Lattice gas automata for flow and transport in geochemical systems

Lattice gas automata models are described, which couple solute transport with chemical reactions at mineral surfaces within pore networks. Diffusion in a box calculations are illustrated, which compare directly with Fickian diffusion. Chemical reactions at solid surfaces, including precipitation/dissolution, sorption, and catalytic reaction, can be examined with the model because hydrodynamic transport, solute diffusion and mineral surface processes are all treated explicitly. The simplicity and flexibility of the approach provides the ability to study the interrelationship between fluid flow and chemical reactions in porous materials, at a level of complexity that has not previously been computationally possible

Dietary Functional Ingredients: Performance of Animals and Quality and Storage Stability of Irradiated Raw Turkey Breast

The objective of this study was to evaluate the effect of dietary functional ingredients vitamin E (VE), Se, and conjugated linoleic acid (CLA), alone or in combination, on the quality of irradiated turkey breast meat. A total of 480 male turkeys (11-wk-old, raised on a cornsoybean basal diet) were randomly allotted to 32 pens and fed 1 of 8 experimental diets (4 pens/treatment) supplemented with none (control), 200 IU/kg of VE (VE), 0.3 ppm Se (Se), 2.5% CLA (CLA), 200 IU/kg of VE + 0.3 ppm Se (VE + Se), 200 IU/kg of VE + 2.5% CLA (VE + CLA), 2.5% CLA + 0.3 ppm Se (CLA + Se), 200 IU/kg of VE + 0.3 ppm Se + 2.5% CLA (VE + Se + CLA) for 4 wk. At 15 wk of age, all birds were slaughtered, and breast muscles of 8 birds from each pen were separated, pooled, and ground. Patties were prepared using the ground meat, aerobically packaged, and irradiated at 0 or 1.5 kGy absorbed dose. Lipid oxidation, color, and volatiles of the patties were measured after 0, 7, and 12 d of storage at 4°C. The content of VE and Se and fatty acid composition of lipids were also determined. Dietary supplementation of VE and CLA increased their concentrations in turkey breast. Dietary CLA decreased monounsaturated and non-CLA polyunsaturated fatty acids content in meat. Irradiation increased (P P This article is published as Yan, H. J., E. J. Lee, K. C. Nam, B. R. Min, and D. U. Ahn. "Dietary functional ingredients: Performance of animals and quality and storage stability of irradiated raw turkey breast." Poultry science 85, no. 10 (2006): 1829-1837. doi:10.1093/ps/85.10.1829.</p

Supplementary Table S6 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

QC sample reporting for Gas chromatography–mass spectrometry (GS-MS)</p

Supplementary Figures S1-S9 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Legends for supplementarytables and supplementary figures. Supplementary Figure S1. Passenger genes are frequently co-amplified with oncogenes in cancers. Supplementary Figure S2. DDX1 is highly expressed when co-amplified with MYCN. Supplementary Figure S3. Neuroblastoma cell lines with DDX1-MYCN co-amplification depend on mTORC1. Supplementary Figure S4. Ectopic DDX1 expression does not alter MYCN-driven tumorigenesis in zebrafish. Supplementary Figure S5.DDX1 expression does not affect tumorigenic properties of cancer cell lines but induces changes in cell size. Supplementary Figure S6. Aberrant DDX1 overexpression results in mTOCR1 pathway activation. Supplementary Figure S7. DDX1 interacts with alpha-KGDH complex members and disruption of the DDX1:DLST interaction reduces mTORC1 pathway activation. Supplementary Figure S8. High DDX1 expression is associated with -KG accumulation and OXPHOS reduction. Supplementary Figure S9. Aberrant DDX1 expression is associated with increased sensitivity to KG and pharmacological mTORC1 inhibition.</p

Supplementary Figures S1-S9 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Legends for supplementarytables and supplementary figures. Supplementary Figure S1. Passenger genes are frequently co-amplified with oncogenes in cancers. Supplementary Figure S2. DDX1 is highly expressed when co-amplified with MYCN. Supplementary Figure S3. Neuroblastoma cell lines with DDX1-MYCN co-amplification depend on mTORC1. Supplementary Figure S4. Ectopic DDX1 expression does not alter MYCN-driven tumorigenesis in zebrafish. Supplementary Figure S5.DDX1 expression does not affect tumorigenic properties of cancer cell lines but induces changes in cell size. Supplementary Figure S6. Aberrant DDX1 overexpression results in mTOCR1 pathway activation. Supplementary Figure S7. DDX1 interacts with alpha-KGDH complex members and disruption of the DDX1:DLST interaction reduces mTORC1 pathway activation. Supplementary Figure S8. High DDX1 expression is associated with α-KG accumulation and OXPHOS reduction. Supplementary Figure S9. Aberrant DDX1 expression is associated with increased sensitivity to αKG and pharmacological mTORC1 inhibition.</p

Figure 3 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

A proof-of-principle study identifies a selective mTOR pathway dependency in cells with DDX1-MYCN coamplification. A, Correlation between DDX1 copy-number and dependency scores (CERES) for RAPTOR in neuroblastoma cell lines (Pearson correlation analysis, R = −0.5996, P = 0.0152, N = 13). B, Western immunoblot of RAPTOR and DDX1 in the KELLY cells transduced with the doxycycline-inducible DDX1-mCherry vectors and with two pairs of sgRNAs targeting RAPTOR (sgRAPTOR) or a nontargeting sgRNA (sgNT) as well as Cas9 in the presence and absence of doxycycline (1 μg/mL). Tubulin serves as a loading control. C, Representative images of cell colonies formed by KELLY cells transduced with the doxycycline-inducible DDX1-mCherry vectors and with two pairs of sgRNA targeting RAPTOR (sgRAPTOR) or nontarget sgRNA (sgNT) as well as Cas9 in the presence and absence of doxycycline (1 μg/mL) and stained with crystal violet (left). Quantification of colony numbers (right, mean ± SE. N = 3 biological replicates; Welch t test, P = 0.564, 0.000117, and 0.00131 for sgNT, sgRAPTOR_1, and sgRAPTOR_2, respectively). D, Gene set enrichment analysis (GSEA) based on a set of genes regulated by mTORC1 measured in genes differentially expressed in tumors with high versus low DDX1 expression. E, GSEA based on a set of genes regulated by mTORC1 measured in genes differentially expressed in KELLY cells harboring a MYCN amplification with versus without ectopic DDX1 expression. F, Western blot of the relative protein expression of mTOR ser2448 phosphorylation and P70-S6K Thr389 phosphorylation in KELLY cell after inducible expression of DDX1 (1,000 ng/mL doxycycline treatment for 48 hours).</p

Supplementary Table S3 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

Gene sets enriched in in cell lines after ectopic DDX1 expression.</p

Supplementary Table S7 from Passenger Gene Coamplifications Create Collateral Therapeutic Vulnerabilities in Cancer

List of antibodies, materials, oligonucleotides, deposited data and software used in this study.</p