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  • 1
    Monograph available for loan
    Monograph available for loan
    Setting standards for european ultraviolet spectroradiometers : final report (1995)
    Brussels [u.a.] : Office for Official Publications of the European Communities
    Associated volumes
    Details Availability
    Call number: AWI A14-96-0020
    In: Air pollution research report
    In: Publication / Commission of the European Communities
    Type of Medium: Monograph available for loan
    Pages: III, 138 S.
    ISBN: 9282654052
    Series Statement: Air pollution research report 53
    Branch Library: AWI Library
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  • 2
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    Neural mechanisms of a genome-wide supported psychosis variant (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Schizophrenia is a devastating, highly heritable brain disorder of unknown etiology. Recently, the first common genetic variant associated on a genome-wide level with schizophrenia and possibly bipolar disorder was discovered in ZNF804A (rs1344706). We show, by using an imaging genetics approach, that healthy carriers of rs1344706 risk genotypes exhibit no changes in regional activity but pronounced gene dosage-dependent alterations in functional coupling (correlated activity) of dorsolateral prefrontal cortex (DLPFC) across hemispheres and with hippocampus, mirroring findings in patients, and abnormal coupling of amygdala. Our findings establish disturbed connectivity as a neurogenetic risk mechanism for psychosis supported by genome-wide association, show that rs1344706 or variation in linkage disequilibrium is functional in human brain, and validate the intermediate phenotype strategy in psychiatry.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Esslinger, Christine -- Walter, Henrik -- Kirsch, Peter -- Erk, Susanne -- Schnell, Knut -- Arnold, Claudia -- Haddad, Leila -- Mier, Daniela -- Opitz von Boberfeld, Carola -- Raab, Kyeon -- Witt, Stephanie H -- Rietschel, Marcella -- Cichon, Sven -- Meyer-Lindenberg, Andreas -- New York, N.Y. -- Science. 2009 May 1;324(5927):605. doi: 10.1126/science.1167768.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, University of Heidelberg, J5, 68159 Mannheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407193" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Affective Symptoms/genetics/physiopathology ; Bipolar Disorder/genetics/physiopathology ; Brain Mapping ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Hippocampus/*physiology ; Humans ; Kruppel-Like Transcription Factors/*genetics ; Magnetic Resonance Imaging ; Male ; Mental Processes ; Phenotype ; *Polymorphism, Single Nucleotide ; Prefrontal Cortex/*physiology ; Schizophrenia/*genetics/physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    RNA editing of Filamin A pre-mRNA regulates vascular contraction and diastolic blood pressure (2018)
    Springer Nature
    Details
    Publication Date: 2018
    Description: 〈p〉Epitranscriptomic events such as adenosine-to-inosine (A-to-I) RNA editing by ADAR can recode mRNAs to translate novel proteins. Editing of the mRNA that encodes actin crosslinking protein Filamin A (FLNA) mediates a Q-to-R transition in the interactive C-terminal region. While FLNA editing is conserved among vertebrates, its physiological function remains unclear. Here, we show that cardiovascular tissues in humans and mice show massive editing and that FLNA RNA is the most prominent substrate. Patient-derived RNA-Seq data demonstrate a significant drop in FLNA editing associated with cardiovascular diseases. Using mice with only impaired FLNA editing, we observed increased vascular contraction and diastolic hypertension accompanied by increased myosin light chain phosphorylation, arterial remodeling, and left ventricular wall thickening, which eventually causes cardiac remodeling and reduced systolic output. These results demonstrate a causal relationship between RNA editing and the development of cardiovascular disease indicating that a single epitranscriptomic RNA modification can maintain cardiovascular health.〈/p〉
    Print ISSN: 0261-4189
    Electronic ISSN: 1460-2075
    Topics: Biology , Medicine
    Published by Springer Nature on behalf of The European Molecular Biology Organization (EMBO).
