TY  - JOUR
A1  - Bousquet, J.
A1  - Farrell, J.
A1  - Crooks, G.
A1  - Hellings, P.
A1  - Bel, E. H.
A1  - Bewick, M.
A1  - Chavannes, N. H.
A1  - Correia de Sousa, J.
A1  - Cruz, A. A.
A1  - Haahtela, T.
A1  - Joos, G.
A1  - Khaltaev, N.
A1  - Malva, J.
A1  - Muraro, A.
A1  - Nogues, M.
A1  - Palkonen, S.
A1  - Pedersen, S.
A1  - Robalo-Cordeiro, C.
A1  - Samolinski, B.
A1  - Strandberg, T.
A1  - Valiulis, A.
A1  - Yorgancioglu, A.
A1  - Zuberbier, T.
A1  - Bedbrook, A.
A1  - Aberer, W.
A1  - Adachi, M.
A1  - Agusti, A.
A1  - Akdis, C. A.
A1  - Akdis, M.
A1  - Ankri, J.
A1  - Alonso, A.
A1  - Annesi-Maesano, I.
A1  - Ansotegui, I. J.
A1  - Anto, J. M.
A1  - Arnavielhe, S.
A1  - Arshad, H.
A1  - Bai, C.
A1  - Baiardini, I.
A1  - Bachert, C.
A1  - Baigenzhin, A. K.
A1  - Barbara, C.
A1  - Bateman, E. D.
A1  - Beghé, B.
A1  - Ben Kheder, A.
A1  - Bennoor, K. S.
A1  - Benson, M.
A1  - Bergmann, K. C.
A1  - Bieber, T.
A1  - Bindslev-Jensen, C.
A1  - Bjermer, L.
A1  - Blain, H.
A1  - Blasi, F.
A1  - Boner, A. L.
A1  - Bonini, M.
A1  - Bonini, S.
A1  - Bosnic-Anticevitch, S.
A1  - Boulet, L. P.
A1  - Bourret, R.
A1  - Bousquet, P. J.
A1  - Braido, F.
A1  - Briggs, A. H.
A1  - Brightling, C. E.
A1  - Brozek, J.
A1  - Buhl, R.
A1  - Burney, P. G.
A1  - Bush, A.
A1  - Caballero-Fonseca, F.
A1  - Caimmi, D.
A1  - Calderon, M. A.
A1  - Calverley, P. M.
A1  - Camargos, P. A. M.
A1  - Canonica, G. W.
A1  - Camuzat, T.
A1  - Carlsen, K. H.
A1  - Carr, W.
A1  - Carriazo, A.
A1  - Casale, T.
A1  - Cepeda Sarabia, A. M.
A1  - Chatzi, L.
A1  - Chen, Y. Z.
A1  - Chiron, R.
A1  - Chkhartishvili, E.
A1  - Chuchalin, A. G.
A1  - Chung, K. F.
A1  - Ciprandi, G.
A1  - Cirule, I.
A1  - Cox, L.
A1  - Costa, D. J.
A1  - Custovic, A.
A1  - Dahl, R.
A1  - Dahlen, S. E.
A1  - Darsow, U.
A1  - De Carlo, G.
A1  - De Blay, F.
A1  - Dedeu, T.
A1  - Deleanu, D.
A1  - De Manuel Keenoy, E.
A1  - Demoly, P.
A1  - Denburg, J. A.
A1  - Devillier, P.
A1  - Didier, A.
A1  - Dinh-Xuan, A. T.
A1  - Djukanovic, R.
A1  - Dokic, D.
A1  - Douagui, H.
A1  - Dray, G.
A1  - Dubakiene, R.
A1  - Durham, S. R.
A1  - Dykewicz, M. S.
A1  - El-Gamal, Y.
A1  - Emuzyte, R.
A1  - Fabbri, L. M.
A1  - Fletcher, M.
A1  - Fiocchi, A.
A1  - Fink Wagner, A.
A1  - Fonseca, J.
A1  - Fokkens, W. J.
A1  - Forastiere, F.
A1  - Frith, P.
A1  - Gaga, M.
A1  - Gamkrelidze, A.
A1  - Garces, J.
A1  - Garcia-Aymerich, J.
A1  - Gemicioğlu, B.
A1  - Gereda, J. E.
A1  - González Diaz, S.
A1  - Gotua, M.
A1  - Grisle, I.
A1  - Grouse, L.
A1  - Gutter, Z.
A1  - Guzmán, M. A.
A1  - Heaney, L. G.
A1  - Hellquist-Dahl, B.
A1  - Henderson, D.
A1  - Hendry, A.
A1  - Heinrich, J.
A1  - Heve, D.
A1  - Horak, F.
A1  - Hourihane, J. O’. B.
A1  - Howarth, P.
A1  - Humbert, M.
A1  - Hyland, M. E.
A1  - Illario, M.
A1  - Ivancevich, J. C.
A1  - Jardim, J. R.
A1  - Jares, E. J.
A1  - Jeandel, C.
A1  - Jenkins, C.
A1  - Johnston, S. L.
A1  - Jonquet, O.
A1  - Julge, K.
A1  - Jung, K. S.
A1  - Just, J.
A1  - Kaidashev, I.
A1  - Kaitov, M. R.
A1  - Kalayci, O.
A1  - Kalyoncu, A. F.
A1  - Keil, T.
A1  - Keith, P. K.
A1  - Klimek, L.
A1  - Koffi N’Goran, B.
A1  - Kolek, V.
A1  - Koppelman, G. H.
A1  - Kowalski, M. L.
A1  - Kull, I.
A1  - Kuna, P.
A1  - Kvedariene, V.
A1  - Lambrecht, B.
A1  - Lau, S.
A1  - Larenas‑Linnemann, D.
A1  - Laune, D.
A1  - Le, L. T. T.
A1  - Lieberman, P.
A1  - Lipworth, B.
A1  - Li, J.
A1  - Lodrup Carlsen, K.
A1  - Louis, R.
A1  - MacNee, W.
A1  - Magard, Y.
A1  - Magnan, A.
A1  - Mahboub, B.
A1  - Mair, A.
A1  - Majer, I.
A1  - Makela, M. J.
A1  - Manning, P.
A1  - Mara, S.
A1  - Marshall, G. D.
A1  - Masjedi, M. R.
A1  - Matignon, P.
A1  - Maurer, M.
