@article{YurdadoganMalschKotsevaetal.2021,
  author    = {Yurdadogan, Tino and Malsch, Carolin and Kotseva, Kornelia and Wood, David and Leyh, Rainer and Ertl, Georg and Karmann, Wolfgang and M{\"u}ller-Scholden, Lara and Morbach, Caroline and Breuning, Margret and Wagner, Martin and Gelbrich, G{\"o}tz and Bots, Michiel L. and Heuschmann, Peter U. and St{\"o}rk, Stefan},
  title     = {Functional versus morphological assessment of vascular age in patients with coronary heart disease},
  series = {Scientific Reports},
  volume    = {11},
  journal   = {Scientific Reports},
  number    = {1},
  doi       = {10.1038/s41598-021-96998-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-265810},
  year      = {2021},
  abstract  = {Communicating cardiovascular risk based on individual vascular age (VA) is a well acknowledged concept in patient education and disease prevention. VA may be derived functionally, e.g. by measurement of pulse wave velocity (PWV), or morphologically, e.g. by assessment of carotid intima-media thickness (cIMT). The purpose of this study was to investigate whether both approaches produce similar results. Within the context of the German subset of the EUROASPIRE IV survey, 501 patients with coronary heart disease underwent (a) oscillometric PWV measurement at the aortic, carotid-femoral and brachial-ankle site (PWVao, PWVcf, PWVba) and derivation of the aortic augmentation index (AIao); (b) bilateral cIMT assessment by high-resolution ultrasound at three sites (common, bulb, internal). Respective VA was calculated using published equations. According to VA derived from PWV, most patients exhibited values below chronological age indicating a counterintuitive healthier-than-anticipated vascular status: for VA(PWVao) in 68\% of patients; for VA\(_{AIao}\) in 52\% of patients. By contrast, VA derived from cIMT delivered opposite results: e.g. according to VA\(_{total-cIMT}\) accelerated vascular aging in 75\% of patients. To strengthen the concept of VA, further efforts are needed to better standardise the current approaches to estimate VA and, thereby, to improve comparability and clinical utility.},
  language  = {en}
}
@article{WinterAndelovicKampfetal.2021,
  author    = {Winter, Patrick M. and Andelovic, Kristina and Kampf, Thomas and Hansmann, Jan and Jakob, Peter Michael and Bauer, Wolfgang Rudolf and Zernecke, Alma and Herold, Volker},
  title     = {Simultaneous measurements of 3D wall shear stress and pulse wave velocity in the murine aortic arch},
  series = {Journal of Cardiovascular Magnetic Resonance},
  volume    = {23},
  journal   = {Journal of Cardiovascular Magnetic Resonance},
  number    = {1},
  doi       = {10.1186/s12968-021-00725-4},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-259152},
  pages     = {34},
  year      = {2021},
  abstract  = {Purpose Wall shear stress (WSS) and pulse wave velocity (PWV) are important parameters to characterize blood flow in the vessel wall. Their quantification with flow-sensitive phase-contrast (PC) cardiovascular magnetic resonance (CMR), however, is time-consuming. Furthermore, the measurement of WSS requires high spatial resolution, whereas high temporal resolution is necessary for PWV measurements. For these reasons, PWV and WSS are challenging to measure in one CMR session, making it difficult to directly compare these parameters. By using a retrospective approach with a flexible reconstruction framework, we here aimed to simultaneously assess both PWV and WSS in the murine aortic arch from the same 4D flow measurement. Methods Flow was measured in the aortic arch of 18-week-old wildtype (n = 5) and ApoE\(^{-/-}\) mice (n = 5) with a self-navigated radial 4D-PC-CMR sequence. Retrospective data analysis was used to reconstruct the same dataset either at low spatial and high temporal resolution (PWV analysis) or high spatial and low temporal resolution (WSS analysis). To assess WSS, the aortic lumen was labeled by semi-automatically segmenting the reconstruction with high spatial resolution. WSS was determined from the spatial velocity gradients at the lumen surface. For calculation of the PWV, segmentation data was interpolated along the temporal dimension. Subsequently, PWV was quantified from the through-plane flow data using the multiple-points transit-time method. Reconstructions with varying frame rates and spatial resolutions were performed to