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  • 1
    Language: English
    In: The Journal of organic chemistry, 21 August 2015, Vol.80(16), pp.8055-64
    Description: A straightforward enantioselective total synthesis algorithm for the preparation of 8 out of 13 macrosphelides within 9-11 steps starting from tert-butyl sorbate is presented. The use of a cyclic sulfate as both protecting and reactivity directing group is the key element within this algorithm. A high-pressure transesterification allows for the selective ring-enlargement of the 15-membered macrosphelides into the 16-membered counterparts. The absolute configurations of the natural products were unambiguously assigned both by the chemical synthesis and by X-ray structure analysis.
    Keywords: Heterocyclic Compounds -- Chemical Synthesis ; Lactones -- Chemical Synthesis
    ISSN: 00223263
    E-ISSN: 1520-6904
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  • 2
    Language: English
    In: Nature, 3/2015, Vol.519(7544), pp.410-411
    ISSN: 0028-0836
    E-ISSN: 1476-4687
    Source: Nature Publishing Group (via CrossRef)
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  • 3
    Language: English
    In: BBA - Molecular Cell Research, April 2011, Vol.1813(4), pp.507-507
    Keywords: Biology ; Chemistry
    ISSN: 0167-4889
    E-ISSN: 1879-2596
    E-ISSN: 00063002
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  • 4
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 11 October 2016, Vol.113(41), pp.E6162-E6171
    Description: Psoriasis is a chronic inflammatory skin disease with a clear genetic contribution, characterized by keratinocyte proliferation and immune cell infiltration. Various closely interacting cell types, including innate immune cells, T cells, and keratinocytes, are known to contribute to inflammation. Innate immune cells most likely initiate the inflammatory process by secretion of IL-23. IL-23 mediates expansion of T helper 17 (Th17) cells, whose effector functions, including IL-17A, activate keratinocytes. Keratinocyte activation in turn results in cell proliferation and chemokine expression, the latter of which fuels the inflammatory process through further immune cell recruitment. One question that remains largely unanswered is how genetic susceptibility contributes to this process and, specifically, which cell type causes disease due to psoriasis-specific genetic alterations. Here we describe a mouse model based on the human psoriasis susceptibility locus TNIP1, also referred to as ABIN1, whose gene product is a negative regulator of various inflammatory signaling pathways, including the Toll-like receptor pathway in innate immune cells. We find that Tnip1-deficient mice recapitulate major features of psoriasis on pathological, genomic, and therapeutic levels. Different genetic approaches, including tissue-specific gene deletion and the use of various inflammatory triggers, reveal that Tnip1 controls not only immune cells, but also keratinocyte biology. Loss of Tnip1 in keratinocytes leads to deregulation of IL-17-induced gene expression and exaggerated chemokine production in vitro and overt psoriasis-like inflammation in vivo. Together, the data establish Tnip1 as a critical regulator of IL-17 biology and reveal a causal role of keratinocytes in the pathogenesis of psoriasis.
    Keywords: Abin1 ; Il-17 ; Tnip1 ; Keratinocytes ; Psoriasis ; Disease Susceptibility ; DNA-Binding Proteins -- Genetics ; Keratinocytes -- Metabolism ; Psoriasis -- Etiology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 5
    Language: English
    In: PLoS ONE, 2011, Vol.6(8), p.e23061
    Description: CD40 is a cell surface receptor important in the activation of antigen-presenting cells during immune responses. In macrophages and dendritic cells, engagement of CD40 by its ligand CD154 provides signals critical for anti-microbial and T cell-mediated immune responses, respectively. In B cells, CD40 signaling has a major role in regulating cell proliferation, antibody production, and memory B cell development. CD40 engagement results in the formation of a receptor-associated complex that mediates activation of NF-κB, stress-activated protein kinases, and other signaling molecules. However, the mechanisms that link CD40 to these signaling events have been only partially characterized. Known components of the CD40 signaling complex include members of the TNF receptor-associated factor (TRAF) family of proteins. We previously showed that the TRAF family member TRAF2 mediates recruitment of HOIL-1L-interacting protein (HOIP) to the cytoplasmic domain of CD40, suggesting that HOIP has a role in the CD40 signaling pathway. To determine the role of HOIP in CD40 signaling, we used somatic cell gene targeting to generate mouse B cell lines deficient in HOIP. We found that the CD40-induced upregulation of CD80 and activation of germline immunoglobulin epsilon transcription were defective in HOIP-deficient cells. We also found that the CD40-mediated activation of NF-κB and c-Jun kinase was impaired. Recruitment of IκB kinase proteins to the CD40 signaling complex was undetectable in HOIP-deficient cells, potentially explaining the defect in NF-κB activation. Restoration of HOIP expression reversed the defects in cellular activation and signaling. These results reveal HOIP as a key component of the CD40 signaling pathway.
