
] |
[
{
"id": "split_0_train_7148_entity",
"type": "progene_text",
"text": [
"glutamine - dependent amidotransferases"
],
"offsets": [
[
66,
105
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4556
|
split_0_train_4556
|
[
{
"id": "split_0_train_4556_passage",
"type": "progene_text",
"text": [
"The mutant ltsA gene has an amber mutation , and the disruption of the ltsA gene caused lysozyme and temperature sensitivity similar to that in the KY9714 mutant ."
],
"offsets": [
[
0,
163
]
]
}
] |
[
{
"id": "split_0_train_7149_entity",
"type": "progene_text",
"text": [
"ltsA"
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"offsets": [
[
11,
15
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"normalized": []
},
{
"id": "split_0_train_7150_entity",
"type": "progene_text",
"text": [
"ltsA"
],
"offsets": [
[
71,
75
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4557
|
split_0_train_4557
|
[
{
"id": "split_0_train_4557_passage",
"type": "progene_text",
"text": [
"L-Glutamate production was induced by elevating growth temperature in the disruptant ."
],
"offsets": [
[
0,
86
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4558
|
split_0_train_4558
|
[
{
"id": "split_0_train_4558_passage",
"type": "progene_text",
"text": [
"These results indicate that the ltsA gene encodes a novel glutamine - dependent amidotransferase that is involved in the mechanisms of formation of rigid cell wall structure and in the L-glutamate production of C. glutamicum ."
],
"offsets": [
[
0,
226
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]
}
] |
[
{
"id": "split_0_train_7151_entity",
"type": "progene_text",
"text": [
"ltsA"
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"offsets": [
[
32,
36
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],
"normalized": []
},
{
"id": "split_0_train_7152_entity",
"type": "progene_text",
"text": [
"glutamine - dependent amidotransferase"
],
"offsets": [
[
58,
96
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],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4559
|
split_0_train_4559
|
[
{
"id": "split_0_train_4559_passage",
"type": "progene_text",
"text": [
"Bivalent sequential binding model of a Bacillus thuringiensis toxin to gypsy moth aminopeptidase N receptor ."
],
"offsets": [
[
0,
109
]
]
}
] |
[
{
"id": "split_0_train_7153_entity",
"type": "progene_text",
"text": [
"aminopeptidase N"
],
"offsets": [
[
82,
98
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4560
|
split_0_train_4560
|
[
{
"id": "split_0_train_4560_passage",
"type": "progene_text",
"text": [
"Specificity for target insects of Bacillus thuringiensis insecticidal Cry toxins is largely determined by toxin affinity for insect midgut receptors ."
],
"offsets": [
[
0,
150
]
]
}
] |
[
{
"id": "split_0_train_7154_entity",
"type": "progene_text",
"text": [
"Cry"
],
"offsets": [
[
70,
73
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4561
|
split_0_train_4561
|
[
{
"id": "split_0_train_4561_passage",
"type": "progene_text",
"text": [
"The mode of binding for one such toxin - receptor complex was investigated by extensive toxin mutagenesis , followed by real - time receptor binding analysis using an optical biosensor ( BIAcore ) ."
],
"offsets": [
[
0,
198
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4562
|
split_0_train_4562
|
[
{
"id": "split_0_train_4562_passage",
"type": "progene_text",
"text": [
"Wild - type Cry1Ac , a three - domain , lepidopteran - specific toxin , bound purified gypsy moth ( Lymantria dispar ) aminopeptidase N ( APN ) biphasically ."
],
"offsets": [
[
0,
158
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]
}
] |
[
{
"id": "split_0_train_7155_entity",
"type": "progene_text",
"text": [
"Cry1Ac"
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"offsets": [
[
12,
18
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],
"normalized": []
},
{
"id": "split_0_train_7156_entity",
"type": "progene_text",
"text": [
"aminopeptidase N"
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"offsets": [
[
119,
135
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"normalized": []
},
{
"id": "split_0_train_7157_entity",
"type": "progene_text",
"text": [
"APN"
],
"offsets": [
[
138,
141
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4563
|
split_0_train_4563
|
[
{
"id": "split_0_train_4563_passage",
"type": "progene_text",
"text": [
"Site 1 displayed fast association and dissociation kinetics , while site 2 possessed slower kinetics , yet tighter affinity ."