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  • 4
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    FADD prevents RIP3-mediated epithelial cell necrosis and chronic intestinal inflammation (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-08-02
    Description: Intestinal immune homeostasis depends on a tightly regulated cross talk between commensal bacteria, mucosal immune cells and intestinal epithelial cells (IECs). Epithelial barrier disruption is considered to be a potential cause of inflammatory bowel disease; however, the mechanisms regulating intestinal epithelial integrity are poorly understood. Here we show that mice with IEC-specific knockout of FADD (FADD(IEC-KO)), an adaptor protein required for death-receptor-induced apoptosis, spontaneously developed epithelial cell necrosis, loss of Paneth cells, enteritis and severe erosive colitis. Genetic deficiency in RIP3, a critical regulator of programmed necrosis, prevented the development of spontaneous pathology in both the small intestine and colon of FADD(IEC-KO) mice, demonstrating that intestinal inflammation is triggered by RIP3-dependent death of FADD-deficient IECs. Epithelial-specific inhibition of CYLD, a deubiquitinase that regulates cellular necrosis, prevented colitis development in FADD(IEC-KO) but not in NEMO(IEC-KO) mice, showing that different mechanisms mediated death of colonic epithelial cells in these two models. In FADD(IEC-KO) mice, TNF deficiency ameliorated colon inflammation, whereas MYD88 deficiency and also elimination of the microbiota prevented colon inflammation, indicating that bacteria-mediated Toll-like-receptor signalling drives colitis by inducing the expression of TNF and other cytokines. However, neither CYLD, TNF or MYD88 deficiency nor elimination of the microbiota could prevent Paneth cell loss and enteritis in FADD(IEC-KO) mice, showing that different mechanisms drive RIP3-dependent necrosis of FADD-deficient IECs in the small and large bowel. Therefore, by inhibiting RIP3-mediated IEC necrosis, FADD preserves epithelial barrier integrity and antibacterial defence, maintains homeostasis and prevents chronic intestinal inflammation. Collectively, these results show that mechanisms preventing RIP3-mediated epithelial cell death are critical for the maintenance of intestinal homeostasis and indicate that programmed necrosis of IECs might be implicated in the pathogenesis of inflammatory bowel disease, in which Paneth cell and barrier defects are thought to contribute to intestinal inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Welz, Patrick-Simon -- Wullaert, Andy -- Vlantis, Katerina -- Kondylis, Vangelis -- Fernandez-Majada, Vanesa -- Ermolaeva, Maria -- Kirsch, Petra -- Sterner-Kock, Anja -- van Loo, Geert -- Pasparakis, Manolis -- England -- Nature. 2011 Jul 31;477(7364):330-4. doi: 10.1038/nature10273.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genetics, Centre for Molecular Medicine, University of Cologne, Zulpicher Str. 47a, 50674 Cologne, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21804564" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Chronic Disease ; Colitis/enzymology/metabolism/*pathology ; Colon/enzymology/metabolism/*pathology ; Cysteine Endopeptidases/metabolism ; Enteritis/enzymology/metabolism/*pathology ; Epithelial Cells/enzymology/metabolism/*pathology ; Fas-Associated Death Domain Protein/deficiency/*metabolism ; Inflammatory Bowel Diseases/enzymology/metabolism/pathology ; Intracellular Signaling Peptides and Proteins/deficiency/metabolism ; Metagenome/physiology ; Mice ; Myeloid Differentiation Factor 88/deficiency/metabolism ; Necrosis ; Paneth Cells/pathology ; Receptor-Interacting Protein Serine-Threonine Kinases/*antagonists & ; inhibitors/*metabolism ; Signal Transduction ; Tumor Necrosis Factors/deficiency
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    City living and urban upbringing affect neural social stress processing in humans (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-06-24
    Description: More than half of the world's population now lives in cities, making the creation of a healthy urban environment a major policy priority. Cities have both health risks and benefits, but mental health is negatively affected: mood and anxiety disorders are more prevalent in city dwellers and the incidence of schizophrenia is strongly increased in people born and raised in cities. Although these findings have been widely attributed to the urban social environment, the neural processes that could mediate such associations are unknown. Here we show, using functional magnetic resonance imaging in three independent experiments, that urban upbringing and city living have dissociable impacts on social evaluative stress processing in humans. Current city living was associated with increased amygdala activity, whereas urban upbringing affected the perigenual anterior cingulate cortex, a key region for regulation of amygdala activity, negative affect and stress. These findings were regionally and behaviourally specific, as no other brain structures were affected and no urbanicity effect was seen during control experiments invoking cognitive processing without stress. Our results identify distinct neural mechanisms for an established environmental risk factor, link the urban environment for the first time to social stress processing, suggest that brain regions differ in vulnerability to this risk factor across the lifespan, and indicate that experimental interrogation of epidemiological associations is a promising strategy in social neuroscience.