Fig 2: Higher expression of IL-33 in cancerous tissues is associated with improved overall and progression-free survival. Expressions of (A) IL-33 and (B) ST2 in the para-carcinoma and carcinoma tissues from patients with ovarian cancer measured using reverse transcription-quantitative PCR (n=10). Survival analysis of the association between the expression of IL-33 and (C) OS and (D) PFS (n=156), and association between the expression of ST2 and (E) OS and (F) PFS (n=156). (G) Co-localization of IL-33 with a-SMA but without PAX8 and CD45 detected by immunofluorescence staining. ***P<0.001. OS, overall survival; PFS, progression-free survival; ST2, interleukin-1 receptor-like 1.

Fig 3: Expression of SPP1, SULT2A1 and MEP1B in the endometrial luminal epithelium in two types of pig uterine samples defined in terms of conceptus localization in the uterus at gestational day 15. (A) Representative images taken from uterine cross-section in which conceptus is located in the mesometrial side (n = 3 gilts). (B,C) Representative images taken from uterine cross-section in which conceptus is located away from the mesometrial side (n = 3 gilts, including uterine cross-sections in which conceptus is located between mesometrial side and anti-mesometrial side and in anti-mesometrial side, respectively.) (a–c) Hematoxylin and eosin-stained whole uterine cross-section. Higher magnification images were taken from the same uterine cross-section and show the localization of the 3 proteins in endometrial regions from the M side ((a11,b11,c11) for SPP1; (a21,b21,c21) for SULT2A1; (a31,b31,c31) for MEP1B), between M and AM side ((a12,b12,c12) for SPP1; (a22,b22,c22) for SULT2A1; (a32,b32,c32) for MEP1B) and AM side ((a13,b13,c13) for SPP1; (a23,b23,c23) for SULT2A1; (a33,b33,c33) for MEP1B) of the uterus, respectively. LE: luminal epithelium; M side: mesometrial side; AM side: anti-mesometrial side. Scale bars = 50 µm.

Fig 4: Mice with ST2-deficiency show a significantly reduced volume of xenograft after transplantation of human-derived primary ovarian cancer cells. Expressions of (A) IL-33 and (B) ST2 were similar between transplant tissues respectively from NOD-SCID WT and NOD-SCID ST2-deficiency mice. (C) Volume of xenograft after transplantation of human-derived primary ovarian cancer cells in the WT and ST2-deficiency mice. (D) Statistical analysis of tumor mass of xenograft after transplantation of human-derived primary ovarian cancer cells in the WT and ST2-deficiency mice. *P<0.05, **P<0.01 and ***P<0.001. WT, wild-type; ST2, interleukin-1 receptor-like 1.

Fig 5: PARP inhibitor PJ34 attenuates APAP metabolism and liver toxicity.C57BL/6J mice were injected intraperitoneally with PJ34, and then administered with 300 mg/kg APAP injection. Blood and tissue were collected at indicated hours after APAP injection. a Representative H&E staining of liver sections from Vehicle, APAP and APAP plus PJ34-treated mice. b Quantification of liver necrosis area. Serum levels of (c) ALT and (d) AST activity. e Mice were treated with a lethal dose of APAP (1 g/kg). Survival was followed for 36 h post-administration. f Total hepatic GSH levels at indicated time points after APAP treatment. g Total hepatic H2O2 concentrations and h APAP-cysteine levels at 6 h after APAP treatment. i The hepatic expressions of Phase I (CYP1A2, CYP2E1 and CYP3A11) and Phase II enzyme genes (GSTa1, GSTp1, UGT1A1 and SULT2A1) were measured by real-time PCR assays. N = 10–12 for each group. *P < 0.01 vs. APAP