Additional file 1: Supplementary Figure 1. ptPDX-derived CTCs are similar in morphology and traditionally defined CTC marker expression to patient CTCs. CTCs from matched patient and ptPDX blood were enriched on a microfilter and stained with CK 8/18/19-FITC, EpCAM-PE, CD45-Cy5 and DAPI for nuclei identification. Arrowhead showing a white blood cell (WBC) captured with CTC. Scale bar, 10 μm. Supplementary Figure 2. Histopathology and immunohistochemistry staining of patient-matched primary tumor, ptPDX and CDX tumor tissues. Immunohistochemical staining of patient-matched primary, ptPDX and CDX tumor tissues. A: Representative images of hematoxylin and eosin (H&E) stained and immunostained (CK7 and Napsin A) patient-matched tumor tissues from MU150. B: Representative images of H&E stained and immunostained (CK5/6 and p40) patient-matched tumor tissues from MU197. For both sets of staining, human aorta served as negative control tissue and IgG served as isotype control. Scale bar, 20 μm. Supplementary Figure 3. Bright field images of extracted nuclei suspension from automated cell counter after staining with trypan blue. Snap-frozen matched ptPDX and CDX tumor tissues were minced on ice and homogenized. Lysate was transferred through 70 μm cell strainer, homogenized again a few strokes, and passed through 40 μm cell strainer. Nuclei were counted after staining with Trypan blue using Countess II FL Automated Cell Counter to check the quality. Supplementary Figure 4. Pre-processing and filtering of snRNA-seq data matrix. Cells were filtered based on RNA transcript count, percentage of mitochondrial (mt)/ribosomal (rb) genes, percentage of mouse reads mapped in alignment to combined human-mouse reference genome. Red dotted line indicates the set cut-off applied to remove outliers. Supplementary Figure 5. Heatmaps using differentially expressed genes (DEGs) of all clusters of ptPDX and CDX tumor tissues for cell type annotation. DEGs (Supplementary file 1) having p adj of less than 0.05 of each cluster expressing cell type canonical markers (Supplementary file 2). DEGs with p adj more than 0.05 were zeroed. Supplementary Figure 6. Heatmaps using differentially expressed genes (DEGs) of all clusters of patient primary and metastatic tumor tissues for cell type annotation. DEGs having p adj of less than 0.05 of each cluster expressing cell type canonical markers (Supplementary file 2). DEGs with p adj more than 0.05 were zeroed. Supplementary Figure 7. Integration of snRNA-seq to determine similarities and variabilities within the models. A: Volcano plot showing the differentially expressed genes (DEGs) between MU150 PDX versus MU150 CDX. Genes were grouped into upregulated (Up), downregulated (down), normal and not significant based on the average log fold change and adjusted p value (p adj). B: Gene set enrichment analysis and pathway enrichment analysis performed using top 100 (up/down regulated) DEGs between MU150 PDX versus MU150 CDX. C: Tumor growth kinetics of MU150 PDX and MU150 CDX. D: Volcano plot showing the DEGs between MU197 PDX versus MU197 CDX. E: Gene set enrichment analysis and pathway enrichment analysis performed using top 100 (up/down regulated) DEGs between MU197 PDX versus MU197. F: Tumor growth kinetics of MU197 PDX and MU197 CDX. DEGs after integration are provided in (Supplementary file 3). Supplementary Figure 8. Integration of snRNA-seq to determine similarities and differences across the models. A: Volcano plot showing the differentially expressed genes (DEGs) between MU150 (PDX + CDX) versus MU197 (PDX + CDX). Genes were grouped into upregulated (Up), downregulated (down), normal and not significant based on the average log fold change and adjusted p value (p adj). B: Heatmap showing top 100 DEGs. C: Gene set enrichment analysis and pathway enrichment analysis performed using top 100 (up/down regulated) DEGs between MU150 (PDX + CDX) versus MU197 (PDX + CDX). D: Volcano plot showing the differentially expressed genes (DEGs) between MU150 CDX versus MU197 CDX. E: Heatmap showing top 100 DEGs. F: Gene set enrichment analysis and pathway enrichment analysis performed using top 100 (up/down regulated) DEGs between MU150 CDX versus MU197 CDX. G: Tumor growth kinetics of MU150/197 PDXs. H: Tumor growth kinetics of MU150/197 CDXs. DEGs after integration are provided in (Supplementary file 3). Supplementary Figure 9. Dose response of drugs against MU150 CDX tumor-derived cells. 0.01 × 106 MU150 CDX tumor-derived cells were seeded in 96 well cell culture dish and treated with increasing concentration of MYC/MAX dimerization blocker (10058-F4) and carboplatin/paclitaxel doublet. Cell proliferation was monitored from day 1 to day 4 by performing cell proliferation assay on each day. A: Effect of increasing concentrations of MYC blocker on cell proliferation (absorbance at 490 nm) measured using the CellTiter 96® Aqueous One solution. B: Effect of increasing concentrations of doublet carboplatin/paclitaxel treatments on cell proliferation.