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lederbogen, Florian -- Kirsch, Peter -- Haddad, Leila -- Streit, Fabian -- Tost, Heike -- Schuch, Philipp -- Wust, Stefan -- Pruessner, Jens C -- Rietschel, Marcella -- Deuschle, Michael -- Meyer-Lindenberg, Andreas -- England -- Nature. 2011 Jun 22;474(7352):498-501. doi: 10.1038/nature10190.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Central Institute of Mental Health, University of Heidelberg/Medical Faculty Mannheim, 68159 Mannheim, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21697947" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/*physiology ; Anxiety Disorders/epidemiology ; *Cities/epidemiology ; Gyrus Cinguli/*physiology ; Humans ; Hydrocortisone/blood ; *Life Style ; Magnetic Resonance Imaging ; Mental Health/statistics & numerical data ; Models, Neurological ; Mood Disorders/epidemiology ; Rural Health/statistics & numerical data ; Sample Size ; Schizophrenia/epidemiology ; Stress, Psychological/blood/epidemiology/*physiopathology ; Time Factors ; Urban Health/statistics & numerical data ; Urbanization
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    RIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis (2014)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2014-08-19
    Description: Necroptosis has emerged as an important pathway of programmed cell death in embryonic development, tissue homeostasis, immunity and inflammation. RIPK1 is implicated in inflammatory and cell death signalling and its kinase activity is believed to drive RIPK3-mediated necroptosis. Here we show that kinase-independent scaffolding RIPK1 functions regulate homeostasis and prevent inflammation in barrier tissues by inhibiting epithelial cell apoptosis and necroptosis. Intestinal epithelial cell (IEC)-specific RIPK1 knockout caused IEC apoptosis, villus atrophy, loss of goblet and Paneth cells and premature death in mice. This pathology developed independently of the microbiota and of MyD88 signalling but was partly rescued by TNFR1 (also known as TNFRSF1A) deficiency. Epithelial FADD ablation inhibited IEC apoptosis and prevented the premature death of mice with IEC-specific RIPK1 knockout. However, mice lacking both RIPK1 and FADD in IECs displayed RIPK3-dependent IEC necroptosis, Paneth cell loss and focal erosive inflammatory lesions in the colon. Moreover, a RIPK1 kinase inactive knock-in delayed but did not prevent inflammation caused by FADD deficiency in IECs or keratinocytes, showing that RIPK3-dependent necroptosis of FADD-deficient epithelial cells only partly requires RIPK1 kinase activity. Epidermis-specific RIPK1 knockout triggered keratinocyte apoptosis and necroptosis and caused severe skin inflammation that was prevented by RIPK3 but not FADD deficiency. These findings revealed that RIPK1 inhibits RIPK3-mediated necroptosis in keratinocytes in vivo and identified necroptosis as a more potent trigger of inflammation compared with apoptosis. Therefore, RIPK1 is a master regulator of epithelial cell survival, homeostasis and inflammation in the intestine and the skin.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206266/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206266/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dannappel, Marius -- Vlantis, Katerina -- Kumari, Snehlata -- Polykratis, Apostolos -- Kim, Chun -- Wachsmuth, Laurens -- Eftychi, Christina -- Lin, Juan -- Corona, Teresa -- Hermance, Nicole -- Zelic, Matija -- Kirsch, Petra -- Basic, Marijana -- Bleich, Andre -- Kelliher, Michelle -- Pasparakis, Manolis -- R01 AI075118/AI/NIAID NIH HHS/ -- R01AI075118/AI/NIAID NIH HHS/ -- T32 AI095213/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Sep 4;513(7516):90-4. doi: 10.1038/nature13608. Epub 2014 Aug 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany [2]. ; Institute for Genetics, Centre for Molecular Medicine (CMMC), and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany. ; Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA. ; Tierforschungszentrum, University of Ulm, Albert-Einstein-Allee 11, D-89081 Ulm, Germany. ; Institute for Laboratory Animal Science, Hannover Medical School, D-30625 Hannover, Germany. ; 1] Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25132550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Caspase 8/metabolism ; Cell Survival ; Epithelial Cells/*cytology/metabolism/*pathology ; Fas-Associated Death Domain Protein/deficiency/metabolism ; Female ; *Homeostasis ; Inflammation/metabolism/pathology ; Intestines/cytology/metabolism/pathology ; Keratinocytes/metabolism/pathology ; Male ; Mice ; Mice, Knockout ; Myeloid Differentiation Factor 88/metabolism ; *Necrosis ; Paneth Cells/metabolism/pathology ; Receptor-Interacting Protein Serine-Threonine ; Kinases/deficiency/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Type I/deficiency/metabolism ; Skin/cytology/metabolism/pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
    Electronic Resource
    Electronic Resource
    Electrical and spectroscopic comparison of HfO2/Si interfaces on nitrided and un-nitrided Si(100) (2002)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 91 (2002), S. 4353-4363 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: The interfacial chemistry of the high-k dielectric HfO2 has been investigated on nitrided and un-nitrided Si(100) using x-ray photoelectron spectroscopy (XPS) and secondary ion mass spectroscopy (SIMS). The samples are prepared by sputter depositing Hf metal and subsequently oxidizing it. A 600 °C densification anneal is critical to completing Hf oxidation. These spectroscopic data complement electrical testing of metal oxide semiconductor capacitors fabricated with ∼50 Å HfO2 on nitrided and un-nitrided Si(100). Capacitors with interfacial nitride show reduced leakage current by a factor of 100 at a −1 V bias. Concurrently, interfacial nitride increased capacitance 12% at saturation. XPS shows that an interfacial layer composed of nonstoichiometric hafnium silicate (HfSixOy), forms at both the HfO2/Si and HfO2/SiNx interfaces. Differences in the Si 2p and O 1s XP spectra suggest more silicate forms at the un-nitrided interface. HfO2 films on un-nitrided Si show more O 1s and Si 2p photoemission intensity characteristic of HfSixOy. SIMS depth profiles through the buried interface are consistent with interfacial silicate formation, as shown by a HfSiO+ ion signal, that is sandwiched between HfO2 and SiNx. SiNx is suggested to minimize interfacial HfSixOy formation by limiting the amount of Si available to interact with the HfO2 layer. © 2002 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1455155
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  • 8
    Electronic Resource
    Electronic Resource
    Chemical and thermal reduction of thin films of copper (II) oxide and copper (I) oxide (2001)
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 90 (2001), S. 4256-4264 
    Details
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Chemical and thermal reduction of copper oxide thin films (∼20 Å) has been studied with x-ray photoelectron spectroscopy (XPS) and temperature programmed desorption (TPD) for application in microelectronic device interconnects. XPS showed that copper (I) oxide (Cu2O) and copper (II) oxide (CuO) were reduced to copper metal at 400 K within a 30 min exposure to deuterium atoms (D*) and molecules at 1×10−4 Torr. Similarly, XPS showed that Cu2O was reduced to copper metal at 400 K within a 30 min exposure to methyl radicals (CH3*) and acetone molecules at 1×10−4 Torr. After D* exposure, TPD showed O leaves the Cu2O surface as D2O from 400 K to 700 K with a peak desorption temperature of 510 K. After CH3* exposure, TPD showed O leaves the Cu2O surface as CO2 over a range from 400 to 700 K with a peak temperature at 590 K. With carbon impurity below the XPS detection limit, thermal reduction of CuO to Cu2O was verified by XPS near 890 K. TPD experiments showed that O leaves the CuO surface as O2 at 890 K. Without surface C, thermal reduction of Cu2O was not observed up to 1073 K. Reduction of Cu2O without reactive radical species (D* or CH3*) was negligible. These results suggest that thin films of copper oxide can be reduced at 400 K with D* and CH3*. © 2001 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1403675
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  • 9
    Electronic Resource
    Electronic Resource
    Organometallic compounds
    Amsterdam : Elsevier
    Journal of Organometallic Chemistry 29 (1971), S. 269-274 
    Details
    ISSN: 0022-328X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0022-328X(00)86136-7
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  • 10
    Electronic Resource
    Electronic Resource
    Quantum yields in photolysis of (diene)tricarbonyliron and bis(diene)carbonyliron complexes
    Amsterdam : Elsevier
    Journal of Organometallic Chemistry 187 (1980), S. 361-373 
    Details
    ISSN: 0022-328X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0022-328X(00)93429-6
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