987 resultados para Genomic library
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This leaflet, no. 7, by Grant C. Miller, of Patton & Miller Architects in Chicago, contains information on how to plan the erection of a new library building. It discusses how to select a librarian, architect, location and surroundings design and layout needed to best serve the library users.
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Includes information on the Iowa State University Academic Library and the resources, services and facilities that if offers.
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Quarterly update for Iowa Library Services/State Library patrons.
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Résumé : Le glioblastome (GBM, WHO grade IV) est la tumeur cérébrale primaire la plus fréquente et la plus maligne, son pronostic reste très réservé et sa réponse aux différents traitements limitée. Récemment, une étude clinique randomisée (EORTC 26981/NCIC CE.3) a démontré que le traitement combiné de temozolomide et radiothérapie (RT/TMZ) est le meilleur dans les cas de GBM nouvellement diagnostiqués [1]. Cependant, seul un sous-groupe de patients bénéficie du traitement RT/TMZ et même parmi eux, leur survie reste très limitée. Pour tenter de mieux comprendre les réponses au traitement RT/TMZ, la biologie du GBM, identifier d'autres facteurs de résistance et découvrir de nouvelles cibles aux traitements, nous avons conduit une analyse moléculaire étendue à 73 patients inclus dans cette étude clinique. Nous avons complété les résultats moléculaires déjà obtenus par un profil génomique du nombre de copies par Array Comparative Genomic Hybridization. Afin d'atteindre nos objectifs, nous avons analysé en parallèle les données cliniques des patients et leurs profils moléculaires. Nos résultats confirment des analyses connues dans le domaine des aberrations du nombre de copies (CNA) et de profils du glioblastome. Nous avons observé une bonne corrélation entre le CNA génomique et l'expression de l'ARN messager dans le glioblastome et identifié un nouveau modèle de CNA du chromosome 7 pouvant présenter un intérêt clinique. Nous avons aussi observé par l'analyse du CNA que moins de 10% des glioblastomes conservent leurs mécanismes de suppression de tumeurs p53 et Rb1. Nous avons aussi observé que l'amplification du CDK4 peut constituer un facteur supplémentaire de résistance au traitement RT/TMZ, cette observation nécessite confirmation sur un plus grand nombre d'analyses. Nous avons montré que dans notre analyse des profils moléculaires et cliniques, il n'est pas possible de différencier le GBM à composante oligodendrogliale (GBM-O) du glioblastome. En superposant les profils moléculaires et les modèles expérimentaux in vitro, nous avons identifié WIF-1 comme un gène suppresseur de tumeur probable et une activation du signal WNT dans la pathologie du glioblastome. Ces observations pourraient servir à une meilleure compréhension de cette maladie dans le futur. Abstract : Glioblastoma, (GBM, WHO grade IV) is the most malignant and most frequent primary brain tumor with a very poor prognosis and response to therapy. A recent randomized clinical trial (EORTC26981/NCIC CE.3) established RT/TMZ as the 1St effective chemo-radiation therapy in newly diagnosed GBM [1]. However only a genetic subgroup of patients benefit from RT/TMZ and even in this subgroup overall survival remains very dismal. To explain the observed response to RT/TMZ, have a better understanding of GBM biology, identify other resistance factors and discover new drugable targets a comprehensive molecular analysis was performed in 73 of these GBM trial cohort. We complemented the available molecular data with a genomic copy number profiling by Array Comparative Genomic Hybridization. We proceeded to align the molecular profiles and the Clinical data, to meet our project objectives. Our data confirm known GBM Copy Number Aberrations and profiles. We observed a good correlation of genomic CN and mRNA expression in GBM, and identified new interesting CNA pattern for chromosome 7 with a potential clinical value. We also observed that by copy number aberration data alone, less than 10% of GBM have an intact p53 and Rb1 tumor .suppressor pathways. We equally observed that CDK4 amplification might constitute an additional RT/TMZ resistant factor, an observation that will need confirmation in a larger data set. We show that the molecular and clinical profiles in our data set, does not support the identification of GBM-O as a new entity in GBM. By combining the molecular profiles and in vitro model experiments we identify WIF1 as a potential GBM TSG and an activated WNT signaling as a pathologic event in GBM worth incorporation in attempts to better understand and impact outcome in this disease.
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ABSTRACT: BACKGROUND: It is accepted that a woman's lifetime risk of developing breast cancer after menopause is reduced by early full term pregnancy and multiparity. This phenomenon is thought to be associated with the development and differentiation of the breast during pregnancy. METHODS: In order to understand the underlying molecular mechanisms of pregnancy induced breast cancer protection, we profiled and compared the transcriptomes of normal breast tissue biopsies from 71 parous (P) and 42 nulliparous (NP) healthy postmenopausal women using Affymetrix Human Genome U133 Plus 2.0 arrays. To validate the results, we performed real time PCR and immunohistochemistry. RESULTS: We identified 305 differentially expressed probesets (208 distinct genes). Of these, 267 probesets were up- and 38 down-regulated in parous breast samples; bioinformatics analysis using gene ontology enrichment revealed that up-regulated genes in the parous breast represented biological processes involving differentiation and development, anchoring of epithelial cells to the basement membrane, hemidesmosome and cell-substrate junction assembly, mRNA and RNA metabolic processes and RNA splicing machinery. The down-regulated genes represented biological processes that comprised cell proliferation, regulation of IGF-like growth factor receptor signaling, somatic stem cell maintenance, muscle cell differentiation and apoptosis. CONCLUSIONS: This study suggests that the differentiation of the breast imprints a genomic signature that is centered in the mRNA processing reactome. These findings indicate that pregnancy may induce a safeguard mechanism at post-transcriptional level that maintains the fidelity of the transcriptional process.
