Kooperativer Bibliotheksverbund

Berlin Brandenburg


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  • 1
    Language: English
    In: Chemosphere, July 2013, Vol.92(5), pp.483-489
    Description: ► The invasive aquatic amphipod is more tolerant to lambda-cyhalothrin than the native one. ► Predation success on Baetis nymphs is substantially higher for than ► may contribute substantially to leaf litter decomposition. Invasive species are considered as one of the major threats for biodiversity worldwide. The Ponto-Caspian species , for instance, spread throughout continental Europe and was recorded for the first time also within Lake Constance in 2003. Although is a highly competitive species it was not capable of replacing the native completely in this ecosystem, especially in the riparian zones of the highly agriculturally used island “Reichenau”. As differences in pesticide sensitivity between both amphipod species may explain their distribution, the present study assessed the implication of the highly toxic pyrethroid lambda-cyhalothrin, which is authorized for application in the Lake Constance region, assuming the invasive species being more sensitive than the native one. However, both the feeding activity bioassays, which measured the leaf consumption over 7 d ( = 20), as well as the predation bioassay, which measured the predation rate upon nymphs in concert with the feeding activity on leaf material over 96 h ( = 13), revealed an up to 5-fold higher tolerance of towards lambda-cyhalothrin. These results suggest the investigated insecticide not being the trigger for the observed distribution pattern of both amphipod species. Hence, other factors like the diversity of habitat structures or the levels of ammonia may have facilitated the coexistence. Nevertheless, the present study uncovered a high leaf-shredding efficacy of the invasive species suggesting that its role in the leaf decomposition process may have been underestimated in the past.
    Keywords: Functional Feeding Group ; Insecticide ; Leaf Litter Decomposition ; Ecosystem Function ; Predator–Prey Interaction ; Freshwater Biodiversity ; Chemistry ; Ecology
    ISSN: 0045-6535
    E-ISSN: 1879-1298
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  • 2
    Language: English
    In: Jostins, Luke, Stephan Ripke, Rinse K Weersma, Richard H Duerr, Dermot P McGovern, Ken Y Hui, James C Lee, et al. 2012. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 491(7422): 119-124.
    Description: Crohn’s disease (CD) and ulcerative colitis (UC), the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry with rising prevalence in other populations1. Genome-wide association studies (GWAS) and subsequent meta-analyses of CD and UC2,3 as separate phenotypes implicated previously unsuspected mechanisms, such as autophagy4, in pathogenesis and showed that some IBD loci are shared with other inflammatory diseases5. Here we expand knowledge of relevant pathways by undertaking a meta-analysis of CD and UC genome-wide association scans, with validation of significant findings in more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional and balancing selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe striking overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.
    Keywords: Colitis, Ulcerative–Genetics ; Colitis, Ulcerative–Immunology ; Colitis, Ulcerative–Microbiology ; Colitis, Ulcerative–Physiopathology ; Crohn Disease–Genetics ; Crohn Disease–Immunology ; Crohn Disease–Microbiology ; Crohn Disease–Physiopathology ; Genetic Predisposition to Disease–Genetics ; Genome, Human–Genetics ; Genome-Wide Association Study–Genetics ; Haplotypes–Genetics ; Host-Pathogen Interactions–Immunology ; Host-Pathogen Interactions–Genetics ; Host-Pathogen Interactions–Immunology ; Host-Pathogen Interactions–Microbiology ; Humans–Physiopathology ; Inflammatory Bowel Diseases–Immunology ; Inflammatory Bowel Diseases–Pathogenicity ; Inflammatory Bowel Diseases–Genetics ; Inflammatory Bowel Diseases–Microbiology ; Mycobacterium–Immunology ; Mycobacterium–Pathogenicity ; Mycobacterium Infections–Genetics ; Mycobacterium Infections–Genetics ; Mycobacterium Tuberculosis–Genetics ; Mycobacterium Tuberculosis–Genetics ; Phenotype–Genetics ; Polymorphism, Single Nucleotide–Genetics ; Reproducibility of Results–Genetics ; Inflammatory Bowel Disease ; Genetics ; Immune System ; Architecture ; Candidates ; Genomes ; Tuberculosis ; Diabetes ; Gene Expression ; Health Risk Assessment;
    ISSN: 0028-0836
    E-ISSN: 14764687
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  • 3
    In: Nature Genetics, 2011, Vol.43(11), p.1131
    Description: Concentrations of liver enzymes in plasma are widely used as indicators of liver disease. We carried out a genome-wide association study in 61,089 individuals, identifying 42 loci associated with concentrations of liver enzymes in plasma, of which 32 are new associations (P = 10 super(-8) to P = 10 super(-190)). We used functional genomic approaches including metabonomic profiling and gene expression analyses to identify probable candidate genes at these regions. We identified 69 candidate genes, including genes involved in biliary transport (ATP8B1 and ABCB11), glucose, carbohydrate and lipid metabolism (FADS1, FADS2, GCKR, JMJD1C, HNF1A, MLXIPL, PNPLA3, PPP1R3B, SLC2A2 and TRIB1), glycoprotein biosynthesis and cell surface glycobiology (ABO, ASGR1, FUT2, GPLD1 and ST3GAL4), inflammation and immunity (CD276, CDH6, GCKR, HNF1A, HPR, ITGA1, RORA and STAT4) and glutathione metabolism (GSTT1, GSTT2 and GGT), as well as several genes of uncertain or unknown function (including ABHD12, EFHD1, EFNA1, EPHA2, MICAL3 and ZNF827). Our results provide new insight into genetic mechanisms and pathways influencing markers of liver function.
    Keywords: Cell Surface ; Liver Diseases ; Gstt1 Protein ; Glutathione ; Glucose ; Enzymes ; Immunity ; Stat4 Protein ; Lipid Metabolism ; Inflammation ; Gene Expression ; Abo System ; Epha2 Protein ; Glycoproteins ; Genomics ; Carbohydrates ; Molecular Genetics ; Miscellaneous;
    ISSN: 1061-4036
    E-ISSN: 15461718
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  • 4
    Language: English
    In: Journal of Investigative Dermatology, August 2014, Vol.134(8), pp.2202-2211
    Description: Patients with resected stage II–III cutaneous melanomas remain at high risk for metastasis and death. Biomarker development has been limited by the challenge of isolating high-quality RNA for transcriptome-wide profiling from formalin-fixed and paraffin-embedded (FFPE) primary tumor specimens. Using NanoString technology, RNA from 40 stage II–III FFPE primary melanomas was analyzed and a 53-immune-gene panel predictive of non-progression (area under the curve (AUC)=0.920) was defined. The signature predicted disease-specific survival (DSS 〈0.001) and recurrence-free survival (RFS 〈0.001). CD2, the most differentially expressed gene in the training set, also predicted non-progression ( 〈0.001). Using publicly available microarray data from 46 primary human melanomas (GSE15605), a coexpression module enriched for the 53-gene panel was then identified using unbiased methods. A Bayesian network of signaling pathways based on this data identified driver genes. Finally, the proposed 53-gene panel was confirmed in an independent test population of 48 patients (AUC=0.787). The gene signature was an independent predictor of non-progression ( 〈0.001), RFS ( 〈0.001), and DSS ( =0.024) in the test population. The identified driver genes are potential therapeutic targets, and the 53-gene panel should be tested for clinical application using a larger data set annotated on the basis of prospectively gathered data.
    Keywords: Medicine
    ISSN: 0022-202X
    E-ISSN: 1523-1747
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