bionlp-ost-19-BB-rel-test  

BB-rel@ldeleger:BB-rel-24474814 JSONTXT

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Below, discontinuous spans are shown in the chain model. You can change it to the bag model.

Id Subject Object Predicate Lexical cue
T6 0-21 Microorganism denotes Group B Streptococcus
T1 0-138 Title denotes Group B Streptococcus β-hemolysin/cytolysin breaches maternal-fetal barriers to cause preterm birth and intrauterine fetal demise in vivo.
T7 53-61 Habitat denotes maternal
T8 62-67 Habitat denotes fetal
T9 104-116 Habitat denotes intrauterine
T10 104-122 Habitat denotes intrauterine fetal
T12 139-147 Habitat denotes Maternal
T11 139-155 Habitat denotes Maternal vaginal
T2 139-404 Paragraph denotes Maternal vaginal colonization with Streptococcus agalactiae (Group B Streptococcus [GBS]) is a precursor to chorioamnionitis, fetal infection, and neonatal sepsis, but the understanding of specific factors in the pathogenesis of ascending infection remains limited.
T13 174-198 Microorganism denotes Streptococcus agalactiae
T14 200-221 Microorganism denotes Group B Streptococcus
T15 223-226 Microorganism denotes GBS
T16 265-270 Habitat denotes fetal
T17 286-294 Habitat denotes neonatal
T18 352-364 Phenotype denotes pathogenesis
T3 405-570 Paragraph denotes We used a new murine model to evaluate the contribution of the pore-forming GBS β-hemolysin/cytolysin (βH/C) to vaginal colonization, ascension, and fetal infection.
T19 419-431 Habitat denotes murine model
T20 468-480 Phenotype denotes pore-forming
T21 481-484 Microorganism denotes GBS
T22 517-524 Habitat denotes vaginal
T23 554-559 Habitat denotes fetal
T4 571-1148 Paragraph denotes Competition assays demonstrated a marked advantage to βH/C-expressing GBS during colonization. Intrauterine fetal demise and/or preterm birth were observed in 54% of pregnant mice colonized with wild-type (WT) GBS and 0% of those colonized with the toxin-deficient cylE knockout strain, despite efficient colonization and ascension by both strains. Robust placental inflammation, disruption of maternal-fetal barriers, and fetal infection were more frequent in animals colonized with WT bacteria. Histopathologic examination revealed bacterial tropism for fetal lung and liver.
T24 625-640 Phenotype denotes βH/C-expressing
T25 641-644 Microorganism denotes GBS
T26 666-678 Habitat denotes Intrauterine
T27 666-684 Habitat denotes Intrauterine fetal
T28 737-750 Habitat denotes pregnant mice
T29 766-775 Phenotype denotes wild-type
T30 777-779 Phenotype denotes WT
T31 781-784 Microorganism denotes GBS
T32 820-835 Phenotype denotes toxin-deficient
T33 820-849 Phenotype denotes toxin-deficient cylE knockout
T34 927-936 Habitat denotes placental
T35 965-973 Habitat denotes maternal
T36 974-979 Habitat denotes fetal
T37 994-999 Habitat denotes fetal
T38 1032-1039 Habitat denotes animals
T39 1055-1057 Phenotype denotes WT
T42 1127-1132 Habitat denotes fetal
T41-0 1127-1132 _FRAGMENT denotes fetal
T40 1127-1137 Habitat denotes fetal lung
T41-1 1142-1147 Habitat denotes liver
T5 1149-1518 Paragraph denotes Preterm birth and fetal demise are likely the direct result of toxin-induced damage and inflammation rather than differences in efficiency of ascension into the upper genital tract. These data demonstrate a distinct contribution of βH/C to GBS chorioamnionitis and subsequent fetal infection in vivo and showcase a model for this most proximal step in GBS pathogenesis.
T43 1167-1172 Habitat denotes fetal
T44 1310-1329 Habitat denotes upper genital tract
T45 1389-1392 Microorganism denotes GBS
T46 1425-1430 Habitat denotes fetal
T47 1501-1504 Microorganism denotes GBS
T48 1505-1517 Phenotype denotes pathogenesis
C-T41-0 T41-1 T41-0 _lexicallyChainedTo liver,fetal