],
"offsets": [
[
0,
125
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4564
|
split_0_train_4564
|
[
{
"id": "split_0_train_4564_passage",
"type": "progene_text",
"text": [
"We empirically determined that two Cry1Ac surface regions are involved in in vivo toxicity and APN binding ."
],
"offsets": [
[
0,
108
]
]
}
] |
[
{
"id": "split_0_train_7158_entity",
"type": "progene_text",
"text": [
"Cry1Ac"
],
"offsets": [
[
35,
41
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],
"normalized": []
},
{
"id": "split_0_train_7159_entity",
"type": "progene_text",
"text": [
"APN"
],
"offsets": [
[
95,
98
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4565
|
split_0_train_4565
|
[
{
"id": "split_0_train_4565_passage",
"type": "progene_text",
"text": [
"Mutations within domain III affected binding rates to APN site 1 , whereas mutations in domain II affected binding rates to APN site 2 ."
],
"offsets": [
[
0,
136
]
]
}
] |
[
{
"id": "split_0_train_7160_entity",
"type": "progene_text",
"text": [
"APN"
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"offsets": [
[
54,
57
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],
"normalized": []
},
{
"id": "split_0_train_7161_entity",
"type": "progene_text",
"text": [
"APN"
],
"offsets": [
[
124,
127
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4566
|
split_0_train_4566
|
[
{
"id": "split_0_train_4566_passage",
"type": "progene_text",
"text": [
"Furthermore , domain III contact is completely inhibited in the presence of N - acetylgalactosamine , indicating loss of domain III binding eliminates all APN binding ."
],
"offsets": [
[
0,
168
]
]
}
] |
[
{
"id": "split_0_train_7162_entity",
"type": "progene_text",
"text": [
"APN"
],
"offsets": [
[
155,
158
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4567
|
split_0_train_4567
|
[
{
"id": "split_0_train_4567_passage",
"type": "progene_text",
"text": [
"Based upon these observations , the following model is proposed ."
],
"offsets": [
[
0,
65
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4568
|
split_0_train_4568
|
[
{
"id": "split_0_train_4568_passage",
"type": "progene_text",
"text": [
"A cavity in lectin - like domain III initiates docking through recognition of an N-acetylgalactosamine moiety on L. dispar APN ."
],
"offsets": [
[
0,
128
]
]
}
] |
[
{
"id": "split_0_train_7163_entity",
"type": "progene_text",
"text": [
"lectin"
],
"offsets": [
[
12,
18
]
],
"normalized": []
},
{
"id": "split_0_train_7164_entity",
"type": "progene_text",
"text": [
"APN"
],
"offsets": [
[
123,
126
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4569
|
split_0_train_4569
|
[
{
"id": "split_0_train_4569_passage",
"type": "progene_text",
"text": [
"Following primary docking , a higher affinity domain II binding mechanism occurs , which is critical for insecticidal activity ."
],
"offsets": [
[
0,
128
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4570
|
split_0_train_4570
|
[
{
"id": "split_0_train_4570_passage",
"type": "progene_text",
"text": [
"Dual effect of IL-4 on resistance to systemic gram - negative infection and production of TNF-alpha ."
