271 research outputs found

    Seventh year projects and activities of the Environmental Remote Sensing Applications Laboratory (ERSAL)

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    There are no author-identified significant results in this report

    Diversity and Distribution of Borrelia hermsii

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    Multilocus sequence analysis and laboratory experiments suggest that birds may play a role in maintaining and dispersing this pathogen

    The comparative evaluation of ERTS-1 imagery for resource inventory in land use planning

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    The author has identified the following significant results. Multidiscipline team interpretation and mapping of resources for Crook County is complete on 1:250,000 scale enlargements of ERTS imagery and 1:120,000 hi-flight photography. Maps of geology, soils, vegetation-land use and land resources units were interpreted to show limitations, suitabilities, and geologic hazards for land use planning. Mapping of lineaments and structures from ERTS imagery has shown a number of features not previously mapped in Oregon. A multistage timber inventory of Ochoco National Forest was made, using ERTS images as the first stage. Inventory of forest clear-cutting practices was successfully demonstrated with color composites. Soil tonal differences in fallow fields correspond with major soil boundaries in loess-mantled terrain. A digital classification system used for discriminating natural vegetation and geologic material classes was successful in separating most major classes around Newberry Caldera, Mt. Washington, and Big Summit Prairie

    Mutational Characterization of the Bile Acid Receptor TGR5 in Primary Sclerosing Cholangitis

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    TGR5, the G protein-coupled bile acid receptor 1 (GPBAR1), has been linked to inflammatory pathways as well as bile homeostasis, and could therefore be involved in primary sclerosing cholangitis (PSC) a chronic inflammatory bile duct disease. We aimed to extensively investigate TGR5 sequence variation in PSC, as well as functionally characterize detected variants. Complete resequencing of TGR5 was performed in 267 PSC patients and 274 healthy controls. Six nonsynonymous mutations were identified in addition to 16 other novel single-nucleotide polymorphisms. To investigate the impact from the nonsynonymous variants on TGR5, we created a receptor model, and introduced mutated TGR5 constructs into human epithelial cell lines. By using confocal microscopy, flow cytometry and a cAMP-sensitive luciferase assay, five of the nonsynonymous mutations (W83R, V178M, A217P, S272G and Q296X) were found to reduce or abolish TGR5 function. Fine-mapping of the previously reported PSC and UC associated locus at chromosome 2q35 in large patient panels revealed an overall association between the TGR5 single-nucleotide polymorphism rs11554825 and PSC (odds ratio = 1.14, 95% confidence interval: 1.03-1.26, p = 0.010) and UC (odds ratio = 1.19, 95% confidence interval 1.11-1.27, p = 8.5 x 10(-7)), but strong linkage disequilibrium precluded demarcation of TGR5 from neighboring genes. Resequencing of TGR5 along with functional investigations of novel variants provided unique insight into an important candidate gene for several inflammatory and metabolic conditions. While significant TGR5 associations were detected in both UC and PSC, further studies are needed to conclusively define the role of TGR5 variation in these diseases

    The immunobiology of primary sclerosing cholangitis

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    Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease histologically characterized by the presence of intrahepatic and/or extrahepatic biliary duct concentric, obliterative fibrosis, eventually leading to cirrhosis. Approximately 75% of patients with PSC have inflammatory bowel disease. The male predominance of PSC, the lack of a defined, pathogenic autoantigen, and the potential role of the innate immune system suggest that it may be due to dysregulation of immunity rather than a classic autoimmune disease. However, PSC is associated with several classic autoimmune diseases, and the strongest genetic link to PSC identified to date is with the human leukocyte antigen DRB01*03 haplotype. The precise immunopathogenesis of PSC is largely unknown but likely involves activation of the innate immune system by bacterial components delivered to the liver via the portal vein. Induction of adhesion molecules and chemokines leads to the recruitment of intestinal lymphocytes. Bile duct injury results from the sustained inflammation and production of inflammatory cytokines. Biliary strictures may cause further damage as a result of bile stasis and recurrent secondary bacterial cholangitis. Currently, there is no effective therapy for PSC and developing a rational therapeutic strategy demands a better understanding of the disease
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