A1  - Mavale‑Manuel, S.
A1  - Melén, E.
A1  - Melo‑Gomes, E.
A1  - Meltzer, E. O.
A1  - Menzies‑Gow, A.
A1  - Merk, H.
A1  - Michel, J. P.
A1  - Miculinic, N.
A1  - Mihaltan, F.
A1  - Milenkovic, B.
A1  - Mohammad, G. M. Y.
A1  - Molimard, M.
A1  - Momas, I.
A1  - Montilla‑Santana, A.
A1  - Morais‑Almeida, M.
A1  - Morgan, M.
A1  - Mösges, R.
A1  - Mullol, J.
A1  - Nafti, S.
A1  - Namazova‑Baranova, L.
A1  - Naclerio, R.
A1  - Neou, A.
A1  - Neffen, H.
A1  - Nekam, K.
A1  - Niggemann, B.
A1  - Ninot, G.
A1  - Nyembue, T. D.
A1  - O’Hehir, R. E.
A1  - Ohta, K.
A1  - Okamoto, Y.
A1  - Okubo, K.
A1  - Ouedraogo, S.
A1  - Paggiaro, P.
A1  - Pali‑Schöll, I.
A1  - Panzner, P.
A1  - Papadopoulos, N.
A1  - Papi, A.
A1  - Park, H. S.
A1  - Passalacqua, G.
A1  - Pavord, I.
A1  - Pawankar, R.
A1  - Pengelly, R.
A1  - Pfaar, O.
A1  - Picard, R.
A1  - Pigearias, B.
A1  - Pin, I.
A1  - Plavec, D.
A1  - Poethig, D.
A1  - Pohl, W.
A1  - Popov, T. A.
A1  - Portejoie, F.
A1  - Potter, P.
A1  - Postma, D.
A1  - Price, D.
A1  - Rabe, K. F.
A1  - Raciborski, F.
A1  - Radier Pontal, F.
A1  - Repka‑Ramirez, S.
A1  - Reitamo, S.
A1  - Rennard, S.
A1  - Rodenas, F.
A1  - Roberts, J.
A1  - Roca, J.
A1  - Rodriguez Mañas, L.
A1  - et al, 
T1  - Scaling up strategies of the chronic respiratory disease programme of the European Innovation Partnership on Active and Healthy Ageing (Action Plan B3: Area 5)
JF  - Clinical and Translational Allergy
N2  - Action Plan B3 of the European Innovation Partnership on Active and Healthy Ageing (EIP on AHA) focuses on the integrated care of chronic diseases. Area 5 (Care Pathways) was initiated using chronic respiratory diseases as a model. The chronic respiratory disease action plan includes (1) AIRWAYS integrated care pathways (ICPs), (2) the joint initiative between the Reference site MACVIA-LR (Contre les MAladies Chroniques pour un VIeillissement Actif) and ARIA (Allergic Rhinitis and its Impact on Asthma), (3) Commitments for Action to the European Innovation Partnership on Active and Healthy Ageing and the AIRWAYS ICPs network. It is deployed in collaboration with the World Health Organization Global Alliance against Chronic Respiratory Diseases (GARD). The European Innovation Partnership on Active and Healthy Ageing has proposed a 5-step framework for developing an individual scaling up strategy: (1) what to scale up: (1-a) databases of good practices, (1-b) assessment of viability of the scaling up of good practices, (1-c) classification of good practices for local replication and (2) how to scale up: (2-a) facilitating partnerships for scaling up, (2-b) implementation of key success factors and lessons learnt, including emerging technologies for individualised and predictive medicine. This strategy has already been applied to the chronic respiratory disease action plan of the European Innovation Partnership on Active and Healthy Ageing.
KW  - EIP on AHA
KW  - European Innovation Partnership on Active and Healthy Ageing
KW  - AIRWAYS ICPs
KW  - MACVIA
KW  - Scaling up
KW  - Chronic respiratory diseases
KW  - ARIA
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-166874
VL  - 6
IS  - 29
ER  - 
TY  - JOUR
A1  - Bousquet, J.
A1  - Anto, J. M.
A1  - Akdis, M.
A1  - Auffray, C.
A1  - Keil, T.
A1  - Momas, I.
A1  - Postma, D. S.
A1  - Valenta, R.
A1  - Wickman, M.
A1  - Cambon-Thomsen, A.
A1  - Haahtela, T.
A1  - Lambrecht, B. N.
A1  - Lodrup Carlsen, K. C.
A1  - Koppelman, G. H.
A1  - Sunyer, J.
A1  - Zuberbier, T.
A1  - Annesi-Maesano, I.
A1  - Arno, A.
A1  - Bindslev-Jensen, C.
A1  - De Carlo, G.
A1  - Forastiere, F.
A1  - Heinrich, J.
A1  - Kowalski, M. L.
A1  - Maier, D.
A1  - Melen, E.
A1  - Palkonen, S.
A1  - Smit, H. A.
A1  - Standl, M.
A1  - Wright, J.
A1  - Asarnoj, A.
A1  - Benet, M.
A1  - Ballardini, N.
A1  - Garcia-Aymerich, J.
A1  - Gehring, U.
A1  - Guerra, S.
A1  - Hohman, C.
A1  - Kull, I.
A1  - Lupinek, C.
A1  - Pinart, M.
A1  - Skrindo, I.
A1  - Westman, M.
A1  - Smagghe, D.
A1  - Akdis, C.
A1  - Albang, R.
A1  - Anastasova, V.
A1  - Anderson, N.
A1  - Bachert, C.
A1  - Ballereau, S.
A1  - Ballester, F.
A1  - Basagana, X.
A1  - Bedbrook, A.
A1  - Bergstrom, A.
A1  - von Berg, A.
A1  - Brunekreef, B.
A1  - Burte, E.
A1  - Carlsen, K.H.
A1  - Chatzi, L.
A1  - Coquet, J.M.
A1  - Curin, M.
A1  - Demoly, P.
A1  - Eller, E.
A1  - Fantini, M.P.
A1  - Gerhard, B.
A1  - Hammad, H.
A1  - von Hertzen, L.
A1  - Hovland, V.
A1  - Jacquemin, B.
A1  - Just, J.
A1  - Keller, T.
A1  - Kerkhof, M.
A1  - Kiss, R.
A1  - Kogevinas, M.
A1  - Koletzko, S.