    Keywords: Research Article ; Biology ; Immunology ; Molecular Biology ; Biochemistry
    E-ISSN: 1932-6203
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  • 6
    Language: English
    In: PLoS ONE, 2011, Vol.6(3), p.e17840
    Description: Streptococcus pneumoniae is the most common pathogen causing non-epidemic bacterial meningitis worldwide. The immune response and inflammatory processes contribute to the pathophysiology. Hence, the anti-inflammatory dexamethasone is advocated as adjuvant treatment although its clinical efficacy remains a question at issue. In experimental models of pneumococcal meningitis, dexamethasone increased neuronal damage in the dentate gyrus. Here, we investigated expressional changes in the hippocampus and cortex at 72 h after infection when dexamethasone was given to infant rats with pneumococcal meningitis. Nursing Wistar rats were intracisternally infected with Streptococcus pneumoniae to induce experimental meningitis or were sham-infected with pyrogen-free saline. Besides antibiotics, animals were either treated with dexamethasone or saline. Expressional changes were assessed by the use of GeneChip® Rat Exon 1.0 ST Arrays and quantitative real-time PCR. Protein levels of brain-derived neurotrophic factor, cytokines and chemokines were evaluated in immunoassays using Luminex xMAP® technology. In infected animals, 213 and 264 genes were significantly regulated by dexamethasone in the hippocampus and cortex respectively. Separately for the cortex and the hippocampus, Gene Ontology analysis identified clusters of biological processes which were assigned to the predefined categories “inflammation”, “growth”, “apoptosis” and others. Dexamethasone affected the expression of genes and protein levels of chemokines reflecting diminished activation of microglia. Dexamethasone-induced changes of genes related to apoptosis suggest the downregulation of the Akt-survival pathway and the induction of caspase-independent apoptosis. Signalling of pro-neurogenic pathways such as transforming growth factor pathway was reduced by dexamethasone resulting in a lack of pro-survival triggers. The anti-inflammatory properties of dexamethasone were observed on gene and protein level in experimental pneumococcal meningitis. Further dexamethasone-induced expressional changes reflect an increase of pro-apoptotic signals and a decrease of pro-neurogenic processes. The findings may help to identify potential mechanisms leading to apoptosis by dexamethasone in experimental pneumococcal meningitis.
    Keywords: Research Article ; Biology ; Medicine ; Genetics And Genomics ; Immunology ; Infectious Diseases ; Neuroscience ; Neurological Disorders
    E-ISSN: 1932-6203
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  • 7
    Language: English
    In: PLoS ONE, 2011, Vol.6(12), p.e28619
    Description: Bacillus cereus causes a uniquely rapid and blinding intraocular infection, endophthalmitis. B. cereus replicates in the eye, synthesizes numerous toxins, and incites explosive intraocular inflammation. The mechanisms involved in the rapid and explosive intraocular immune response have not been addressed. Because Toll-like receptors (TLRs) are integral to the initial recognition of organisms during infection, we hypothesized that the uniquely explosive immune response observed during B. cereus endophthalmitis is directly influenced by the presence of TLR2, a known Gram-positive pathogen recognition receptor. To address this hypothesis, we compared the courses of experimental B. cereus endophthalmitis in wild type C57BL/6J mice to that of age-matched homozygous TLR2 -/- mice. Output parameters included analysis of bacterial growth, inflammatory cell (PMN) infiltration, cytokine/chemokine kinetics, retinal function testing, and histology, with N≥4 eyes/assay/time point/mouse strain. B. cereus grew at similar rates to10 8 CFU/eye by 12 h, regardless of the mouse strain. Retinal function was preserved to a greater degree in infected TLR2 -/- eyes compared to that of infected wild type eyes, but infected eyes of both mouse strains lost significant function. Retinal architecture was preserved in infected TLR2 -/- eyes, with limited retinal and vitreal cellular infiltration compared to that of infected wild type eyes. Ocular myeloperoxidase activities corroborated these results. In general, TNFα, IFNγ, IL6, and KC were detected in greater concentrations in infected wild type eyes than in infected TLR2 -/- eyes. The absence of TLR2 resulted in decreased intraocular proinflammatory cytokine/chemokine levels and altered recruitment of inflammatory cells into the eye, resulting in less intraocular inflammation and preservation of retinal architecture, and a slightly greater degree of retinal function. These results demonstrate TLR2 is an important component of the initial ocular response to B. cereus endophthalmitis.