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The discovery of early manuscript reports of Territorial and State Librarians, buried in the mass of old official papers transferred from the several departments of State to the new Department of Archives in the Historical Building, has suggested the propriety of completing as far as possible, the historical record of Iowa's State Library, "from the earliest period to the present time." After a thorough research through the papers on file in the Archives Department, the published Journals and departmental reports in the State Library and documents and private papers loaned me by Mr. Newton R. Parvin, librarian of the Iowa Masonic Library, Cedar Rapids. I am now able to present the following historical sketch, Supplemented by the hitherto unpublished papers referred to this filling a gap in the history of a State institution which from very small beginnings has grown to large proportions and has made for itself a firm place in the respect and esteem of every citizen of Iowa.
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Quarterly update for Iowa Library Services/State Library patrons.
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Isolated gonadotropin-releasing hormone (GnRH) deficiency is a treatable albeit rare form of reproductive failure that has revealed physiological mechanisms controlling human reproduction, but despite substantial progress in discovering pathogenic single-gene defects, most of the genetic basis of GnRH deficiency remains uncharted. Although unbiased genetic investigations of affected families have identified mutations in previously unsuspected genes as causes of this disease in some cases, their application has been severely limited because of the negative effect of GnRH deficiency on fertility; moreover, relatively few of the many candidate genes nominated because of biological plausibility from in vitro or animal model experiments were subsequently validated in patients. With the advent of exciting technological platforms for sequencing, homozygosity mapping, and detection of structural variation at the whole-genome level, human investigations are again assuming the leading role for gene discovery. Using human GnRH deficiency as a paradigm and presenting original data from the screening of numerous candidate genes, we discuss the emerging model of patient-focused clinical genetic research and its complementarities with basic approaches in the near future.
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SNAP(c) is one of a few basal transcription factors used by both RNA polymerase (pol) II and pol III. To define the set of active SNAP(c)-dependent promoters in human cells, we have localized genome-wide four SNAP(c) subunits, GTF2B (TFIIB), BRF2, pol II, and pol III. Among some seventy loci occupied by SNAP(c) and other factors, including pol II snRNA genes, pol III genes with type 3 promoters, and a few un-annotated loci, most are primarily occupied by either pol II and GTF2B, or pol III and BRF2. A notable exception is the RPPH1 gene, which is occupied by significant amounts of both polymerases. We show that the large majority of SNAP(c)-dependent promoters recruit POU2F1 and/or ZNF143 on their enhancer region, and a subset also recruits GABP, a factor newly implicated in SNAP(c)-dependent transcription. These activators associate with pol II and III promoters in G1 slightly before the polymerase, and ZNF143 is required for efficient transcription initiation complex assembly. The results characterize a set of genes with unique properties and establish that polymerase specificity is not absolute in vivo.
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How phenomena like helping, dispersal, or the sex ratio evolve depends critically on demographic and life-history factors. One phenotype that is of particular interest to biologists is genomic imprinting, which results in parent-of-origin-specific gene expression and thus deviates from the predictions of Mendel's rules. The most prominent explanation for the evolution of genomic imprinting, the kinship theory, originally specified that multiple paternity can cause the evolution of imprinting when offspring affect maternal resource provisioning. Most models of the kinship theory do not detail how population subdivision, demography, and life history affect the evolution of imprinting. In this work, we embed the classic kinship theory within an island model of population structure and allow for diverse demographic and life-history features to affect the direction of selection on imprinting. We find that population structure does not change how multiple paternity affects the evolution of imprinting under the classic kinship theory. However, if the degree of multiple paternity is not too large, we find that sex-specific migration and survival and generation overlap are the primary factors determining which allele is silenced. This indicates that imprinting can evolve purely as a result of sex-related asymmetries in the demographic structure or life history of a species.
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A novel approach for the identification of tumor antigen-derived sequences recognized by CD8(+) cytolytic T lymphocytes (CTL) consists in using synthetic combinatorial peptide libraries. Here we have screened a library composed of 3.1 x 10(11) nonapeptides arranged in a positional scanning format, in a cytotoxicity assay, to search the antigen recognized by melanoma-reactive CTL of unknown specificity. The results of this analysis enabled the identification of several optimal peptide ligands, as most of the individual nonapeptides deduced from the primary screening were efficiently recognized by the CTL. The results of the library screening were also analyzed with a mathematical approach based on a model of independent and additive contribution of individual amino acids to antigen recognition. This biometrical data analysis enabled the retrieval, in public databases, of the native antigenic peptide SSX-2(41-49), whose sequence is highly homologous to the ones deduced from the library screening, among the ones with the highest stimulatory score. These results underline the high predictive value of positional scanning synthetic combinatorial peptide library analysis and encourage its use for the identification of CTL ligands.
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A short booklet from the Iowa Library Commission containing advice on how small towns can start and set up public libraries for their communities.
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Information technology will affect academic activities as well as the nature of the high education sector. This sector besides the need to assimilate these technologies will need to attend the requisites of market globalization and, as consequence, all theses changes will be reflected in the university library. Prospectives impacts will affect the structure (emphasis in user services, outsourcing of several services), in the financing aspect (growing of consortia in order to reduce costs), in services (electronic reference, support to long distance education programs, intelligent agents) and in the clientele (attending the great demand por high education which implies a diversity of people).