This dataset contains a summary of somatic variants, including variants of uncertain significance (VUS), identified through FoundationOne CDx testing in patients with papillary thyroid carcinoma. The data include gene names, mutation contexts and types, and their interpretations.All patient-identifiable information has been removed.

Brachionus leydigii (Monogononta: Ploima) reported from the western basin of Lake Erie. This dataset is not publicly accessible because: 1 specimen was reported; images available in the manuscript; water quality data and station information for EPA monitoring station where specimen was collected is available online via EPA's CDX GLENDA portal. It can be accessed through the following means: 1 specimen was reported; images available in the manuscript; water quality data and station information for EPA monitoring station where specimen was collected is available online via EPA's CDX GLENDA portal. Format: 1 specimen was reported; images available in the manuscript; water quality data and station information for EPA monitoring station where specimen was collected is available online via EPA's CDX GLENDA portal. Citation information for this dataset can be found in the EDG's Metadata Reference Information section and Data.gov's References section.

Protein-Protein, Genetic, and Chemical Interactions for Pilon N (2006):Cdx4 is a direct target of the canonical Wnt pathway. curated by BioGRID (https://thebiogrid.org); ABSTRACT: There is considerable evidence that the Cdx gene products impact on vertebral patterning by direct regulation of Hox gene expression. Data from a number of vertebrate model systems also suggest that Cdx1, Cdx2 and Cdx4 are targets of caudalizing signals such as RA, Wnt and FGF. These observations have lead to the hypothesis that Cdx members serve to relay information from signaling pathways involved in posterior patterning to the Hox genes. Regulation of Cdx1 expression by RA and Wnt in the mouse has been well characterized; however, the means by which Cdx2 and Cdx4 are regulated is less well understood. In the present study, we present data suggesting that Cdx4 is a direct target of the canonical Wnt pathway. We found that Cdx4 responds to exogenous Wnt3a in mouse embryos ex vivo, and conversely, that its expression is down-regulated in Wnt3a(vt/vt) embryos and in embryos cultured in the presence of Wnt inhibitors. We also found that the Cdx4 promoter responds to Wnt signaling in P19 embryocarcinoma cells and have identified several putative LEF/TCF response elements mediating this effect. Consistent with these data, chromatin immunoprecipitation assays from either embryocarcinoma cells or from the tail bud of embryos revealed that LEF1 and beta-catenin co-localize with the Cdx4 promoter. Taken together, these results suggest that Cdx4, like Cdx1, is a direct Wnt target.

Mean bacterial counts (log10 cells/g) per 1 g of feces from four mice in each group.Fecal bacteria in mice treated with chlorinated or tap water.

Graph and download economic data for ICE BofA US Corporate Index Option-Adjusted Spread (BAMLC0A0CM) from 1996-12-31 to 2025-07-15 about option-adjusted spread, corporate, and USA.

View the spread between a computed option-adjusted index of all BBB-rated bonds and a spot Treasury curve.

A rise in atmospheric CO2 levels, following years of burning fossil fuels, has brought about increase in global temperatures and climate change due to the greenhouse effect. As such, recent efforts in addressing this problem have been directed to the use of CO2 as a non-expensive and non-toxic single carbon, C1, source for making chemical products. Herein, we report on the use of tetrazolyl complexes as catalyst precursors for hydrogenation of CO2. Specifically, tetrazolyl compounds bearing P–S bonds have been synthesized with the view of using these as P∧N bidentate tetrazolyl ligands (1–3) that can coordinate to iridium(III), thereby forming heteroatomic five-member complexes. Interestingly, reacting the P,N′-bidentate tetrazolyl ligands with [Ir(C5Me5)Cl2]2 led to serendipitous isolation of chiral-at-metal iridium(III) half-sandwich complexes (7–9) instead. Complexes 7–9 were obtained via prior formation of non-chiral iridium(III) half-sandwich complexes (4–6). The complexes undergo prior P–S bond heterolysis of the precursor ligands, which then ultimately results in new half-sandwich iridium(III) complexes featuring monodentate phosphine co-ligands with proton-responsive P-OH groups. Conditions necessary to significantly affect the rate of P–S bond heterolysis in the precursor ligand and the subsequent coordination to iridium have been reported. The complexes served as catalyst precursors and exhibited activity in CO2 and bicarbonate hydrogenation in excellent catalytic activity, at low catalyst loadings (1 μmol or 0.07 mol% with respect to base), producing concentrated formate solutions (ca 180 mM) exclusively. Catalyst precursors with proton-responsive P-OH groups were found to influence catalytic activity when present as racemates, while ease of dissociation of the ligand from the iridium center was observed to influence activity in spite of the presence of electron-donating ligands. A test for homogeneity indicated that hydrogenation of CO2 proceeded by homogeneous means. Subsequently, the mechanism of the reaction by the iridium(III) catalyst precursors was studied using 1H NMR techniques. This revealed that a chiral-at-metal iridium hydride species generated in situ served as the active catalyst.