A1  - Lau, S.
A1  - Lehmann, I.
A1  - Lemonnier, N.
A1  - McEachan, R.
A1  - Makela, M.
A1  - Mestres, J.
A1  - Minina, E.
A1  - Mowinckel, P.
A1  - Nadif, R.
A1  - Nawijn, M.
A1  - Oddie, S.
A1  - Pellet, J.
A1  - Pin, I.
A1  - Porta, D.
A1  - Rancière, F.
A1  - Rial-Sebbag, A.
A1  - Schuijs, M.J.
A1  - Siroux, V.
A1  - Tischer, C.G.
A1  - Torrent, M.
A1  - Varraso, R.
A1  - De Vocht, J.
A1  - Wenger, K.
A1  - Wieser, S.
A1  - Xu, C.
T1  - Paving the way of systems biology and precision medicine in allergic diseases: the MeDALL success story 
Mechanisms of the Development of ALLergy; EUFP7-CP-IP; Project No: 261357; 2010-2015
JF  - Allergy
N2  - MeDALL (Mechanisms of the Development of ALLergy; EU FP7-CP-IP; Project No: 261357; 2010-2015) has proposed an innovative approach to develop early indicators for the prediction, diagnosis, prevention and targets for therapy. MeDALL has linked epidemiological, clinical and basic research using a stepwise, large-scale and integrative approach: MeDALL data of precisely phenotyped children followed in 14 birth cohorts spread across Europe were combined with systems biology (omics, IgE measurement using microarrays) and environmental data. Multimorbidity in the same child is more common than expected by chance alone, suggesting that these diseases share causal mechanisms irrespective of IgE sensitization. IgE sensitization should be considered differently in monosensitized and polysensitized individuals. Allergic multimorbidities and IgE polysensitization are often associated with the persistence or severity of allergic diseases. Environmental exposures are relevant for the development of allergy-related diseases. To complement the population-based studies in children, MeDALL included mechanistic experimental animal studies and in vitro studies in humans. The integration of multimorbidities and polysensitization has resulted in a new classification framework of allergic diseases that could help to improve the understanding of genetic and epigenetic mechanisms of allergy as well as to better manage allergic diseases. Ethics and gender were considered. MeDALL has deployed translational activities within the EU agenda.
KW  - asthma
KW  - birth cohort
KW  - atopic-dermatitis
KW  - immune-responses
KW  - IgE
KW  - multimorbidity
KW  - polysensitization
KW  - rhinitis
KW  - chronic respiratory-diseases
KW  - childhood asthma
KW  - immunological reactivity
KW  - IgE sensitazion
KW  - immunoglobulin-e
KW  - integraed care
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-186858
VL  - 71
IS  - 11
ER  - 
TY  - JOUR
A1  - Drenckhahn, Detlev
A1  - Drenckhahn, Helga
A1  - Weber, Heinrich E.
A1  - Jansen, Werner
A1  - Weber, Heinrich E.
A1  - Zonnenveld, Ben J. M.
ED  - Meierott, Lenz
ED  - Drenckhahn, Detlev
ED  - Dunkel, Franz G.
ED  - Ewald, Jörg
ED  - Fleischmann, Andreas
T1  - Forum Geobotanicum Vol. 8 (2018/2019)
N2  - Forum Geobotanicum is an electronic journal devoted to disseminate information concerning geographical distribution, ecology, morphology, taxonomy and conservation of vascular plants in the European Union with a main focus on middle Europe. It covers from molecular biology to environmental aspects. The focus is to publish original papers, reviews and announcements for the educated generalist as well as the specialist in this broad field. Forum Geobotanicum does not aim to supplant existing paper journals, but will be much more flexible in format, publication time and world-wide distribution than paper journals. Many important studies are being currently published in local journals and booklets and some of them are published privately. Hence, these studies will become aware to only a limited readership. Forum Geobotanicum will encourage authors of such papers to submit them as special issues of the journal. Moreover, the journal is planning to build up an E-mail-address section to support communication between geobotanists in Europe. The editors are optimistic that this electronic journal will develop to a widely used communication forum that will help to stimulate activities in the entire field of geobotany in middle Europe. To overcome problems of long term archivation and effective taxonomic publication of articles published electronically in Forum Geobotanicum, print versions of each volume of the journal and appropriate digital storage devices will be delivered freely to selected university libraries and state libraries in middle Europe.
N2  - Forum Geobotanicum ist eine elektronische Plattform, deren Zielsetzung darin besteht, neue Erkenntnisse der geobotanischen Forschung in der Europäischen Union mit Schwerpunkt Mitteleuropa umfassend zu verbreiten. Das Journal befasst sich mit allen Fragen von Verbreitung, Ökologie, Morphologie und Taxonomie von Gefäßpflanzen und soll das gesamte Spektrum der Geobotanik von molekularbiologischen Aspekten bis zu Umwelt- und Naturschutzfragen abdecken. Der Hauptfokus liegt auf der Publikation von Originaluntersuchungen und Übersichtsartikeln sowie Behandlung aktueller Fragen des Naturschutzes. Die Zielgruppen sind Personen mit Allgemeinkenntnissen in der Botanik und Floristik sowie Spezialisten auf den Gebieten der Geobotanik und Pflanzensystematik.
Das Journal soll keine Zeitschrift in Druckform ersetzen, sondern eine Ergänzung zu den traditionellen Publikationsorganen bilden. Der Vorteil der Zeitschrift liegt in ihrer Flexibilität und raschen Publikationszeit nach Begutachtung der eingereichten Manuskripte und den Möglichkeiten, in größerem Umfang Fotografien und andere Abbildungen zu veröffentlichen. Der Vorteil einer elektronischen Zeitschrift besteht weiterhin darin, dass die Veröffentlichungen weltweit jedermann sofort zugänglich sind. Viele durchaus wichtige Untersuchungen aus dem Bereich der Geobotanik erscheinen in lokalen Publikationsorganen, wie Jahrbüchern und Heimatkalendern, oder auch im Eigenverlag. Da solche Veröffentlichungen bibliographisch kaum erfasst werden, können sie auch nicht in adäquater Weise wahrgenommen werden. Forum Geobotanicum soll ermöglichen, dass auch solche Publikationen in einer Literaturrubrik bekannt gemacht werden und ggf. nach Klärung von Copyright-Fragen als Supplemente der Zeitschrift ins Netz gestellt werden. Forum Geobotanicum nutzt die Vorteile des Internets, indem es abrufbare Hilfen, wie ein Verzeichnis von Adressen, Pflanzenlisten etc. zur Verfügung stellt. Insgesamt soll die Kommunikation zwischen Geobotanikern in Mitteleuropa erleichtert und eine Kommunikationsplattform etabliert werden, die die Aktivitäten auf dem gesamten Wissenschaftsgebiet stimuliert.
