| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T53 |
0-18 |
Sentence |
denotes |
E-series resolvins |
| T54 |
19-66 |
Sentence |
denotes |
RvE is a di- or tri-hydroxyl metabolite of EPA. |
| T55 |
67-140 |
Sentence |
denotes |
To date, four RvEs (RvE1, 18S-RvE1, RvE2, and RvE3) have been discovered. |
| T56 |
141-282 |
Sentence |
denotes |
COX-2, acetylated by aspirin in hypoxic endothelial cells, introduces oxygen groups into 18R-hydro (peroxy)-eicosapentaenoic acid (18R-HEPE). |
| T57 |
283-404 |
Sentence |
denotes |
Activated PMN uses 5-LOX to convert 18R-HEPE to 5S (6)-epoxy-18R-HEPE, which is further hydrolyzed to RvE1 (Serhan et al. |
| T58 |
405-411 |
Sentence |
denotes |
2000). |
| T59 |
412-531 |
Sentence |
denotes |
RvE2 is produced by reduction of 18R HEPE products by 5-LOX to 5S-hydroperoxy, 18-hydroxy-EPE in whole blood (Oh et al. |
| T60 |
532-538 |
Sentence |
denotes |
2012). |
| T61 |
539-652 |
Sentence |
denotes |
Unlike RvE1, RvE2 and RvE3 are biosynthesized from 18-HEPE via the 12/15-LOX pathway in eosinophils (Isobe et al. |
| T62 |
653-660 |
Sentence |
denotes |
2012b). |
| T63 |
661-793 |
Sentence |
denotes |
Endogenous RvE1 has been shown to accumulate for between 48 and 72 hours, which is a delayed time point of inflammation (Hong et al. |
| T64 |
794-800 |
Sentence |
denotes |
2008). |
| T65 |
801-968 |
Sentence |
denotes |
RvE2 appeared at the time point corresponding to initial PMN infiltration in rat peritoneal exudate stimulated by zymosan A and decreased within 24 hours (Isobe et al. |
| T66 |
969-976 |
Sentence |
denotes |
2012a). |
| T67 |
977-1066 |
Sentence |
denotes |
18S-RvE1 is produced by 5-LOX and LTA4 hydrolase using 18S-HEPE as a substrate (Oh et al. |
| T68 |
1067-1073 |
Sentence |
denotes |
2011). |
