TY  - THES
A1  - Schmidt, Marco
T1  - Ground Station Networks for Efficient Operation of Distributed Small Satellite Systems
T1  - Effizienter Betrieb von Verteilten Kleinsatelliten-Systemen mit Bodenstationsnetzwerken
N2  - The field of small satellite formations and constellations attracted growing attention, based on recent advances in small satellite engineering. The utilization of distributed space systems allows the realization of innovative applications and will enable improved temporal and spatial resolution in observation scenarios. On the other side, this new paradigm imposes a variety of research challenges. In this monograph new networking concepts for space missions are presented, using networks of ground stations. The developed approaches combine ground station resources in a coordinated way to achieve more robust and efficient communication links. Within this thesis, the following topics were elaborated to improve the performance in distributed space missions: Appropriate scheduling of contact windows in a distributed ground system is a necessary process to avoid low utilization of ground stations. The theoretical basis for the novel concept of redundant scheduling was elaborated in detail. Additionally to the presented algorithm was a scheduling system implemented, its performance was tested extensively with real world scheduling problems. In the scope of data management, a system was developed which autonomously synchronizes data frames in ground station networks and uses this information to detect and correct transmission errors. The system was validated with hardware in the loop experiments, demonstrating the benefits of the developed approach.
N2  - Satellitenformationen und Konstellationen rücken immer mehr in den Fokus aktueller Forschung, ausgelöst durch die jüngsten Fortschritte in der Kleinsatelliten-Entwicklung. Der Einsatz von verteilten Weltraumsystemen ermöglicht die Realisierung von innovativen Anwendungen auf Basis von hoher zeitlicher und räumlicher Auflösung in Observationsszenarien. Allerdings bringt dieses neue Paradigma der Raumfahrttechnik auch Herausforderungen in verschiedenen Forschungsfeldern mit sich. In dieser Dissertation werden neue Netzwerk-Konzepte für Raumfahrtmissionen unter Einsatz von Bodenstationnetzwerken vorgestellt. Die präsentierten Verfahren koordinieren verfügbare Bodenstationsressourcen um einen robusten und effizienten Kommunikationslink zu ermöglichen. In dieser Arbeit werden dabei folgende Themenfelder behandelt um die Performance in verteilten Raumfahrtmissionen zu steigern: Das Verteilen von Kontaktfenster (sogenanntes Scheduling) in verteilten Bodenstationssystem ist ein notwendiger Prozess um eine niedrige Auslastung der Stationen zu vermeiden. Die theoretische Grundlage für das Konzept des redundanten Scheduling wurde erarbeitet. Zusätztlich wurde das Verfahren in Form eines Scheduling Systems implementiert und dessen Performance ausführlich an real-world Szenarien getestet. Im Rahmen des Themenfeldes Data Management wurde ein System entwickelt, welches autonom Datenframes in Bodenstationsnetzwerken synchronisieren kann. Die in den Datenframes enthaltene Information wird genutzt um Übertragungsfehler zu erkennen und zu korrigieren. Das System wurde mit Hardware-in-the-loop Experimenten validiert und die Vorteile des entwickelten Verfahrens wurden gezeigt.
T3  - Forschungsberichte in der Robotik = Research Notes in Robotics - 6 
KW  - Kleinsatellit
KW  - Bodenstation
KW  - Verteiltes System
KW  - Scheduling
KW  - Ground Station Networks
KW  - Small Satellites
KW  - Distributed Space Systems
Y1  - 2011
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-64999
SN  - 978-3-923959-77-8
ER  - 
TY  - JOUR
A1  - Wohlfarth, Carolin
A1  - Schmitteckert, Stefanie
A1  - Härtle, Janina D.
A1  - Houghton, Lesley A.
A1  - Dweep, Harsh
A1  - Fortea, Marina
A1  - Assadi, Ghazaleh
A1  - Braun, Alexander
A1  - Mederer, Tanja
A1  - Pöhner, Sarina
A1  - Becker, Philip P.
A1  - Fischer, Christine
A1  - Granzow, Martin
A1  - Mönnikes, Hubert
A1  - Mayer, Emeran A.
A1  - Sayuk, Gregory
A1  - Boeckxstaens, Guy
A1  - Wouters, Mira M.
