TY  - JOUR
A1  - Dech, Stefan
A1  - Holzwarth, Stefanie
A1  - Asam, Sarah
A1  - Andresen, Thorsten
A1  - Bachmann, Martin
A1  - Boettcher, Martin
A1  - Dietz, Andreas
A1  - Eisfelder, Christina
A1  - Frey, Corinne
A1  - Gesell, Gerhard
A1  - Gessner, Ursula
A1  - Hirner, Andreas
A1  - Hofmann, Matthias
A1  - Kirches, Grit
A1  - Klein, Doris
A1  - Klein, Igor
A1  - Kraus, Tanja
A1  - Krause, Detmar
A1  - Plank, Simon
A1  - Popp, Thomas
A1  - Reinermann, Sophie
A1  - Reiners, Philipp
A1  - Roessler, Sebastian
A1  - Ruppert, Thomas
A1  - Scherbachenko, Alexander
A1  - Vignesh, Ranjitha
A1  - Wolfmueller, Meinhard
A1  - Zwenzner, Hendrik
A1  - Kuenzer, Claudia
T1  - Potential and challenges of harmonizing 40 years of AVHRR data: the TIMELINE experience
JF  - Remote Sensing
N2  - Earth Observation satellite data allows for the monitoring of the surface of our planet at predefined intervals covering large areas. However, there is only one medium resolution sensor family in orbit that enables an observation time span of 40 and more years at a daily repeat interval. This is the AVHRR sensor family. If we want to investigate the long-term impacts of climate change on our environment, we can only do so based on data that remains available for several decades. If we then want to investigate processes with respect to climate change, we need very high temporal resolution enabling the generation of long-term time series and the derivation of related statistical parameters such as mean, variability, anomalies, and trends. The challenges to generating a well calibrated and harmonized 40-year-long time series based on AVHRR sensor data flown on 14 different platforms are enormous. However, only extremely thorough pre-processing and harmonization ensures that trends found in the data are real trends and not sensor-related (or other) artefacts. The generation of European-wide time series as a basis for the derivation of a multitude of parameters is therefore an extremely challenging task, the details of which are presented in this paper.
KW  - AVHRR
KW  - Earth Observation
KW  - harmonization
KW  - time series analysis
KW  - climate related trends
KW  - automatic processing
KW  - Europe
KW  - TIMELINE
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-246134
SN  - 2072-4292
VL  - 13
IS  - 18
ER  - 
TY  - JOUR
A1  - Göbel, Kerstin
A1  - Pankratz, Susann
A1  - Asaridou, Chloi-Magdalini
A1  - Herrmann, Alexander M.
A1  - Bittner, Stefan
A1  - Merker, Monika
A1  - Ruck, Tobias
A1  - Glumm, Sarah
A1  - Langhauser, Friederike
A1  - Kraft, Peter
A1  - Krug, Thorsten F.
A1  - Breuer, Johanna
A1  - Herold, Martin
A1  - Gross, Catharina C.
A1  - Beckmann, Denise
A1  - Korb-Pap, Adelheid
A1  - Schuhmann, Michael K.
A1  - Kuerten, Stefanie
A1  - Mitroulis, Ioannis
A1  - Ruppert, Clemens
A1  - Nolte, Marc W.
A1  - Panousis, Con
A1  - Klotz, Luisa
A1  - Kehrel, Beate
A1  - Korn, Thomas
A1  - Langer, Harald F.
A1  - Pap, Thomas
A1  - Nieswandt, Bernhard
A1  - Wiendl, Heinz
A1  - Chavakis, Triantafyllos
A1  - Kleinschnitz, Christoph
A1  - Meuth, Sven G.
T1  - Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells
JF  - Nature Communications
N2  - Aberrant immune responses represent the underlying cause of central nervous system (CNS) autoimmunity, including multiple sclerosis (MS). Recent evidence implicated the crosstalk between coagulation and immunity in CNS autoimmunity. Here we identify coagulation factor XII (FXII), the initiator of the intrinsic coagulation cascade and the kallikrein–kinin system, as a specific immune cell modulator. High levels of FXII activity are present in the plasma of MS patients during relapse. Deficiency or pharmacologic blockade of FXII renders mice less susceptible to experimental autoimmune encephalomyelitis (a model of MS) and is accompanied by reduced numbers of interleukin-17A-producing T cells. Immune activation by FXII is mediated by dendritic cells in a CD87-dependent manner and involves alterations in intracellular cyclic AMP formation. Our study demonstrates that a member of the plasmatic coagulation cascade is a key mediator of autoimmunity. FXII inhibition may provide a strategy to combat MS and other immune-related disorders.
KW  - blood coagulation
KW  - factor XII
KW  - neuroinflammation
KW  - dendric cells
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-165503
VL  - 7
IS  - 11626
ER  - 
TY  - JOUR
A1  - Schulz, Herbert
A1  - Ruppert, Ann-Kathrin
A1  - Herms, Stefan
A1  - Wolf, Christiane
A1  - Mirza-Schreiber, Nazanin
A1  - Stegle, Oliver
A1  - Czamara, Darina
A1  - Forstner, Andreas J.
A1  - Sivalingam, Sugirthan
A1  - Schoch, Susanne
A1  - Moebus, Susanne
A1  - Pütz, Benno
A1  - Hillmer, Axel
A1  - Fricker, Nadine
A1  - Vatter, Hartmut
A1  - Müller-Myhsok, Bertram
A1  - Nöthen, Markus M.
A1  - Becker, Albert J.
A1  - Hoffmann, Per
A1  - Sander, Thomas
A1  - Cichon, Sven
T1  - Genome-wide mapping of genetic determinants influencing DNA methylation and gene expression in human hippocampus
JF  - Nature Communications
N2  - Emerging evidence emphasizes the strong impact of regulatory genomic elements in neurodevelopmental processes and the complex pathways of brain disorders. The present genome-wide quantitative trait loci analyses explore the \(cis\)-regulatory effects of single-nucleotide polymorphisms (SNPs) on DNA methylation (meQTL) and gene expression (eQTL) in 110 human hippocampal biopsies. We identify \(cis\)-meQTLs at 14,118 CpG methylation sites and \(cis\)-eQTLs for 302 3′-mRNA transcripts of 288 genes. Hippocampal \(cis\)-meQTL-CpGs are enriched in flanking regions of active promoters, CpG island shores, binding sites of the transcription factor CTCF and brain eQTLs. \(Cis\)-acting SNPs of hippocampal meQTLs and eQTLs significantly overlap schizophrenia-associated SNPs. Correlations of CpG methylation and RNA expression are found for 34 genes. Our comprehensive maps of \(cis\)-acting hippocampal meQTLs and eQTLs provide a link between disease-associated SNPs and the regulatory genome that will improve the functional interpretation of non-coding genetic variants in the molecular genetic dissection of brain disorders.
KW  - psychiatry
KW  - epigenetics in the nervous system
KW  - epigenomics
KW  - gene expression
KW  - neurological disorders
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-173168
VL  - 8
ER  -