investigate the influence of spatiotemporal resolution on the PWV and WSS quantification. Results 4D flow measurements were conducted in an acquisition time of only 35 min. Increased peak flow and peak WSS values and lower errors in PWV estimation were observed in the reconstructions with high temporal resolution. Aortic PWV was significantly increased in ApoE\(^{-/-}\) mice compared to the control group (1.7 ± 0.2 versus 2.6 ± 0.2 m/s, p < 0.001). Mean WSS magnitude values averaged over the aortic arch were (1.17 ± 0.07) N/m\(^2\) in wildtype mice and (1.27 ± 0.10) N/m\(^2\) in ApoE\(^{-/-}\) mice. Conclusion The post processing algorithm using the flexible reconstruction framework developed in this study permitted quantification of global PWV and 3D-WSS in a single acquisition. The possibility to assess both parameters in only 35 min will markedly improve the analyses and information content of in vivo measurements.},
  language  = {en}
}
@phdthesis{Steiner2003,
  author    = {Steiner, Martin},
  title     = {Langzeitergebnisse nach radiologischen Interventionen der Becken- und Beinarterien},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-8161},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2003},
  abstract  = {Retrospektive Studie (1995-1999) aus dem Institut f{\"u}r R{\"o}ntgendiagnostik der Universit{\"a}t W{\"u}rzburg mit insgesamt 206 Patienten. Die Offenheitsraten der insg. 535 radiologischen Interventionen (PTA, Stentimplantationen) der Becken- und Beinarterien wurden in einer statistischen Auswertung nach Kaplan-Meier dargestellt. Dabei wurden die Ergebnisse auf die unterschiedlichen Grundparameter (Alter, Geschlecht, Risikofaktoren, Fontaine-Stadium, Gef{\"a}ßlokalisation, Runoff, Stenosenart, Stenosenanzahl, Interventionsart...) bezogen.},
  language  = {de}
}
@article{SoehnleinDrechslerDoeringetal.2013,
  author    = {Soehnlein, Oliver and Drechsler, Maik and D{\"o}ring, Yvonne and Lievens, Dirk and Hartwig, Helene and Kemmerich, Klaus and Ortega-G{\´o}mez, Almudena and Mandl, Manuela and Vijayan, Santosh and Projahn, Delia and Garlichs, Christoph D. and Koenen, Rory R. and Hristov, Mihail and Lutgens, Esther and Zernecke, Alma and Weber, Christian},
  title     = {Distinct functions of chemokine receptor axes in the atherogenic mobilization and recruitment of classical monocytes},
  series = {EMBO Molecular Medicine},
  volume    = {5},
  journal   = {EMBO Molecular Medicine},
  issn      = {1757-4676},
  doi       = {10.1002/emmm.201201717},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-122204},
  pages     = {471-481},
  year      = {2013},
  abstract  = {We used a novel approach of cytostatically induced leucocyte depletion and subsequent reconstitution with leucocytes deprived of classical \((inflammatory/Gr1^{hi})\) or non-classical \((resident/Gr1^{lo})\) monocytes to dissect their differential role in atheroprogression under high-fat diet (HFD). Apolipoprotein E-deficient \((Apoe^{-/-})\) mice lacking classical but not non-classical monocytes displayed reduced lesion size and macrophage and apoptotic cell content. Conversely, HFD induced a selective expansion of classical monocytes in blood and bone marrow. Increased CXCL1 levels accompanied by higher expression of its receptor CXCR2 on classical monocytes and inhibition of monocytosis by CXCL1-neutralization indicated a preferential role for the CXCL1/CXCR2 axis in mobilizing classical monocytes during hypercholesterolemia. Studies correlating circulating and lesional classical monocytes in gene-deficient \(Apoe^{-/-}\) mice, adoptive transfer of gene-deficient cells and pharmacological modulation during intravital microscopy of the carotid artery revealed a crucial function of CCR1 and CCR5 but not CCR2 or \(CX_3CR1\) in classical monocyte recruitment to atherosclerotic vessels. Collectively, these data establish the impact of classical monocytes on atheroprogression, identify a sequential role of CXCL1 in their mobilization and CCR1/CCR5 in their recruitment.},
  language  = {en}
}
@article{SchaeferZernecke2020,
  author    = {Sch{\"a}fer, Sarah and Zernecke, Alma},
  title     = {CD8\(^+\) T cells in atherosclerosis},
  series = {Cells},
  volume    = {10},
  journal   = {Cells},
  number    = {1},
  issn      = {2073-4409},
  doi       = {10.3390/cells10010037},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-220170},
  year      = {2020},