Das Journal ist uneigennützig und für Autoren und Benutzer kostenfrei. Für die Kostendeckung sind Sponsoren erwünscht, denen eine begrenzte Möglichkeit zur Darstellung eingeräumt werden kann. In der Anfangsphase wird das Journal von einem kleinen Herausgebergremiumbetrieben. Sollte sich Forum Geobotanicum erfolgreich weiter entwickeln, ist an eine Erweiterung des Herausgebergremiums auf Experten aus allen Nationen des mitteleuropäischen Raums gedacht. Um eine langfristige Verfügbarkeit der Publikationen zu gewährleisten, wird jeder Jahrgang von Forum Geobotanicum ausgedruckt, gebunden und mit digitalem Datenträger versehen an ausgewählte Universitätsbibliotheken, Landes- und Staatsbibliotheken Deutschlands und wichtiger Städte Mitteleuropas zur Archivierung und Ausleihe versandt.
KW  - Geobotanik
KW  - Pflanzengeographie
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-175292
SN  - 1867-9315
VL  - 8(2018/2019)
ER  - 
TY  - JOUR
A1  - Jarick, I.
A1  - Volckmar, A. L.
A1  - Pütter, C.
A1  - Pechlivanis, S.
A1  - Nguyen, T. T.
A1  - Dauvermann, M. R.
A1  - Beck, S.
A1  - Albayrak, Ö.
A1  - Scherag, S.
A1  - Gilsbach, S.
A1  - Cichon, S.
A1  - Hoffmann, P.
A1  - Degenhardt, F.
A1  - Nöthen, M. M.
A1  - Schreiber, S.
A1  - Wichmann, H. E.
A1  - Jöckel, K. H.
A1  - Heinrich, J.
A1  - Tiesler, C. M. T.
A1  - Faraone, S. V.
A1  - Walitza, S.
A1  - Sinzig, J.
A1  - Freitag, C.
A1  - Meyer, J.
A1  - Herpertz-Dahlmann, B.
A1  - Lehmkuhl, G.
A1  - Renner, T. J.
A1  - Warnke, A.
A1  - Romanos, M.
A1  - Lesch, K. P.
A1  - Reif, A.
A1  - Schimmelmann, B. G.
A1  - Hebebrand, J.
A1  - Scherag, A.
A1  - Hinney, A.
T1  - Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder
JF  - Molecular Psychiatry
N2  - Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency ≤1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls \((P=2.8 × 10^{-4})\) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients \((P=1.2 × 10^{-3})\) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control \((P=4.3 × 10^{-2})\). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.
KW  - children
KW  - ADHD
KW  - CNVs
KW  - GWAS
KW  - PARK2
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121131
VL  - 19
IS  - 19
ER  - 
TY  - JOUR
A1  - Wilson, Duncan
A1  - Ambler, Gareth
A1  - Lee, Keon-Joo
A1  - Lim, Jae-Sung
A1  - Shiozawa, Masayuki
A1  - Koga, Masatoshi
A1  - Li, Linxin
A1  - Lovelock, Caroline
A1  - Chabriat, Hugues
A1  - Hennerici, Michael
A1  - Wong, Yuen Kwun
A1  - Mak, Henry Ka Fung
A1  - Prats-Sánchez, Luis
A1  - Martínez-Domeño, Alejandro
A1  - Inamura, Shigeru
A1  - Yoshifuji, Kazuhisa
A1  - Arsava, Ethem Murat
A1  - Horstmann, Solveig
A1  - Purrucker, Jan
A1  - Lam, Bonnie Yin Ka
A1  - Wong, Adrian
A1  - Kim, Young Dae
A1  - Song, Tae-Jin
A1  - Schrooten, Maarten
A1  - Lemmens, Robin
A1  - Eppinger, Sebastian
A1  - Gattringer, Thomas
A1  - Uysal, Ender
A1  - Tanriverdi, Zeynep
A1  - Bornstein, Natan M
A1  - Ben Assayag, Einor
A1  - Hallevi, Hen
A1  - Tanaka, Jun
A1  - Hara, Hideo
A1  - Coutts, Shelagh B
A1  - Hert, Lisa
A1  - Polymeris, Alexandros
A1  - Seiffge, David J
A1  - Lyrer, Philippe
A1  - Algra, Ale
A1  - Kappelle, Jaap
A1  - Salman, Rustam Al-Shahi
A1  - Jäger, Hans R
A1  - Lip, Gregory Y H
A1  - Mattle, Heinrich P
A1  - Panos, Leonidas D
A1  - Mas, Jean-Louis
A1  - Legrand, Laurence
A1  - Karayiannis, Christopher
A1  - Phan, Thanh
A1  - Gunkel, Sarah
A1  - Christ, Nicolas
A1  - Abrigo, Jill
A1  - Leung, Thomas
A1  - Chu, Winnie
A1  - Chappell, Francesca
A1  - Makin, Stephen
A1  - Hayden, Derek
A1  - Williams, David J
A1  - Kooi, M Eline
A1  - van Dam-Nolen, Dianne H K
A1  - Barbato, Carmen
A1  - Browning, Simone
A1  - Wiegertjes, Kim
A1  - Tuladhar, Anil M
A1  - Maaijwee, Noortje
A1  - Guevarra, Christine
A1  - Yatawara, Chathuri
A1  - Mendyk, Anne-Marie
A1  - Delmaire, Christine
A1  - Köhler, Sebastian
A1  - van Oostenbrugge, Robert
A1  - Zhou, Ying
A1  - Xu, Chao
A1  - Hilal, Saima
A1  - Gyanwali, Bibek
A1  - Chen, Christopher
A1  - Lou, Min
A1  - Staals, Julie
A1  - Bordet, Régis
A1  - Kandiah, Nagaendran
A1  - de Leeuw, Frank-Erik
A1  - Simister, Robert
A1  - van der Lugt, Aad
A1  - Kelly, Peter J
A1  - Wardlaw, Joanna M
A1  - Soo, Yannie
A1  - Fluri, Felix
A1  - Srikanth, Velandai
A1  - Calvet, David
A1  - Jung, Simon
A1  - Kwa, Vincent I H
A1  - Engelter, Stefan T
A1  - Peters, Nils
A1  - Smith, Eric E
A1  - Yakushiji, Yusuke
A1  - Necioglu Orken, Dilek
A1  - Fazekas, Franz
A1  - Thijs, Vincent
A1  - Heo, Ji Hoe
A1  - Mok, Vincent
A1  - Veltkamp, Roland
A1  - Ay, Hakan
A1  - Imaizumi, Toshio
A1  - Gomez-Anson, Beatriz
A1  - Lau, Kui Kai
A1  - Jouvent, Eric
A1  - Rothwell, Peter M
A1  - Toyoda, Kazunori
A1  - Bae, Hee-Yoon
A1  - Marti-Fabregas, Joan
A1  - Werring, David J
T1  - Cerebral microbleeds and stroke risk after ischaemic stroke or transient ischaemic attack: a pooled analysis of individual patient data from cohort studies
JF  - The Lancet Neurology
N2  - Background
Cerebral microbleeds are a neuroimaging biomarker of stroke risk. A crucial clinical question is whether cerebral microbleeds indicate patients with recent ischaemic stroke or transient ischaemic attack in whom the rate of future intracranial haemorrhage is likely to exceed that of recurrent ischaemic stroke when treated with antithrombotic drugs. We therefore aimed to establish whether a large burden of cerebral microbleeds or particular anatomical patterns of cerebral microbleeds can identify ischaemic stroke or transient ischaemic attack patients at higher absolute risk of intracranial haemorrhage than ischaemic stroke.