],
"offsets": [
[
0,
101
]
]
}
] |
[
{
"id": "split_0_train_7165_entity",
"type": "progene_text",
"text": [
"IL-4"
],
"offsets": [
[
15,
19
]
],
"normalized": []
},
{
"id": "split_0_train_7166_entity",
"type": "progene_text",
"text": [
"TNF-alpha"
],
"offsets": [
[
90,
99
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4571
|
split_0_train_4571
|
[
{
"id": "split_0_train_4571_passage",
"type": "progene_text",
"text": [
"To determine the effect of interleukin 4 ( IL-4 ) administration in a live sepsis model characterised by high - level production of tumour necrosis factor a ( TNF-alpha ) , mice infected systemically with lethal or sublethal inocula of Pseudomonas aeruginosa were given the recombinant cytokine at different times before infection ."
],
"offsets": [
[
0,
332
]
]
}
] |
[
{
"id": "split_0_train_7167_entity",
"type": "progene_text",
"text": [
"interleukin 4"
],
"offsets": [
[
27,
40
]
],
"normalized": []
},
{
"id": "split_0_train_7168_entity",
"type": "progene_text",
"text": [
"IL-4"
],
"offsets": [
[
43,
47
]
],
"normalized": []
},
{
"id": "split_0_train_7169_entity",
"type": "progene_text",
"text": [
"tumour necrosis factor a"
],
"offsets": [
[
132,
156
]
],
"normalized": []
},
{
"id": "split_0_train_7170_entity",
"type": "progene_text",
"text": [
"TNF-alpha"
],
"offsets": [
[
159,
168
]
],
"normalized": []
},
{
"id": "split_0_train_7171_entity",
"type": "progene_text",
"text": [
"cytokine"
],
"offsets": [
[
286,
294
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4572
|
split_0_train_4572
|
[
{
"id": "split_0_train_4572_passage",
"type": "progene_text",
"text": [
"Improved survival and decreased TNF-alpha production were observed in lethally infected mice treated with the cytokine 1 day before challenge ."
],
"offsets": [
[
0,
143
]
]
}
] |
[
{
"id": "split_0_train_7172_entity",
"type": "progene_text",
"text": [
"TNF-alpha"
],
"offsets": [
[
32,
41
]
],
"normalized": []
},
{
"id": "split_0_train_7173_entity",
"type": "progene_text",
"text": [
"cytokine"
],
"offsets": [
[
110,
118
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4573
|
split_0_train_4573
|
[
{
"id": "split_0_train_4573_passage",
"type": "progene_text",
"text": [
"In contrast , increased mortality and overproduction of TNF-alpha were observed in sublethally infected mice given IL-4 at the time of infection ."
],
"offsets": [
[
0,
146
]
]
}
] |
[
{
"id": "split_0_train_7174_entity",
"type": "progene_text",
"text": [
"TNF-alpha"
],
"offsets": [
[
56,
65
]
],
"normalized": []
},
{
"id": "split_0_train_7175_entity",
"type": "progene_text",
"text": [
"IL-4"
],
"offsets": [
[
115,
119
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4574
|
split_0_train_4574
|
[
{
"id": "split_0_train_4574_passage",
"type": "progene_text",
"text": [
"Bradykinin B2 - receptor antagonism attenuates fatal cardiocirculatory breakdown induced by severe experimental pancreatitis ."
],
"offsets": [
[
0,
126
]
]
}
] |
[
{
"id": "split_0_train_7176_entity",
"type": "progene_text",
"text": [
"Bradykinin B2 - receptor"
],
"offsets": [
[
0,
24
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4575
|
split_0_train_4575
|
[
{
"id": "split_0_train_4575_passage",
"type": "progene_text",
"text": [
"OBJECTIVES :"
],
"offsets": [
[
0,
12
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4576
|
split_0_train_4576
|
[
{
"id": "split_0_train_4576_passage",
"type": "progene_text",
"text": [
"To investigate the impact of the long - acting bradykinin B2 receptor antagonist HOE 140 ( Icatibant ) on survival time in a model of severe porcine pancreatitis ."