  abstract  = {Atherosclerotic lesions are populated by cells of the innate and adaptive immune system, including CD8\(^+\) T cells. The CD8\(^+\) T cell infiltrate has recently been characterized in mouse and human atherosclerosis and revealed activated, cytotoxic, and possibly dysfunctional and exhausted cell phenotypes. In mouse models of atherosclerosis, antibody-mediated depletion of CD8\(^+\) T cells ameliorates atherosclerosis. CD8\(^+\) T cells control monopoiesis and macrophage accumulation in early atherosclerosis. In addition, CD8\(^+\) T cells exert cytotoxic functions in atherosclerotic plaques and contribute to macrophage cell death and necrotic core formation. CD8\(^+\) T cell activation may be antigen-specific, and epitopes of atherosclerosis-relevant antigens may be targets of CD8\(^+\) T cells and their cytotoxic activity. CD8\(^+\) T cell functions are tightly controlled by costimulatory and coinhibitory immune checkpoints. Subsets of regulatory CD25\(^+\)CD8\(^+\) T cells with immunosuppressive functions can inhibit atherosclerosis. Importantly, local cytotoxic CD8\(^+\) T cell responses may trigger endothelial damage and plaque erosion in acute coronary syndromes. Understanding the complex role of CD8\(^+\) T cells in atherosclerosis may pave the way for defining novel treatment approaches in atherosclerosis. In this review article, we discuss these aspects, highlighting the emerging and critical role of CD8\(^+\) T cells in atherosclerosis.},
  language  = {en}
}
@phdthesis{Schwarz2001,
  author    = {Schwarz, Ulrike},
  title     = {Biochemische und Molekularbiologische Charakterisierung der Wechselwirkungen zwischen Humanen Thrombozyten und Endothelzellen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-2030},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2001},
  abstract  = {Der Blutkreislauf ist als wichtigstes Transportsystem im menschlichen K{\"o}rper essentiell f{\"u}r die Versorgung der Gewebe und Organe mit Sauerstoff, N{\"a}hrstoffen, Hormonen etc. Zwei Zelltypen, die eine wichtige Rolle bei der Aufrechterhaltung eines funktionell intakten Blutgef{\"a}ßsystems spielen, sind Thrombozyten, die zentralen Mediatoren der Blutgerinnung, und Endothelzellen, welche die luminale Seite der Gef{\"a}ßw{\"a}nde auskleiden. Diese beiden Zellen sind aber auch wesentlich an der Pathologie der Atherosklerose und kardiovaskul{\"a}rer Erkrankungen beteiligt. Durch direkte und indirekte Interaktionen beeinflussen sich diese beiden Zelltypen gegenseitig und regulieren ihre Aktivit{\"a}t. Im Rahmen dieser Arbeit wurde eine Analysenmethode entwickelt, welche den Funktionszustand der Thrombozyten quantitativ erfaßt. Sowohl die Aktivierung als auch die Hemmung humaner Thrombozyten wird durch die Phosphorylierung spezifischer Signalproteine reguliert. Basierend auf der Verwendung phosphorylierungsspezifischer Antik{\"o}rper und der Durchflußzytometrie wurde eine Methode etabliert, welche die Proteinphosphorylierung auf Einzelzellebene erfaßt, schnell quantifizierbare Ergebnisse liefert und f{\"u}r die Analyse im Vollblut geeignet ist. Da die Sekretion von Endothelfaktoren den Phosphorylierungszustand dieser Proteine in den Thrombozyten beeinflußt, kann die Methode auch dazu verwendet werden, indirekt R{\"u}ckschl{\"u}sse auf den Funktionszustand der Endothelzellen zu gewinnen. In einer ersten klinischen Anwendung wurde die Methode eingesetzt, um den Therapieverlauf der antithrombotischen Medikamente Ticlopidin und Clopidogrel, welche gezielt die ADP-induzierte Thrombozytenaktivierung hemmen, zu verfolgen und das Antwortverhalten von Patienten auf diese Medikamente zu messen. Mehrere Personen, bei denen Ticlopidin und Clopidogrel keine Wirkung zeigten, wurden gefunden, ein Hinweis darauf, daß eine Resistenz gegen Thienopyridine vorkommt. Es ist bekannt, daß Endothelfaktoren bestimmte Aspekte der Thrombozytenaktivierung hemmen. In dieser Arbeit wurde gezeigt, daß die Phosphorylierung der p38 und p42 Mitogen-aktivierten Proteinkinasen, die im Verlauf der Thrombozytenaktivierung von zahlreichen Agonisten induziert wird, ebenfalls durch die endothelialen Vasodilatatoren NO (Stickstoffmonoxid) und Prostaglandin gehemmt wurde. Außerdem hemmten diese Substanzen die Translokation der inflammatorischen Molek{\"u}le P-Selektin und CD40 Ligand (CD40L) aus intrazellul{\"a}ren Speicherorganellen auf die Thrombozytenoberfl{\"a}che. P-Selektin