DataSheet1_Sedimentary CaCO3 Accumulation in the Deep West Pacific Ocean.pdf

Distribution of calcium carbonate (CaCO3) in marine sediment has been studied over the last century, and influence by multiple factors with regard to dissolution and dilution of sedimentary CaCO3 has long been established. There is still lack of quantification on the influence of those factors, so it remains elusive to determine which specific process is driving the down-core variation of CaCO3 content (wtCaCO3%) records. Here, based on a newly compiled CaCO3 data set and a carbonate model, depth-profiles of sedimentary wtCaCO3% from the West Pacific Ocean can be well illustrated, and influence from different factors on their distribution features can be quantified. The deep ocean circulation is found to largely shape the inter-basin disparity in sedimentary wtCaCO3% distribution between the equatorial regions (e.g., the Western Equatorial Pacific Ocean and the Central Pacific Ocean) and the north–west regions (the Philippine Sea and the Northwest Pacific Ocean) in our study region. Moreover, the slow carbonate dissolution rate in the deep Central Pacific Ocean guarantees better accumulation of CaCO3 at depth compared to that in other regions. However, enhanced dilution by non-carbonate materials of sedimentary CaCO3 on a topographic complex can potentially obstruct the dissolution profiles constituted by sedimentary wtCaCO3% in the pelagic ocean. The aforementioned assertion suggests that changes of wtCaCO3% accumulation in marine sediment in the West Pacific Ocean can be used to dictate past changes of the deep ocean circulation (2,500 to 3,000 m) in this area but constraint on the non-carbonate flux, especially on the topographic complex, should be necessary.</p

Supplementary Methods and Figure Legends from LY2875358, a Neutralizing and Internalizing Anti-MET Bivalent Antibody, Inhibits HGF-Dependent and HGF-Independent MET Activation and Tumor Growth

Supplementary Methods and Supplementary Figure Legends</p

Supplementary Tables from LY2875358, a Neutralizing and Internalizing Anti-MET Bivalent Antibody, Inhibits HGF-Dependent and HGF-Independent MET Activation and Tumor Growth

Supplementary Tables. Supplementary Table S1. Summary of cell lines used. Supplementary Table S2. Summary of Repeat-Dose Toxicity Study with LY2875358</p

Supplementary Figures from LY2875358, a Neutralizing and Internalizing Anti-MET Bivalent Antibody, Inhibits HGF-Dependent and HGF-Independent MET Activation and Tumor Growth

Supplementary Figures. Figure S1. Binding of LY2875358 to human and cynomolgus monkey MET-ECD and the blocking of HGF binding to MET-ECD by LY2875358 as determined by Biacore and ELISA assays Figure S2: Binding epitope regions of LY2875358 determined by H/D mass spectrometry were shown on the crystal structure of ternary complex MET-Sema-PSI with onartuzumab and HGFβ Figure S3. Effect of LY2875358 on HGF-induced cell migration compared to huOA-5D5. Figure S4. Effect of LY2875358 on pan-AKT phosphorylation in Caki-1, H441, and HepG2 cells. Figure S5. Effect of LY2875358 on Caki-1 cell proliferation. Figure S6. Effect of LY2875358 on HepG2 tubulogenesis. Figure S7. Effect of LY2875358 on staurosporin (STS) induced cell apoptosis. Figure S8. Effect of lysosome inhibitor leupeptin on LY2875358-induced MET localization to the lysosome. Figure S9. Effect of LY2875358 and Fab fragment of LY2875358 on HGF binding to MET, depletion of cell surface MET, and proliferation of MET amplified cell lines.</p