http://demo.openrepository.com/demo Open Repository captures, stores, indexes, preserves, and distributes digital research material. Search the Channel search http://demo.openrepository.com/demo/simple-search http://hdl.handle.net/2384/93745 Title: Mutations in genes required for T-cell development: IL7R, CD45, IL2RG, JAK3, RAG1, RAG2, ARTEMIS, and ADA and severe combined immunodeficiency: HuGE review.<br/><br/>Authors: Kalman, Lisa; Lindegren, Mary Lou; Kobrynski, Lisa; Vogt, Robert; Hannon, Harry; Howard, Joelyn Tonkin; Buckley, Rebecca<br/><br/>Abstract: Severe combined immunodeficiency (SCID) is an inherited immune disorder characterized by T-cell lymphopenia (TCLP), a profound lack of cellular (T-cell) and humoral (B-cell) immunity and, in some cases, decreased NK-cell number and function. Affected children develop severe bacterial and viral infections within the first 6 months of life and die before 1 year of age without treatment. Mutations in any of eight known genes: IL2RG, ARTEMIS, RAG1, RAG2, ADA, CD45, JAK3, and IL7R cause SCID. Mutations in unidentified genes may also cause SCID. Population-based genotype and allelic frequencies of these gene defects have not been measured. Some minimal estimates of SCID prevalence are presented. Currently, hematopoietic stem cell transplants are the standard treatment. In clinical trials, gene therapy has been used to reconstitute immune function in patients with IL2RG and ADA defects. The availability of effective therapies, plus the short asymptomatic period after birth, (when stem-cell transplantation is most effective), make SCID a potentially good candidate for newborn screening. Dried blood spots are currently collected from all infants at birth for newborn metabolic screening. Tests for TCLP on dried blood spots could be developed as a screen for SCID. Because SCID may be unrecognized, with infant deaths from infection attributed to other causes, newborn screening is the only way to ascertain true birth prevalence. Validated tests and pilot population studies are necessary to determine newborn screening's potential for identifying infants with SCID.<br/><br/>Description: This is an article about Genomics Fri, 05 Mar 2010 11:50:01 GMT http://hdl.handle.net/2384/90681 Title: san interop guide<br/><br/>Abstract: Historically, finding interoperability information required endless hours of searching supplier websites or contacting suppliers to obtain interoperability information relating to their products. QLogic Corporation has addressed this challenge by incorporating interoperability information from multiple suppliers within this single publication. To save you valuable time, QLogic Corporation provides wide-ranging interoperability information from the major storage area network (SAN) suppliers in this SAN interoperability guide. Fri, 28 Sep 2007 22:58:59 GMT http://hdl.handle.net/2384/86913 Title: Test submission<br/><br/>Authors: Orme, Susan Wed, 25 Nov 2009 16:17:56 GMT http://hdl.handle.net/2384/86863 Title: test50 Wed, 25 Nov 2009 11:42:46 GMT http://hdl.handle.net/2384/85096 Title: 'Systems toxicology' approach identifies coordinated metabolic responses to copper in a terrestrial non-model invertebrate, the earthworm Lumbricus rubellus.<br/><br/>Authors: Bundy, Jacob G; Sidhu, Jasmin K; Rana, Faisal; Spurgeon, David J; Svendsen, Claus; Wren, Jodie F; Stürzenbaum, Stephen R; Morgan, A John; Kille, Peter<br/><br/>Abstract: BACKGROUND: New methods are needed for research into non-model organisms, to monitor the effects of toxic disruption at both the molecular and functional organism level. We exposed earthworms (Lumbricus rubellus Hoffmeister) to sub-lethal levels of copper (10-480 mg/kg soil) for 70 days as a real-world situation, and monitored both molecular (cDNA transcript microarrays and nuclear magnetic resonance-based metabolic profiling: metabolomics) and ecological/functional endpoints (reproduction rate and weight change, which have direct relevance to population-level impacts). RESULTS: Both of the molecular endpoints, metabolomics and transcriptomics, were highly sensitive, with clear copper-induced differences even at levels below those that caused a reduction in reproductive parameters. The microarray and metabolomic data provided evidence that the copper exposure led to a disruption of energy metabolism: transcripts of enzymes from oxidative phosphorylation were significantly over-represented, and increases in transcripts of carbohydrate metabolising enzymes (maltase-glucoamylase, mannosidase) had corresponding decreases in small-molecule metabolites (glucose, mannose). Treating both enzymes and metabolites as functional cohorts led to clear inferences about changes in energetic metabolism (carbohydrate use and oxidative phosphorylation), which would not have been possible by taking a 'biomarker' approach to data analysis. CONCLUSION: Multiple post-genomic techniques can be combined to provide mechanistic information about the toxic effects of chemical contaminants, even for non-model organisms with few additional mechanistic toxicological data. With 70-day no-observed-effect and lowest-observed-effect concentrations (NOEC and LOEC) of 10 and 40 mg kg-1 for metabolomic and microarray profiles, copper is shown to interfere with energy metabolism in an important soil organism at an ecologically and functionally relevant level. Mon, 29 Oct 2007 22:58:59 GMT http://hdl.handle.net/2384/84534 Title: saas prueba Tue, 20 Oct 2009 23:54:26 GMT http://hdl.handle.net/2384/84553 Title: saas 2 Tue, 20 Oct 2009 23:26:57 GMT http://hdl.handle.net/2384/84533 Title: saas Tue, 20 Oct 2009 23:20:15 GMT http://hdl.handle.net/2384/83434 Title: HMS Beagle<br/><br/>Authors: Martens, Conrad Sun, 04 Oct 2009 18:31:19 GMT http://hdl.handle.net/2384/76656 Title: check Fri, 07 Aug 2009 10:27:19 GMT