A1  - Simrén, Magnus
A1  - Lindberg, Greger
A1  - Ohlsson, Bodil
A1  - Schmidt, Peter Thelin
A1  - Dlugosz, Aldona
A1  - Agreus, Lars
A1  - Andreasson, Anna
A1  - D'Amato, Mauro
A1  - Burwinkel, Barbara
A1  - Bermejo, Justo Lorenzo
A1  - Röth, Ralph
A1  - Lasitschka, Felix
A1  - Vicario, Maria
A1  - Metzger, Marco
A1  - Santos, Javier
A1  - Rappold, Gudrun A.
A1  - Martinez, Cristina
A1  - Niesler, Beate
T1  - miR-16 and miR-103 impact 5-HT4 receptor signalling and correlate with symptom profile in irritable bowel syndrome
JF  - Scientific Reports
N2  - Irritable bowel syndrome (IBS) is a gut-brain disorder involving alterations in intestinal sensitivity and motility. Serotonin 5-HT4 receptors are promising candidates in IBS pathophysiology since they regulate gut motor function and stool consistency, and targeted 5-HT4R selective drug intervention has been proven beneficial in subgroups of patients. We identified a single nucleotide polymorphism (SNP) (rs201253747) c.*61 T > C within the 5-HT4 receptor gene \(HTR4\) to be predominantly present in diarrhoea-IBS patients (IBS-D). It affects a binding site for the miR-16 family and miR-103/miR-107 within the isoforms \({HTR4b/i}\) and putatively impairs \(HTR4\) expression. Subsequent miRNA profiling revealed downregulation of miR-16 and miR-103 in the jejunum of IBS-D patients correlating with symptoms. \(In\) \(vitro\) assays confirmed expression regulation via three 3′UTR binding sites. The novel isoform \(HTR4b\_2\) lacking two of the three miRNA binding sites escapes miR-16/103/107 regulationin SNP carriers. We provide the first evidence that \(HTR4\) expression is fine-tuned by miRNAs, and that this regulation is impaired either by the SNP c.*61 T > C or bydiminished levels of miR-16 and miR-103 suggesting that \(HTR4\) might be involved in the development of IBS-D.
KW  - Medicine
KW  - Gene regulation
KW  - Irritable bowel syndrome
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-173478
VL  - 7
ER  - 
TY  - JOUR
A1  - Trujillo‐Viera, Jonathan
A1  - El‐Merahbi, Rabih
A1  - Schmidt, Vanessa
A1  - Karwen, Till
A1  - Loza‐Valdes, Angel
A1  - Strohmeyer, Akim
A1  - Reuter, Saskia
A1  - Noh, Minhee
A1  - Wit, Magdalena
A1  - Hawro, Izabela
A1  - Mocek, Sabine
A1  - Fey, Christina
A1  - Mayer, Alexander E.
A1  - Löffler, Mona C.
A1  - Wilhelmi, Ilka
A1  - Metzger, Marco
A1  - Ishikawa, Eri
A1  - Yamasaki, Sho
A1  - Rau, Monika
A1  - Geier, Andreas
A1  - Hankir, Mohammed
A1  - Seyfried, Florian
A1  - Klingenspor, Martin
A1  - Sumara, Grzegorz
T1  - Protein Kinase D2 drives chylomicron‐mediated lipid transport in the intestine and promotes obesity
JF  - EMBO Molecular Medicine
N2  - Lipids are the most energy‐dense components of the diet, and their overconsumption promotes obesity and diabetes. Dietary fat content has been linked to the lipid processing activity by the intestine and its overall capacity to absorb triglycerides (TG). However, the signaling cascades driving intestinal lipid absorption in response to elevated dietary fat are largely unknown. Here, we describe an unexpected role of the protein kinase D2 (PKD2) in lipid homeostasis. We demonstrate that PKD2 activity promotes chylomicron‐mediated TG transfer in enterocytes. PKD2 increases chylomicron size to enhance the TG secretion on the basolateral side of the mouse and human enterocytes, which is associated with decreased abundance of APOA4. PKD2 activation in intestine also correlates positively with circulating TG in obese human patients. Importantly, deletion, inactivation, or inhibition of PKD2 ameliorates high‐fat diet‐induced obesity and diabetes and improves gut microbiota profile in mice. Taken together, our findings suggest that PKD2 represents a key signaling node promoting dietary fat absorption and may serve as an attractive target for the treatment of obesity.
KW  - chylomicron
KW  - fat absorption
KW  - intestine
KW  - obesity
KW  - protein kinase D2/PKD2/PRKD2
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-239018
VL  - 13
IS  - 5
ER  - 
TY  - JOUR
A1  - Ferreira, Manuel A.
