bionlp-ost-19-BB-rel-test  

BB-rel@ldeleger:BB-rel-12443829 JSONTXT

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Id Subject Object Predicate Lexical cue
T1 0-118 Title denotes Subtyping of Shiga toxin 2 variants in human-derived Shiga toxin-producing Escherichia coli strains isolated in Japan.
T3 39-44 Habitat denotes human
T4 53-74 Phenotype denotes Shiga toxin-producing
T5 75-91 Microorganism denotes Escherichia coli
T6 112-117 Geographical denotes Japan
T2 119-1177 Paragraph denotes Shiga toxin 2 (Stx2) variants have been found to exhibit not only antigenic divergence, but also differences in toxicity for tissue culture cells and animals. To clarify whether all or just a subset of Stx2 variants are important for the virulence of Shiga toxin-producing Escherichia coli, we designed PCR primers to detect and type all reported variants. We classified them into four groups according to the nucleotide sequences of the Stx2 family; for example, group 1 (G1) contains VT2vha and group 2 (G2) contains VT2d-Ount. The 120 strains of Shiga toxin-producing E. coli used in this study were isolated from humans in Japan between 1986 and 1999. Among the four variant groups, the G1 gene only was detected in 23 of the 120 clinical strains (19.2%) and all belonged to the O157 serotype. G1 is considered the most important Stx2 variant group in terms of human pathogenicity. A multiplex PCR that can detect the stx1, stx2, and G1 genes was developed as a means of rapid and easy typing to better understand the roles of the different types of Stx.
T7 244-264 Habitat denotes tissue culture cells
T8 269-276 Habitat denotes animals
T9 357-366 Phenotype denotes virulence
T10 370-391 Phenotype denotes Shiga toxin-producing
T11 392-408 Microorganism denotes Escherichia coli
T12 668-689 Phenotype denotes Shiga toxin-producing
T13 690-697 Microorganism denotes E. coli
T14 736-742 Habitat denotes humans
T15 746-751 Geographical denotes Japan
T16 853-861 Habitat denotes clinical
T17 902-906 Microorganism denotes O157
T19 984-989 Habitat denotes human
T18 984-1003 Phenotype denotes human pathogenicity