Methods
We did a pooled analysis of individual patient data from cohort studies in adults with recent ischaemic stroke or transient ischaemic attack. Cohorts were eligible for inclusion if they prospectively recruited adult participants with ischaemic stroke or transient ischaemic attack; included at least 50 participants; collected data on stroke events over at least 3 months follow-up; used an appropriate MRI sequence that is sensitive to magnetic susceptibility; and documented the number and anatomical distribution of cerebral microbleeds reliably using consensus criteria and validated scales. Our prespecified primary outcomes were a composite of any symptomatic intracranial haemorrhage or ischaemic stroke, symptomatic intracranial haemorrhage, and symptomatic ischaemic stroke. We registered this study with the PROSPERO international prospective register of systematic reviews, number CRD42016036602.

Findings
Between Jan 1, 1996, and Dec 1, 2018, we identified 344 studies. After exclusions for ineligibility or declined requests for inclusion, 20 322 patients from 38 cohorts (over 35 225 patient-years of follow-up; median 1·34 years [IQR 0·19–2·44]) were included in our analyses. The adjusted hazard ratio [aHR] comparing patients with cerebral microbleeds to those without was 1·35 (95% CI 1·20–1·50) for the composite outcome of intracranial haemorrhage and ischaemic stroke; 2·45 (1·82–3·29) for intracranial haemorrhage and 1·23 (1·08–1·40) for ischaemic stroke. The aHR increased with increasing cerebral microbleed burden for intracranial haemorrhage but this effect was less marked for ischaemic stroke (for five or more cerebral microbleeds, aHR 4·55 [95% CI 3·08–6·72] for intracranial haemorrhage vs 1·47 [1·19–1·80] for ischaemic stroke; for ten or more cerebral microbleeds, aHR 5·52 [3·36–9·05] vs 1·43 [1·07–1·91]; and for ≥20 cerebral microbleeds, aHR 8·61 [4·69–15·81] vs 1·86 [1·23–2·82]). However, irrespective of cerebral microbleed anatomical distribution or burden, the rate of ischaemic stroke exceeded that of intracranial haemorrhage (for ten or more cerebral microbleeds, 64 ischaemic strokes [95% CI 48–84] per 1000 patient-years vs 27 intracranial haemorrhages [17–41] per 1000 patient-years; and for ≥20 cerebral microbleeds, 73 ischaemic strokes [46–108] per 1000 patient-years vs 39 intracranial haemorrhages [21–67] per 1000 patient-years).

Interpretation
In patients with recent ischaemic stroke or transient ischaemic attack, cerebral microbleeds are associated with a greater relative hazard (aHR) for subsequent intracranial haemorrhage than for ischaemic stroke, but the absolute risk of ischaemic stroke is higher than that of intracranial haemorrhage, regardless of cerebral microbleed presence, antomical distribution, or burden.
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-233710
VL  - 18
ER  - 
TY  - JOUR
A1  - Heinrich, T.
A1  - Nanda, I.
A1  - Rehn, M.
A1  - Zollner, U.
A1  - Frieauff, E.
A1  - Wirbelauer, J.
A1  - Grimm, T.
A1  - Schmid, M.
T1  - Live-Born Trisomy 22: Patient Report and Review
JF  - Molecular Syndromology
N2  - Trisomy 22 is a common trisomy in spontaneous abortions. In contrast, live-born trisomy 22 is rarely seen due to severe organ malformations associated with this condition. Here, we report on a male infant with complete, non-mosaic trisomy 22 born at 35 + 5 weeks via caesarean section. Peripheral blood lymphocytes and fibroblasts showed an additional chromosome 22 in all metaphases analyzed (47,XY,+22). In addition, array CGH confirmed complete trisomy 22. The patient’s clinical features included dolichocephalus, hypertelorism, flattened nasal bridge, dysplastic ears with preauricular sinuses and tags, medial cleft palate, anal atresia, and coronary hypospadias with scrotum bipartitum. Essential treatment was implemented in close coordination with the parents. The child died 29 days after birth due to respiratory insufficiency and deterioration of renal function. Our patient’s history complements other reports illustrating that children with complete trisomy 22 may survive until birth and beyond.
KW  - chromosomal abnormality
KW  - live-born
KW  - non-mosaic
KW  - trisomy 22
Y1  - 2013
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-196535
SN  - 1661-8769
SN  - 1661-8777
N1  - This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.
VL  - 3
IS  - 6
ER  - 
TY  - JOUR
A1  - Mousset, Sabine
A1  - Buchheidt, Dieter
A1  - Heinz, Werner
A1  - Ruhnke, Markus
A1  - Cornely, Oliver A.