A1  - Gamazon, Eric R.
A1  - Al-Ejeh, Fares
A1  - Aittomäki, Kristiina
A1  - Andrulis, Irene L.
A1  - Anton-Culver, Hoda
A1  - Arason, Adalgeir
A1  - Arndt, Volker
A1  - Aronson, Kristan J.
A1  - Arun, Banu K.
A1  - Asseryanis, Ella
A1  - Azzollini, Jacopo
A1  - Balmaña, Judith
A1  - Barnes, Daniel R.
A1  - Barrowdale, Daniel
A1  - Beckmann, Matthias W.
A1  - Behrens, Sabine
A1  - Benitez, Javier
A1  - Bermisheva, Marina
A1  - Bialkowska, Katarzyna
A1  - Blomqvist, Carl
A1  - Bogdanova, Natalia V.
A1  - Bojesen, Stig E.
A1  - Bolla, Manjeet K.
A1  - Borg, Ake
A1  - Brauch, Hiltrud
A1  - Brenner, Hermann
A1  - Broeks, Annegien
A1  - Burwinkel, Barbara
A1  - Caldés, Trinidad
A1  - Caligo, Maria A.
A1  - Campa, Daniele
A1  - Campbell, Ian
A1  - Canzian, Federico
A1  - Carter, Jonathan
A1  - Carter, Brian D.
A1  - Castelao, Jose E.
A1  - Chang-Claude, Jenny
A1  - Chanock, Stephen J.
A1  - Christiansen, Hans
A1  - Chung, Wendy K.
A1  - Claes, Kathleen B. M.
A1  - Clarke, Christine L.
A1  - Couch, Fergus J.
A1  - Cox, Angela
A1  - Cross, Simon S.
A1  - Czene, Kamila
A1  - Daly, Mary B.
A1  - de la Hoya, Miguel
A1  - Dennis, Joe
A1  - Devilee, Peter
A1  - Diez, Orland
A1  - Dörk, Thilo
A1  - Dunning, Alison M.
A1  - Dwek, Miriam
A1  - Eccles, Diana M.
A1  - Ejlertsen, Bent
A1  - Ellberg, Carolina
A1  - Engel, Christoph
A1  - Eriksson, Mikael
A1  - Fasching, Peter A.
A1  - Fletcher, Olivia
A1  - Flyger, Henrik
A1  - Friedman, Eitan
A1  - Frost, Debra
A1  - Gabrielson, Marike
A1  - Gago-Dominguez, Manuela
A1  - Ganz, Patricia A.
A1  - Gapstur, Susan M.
A1  - Garber, Judy
A1  - García-Closas, Montserrat
A1  - García-Sáenz, José A.
A1  - Gaudet, Mia M.
A1  - Giles, Graham G.
A1  - Glendon, Gord
A1  - Godwin, Andrew K.
A1  - Goldberg, Mark S.
A1  - Goldgar, David E.
A1  - González-Neira, Anna
A1  - Greene, Mark H.
A1  - Gronwald, Jacek
A1  - Guenél, Pascal
A1  - Haimann, Christopher A.
A1  - Hall, Per
A1  - Hamann, Ute
A1  - He, Wei
A1  - Heyworth, Jane
A1  - Hogervorst, Frans B. L.
A1  - Hollestelle, Antoinette
A1  - Hoover, Robert N.
A1  - Hopper, John L.
A1  - Hulick, Peter J.
A1  - Humphreys, Keith
A1  - Imyanitov, Evgeny N.
A1  - Isaacs, Claudine
A1  - Jakimovska, Milena
A1  - Jakubowska, Anna
A1  - James, Paul A.
A1  - Janavicius, Ramunas
A1  - Jankowitz, Rachel C.
A1  - John, Esther M.
A1  - Johnson, Nichola
A1  - Joseph, Vijai
A1  - Karlan, Beth Y.
A1  - Khusnutdinova, Elza
A1  - Kiiski, Johanna I.
A1  - Ko, Yon-Dschun
A1  - Jones, Michael E.
A1  - Konstantopoulou, Irene
A1  - Kristensen, Vessela N.
A1  - Laitman, Yael
A1  - Lambrechts, Diether
A1  - Lazaro, Conxi
A1  - Leslie, Goska
A1  - Lester, Jenny
A1  - Lesueur, Fabienne
A1  - Lindström, Sara
A1  - Long, Jirong
A1  - Loud, Jennifer T.