],
"offsets": [
[
0,
163
]
]
}
] |
[
{
"id": "split_0_train_7177_entity",
"type": "progene_text",
"text": [
"bradykinin B2 receptor"
],
"offsets": [
[
47,
69
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4577
|
split_0_train_4577
|
[
{
"id": "split_0_train_4577_passage",
"type": "progene_text",
"text": [
"DESIGN :"
],
"offsets": [
[
0,
8
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4578
|
split_0_train_4578
|
[
{
"id": "split_0_train_4578_passage",
"type": "progene_text",
"text": [
"Randomized , controlled intervention trial ."
],
"offsets": [
[
0,
44
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4579
|
split_0_train_4579
|
[
{
"id": "split_0_train_4579_passage",
"type": "progene_text",
"text": [
"SUBJECTS :"
],
"offsets": [
[
0,
10
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4580
|
split_0_train_4580
|
[
{
"id": "split_0_train_4580_passage",
"type": "progene_text",
"text": [
"Thirty domestic pigs of either gender anesthetized by intravenous application of piritramide , midazolam , and pancuronium and mechanically ventilated ."
],
"offsets": [
[
0,
152
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4581
|
split_0_train_4581
|
[
{
"id": "split_0_train_4581_passage",
"type": "progene_text",
"text": [
"INTERVENTIONS :"
],
"offsets": [
[
0,
15
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4582
|
split_0_train_4582
|
[
{
"id": "split_0_train_4582_passage",
"type": "progene_text",
"text": [
"Pancreatitis was induced by an injection of sodium taurocholate ( 5 % , 1 mL / kg body weight [ BW ] ) and enterokinase ( 10 U / kg BW ) ."
],
"offsets": [
[
0,
138
]
]
}
] |
[
{
"id": "split_0_train_7178_entity",
"type": "progene_text",
"text": [
"enterokinase"
],
"offsets": [
[
107,
119
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4583
|
split_0_train_4583
|
[
{
"id": "split_0_train_4583_passage",
"type": "progene_text",
"text": [
"Control animals ( group 1 , n = 10 ) underwent the spontaneous course of the disease ."
],
"offsets": [
[
0,
86
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4584
|
split_0_train_4584
|
[
{
"id": "split_0_train_4584_passage",
"type": "progene_text",
"text": [
"In two treatment groups , Icatibant was administered either in a low ( 100 nmol / kg BW ; group 2 , n = 10 ) or in a high dosage ( 5000 nmol / kg BW ; group 3 , n = 10 ) ."
],
"offsets": [
[
0,
171
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4585
|
split_0_train_4585
|
[
{
"id": "split_0_train_4585_passage",
"type": "progene_text",
"text": [
"MEASUREMENTS AND MAIN RESULTS :"
],
"offsets": [
[
0,
31
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4586
|
split_0_train_4586
|
[
{
"id": "split_0_train_4586_passage",
"type": "progene_text",
"text": [
"Mean survival time was significantly prolonged by Icatibant ( controls , 6.6 hrs ; group 2 , 9.8 hrs ; p = .022 ; group 3 , 10.9 hrs ; p = .007 ) ."
],
"offsets": [
[
0,
147
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4587
|
split_0_train_4587
|
[
{
"id": "split_0_train_4587_passage",
"type": "progene_text",
"text": [
"Six hours postinduction , the decline of total peripheral resistance ( 52 % of baseline ) and cardiac index ( 92 % of baseline ) in controls was significantly improved by Icatibant , both in the low ( 16 % and 44 % ; p < .05 ) and high ( 6 % and 45 % ; p < .05 ) dosage ."
],
"offsets": [
[
0,
271
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4588
|
split_0_train_4588
|
[
{
"id": "split_0_train_4588_passage",
"type": "progene_text",
"text": [
"The concentrations of free , nonreceptor - bound kinin in plasma 6 hrs postinduction were significantly lower in controls than in groups 2 and 3 animals ( 111 + / - 50 vs. 208 +/- 40 and 237 + / - 52 fmol / mL , respectively ) ."