A1  - Egerer, Gerlinde
A1  - Krüger, William
A1  - Link, Hartmut
A1  - Neumann, Silke
A1  - Ostermann, Helmut
A1  - Panse, Jens
A1  - Penack, Olaf
A1  - Rieger, Christina
A1  - Schmidt-Hieber, Martin
A1  - Silling, Gerda
A1  - Südhoff, Thomas
A1  - Ullmann, Andrew J.
A1  - Wolf, Hans-Heinrich
A1  - Maschmeyer, Georg
A1  - Böhme, Angelika
T1  - Treatment of invasive fungal infections in cancer patients—updated recommendations of the Infectious Diseases Working Party (AGIHO) of the German Society of Hematology and Oncology (DGHO)
JF  - Annals of Hematology
N2  - Invasive fungal infections are a main cause of morbidity and mortality in cancer patients undergoing intensive chemotherapy regimens. Early antifungal treatment is mandatory to improve survival. Today, a number of effective and better-tolerated but more expensive antifungal agents compared to the former gold standard amphotericin B deoxycholate are available. Clinical decision-making must consider results from numerous studies and published guidelines, as well as licensing status and cost pressure. New developments in antifungal prophylaxis improving survival rates result in a continuous need for actualization. The treatment options for invasive Candida infections include fluconazole, voriconazole, and amphotericin B and its lipid formulations, as well as echinocandins. Voriconazole, amphotericin B, amphotericin B lipid formulations, caspofungin, itraconazole, and posaconazole are available for the treatment of invasive aspergillosis. Additional procedures, such as surgical interventions, immunoregulatory therapy, and granulocyte transfusions, have to be considered. The Infectious Diseases Working Party of the German Society of Hematology and Oncology here presents its 2008 recommendations discussing the dos and do-nots, as well as the problems and possible solutions, of evidence criteria selection.
KW  - cancer
KW  - invasive fungal infections
KW  - antifungals
KW  - mycoses
KW  - hematologic malignancies
KW  - aspergillosis
KW  - antifungal agents
KW  - invasive candidiasis
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-121340
VL  - 96
ER  - 
TY  - JOUR
A1  - Leistner, Stefanie
A1  - Benik, Steffen
A1  - Laumeier, Inga
A1  - Ziegler, Annerose
A1  - Nieweler, Gabriele
A1  - Nolte, Christian H.
A1  - Heuschmann, Peter U.
A1  - Audebert, Heinrich J.
T1  - Secondary Prevention after Minor Stroke and TIA - Usual Care and Development of a Support Program
JF  - PLoS One
N2  - Background: Effective methods of secondary prevention after stroke or TIA are available but adherence to recommended evidence-based treatments is often poor. The study aimed to determine the quality of secondary prevention in usual care and to develop a stepwise modeled support program. 
Methods: Two consecutive cohorts of patients with acute minor stroke or TIA undergoing usual outpatient care versus a secondary prevention program were compared. Risk factor control and medication adherence were assessed in 6-month follow-ups (6M-FU). Usual care consisted of detailed information concerning vascular risk factor targets given at discharge and regular outpatient care by primary care physicians. The stepwise modeled support program additionally employed up to four outpatient appointments. A combination of educational and behavioral strategies was employed. 
Results: 168 patients in the observational cohort who stated their openness to participate in a prevention program (mean age 64.7 y, admission blood pressure (BP): 155/84 mmHg) and 173 patients participating in the support program (mean age 67.6 y, BP: 161/84 mmHg) were assessed at 6 months. Proportions of patients with BP according to guidelines were 50% in usual-care and 77% in the support program (p<0.01). LDL<100 mg/dl was measured in 62 versus 71% (p = 0.12). Proportions of patients who stopped smoking were 50 versus 79% (p<0.01). 72 versus 89% of patients with atrial fibrillation were on oral anticoagulation (p = 0.09).
Conclusions: Risk factor control remains unsatisfactory in usual care. Targets of secondary prevention were met more often within the supported cohort. Effects on (cerebro-)vascular recurrence rates are going to be assessed in a multicenter randomized trial.
KW  - atherothrombosis
KW  - multifactorial
KW  - clinical trial
KW  - hypertension
KW  - disease
KW  - transient ischemic attack
KW  - randomized controlled trial
KW  - cardiovascular risk factors
KW  - blood pressure
KW  - event rates
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-135247
VL  - 7
IS  - 12
ER  - 
TY  - JOUR
A1  - Mitchell, Anna L.
A1  - Macarthur, Katie D. R.
A1  - Gan, Earn H.
A1  - Baggott, Lucy E.
A1  - Wolff, Anette S. B.
A1  - Skinningsrud, Beate
A1  - Platt, Hazel
A1  - Short, Andrea
A1  - Lobell, Anna
A1  - Kampe, Olle
A1  - Bensing, Sophie
A1  - Betterle, Corrado
A1  - Kasperlik-Zaluska, Anna
A1  - Zurawek, Magdalena
A1  - Fichna, Marta
A1  - Kockum, Ingrid
A1  - Eriksson, Gabriel Nordling
A1  - Ekwall, Olov
A1  - Wahlberg, Jeanette
A1  - Dahlqvist, Per
A1  - Hulting, Anna-Lena
A1  - Penna-Martinez, Marissa
A1  - Meyer, Gesine
A1  - Kahles, Heinrich
A1  - Badenhoop, Klaus
A1  - Hahner, Stephanie
A1  - Quinkler, Marcus
A1  - Falorni, Alberto
A1  - Phipps-Green, Amanda
A1  - Merriman, Tony R.
A1  - Ollier, William
A1  - Cordell, Heather J.
A1  - Undlien, Dag
A1  - Czarnocka, Barbara
A1  - Husebye, Eystein
A1  - Pearce, Simon H. S.
T1  - Association of Autoimmune Addison's Disease with Alleles of STAT4 and GATA3 in European Cohorts
JF  - PLOS ONE
N2  - Background: Gene variants known to contribute to Autoimmune Addison's disease (AAD) susceptibility include those at the MHC, MICA, CIITA, CTLA4, PTPN22, CYP27B1, NLRP-1 and CD274 loci. The majority of the genetic component to disease susceptibility has yet to be accounted for. 
Aim: To investigate the role of 19 candidate genes in AAD susceptibility in six European case-control cohorts. 
