Can We Possibly Derive Sediment Quality Guidelines for Chemical Mixtures ?

for their great contribution to this work. Concluding Remarks: • Chemical mixtures do matter as reflected by the fact that 78% cases for mixtures of antifouling biocides would result in additive or synergistic effects to marine organisms. • It is possible to use TEQ-based approach to derive SQGs for mixtures consisting chemicals with a similar mode of toxic action. • For mixtures containing chemicals with different modes of toxic action, the multidimensional SSD approach maybe adopted. But this method is time-consuming and not cost-effective. • Field based approaches such as f-SSD and f-CSD potentially serve as an alternative way to derive SQGs and account for interacting effects of chemicals and biological interaction. • There is no perfect solution but we can always find a better one

Short-term tissue decomposition alters stable isotope values and C:N ratio, but does not change relationships between lipid content, C:N ratio, and Δδ13C in marine animals

Measures (e.g. δ15N, δ13C, %C, %N and C:N) derived from animal tissues are commonlyused to estimate diets and trophic interactions. Since tissue samples are often exposed toair or kept chilled in ice over a short-term during sample preparation, they may degrade.Herein, we hypothesize that tissue decomposition will cause changes in these measures. Inthis study, we kept marine fish, crustacean and mollusc tissues in air or ice over 120 h (5days). We found that tissue decomposition in air enriched δ15N (range 0.6½ to 1.3½) andδ13C (0.2½ to 0.4½), decreased %N (0.47 to 3.43 percentage points from staring values of~13%) and %C (4.53 to 8.29 percentage points from starting values of ~43%), and subsequentlyincreased C:N ratio (0.14 to 0.75). In air, while such changes to δ13C were relativelyminor and therefore likely tolerable, changes in δ15N, %N, %C and C:N ratio should be interpretedwith caution. Ice effectively reduced the extent to which decomposition enrichedδ15N ( 0.4½) and δ13C ( 0.2½), and eliminated decomposition in C:N ratio, %N and %C.In our second experiment, for fish tissues in either air or ice over 120 h, we observed noeffects of decomposition on relationships between lipid content, C:N ratio, and Δδ13C(change in δ13C after lipid removal), which are employed to correct δ13C for samples containinglipid. We also confirmed that lipid in tissues caused large errors when estimatingδ13C (mean ± standard error = -1.8½ ± 0.1½, range -0.6½ to -3.8½), and showed both lipidextraction and mathematical correction performed equally well to correct for lipids when estimatingδ13C. We, therefore, recommend that specimens of marine animals should be keptin ice during sample preparation for a short-term, as it is an effective means for minimizingchanges of the stable isotope measures in their tissue

N-cadherin is key to expression of the nucleus pulposus cell phenotype under selective substrate culture conditions

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House Market in Chinese Cities: Dynamic Modeling, In-Sampling Fitting and Out-of-Sample Forecasting

This paper attempts to contribute in several ways. Theoretically, it proposes simple models of house price dynamics and construction dynamics, all based on forward-looking agents’ maximization problems, which may carry independent interests. Simplified version of the model implications are estimated with the data from four major cities in China. Both price and construction dynamics exhibit strong persistence in al cities. Significant heterogeneity across cities is found. Our models out-perform widely used alternatives in in-sample-fitting for all cities, although similar success only limited to highly developed cities in out-of-sample forecasting. Policy implications and future research directions are also discussed

Co-regulatory expression quantitative trait loci mapping: method and application to endometrial cancer

<p>Abstract</p> <p>Background</p> <p>Expression quantitative trait loci (eQTL) studies have helped identify the genetic determinants of gene expression. Understanding the potential interacting mechanisms underlying such findings, however, is challenging.</p> <p>Methods</p> <p>We describe a method to identify the <it>trans-</it>acting drivers of multiple gene co-expression, which reflects the action of regulatory molecules. This method-termed <it>co-regulatory expression quantitative trait locus </it>(creQTL) <it>mapping</it>-allows for evaluation of a more focused set of phenotypes within a clear biological context than conventional eQTL mapping.</p> <p>Results</p> <p>Applying this method to a study of endometrial cancer revealed regulatory mechanisms supported by the literature: a creQTL between a locus upstream of STARD13/DLC2 and a group of seven IFNβ-induced genes. This suggests that the Rho-GTPase encoded by STARD13 regulates IFNβ-induced genes and the DNA damage response.</p> <p>Conclusions</p> <p>Because of the importance of IFNβ in cancer, our results suggest that creQTL may provide a finer picture of gene regulation and may reveal additional molecular targets for intervention. An open source R implementation of the method is available at <url>http://sites.google.com/site/kenkompass/</url>.</p

Speech Communication

Contains reports on five research projects.C.J. Lebel FellowshipNational Institutes of Health (Grant 5 T32 NS07040)National Institutes of Health (Grant 5 R01 NS04332)National Science Foundation (Grant 1ST 80-17599)U.S. Navy - Naval Electronic Systems Command Contract (N00039-85-C-0254)U.S. Navy - Naval Electronic Systems Command Contract (N00039-85-C-0341)U.S. Navy - Naval Electronic Systems Command Contract (N00039-85-C-0290

Engineering HIV-Resistant Human CD4+ T Cells with CXCR4-Specific Zinc-Finger Nucleases

HIV-1 entry requires the cell surface expression of CD4 and either the CCR5 or CXCR4 coreceptors on host cells. Individuals homozygous for the ccr5Δ32 polymorphism do not express CCR5 and are protected from infection by CCR5-tropic (R5) virus strains. As an approach to inactivating CCR5, we introduced CCR5-specific zinc-finger nucleases into human CD4+ T cells prior to adoptive transfer, but the need to protect cells from virus strains that use CXCR4 (X4) in place of or in addition to CCR5 (R5X4) remains. Here we describe engineering a pair of zinc finger nucleases that, when introduced into human T cells, efficiently disrupt cxcr4 by cleavage and error-prone non-homologous DNA end-joining. The resulting cells proliferated normally and were resistant to infection by X4-tropic HIV-1 strains. CXCR4 could also be inactivated in ccr5Δ32 CD4+ T cells, and we show that such cells were resistant to all strains of HIV-1 tested. Loss of CXCR4 also provided protection from X4 HIV-1 in a humanized mouse model, though this protection was lost over time due to the emergence of R5-tropic viral mutants. These data suggest that CXCR4-specific ZFNs may prove useful in establishing resistance to CXCR4-tropic HIV for autologous transplant in HIV-infected individuals