],
"offsets": [
[
0,
228
]
]
}
] |
[
{
"id": "split_0_train_7179_entity",
"type": "progene_text",
"text": [
"kinin"
],
"offsets": [
[
49,
54
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4589
|
split_0_train_4589
|
[
{
"id": "split_0_train_4589_passage",
"type": "progene_text",
"text": [
"Six hours postinduction , the pretreatment with Icatibant was associated with significantly higher plasma concentrations of phospholipase A2 ( controls , + 1194 % ; group 2 , + 2000 % ; group 3 , + 2285 % of baseline values ) and interleukin-1 receptor antagonist ( controls , 1900 + / - 800 ; group 2 , 3100 + / - 800 ; group 3 , 3600 + / - 800 pg / mL ) ."
],
"offsets": [
[
0,
357
]
]
}
] |
[
{
"id": "split_0_train_7180_entity",
"type": "progene_text",
"text": [
"phospholipase A2"
],
"offsets": [
[
124,
140
]
],
"normalized": []
},
{
"id": "split_0_train_7181_entity",
"type": "progene_text",
"text": [
"interleukin-1 receptor antagonist"
],
"offsets": [
[
230,
263
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4590
|
split_0_train_4590
|
[
{
"id": "split_0_train_4590_passage",
"type": "progene_text",
"text": [
"In contrast , the increase of urinary trypsinogen activation peptides indicating local pancreatic damage ( 589 + / - 114 nmol / L in controls ) was substantially attenuated by pretreatment with Icatibant ( group 2 , 467 + / - 102 , NS ; 352+ / - 91 nmol / L in group 3 ; p = .022 vs. controls ) ."
],
"offsets": [
[
0,
296
]
]
}
] |
[
{
"id": "split_0_train_7182_entity",
"type": "progene_text",
"text": [
"trypsinogen"
],
"offsets": [
[
38,
49
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4591
|
split_0_train_4591
|
[
{
"id": "split_0_train_4591_passage",
"type": "progene_text",
"text": [
"Systemic inflammatory reactions , however , as quantified by C - reactive protein and the extracellularly discharged neutrophil cytosolic inhibitor leukocyte neutral proteinase inhibitor were not influenced by the bradykinin B2 - receptor antagonist ."
],
"offsets": [
[
0,
251
]
]
}
] |
[
{
"id": "split_0_train_7183_entity",
"type": "progene_text",
"text": [
"C - reactive protein"
],
"offsets": [
[
61,
81
]
],
"normalized": []
},
{
"id": "split_0_train_7184_entity",
"type": "progene_text",
"text": [
"neutral proteinase"
],
"offsets": [
[
158,
176
]
],
"normalized": []
},
{
"id": "split_0_train_7185_entity",
"type": "progene_text",
"text": [
"bradykinin B2 - receptor"
],
"offsets": [
[
214,
238
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4592
|
split_0_train_4592
|
[
{
"id": "split_0_train_4592_passage",
"type": "progene_text",
"text": [
"CONCLUSIONS :"
],
"offsets": [
[
0,
13
]
]
}
] |
[] |
[] |
[] |
[] |
split_0_train_4593
|
split_0_train_4593
|
[
{
"id": "split_0_train_4593_passage",
"type": "progene_text",
"text": [
"Pretreatment with the bradykinin B2 receptor antagonist Icatibant resulted in prolonged survival time and in delayed impairment of major macrocirculatory and pulmonary variables ."
],
"offsets": [
[
0,
179
]
]
}
] |
[
{
"id": "split_0_train_7186_entity",
"type": "progene_text",
"text": [
"bradykinin B2 receptor"
],
"offsets": [
[
22,
44
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4594
|
split_0_train_4594
|
[
{
"id": "split_0_train_4594_passage",
"type": "progene_text",
"text": [
"Icatibant resulted in elevated concentrations of free , circulating kinin ."