A1  - Lubiński, Jan
A1  - Makalic, Enes
A1  - Mannermaa, Arto
A1  - Manoochehri, Mehdi
A1  - Margolin, Sara
A1  - Maurer, Tabea
A1  - Mavroudis, Dimitrios
A1  - McGuffog, Lesley
A1  - Meindl, Alfons
A1  - Menon, Usha
A1  - Michailidou, Kyriaki
A1  - Miller, Austin
A1  - Montagna, Marco
A1  - Moreno, Fernando
A1  - Moserle, Lidia
A1  - Mulligan, Anna Marie
A1  - Nathanson, Katherine L.
A1  - Neuhausen, Susan L.
A1  - Nevanlinna, Heli
A1  - Nevelsteen, Ines
A1  - Nielsen, Finn C.
A1  - Nikitina-Zake, Liene
A1  - Nussbaum, Robert L.
A1  - Offit, Kenneth
A1  - Olah, Edith
A1  - Olopade, Olufunmilayo I.
A1  - Olsson, Håkan
A1  - Osorio, Ana
A1  - Papp, Janos
A1  - Park-Simon, Tjoung-Won
A1  - Parsons, Michael T.
A1  - Pedersen, Inge Sokilde
A1  - Peixoto, Ana
A1  - Peterlongo, Paolo
A1  - Pharaoh, Paul D. P.
A1  - Plaseska-Karanfilska, Dijana
A1  - Poppe, Bruce
A1  - Presneau, Nadege
A1  - Radice, Paolo
A1  - Rantala, Johanna
A1  - Rennert, Gad
A1  - Risch, Harvey A.
A1  - Saloustros, Emmanouil
A1  - Sanden, Kristin
A1  - Sawyer, Elinor J.
A1  - Schmidt, Marjanka K.
A1  - Schmutzler, Rita K.
A1  - Sharma, Priyanka
A1  - Shu, Xiao-Ou
A1  - Simard, Jaques
A1  - Singer, Christian F.
A1  - Soucy, Penny
A1  - Southey, Melissa C.
A1  - Spinelli, John J.
A1  - Spurdle, Amanda B.
A1  - Stone, Jennifer
A1  - Swerdlow, Anthony J.
A1  - Tapper, William J.
A1  - Taylor, Jack A.
A1  - Teixeira, Manuel R.
A1  - Terry, Mary Beth
A1  - Teulé, Alex
A1  - Thomassen, Mads
A1  - Thöne, Kathrin
A1  - Thull, Darcy L.
A1  - Tischkowitz, Marc
A1  - Toland, Amanda E.
A1  - Torres, Diana
A1  - Truong, Thérèse
A1  - Tung, Nadine
A1  - Vachon, Celine M.
A1  - van Asperen, Christi J.
A1  - van den Ouweland, Ans M. W.
A1  - van Rensburg, Elizabeth J.
A1  - Vega, Ana
A1  - Viel, Alexandra
A1  - Wang, Qin
A1  - Wappenschmidt, Barbara
A1  - Weitzel, Jeffrey N.
A1  - Wendt, Camilla
A1  - Winqvist, Robert
A1  - Yang, Xiaohong R.
A1  - Yannoukakos, Drakoulis
A1  - Ziogas, Argyrios
A1  - Kraft, Peter
A1  - Antoniou, Antonis C.
A1  - Zheng, Wei
A1  - Easton, Douglas F.
A1  - Milne, Roger L.
A1  - Beesley, Jonathan
A1  - Chenevix-Trench, Georgia
T1  - Genome-wide association and transcriptome studies identify target genes and risk loci for breast cancer
JF  - Nature Communications
N2  - Genome-wide association studies (GWAS) have identified more than 170 breast cancer susceptibility loci. Here we hypothesize that some risk-associated variants might act in non-breast tissues, specifically adipose tissue and immune cells from blood and spleen. Using expression quantitative trait loci (eQTL) reported in these tissues, we identify 26 previously unreported, likely target genes of overall breast cancer risk variants, and 17 for estrogen receptor (ER)-negative breast cancer, several with a known immune function. We determine the directional effect of gene expression on disease risk measured based on single and multiple eQTL. In addition, using a gene-based test of association that considers eQTL from multiple tissues, we identify seven (and four) regions with variants associated with overall (and ER-negative) breast cancer risk, which were not reported in previous GWAS. Further investigation of the function of the implicated genes in breast and immune cells may provide insights into the etiology of breast cancer.
KW  - cancer
KW  - genetics
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-228024
VL  - 10
ER  -