Nitrogen leaching in croplands is a worldwide problem with implications both on human health and on the environment. Efforts should be taken to increase nutrient use efficiency and minimize N losses from terrestrial to water ecosystems. Soil-applied biochar has been reported to increase soil fertility and decrease nutrient leaching in tropical soils and under laboratory conditions. Our objective was to evaluate the effect of biochar addition on short-term N leaching from A soil horizon in a mature apple orchard growing on subalkaline soils located in the Po Valley (Italy). In spring 2009, 10 Mg of biochar per hectare was incorporated into the surface 20-cm soil layer by soil plowing. Cumulative nitrate (NO) and ammonium (NH) leaching was measured in treated and control plots 4 mo after the addition of biochar and the following year by using ion-exchange resin lysimeters installed below the plowed soil layer. Cumulative NO leaching was not affected by biochar after 4 mo, whereas in the following year it was significantly ( < 0.05) reduced by 75% over the control (from 5.5 to 1.4 kg ha). Conversely, NH leaching was very low and unaffected by soil biochar treatment. The present study shows that soil biochar addition can significantly decrease short-term nitrate leaching from the surface layer of a subalkaline soil under temperate climatic conditions.
High-throughput genomic technologies enable researchers to identify genes that are co-regulated with respect to specific experimental conditions. Numerous statistical approaches have been developed to identify differentially expressed genes. Because each approach can produce distinct gene sets, it is difficult for biologists to determine which statistical approach yields biologically relevant gene sets and is appropriate for their study. To address this issue, we implemented Latent Semantic Indexing (LSI) to determine the functional coherence of gene sets. An LSI model was built using over 1 million Medline abstracts for over 20,000 mouse and human genes annotated in Entrez Gene. The gene-to-gene LSI-derived similarities were used to calculate a literature cohesion p-value (LPv) for a given gene set using a Fisher's exact test. We tested this method against genes in more than 6,000 functional pathways annotated in Gene Ontology (GO) and found that approximately 75% of gene sets in GO biological process category and 90% of the gene sets in GO molecular function and cellular component categories were functionally cohesive (LPv<0.05). These results indicate that the LPv methodology is both robust and accurate. Application of this method to previously published microarray datasets demonstrated that LPv can be helpful in selecting the appropriate feature extraction methods. To enable real-time calculation of LPv for mouse or human gene sets, we developed a web tool called Gene-set Cohesion Analysis Tool (GCAT). GCAT can complement other gene set enrichment approaches by determining the overall functional cohesion of data sets, taking into account both explicit and implicit gene interactions reported in the biomedical literature.AvailabilityGCAT is freely available at http://binf1.memphis.edu/gcat
SllmmaryPresentation of antigenic peptides by major histocompatibility complex (MHC) class I molecules requires MHC-encoded molecules of the adenosine triphosphate binding cassette (ABC) family. Defects in these proteins represent a potential risk, since they are essential links in the machinery of T cell-mediated surveillance which continuously scrutinizes peptide samples of cellular proteins. Nevertheless, transfection of the mouse lymphoma mutant RMA-S with the rat ABC gene mtp2 ~ (homologue to mouse HAM2 and human RINGI1), commonly termed TAP-2 genes, led to a marked increase in tumor outgrowth potential in vivo. This occurred despite restored antigen presentation and sensitivity to cytotoxic T lymphocytes, and was found to be due to escape from natural killer (NK) cell-mediated rejection. It has previously been proposed that adequate expression of sdf-MHC dass I is one important mechanism to avoid dimination by NK cells. Our data argue that a defect in the machinery responsible for processing and loading of peptides into MHC class I molecules is sufficient to render cells sensitive to elimination by NK cells. The latter thus appear to function as a surveillance of the peptide surveillance machinery.M HC class I molecules present short antigenic peptides to CD8 + cytotoxic T cells (1-3). The peptides presented are derived from cytosolic proteins, usually translated endogenously (2). There are at least two genes in the MHC that code for products involved in peptide supply to MHC class I molecules, termed TAP-I and TAP-2. These products are homologous to the transport proteins in the ATP binding cassette (ABC) family, and are thought to mediate transport from the cytoplasm to the endoplasmic reticulum, either of peptides or a cofactor essential for peptide loading into MHC class I molecules (4-13). The mouse lymphoma mutant RMA-S has a profound (14-16), but not total (17-19), peptide presentation defect in the MHC class I presentation pathway, which is due to a premature stop in the message of the mouse TAP-2 gene HAM2 (19a). The phenotype was restored to normal by transfection of TAP-2 genes from different species, first the ratp2 ~ rat gene (9) and then the HAM2 mouse gene (12) and the RINGII human gene (A. Townsend, personal communication); the mtp2" transfectant (RMA-S.mtp2') was able to process and present influenza virus epitopes to CD8 + T cells (9). This transfectant system has now made it possible to investigate directly the role of TAP genes for in vivo phenomena such as tumorigenicity and transplant rejection. The aim of the present study was to investigate the effects on in vivo immunobiology of RMA-S after restoration of its antigen presentation defect by the rat TAP-2 gene. Materials and MethodsAnimals. C57BL/6 mice were bred and maintained at the Department of Tumor Biology, Karolinska Institutet. Athymic nu/nu C57BL/6 mice were purchased from Bomholtgaarden, Denmark. All mice were 4-8 wk old at the start of the experiments.Tumor Cell Lines. RMA (derived from RBL-5 after mutagenization, nonselec...
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