Methods: A sequential association study design was employed with genotyping using Sequenom iPlex technology. In phase one, 85 SNPs in 19 genes were genotyped in UK and Norwegian AAD cohorts (691 AAD, 715 controls). In phase two, 21 SNPs in 11 genes were genotyped in German, Swedish, Italian and Polish cohorts (1264 AAD, 1221 controls). In phase three, to explore association of GATA3 polymorphisms with AAD and to determine if this association extended to other autoimmune conditions, 15 SNPs in GATA3 were studied in UK and Norwegian AAD cohorts, 1195 type 1 diabetes patients from Norway, 650 rheumatoid arthritis patients from New Zealand and in 283 UK Graves' disease patients. Meta-analysis was used to compare genotype frequencies between the participating centres, allowing for heterogeneity. 
Results: We report significant association with alleles of two STAT4 markers in AAD cohorts (rs4274624: P = 0.00016; rs10931481: P = 0.0007). In addition, nominal association of AAD with alleles at GATA3 was found in 3 patient cohorts and supported by meta-analysis. Association of AAD with CYP27B1 alleles was also confirmed, which replicates previous published data. Finally, nominal association was found at SNPs in both the NF-kappa B1 and IL23A genes in the UK and Italian cohorts respectively. 
Conclusions: Variants in the STAT4 gene, previously associated with other autoimmune conditions, confer susceptibility to AAD. Additionally, we report association of GATA3 variants with AAD: this adds to the recent report of association of GATA3 variants with rheumatoid arthritis.
KW  - Graves disease
KW  - identical twins
KW  - hashimotos-thyroiditis
KW  - population
KW  - gene
KW  - polymorphism
KW  - susceptibility
KW  - prevalence
KW  - haplotype
KW  - rheumatoid arthritis
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-117105
VL  - 9
IS  - 3
ER  - 
TY  - JOUR
A1  - Ellgring, Johann Heinrich
A1  - Schneider, F.
A1  - Friedrich, J.
A1  - Fus, I.
A1  - Beyer, T.
A1  - Heimann, H.
A1  - Himer, W.
T1  - The effects of neuroleptics on facial action in schizophrenic patients
N2  - This paper describes the influence of neuroleptic therapy on facial action in drug-naive schizophrenics. In a comparative study of medicated and unmedicated schizophrenic patients, the coordinates of 12 small light-reflecting points, attached to subjects' faces, were computer-recorded and analyzed automatically during a semistandardized clinical interview. In addition, facial activity in videotaped interviews was coded using the Facial Action Coding System (FACS). Each sample group comprised of eight patients with the DSMIII- R diagnostic criteria "schizophrenia" or "schizophreniform disorder". Subjects were studied on two occasions, one shortly after admission to the hospital, the other three weeks later. Group I was unmedicated during the first session, whereas group2 was medicated throughout the study. Three weeks after the start of medication, at the second interview, both recording methods showed a reduction in facial activity and facial expression across all subjects in group 1. The facial action of patients in group2, however, remained unchanged.
N2  - Ziel der vorliegenden Arbeit war die Untersuchung des Einflusses von Neuroleptika auf die Mimik von unmedizierten schizophrenen Patienten. Wiihrend eines halbstandardisierten klinischen Interviews worde die Beweglichkeit von zwolf kleinen, licht-reflektierenden Punkten, die in das Gesicht von medizierten und unmedizierten schizophrenen Patienten geklebt worden, automatisch im Zeitverlauf gemessen. Erganzend wurde der mirnische Ausdruck mit dem Facial Action Coding System (FACS) kodiert, wofiir die Patienten gleichzeitig mit Video aufgenommen worden. Jede der beiden Gruppen bestand aus acht Patienten mit den DSM-IIIR- Diagnosen "Schizophrenie" oder "Schizophrenieforme Storung". Die Patienten worden einmal direkt nach der stationaren Aufnahme und ein zweites Mal nach drei Wochen untersucht. Die Patienten der ersten Gruppe waren zum ersten Zeitpunkt nicht mit Neuroleptika mediziert, wiihrend die der zweiten Gruppe schon zu diesem Zeitpunkt entsprechende Medikamente einnahmen. Es konnte eine Reduktion der mimischen Beweglichkeit des gesamten Gesichtes im Sinne einer neuroleptisch bedingten Hypornimie der primiir Neuroleptika-unbehandelten Patienten bei der zweiten Untersuchung beobachtet werden. Die andere Gruppe Schizophrener, die zu beiden Zeitpunkten mit Neuroleptika behandelt waren, zeigte keine Veriinderung in ihrer mimischen Beweglichkeit.
Y1  - 1992
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-43269
ER  - 
TY  - JOUR
A1  - Scheitz, Jan F.
A1  - Lim, Jess
A1  - Broersen, Leonie H. A.
A1  - Ganeshan, Ramanan
A1  - Huo, Shufan
A1  - Sperber, Pia S.
A1  - Piper, Sophie K.
A1  - Heuschmann, Peter U.
A1  - Audebert, Heinrich J.
A1  - Nolte, Christian H.
A1  - Siegerink, Bob
A1  - Endres, Matthias
A1  - Liman, Thomas G.
T1  - High‐Sensitivity Cardiac Troponin T and Recurrent Vascular Events After First Ischemic Stroke
JF  - Journal of the American Heart Association
N2  - Background
Recent evidence suggests cardiac troponin levels to be a marker of increased vascular risk. We aimed to assess whether levels of high‐sensitivity cardiac troponin T (hs‐cTnT) are associated with recurrent vascular events and death in patients with first‐ever, mild to moderate ischemic stroke.

Methods and Results
We used data from the PROSCIS‐B (Prospective Cohort With Incident Stroke Berlin) study. We computed Cox proportional hazards regression analyses to assess the association between hs‐cTnT levels upon study entry (Roche Elecsys, upper reference limit, 14 ng/L) and the primary outcome (composite of recurrent stroke, myocardial infarction, and all‐cause death). A total of 562 patients were analyzed (mean age, 67 years [SD 13]; 38.6% women; median National Institutes of Health Stroke Scale=2; hs‐cTnT above upper reference limit, 39.2%). During a mean follow‐up of 3 years, the primary outcome occurred in 89 patients (15.8%), including 40 (7.1%) recurrent strokes, 4 (0.7%) myocardial infarctions, and 51 (9.1%) events of all‐cause death. The primary outcome occurred more often in patients with hs‐cTnT above the upper reference limit (27.3% versus 10.2%; adjusted hazard ratio, 2.0; 95% CI, 1.3–3.3), with a dose‐response relationship when the highest and lowest hs‐cTnT quartiles were compared (15.2 versus 1.8 events per 100 person‐years; adjusted hazard ratio, 4.8; 95% CI, 1.9–11.8). This association remained consistent in sensitivity analyses, which included age matching and stratification for sex.

