Fig 2: Immunohistochemical characterization of Wilms tumor tissue for expression of a Glut 1, b fatty acid synthetase (FASN), c Ki67 (proliferating cells), and d CD34+ microvasculature.

Fig 3: Bovine and porcine pericardial patches, day 30. A) Representative photomicrographs of bovine and porcine patches, low (10x) and high (40x) magnification, scale bar 80 and 30 (porcine, 40) microns. Arrow shows the neointima; arrowhead shows the patch; L, lumen. B) Bar graph of mean neointimal thickness, bovine and porcine patches, day 30. C) Photomicrographs of immunofluorescence: blue color, DAPI; green color, CD34; red color, Ephrin-B2 or VEGFR2; merge, green + red. n = 2; representative pictures are shown. Scale bar, 10 microns. D) Western blot of Ephrin-B2 or CD34, in bovine or porcine pericardial patch, day 0 (preimplantation) or day 30; n = 2.

Fig 4: Ischemic injury stimulates TNKS1 in non-cardiomyocytes and TNKS2 in cardiomyocytes in the infarct area in rat hearts. (A–D) Representative immunohistochemical staining of TNKS1 (in red) and MHC (in green) in ventricular sections from sham-operated and MI rat hearts at 2, 4, and 8 weeks post-MI. The TNKS1-positive signal is visualized in the vasculature (arrow) in sham-operated hearts (A,A’) and in non-cardiomyocytes (examples indicated by arrows) in the infarct area at the examined time points (B–D). (A’) Inset: magnified image of TNKS1-positive cells within the vasculature. (E–G) Representative images of immunohistochemical staining showing the TNKS1-positive signal in granulocytes-like cells (E), fibroblasts (F), and endothelium-like cells (G) indicated by the arrow in the infarct area. (H,I) Representative immunohistochemical staining of TNKS1 (in green) and vimentin (in red) showing accumulation of TNKS1 in vimentin-positive fibroblasts (arrow in H), EMT cells (arrow in I), and vascular endothelial cells (arrowhead in I) in the infarct area at 2 weeks post-MI. Stars (* in I) indicate the epicardium. (J,K) Representative immunohistochemical staining of TNKS1 (in green) and CD34 (in red) showing accumulation of TNKS1 in CD34-positive (arrow) vascular endothelial cells (J) and circulating cells (K) in the infarct area at 2 weeks post-MI. (L–O) Representative immunohistochemical staining of TNKS2 (in red) and MHC (in green) in ventricular sections from sham-operated and infarcted rat hearts at 2, 4, and 8 weeks post-MI. The co-localization of TNKS2 and MHC is visualized in cardiomyocytes (arrowhead) in the infarct area at the examined time points. Scale bars: 20 μm.

Fig 5: Adjuvant nanoparticle anti-IL6 siRNA suppresses hepatic ablation-induced distant subcutaneous R3230 tumor growth via reduction in VEGF-mediated angiogenesis. (A) Tissue levels of VEGF (Y-axis2, dark gray columns) in the periablational tissue surrounding the ablation zone were quantified at 72hr after different treatments (mean ± standard deviation, n = 3–4 animals/arm). Hepatic thermal ablation increased periablational VEGF levels, which were then suppressed with adjuvant MNP anti-IL6 siRNA (p<0.05 for all comparisons). (B-E) Similarly, hepatic thermal ablation led to increased microvascular density/angiogenesis (immunohistochemistry for CD34, A: Y-axis1, light gray columns) in distant subcutaneous R3230 tumor that was also suppressed with adjuvant anti-IL6 siRNA (n = 6–7 animals/arm).