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Träfflista för sökning "WFRF:(Higgins A.) srt2:(2005-2009)"

Sökning: WFRF:(Higgins A.) > (2005-2009)

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  • Sankaran, M, et al. (författare)
  • Determinants of woody cover in African savannas
  • 2005
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 438:7069, s. 846-849
  • Tidskriftsartikel (refereegranskat)abstract
    • Savannas are globally important ecosystems of great significance to human economies. In these biomes, which are characterized by the co-dominance of trees and grasses, woody cover is a chief determinant of ecosystem properties(1-3). The availability of resources ( water, nutrients) and disturbance regimes ( fire, herbivory) are thought to be important in regulating woody cover(1,2,4,5), but perceptions differ on which of these are the primary drivers of savanna structure. Here we show, using data from 854 sites across Africa, that maximum woody cover in savannas receiving a mean annual precipitation (MAP) of less than similar to 650 mm is constrained by, and increases linearly with, MAP. These arid and semi-arid savannas may be considered 'stable' systems in which water constrains woody cover and permits grasses to coexist, while fire, herbivory and soil properties interact to reduce woody cover below the MAP-controlled upper bound. Above a MAP of similar to 650 mm, savannas are 'unstable' systems in which MAP is sufficient for woody canopy closure, and disturbances ( fire, herbivory) are required for the coexistence of trees and grass. These results provide insights into the nature of African savannas and suggest that future changes in precipitation(6) may considerably affect their distribution and dynamics.
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  • Williams, Ariel A, et al. (författare)
  • CD9 and vimentin distinguish clear cell from chormophobe renal cell carcinoma.
  • 2009
  • Ingår i: BMC Clinical Pathology. - : Springer Science and Business Media LLC. - 1472-6890. ; 9:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Clear cell renal cell carcinoma (ccRCC) and chromophobe renal cell carcinoma(chRCC) can usually be distinguished by histologic characteristics. Occasionally, diagnosis proveschallenging and diagnostic difficulty will likely increase as needle biopsies of renal lesions becomemore common.Methods: To identify markers that aid in differentiating ccRCC from chRCC, we used geneexpression profiles to identify candidate markers that correlate with histology. 39 antisera andantibodies, including 35 for transcripts identified from gene expression profiling, were evaluated.Promising markers were tested on a tissue microarray (TMA) containing 428 renal neoplasms.Strength of staining of each core on the TMA was formally scored and the distribution of stainingacross different types of renal neoplasms was analyzed.Results: Based on results from initial immunohistochemical staining of multitissue titer arrays, 23of the antisera and antibodies were selected for staining of the TMA. For 7 of these markers,strength of staining of each core on the TMA was formally scored. Vimentin (positive in ccRCC)and CD9 (positive in chRCC) best distinguished ccRCC from chRCC. The combination of vimentinnegativity and CD9 positivity was found to distinguish chRCC from ccRCC with a sensitivity of100.0% and a specificity of 95.2%.Conclusion: Based on gene expression analysis, we identify CD9 and vimentin as candidatemarkers for distinguishing between ccRCC and chRCC. In difficult cases and particularly when theamount of diagnostic tissue is limited, vimentin and CD9 staining could serve as a useful adjunct inthe differential diagnosis of ccRCC and chRCC.
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  • Yusta, Bernardo, et al. (författare)
  • ErbB Signaling Is Required for the Proliferative Actions of GLP-2 in the Murine Gut
  • 2009
  • Ingår i: Gastroenterology. - : Elsevier BV. - 0016-5085. ; 137:3, s. 986-996
  • Tidskriftsartikel (refereegranskat)abstract
    • Background & Aims: Glucagon-like peptide-2 (GLP-2) is a 33-amino acid peptide hormone secreted by enteroendocrine cells in response to nutrient ingestion. GLP-2 stimulates crypt cell proliferation leading to expansion of the mucosal epithelium; however, the mechanisms transducing the trophic effects of GLP-2 are incompletely understood. Methods: We examined the gene expression profiles and growth-promoting actions of GLP-2 in normal mice in the presence or absence of an inhibitor of ErbB receptor signaling, in Glp2r-/- mice and in Egfrwa2 mice harboring a hypomorphic point mutation in the epidermal growth factor receptor. Results: Exogenous GLP-2 administration rapidly induced the expression of a subset of ErbB ligands including amphiregulin, epiregulin, and heparin binding (HB)-epidermal growth factor, in association with induction of immediate early gene expression in the small and large bowel. These actions of GLP-2 required a functional GLP-2 receptor because they were eliminated in Glp2r-/- mice. In contrast, insulin-like growth factor-I and keratinocyte growth factor, previously identified mediators of GLP-2 action, had no effect on the expression of these ErbB ligands. The GLP-2-mediated induction of ErbB ligand expression was not metalloproteinase inhibitor sensitive but was significantly diminished in Egfrwa2 mice and completed abrogated in wild-type mice treated with the pan-ErbB inhibitor CI-1033. Furthermore, the stimulatory actions of GLP-2 on crypt cell proliferation and bowel growth were eliminated in the presence of CI-1033. Conclusions: These findings identify the ErbB signaling network as a target for GLP-2 action leading to stimulation of growth factor-dependent signal transduction and bowel growth in vivo.
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