und CD40L werden auf aktivierten Thrombozyten exprimiert und sind direkt an der Interaktion von Thrombozyten mit Leukozyten und Endothelzellen beteiligt. Um die Auswirkung von CD40L, P-Selektin und weiteren Faktoren aktivierter Thrombozyten auf humane Endothelzellen zu untersuchen, wurde mit Hilfe von cDNA-Arrays die differentielle Genexpression in Endothelzellen nach Koinkubation mit aktivierten Thrombozyten analysiert. Neben einer bereits bekannten Hochregulierung von Faktoren, die an inflammatorischen Prozessen beteiligt sind, wurde eine verst{\"a}rkte Expression von Transkriptionsfaktoren (c-Jun, Egr1, CREB2), Wachstumsfaktoren (PDGF) sowie von Adh{\"a}sionsrezeptoren f{\"u}r extrazellul{\"a}re Matrixproteine (Integrin av, Integrin b1) gefunden. Diese Faktoren weisen darauf hin, daß aktivierte Thrombozyten die Migration und Proliferation der Endothelzellen anregen und damit die Wundheilung, aber auch pathophysiologische Prozesse wie die Ausbildung atherosklerotischer Plaques induzieren k{\"o}nnten.},
  subject      = {Thrombozyt},
  language  = {de}
}
@article{PaudelFusiSchmidt2021,
  author    = {Paudel, Rupesh and Fusi, Lorenza and Schmidt, Marc},
  title     = {The MEK5/ERK5 pathway in health and disease},
  series = {International Journal of Molecular Sciences},
  volume    = {22},
  journal   = {International Journal of Molecular Sciences},
  number    = {14},
  issn      = {1422-0067},
  doi       = {10.3390/ijms22147594},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-261638},
  year      = {2021},
  abstract  = {The MEK5/ERK5 mitogen-activated protein kinases (MAPK) cascade is a unique signaling module activated by both mitogens and stress stimuli, including cytokines, fluid shear stress, high osmolarity, and oxidative stress. Physiologically, it is mainly known as a mechanoreceptive pathway in the endothelium, where it transduces the various vasoprotective effects of laminar blood flow. However, it also maintains integrity in other tissues exposed to mechanical stress, including bone, cartilage, and muscle, where it exerts a key function as a survival and differentiation pathway. Beyond its diverse physiological roles, the MEK5/ERK5 pathway has also been implicated in various diseases, including cancer, where it has recently emerged as a major escape route, sustaining tumor cell survival and proliferation under drug stress. In addition, MEK5/ERK5 dysfunction may foster cardiovascular diseases such as atherosclerosis. Here, we highlight the importance of the MEK5/ERK5 pathway in health and disease, focusing on its role as a protective cascade in mechanical stress-exposed healthy tissues and its function as a therapy resistance pathway in cancers. We discuss the perspective of targeting this cascade for cancer treatment and weigh its chances and potential risks when considering its emerging role as a protective stress response pathway.},
  language  = {en}
}
@phdthesis{Parczyk2010,
  author    = {Parczyk, Marco},
  title     = {In vivo NMR-methods to study effects of atherosclerosis in mice},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-53302},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2010},
  abstract  = {Background Transgenic mouse models are increasingly used to study the pathophysiology of human cardiovascular diseases. The aortic pulse wave velocity (PWV) is an indirect measure for vascular stiffness and a marker for cardiovascular risk. Results This work presents three MR-methods that allow the determination of the PWV in the descending murine aorta by analyzing blood flow waveforms, arterial distension waveforms, and a method that uses the combination of flow and distension waveforms. Systolic flow pulses were recorded with a temporal resolution of 1 ms applying phase velocity encoding. In a first step, the MR methods were validated by pressure waveform measurements on pulsatile elastic vessel phantoms. In a second step, the MR methods were applied to measure PWVs in a group of five eight-month-old apolipoprotein E deficient (ApoE(-/-)) mice and an age matched group of four C57Bl/6J mice. The ApoE(-/-) group had a higher mean PWV than the C57Bl/6J group. Depending on the measurement technique, the differences were or were not statistically significant. Conclusions The findings of this study demonstrate that high field MRI is applicable to non-invasively determine and distinguish PWVs in the arterial system of healthy and diseased groups of mice.},