],
"offsets": [
[
0,
75
]
]
}
] |
[
{
"id": "split_0_train_7187_entity",
"type": "progene_text",
"text": [
"kinin"
],
"offsets": [
[
68,
73
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4595
|
split_0_train_4595
|
[
{
"id": "split_0_train_4595_passage",
"type": "progene_text",
"text": [
"This was associated with increased concentrations of phospholipase A2 and interleukin-1 receptor antagonist , suggesting that circulating kinins strengthen the activation of some mediator cascades , the association of which with the kinin metabolism requires further experimental clarification ."
],
"offsets": [
[
0,
295
]
]
}
] |
[
{
"id": "split_0_train_7188_entity",
"type": "progene_text",
"text": [
"phospholipase A2"
],
"offsets": [
[
53,
69
]
],
"normalized": []
},
{
"id": "split_0_train_7189_entity",
"type": "progene_text",
"text": [
"interleukin-1 receptor antagonist"
],
"offsets": [
[
74,
107
]
],
"normalized": []
},
{
"id": "split_0_train_7190_entity",
"type": "progene_text",
"text": [
"kinins"
],
"offsets": [
[
138,
144
]
],
"normalized": []
},
{
"id": "split_0_train_7191_entity",
"type": "progene_text",
"text": [
"kinin"
],
"offsets": [
[
233,
238
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4596
|
split_0_train_4596
|
[
{
"id": "split_0_train_4596_passage",
"type": "progene_text",
"text": [
"Other variables indicating a systemic inflammatory response ( C - reactive protein , leukocyte neutral proteinase inhibitor ) remained unaffected by Icatibant ."
],
"offsets": [
[
0,
160
]
]
}
] |
[
{
"id": "split_0_train_7192_entity",
"type": "progene_text",
"text": [
"C - reactive protein"
],
"offsets": [
[
62,
82
]
],
"normalized": []
},
{
"id": "split_0_train_7193_entity",
"type": "progene_text",
"text": [
"neutral proteinase"
],
"offsets": [
[
95,
113
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4597
|
split_0_train_4597
|
[
{
"id": "split_0_train_4597_passage",
"type": "progene_text",
"text": [
"Bradykinin antagonism distinctly ameliorated the local pancreatic damage , indicated by increased urinary concentrations of trypsinogen activation peptides ."
],
"offsets": [
[
0,
157
]
]
}
] |
[
{
"id": "split_0_train_7194_entity",
"type": "progene_text",
"text": [
"Bradykinin"
],
"offsets": [
[
0,
10
]
],
"normalized": []
},
{
"id": "split_0_train_7195_entity",
"type": "progene_text",
"text": [
"trypsinogen"
],
"offsets": [
[
124,
135
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4598
|
split_0_train_4598
|
[
{
"id": "split_0_train_4598_passage",
"type": "progene_text",
"text": [
"It is concluded that the kinin metabolism plays an important role in the pathophysiology of systemic complications after severe experimental pancreatitis ."
],
"offsets": [
[
0,
155
]
]
}
] |
[
{
"id": "split_0_train_7196_entity",
"type": "progene_text",
"text": [
"kinin"
],
"offsets": [
[
25,
30
]
],
"normalized": []
}
] |
[] |
[] |
[] |
split_0_train_4599
|
split_0_train_4599
|
[
{
"id": "split_0_train_4599_passage",
"type": "progene_text",
"text": [
"Genetic analysis of insulin - like growth factor II and HLA-G in pre - eclampsia ."
],
"offsets": [
[
0,
82
]
]
}
] |
[
{
"id": "split_0_train_7197_entity",
"type": "progene_text",
"text": [
"insulin - like growth factor II"
],
"offsets": [
[
20,
51
]
],
"normalized": []
},
{
"id": "split_0_train_7198_entity",
"type": "progene_text",
"text": [
"HLA-G"
],
"offsets": [
[
56,
61
]
],
"normalized": []
}
] |
[] |
[] |
[] |
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