Conclusions
Hs‐cTnT is dose‐dependently associated with an increased risk of recurrent vascular events and death within 3 years after first‐ever, mild to moderate ischemic stroke. These findings support further studies of the utility of hs‐cTnT for individualized risk stratification after stroke.
KW  - epidemiology
KW  - ischemic stroke
KW  - mortality/survival
KW  - troponin
KW  - vascular disease
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-239039
VL  - 10
IS  - 10
ER  - 
TY  - JOUR
A1  - Schleicher, Ulrike
A1  - Paduch, Katrin
A1  - Debus, Andrea
A1  - Obermeyer, Stephanie
A1  - König, Till
A1  - Kling, Jessica C.
A1  - Ribechini, Eliana
A1  - Dudziak, Diana
A1  - Mougiakakos, Dimitrios
A1  - Murray, Peter J.
A1  - Ostuni, Renato
A1  - Körner, Heinrich
A1  - Bogdan, Christian
T1  - TNF-Mediated Restriction of Arginase 1 Expression in Myeloid Cells Triggers Type 2 NO Synthase Activity at the Site of Infection
JF  - Cell Reports
N2  - Neutralization or deletion of tumor necrosis factor (TNF) causes loss of control of intracellular pathogens in mice and humans, but the underlying mechanisms are incompletely understood. Here, we found that TNF antagonized alternative activation of macrophages and dendritic cells by IL-4. TNF inhibited IL-4-induced arginase 1 (Arg1) expression by decreasing histone acetylation, without affecting STAT6 phosphorylation and nuclear translocation. In Leishmania major-infected C57BL/6 wild-type mice, type 2 nitric oxide (NO) synthase (NOS2) was detected in inflammatory dendritic cells or macrophages, some of which co-expressed Arg1. In TNF-deficient mice, Arg1 was hyperexpressed, causing an impaired production of NO in situ. A similar phenotype was seen in L. major-infected BALB/c mice. Arg1 deletion in hematopoietic cells protected these mice from an otherwise lethal disease, although their disease-mediating T cell response (Th2, Treg) was maintained. Thus, deletion or TNF-mediated restriction of Arg1 unleashes the production of NO by NOS2, which is critical for pathogen control.
KW  - TNF
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-164897
VL  - 15
IS  - 5
ER  - 
TY  - JOUR
A1  - Kremer, Mark
A1  - Biesenthal, Tobias
A1  - Maczewsky, Lukas J.
A1  - Heinrich, Matthias
A1  - Thomale, Ronny
A1  - Szameit, Alexander
T1  - Demonstration of a two-dimensional PT-symmetric crystal
JF  - Nature Communications
N2  - With the discovery of PT-symmetric quantum mechanics, it was shown that even non-Hermitian systems may exhibit entirely real eigenvalue spectra. This finding did not only change the perception of quantum mechanics itself, it also significantly influenced the field of photonics. By appropriately designing one-dimensional distributions of gain and loss, it was possible to experimentally verify some of the hallmark features of PT-symmetry using electromagnetic waves. Nevertheless, an experimental platform to study the impact of PT-symmetry in two spatial dimensions has so far remained elusive. We break new grounds by devising a two-dimensional PT-symmetric system based on photonic waveguide lattices with judiciously designed refractive index landscape and alternating loss. With this system at hand, we demonstrate a non-Hermitian two-dimensional topological phase transition that is closely linked to the emergence of topological mid-gap edge states.
KW  - micro-optics
KW  - optical materials and structures
KW  - topological matter
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-230132
VL  - 10
ER  - 
TY  - JOUR
A1  - Schurig, Johannes
A1  - Haeusler, Karl Georg
A1  - Grittner, Ulrike
A1  - Nolte, Christian H.
A1  - Fiebach, Jochen B.
A1  - Audebert, Heinrich J.
A1  - Endres, Matthias
A1  - Rocco, Andrea
T1  - Frequency of Hemorrhage on Follow Up Imaging in Stroke Patients Treated With rt-PA Depending on Clinical Course
JF  - Frontiers in Neurology
N2  - Background: According to current guidelines, stroke patients treated with rt-PA should undergo brain imaging to exclude intracerebral bleeding 24 h after thrombolysis, before the start of medical secondary prevention. However, the usefulness of routine follow-up imaging with regard to changes in therapeutic management in patients without neurological deterioration is unclear. We hypothesized that follow up brain imaging solely to exclude bleeding in patients who clinically improved after rt-PA application may not be necessary.

Methods: Retrospective single-center analysis including stroke patients treated with rt-PA. Records were reviewed for hemorrhagic transformation one day after systemic thrombolysis and brain imaging-based changes in therapeutic management. Twenty-four hour after thrombolysis patients were divided into four groups: (1) increased NIHSS score; (2) unchanged NIHSS score; (3) improved NIHSS score and; (4) NIHSS score = 0.

Results: Out of 188 patients (mean age 73 years, 100 female) receiving rt-PA, 32 (17%) had imaging-proven hemorrhagic transformation including 11 (6%) patients with parenchymal hemorrhage. Patients in group (1, 2) more often had hypertension (p = 0.015) and more often had parenchymal hemorrhage (9 vs. 4%; p < 0.206) compared to group (3, 4) and imaging-based changes in therapeutic management were more frequent (19% vs. 6%; p = 0.007). Patients of group (3, 4) had no changes in therapeutic management in 94% of the cases. Patients in group (4) had no hemorrhagic transformation in routine follow-up brain imaging.

Conclusions: Frequency of hemorrhagic transformation in Routine follow-up brain imaging and consecutive changes in therapeutic management were different depending on clinical course measured by NHISS score.
KW  - thrombolysis
KW  - stroke
KW  - stroke management
KW  - magnetic resonance imaging
KW  - computerized tomography
KW  - intracerebral hemorrhage
Y1  - 2019
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-234947
VL  - 10
ER  -