    Keywords: Research Article ; Biology ; Medicine ; Immunology ; Ophthalmology ; Microbiology
    E-ISSN: 1932-6203
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  • 8
    Language: English
    In: Pediatric Surgery International, 2011, Vol.27(6), pp.623-627
    Description: Byline: Frank-Martin Haecker (1) Keywords: Pectus excavatum; Conservative treatment; Vacuum bell Abstract: Objective Surgical repair of pectus excavatum (PE) in childhood is a well-established procedure. Previously used operative techniques to correct PE were largely based on the Ravitch technique. Since about 10 years, the minimally invasive repair (MIRPE) by Nuss is well established. Conservative treatment with the vacuum bell to elevate the funnel in patients with PE represents a potential alternative to surgery in selected patients. Methods A suction cup is used to create a vacuum at the anterior chest wall. Three different sizes of vacuum bell exist which are selected according to the individual patients age. When creating the vacuum, the lift of the sternum is obvious and remains for a different time period. The device should be used for a minimum of 30 min (twice/day), and may be used up to a maximum of several hours daily. Results One hundred and thirty-three patients (110 males, 23 females) aged from 3 to 61 years (median 16.21 years) used the vacuum bell for 1 to a maximum of 36 months. Computed tomographic scans showed that the device lifted the sternum and ribs immediately. In addition, this was confirmed thoracoscopically during the MIRPE procedure. One hundred and five patients showed a permanent lift of the sternum for more than 1 cm after 3 months of daily application. Thirteen patients stopped the application and underwent MIRPE. Relevant side effects were not noted. Conclusion The vacuum bell has proved to be an alternative therapeutic option in selected patients suffering from PE. The initial results proved to be dramatic, but long-term results are so far lacking, and further evaluation and follow-up studies are necessary. Author Affiliation: (1) Department of Pediatric Surgery, University Children's Hospital, Spitalstrasse 33, 4056, Basel, Switzerland Article History: Registration Date: 29/12/2010 Online Date: 15/01/2011
    Keywords: Pectus excavatum ; Conservative treatment ; Vacuum bell
    ISSN: 0179-0358
    E-ISSN: 1437-9813
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  • 9
    Language: English
    In: Nanotechnology, 2013, Vol.24(28), p.285101 (7pp)
    Description: Engineered nanoparticles have been under increasing scrutiny in recent years. High aspect ratio nanoparticles such as carbon nanotubes and nanowires have raised safety concerns due to their geometrical similarity to asbestos fibers. III–V epitaxial semiconductor nanowires are expected to be utilized in devices such as LEDs and solar cells and will thus be available to the public. In addition, clean-room staff fabricating and characterizing the nanowires are at risk of exposure, emphasizing the importance of investigating their possible toxicity. Here we investigated the effects of gallium phosphide nanowires on the fruit fly Drosophila melanogaster . Drosophila larvae and/or adults were exposed to gallium phosphide nanowires by ingestion with food. The toxicity and tissue interaction of the nanowires was evaluated by investigating tissue distribution, activation of immune response, genome-wide gene expression, life span, fecundity and somatic mutation rates. Our results show that gallium phosphide nanowires applied through the diet are not taken up into Drosophila tissues, do not elicit a measurable immune response or changes in genome-wide gene expression and do not significantly affect life span or somatic mutation rate.
    Keywords: Gene Expression ; Life Span ; Semiconductors ; Nanowires ; Gallium Phosphides ; Toxicity ; Ingestion ; Drosophila ; Microstructure (So) ; Crystal Properties (MD) ; Microstructure (Ep) ; Microstructure (Ed) ; Microstructure (EC) ; (An);
    ISSN: 0957-4484
    E-ISSN: 1361-6528
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  • 10
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 01 November 2011, Vol.108(44), pp.E998-1006
    Description: Toll-like receptors (TLRs) are expressed on innate immune cells and trigger inflammation upon detection of pathogens and host tissue injury. TLR-mediated proinflammatory-signaling pathways are counteracted by partially characterized anti-inflammatory mechanisms that prevent exaggerated inflammation and host tissue damage as manifested in inflammatory diseases. We biochemically identified a component of TLR-signaling pathways, A20-binding inhibitor of NF-κB (ABIN1), which recently has been linked by genome-wide association studies to the inflammatory diseases systemic lupus erythematosus and psoriasis. We generated ABIN1-deficient mice to study the function of ABIN1 in vivo and during TLR activation. Here we show that ABIN1-deficient mice develop a progressive, lupus-like inflammatory disease characterized by expansion of myeloid cells, leukocyte infiltrations in different parenchymatous organs, activated T and B lymphocytes, elevated serum Ig levels, and the appearance of autoreactive antibodies. Kidneys develop glomerulonephritis and proteinuria, reflecting tissue injury. Surprisingly, ABIN1-deficient macrophages exhibit normal regulation of major proinflammatory signaling pathways and mediators but show selective deregulation of the transcription factor CCAAT/enhancer binding protein β (C/EBPβ) and its target genes, such as colony-stimulating factor 3 (Csf3), nitric oxide synthase, inducible (Nos2), and S100 calcium-binding protein A8 (S100a8). Their gene products, which are intimately linked to innate immune cell expansion (granulocyte colony-stimulating factor), cytotoxicity (inducible nitric oxide synthase), and host factor-derived inflammation (S100A8), may explain, at least in part, the inflammatory phenotype observed. Together, our data reveal ABIN1 as an essential anti-inflammatory component of TLR-signaling pathways that controls C/EBPβ activity.
    Keywords: Adaptor Proteins, Signal Transducing -- Physiology ; Ccaat-Enhancer-Binding Protein-Beta -- Metabolism ; Lupus Erythematosus, Systemic -- Prevention & Control ; Nf-Kappa B -- Antagonists & Inhibitors ; Psoriasis -- Prevention & Control ; Toll-Like Receptors -- Physiology
    ISSN: 00278424
    E-ISSN: 1091-6490
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