  subject      = {Arteriosklerose},
  language  = {en}
}
@phdthesis{Padmapriya2008,
  author    = {Padmapriya, Ponnuswamy},
  title     = {Insight into oxidative stress mediated by nitric oxide synthase (NOS) isoforms in atherosclerosis},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-30659},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2008},
  abstract  = {The principle product of each NOS is nitric oxide. However, under conditions of substrate and cofactor deficiency the enzymes directly catalyze superoxide formation. Considering this alternative chemistry of each NOS, the effects of each single enzyme on key events of atherosclerosis are difficult to predict. Here, we evaluate nitric oxide and superoxide production by all three NOS isoforms in atherosclerosis. ESR measurements of circulating and vascular wall nitric oxide production showed significantly reduced nitric oxide levels in apoE/eNOS double knockout (dko) and apoE/iNOS dko animals but not in apoE/nNOS dko animals suggesting that eNOS and iNOS majorly contribute to vascular nitric oxide production in atherosclerosis. Pharmacological inhibition and genetic deletion of eNOS and iNOS reduced vascular superoxide production suggesting that eNOS and iNOS are uncoupled in atherosclerotic vessels. Though genetic deletion of nNOS did not alter superoxide production, acute inhibition of nNOS showed that nNOS contributes significantly to superoxide production. In conclusion, uncoupling of eNOS occurs in apoE ko atherosclerosis but eNOS mediated superoxide production does not outweigh the protective effects of eNOS mediated nitric oxide production. We show that although nNOS is not a major contributor of the vascular nitric oxide formation, it prevents atherosclerosis development. Acute inhibition of nNOS showed a significant reduction of superoxide formation suggesting that nNOS is uncoupled. The exact mechanism of action of nNOS in atheroprotection is yet to be elucidated. Genetic deletion of iNOS reduced NADPH oxidase activity. Thus, iNOS has both direct and indirect proatherosclerotic effects, as it directly generates both nitric oxide and superoxide simultaneously resulting in peroxynitrite formation and indirectly modulates NADPH oxidase activity. We hypothesize that eNOS is coupled in the disease free regions of the vessel and contributes to nitric oxide generation whereas in the diseased region of the vessel it is uncoupled to produce superoxide (Figure 16). nNOS expressed in the smooth muscle cells of the plaque contributes to the local superoxide generation. iNOS expressed in smooth muscle cells and leukocytes of the plaque generates superoxide and nitric oxide simultaneously to produce the strong oxidant peroxynitrite.},
  subject      = {atherosclerosis},
  language  = {en}
}
@phdthesis{Offenberger2009,
  author    = {Offenberger, Wolfgang},
  title     = {Hochaufgel{\"o}ste Magnetresonanz-Bildgebung der M{\"a}useaorta zur Bestimmung der Dynamik funktioneller Parameter durch Laufrad-Training bei ApoE-Knock-Out-M{\"a}usen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-35146},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2009},
  abstract  = {Einf{\"u}hrung: Atherosklerose ist eine f{\"u}hrende Ursache von Morbidit{\"a}t und Mortalit{\"a}t weltweit. Die ApoE-Knock-Out-Maus (ApoE-/-) ist das wichtigste Tiermodell f{\"u}r das Studium der Atherosklerose und von Interventionen auf diese Erkrankung. Mittels hochaufgel{\"o}ster Magnet-Resonanz-Bildgebung ist es m{\"o}glich, eine nicht-invasive in-vivo Gef{\"a}ß-Charakterisierung bei M{\"a}usen durchzuf{\"u}hren. In dieser Arbeit wurden die Auswirkungen von Sport auf die Gef{\"a}ßfunktion der Aorta ascendens und abdominalis bei ApoE-/--M{\"a}usen mittels hochaufgel{\"o}ster MR-Cine-FLASH-Bildgebung untersucht. Methodik und Ergebnisse: 18 ApoE-/--M{\"a}use mit oder ohne Lipid-reicher „Western Type Diet" (WTD) f{\"u}hrten 4-6 Wochen lang Laufrad-Training durch. Vor Laufrad-Training wurde zweimal (Validit{\"a}t) und nach Laufrad-Training einmal mittels EKG- und Atmungs-getriggerter Magnet-Resonanz-Cine-FLASH-Bildgebung an einem 7-Tesla-Scanner unter Isofluran-Inhalationsnarkose die Compliance von Aorta ascendens und abdominalis gemessen. Aufnahme-Parameter: TR/TE = 4,3/1,4 ms; Field of View (FOV) = 3,0 x 3,0 cm2; Matrixgr{\"o}ße = 256 x 256; Pixel-Gr{\"o}ße = (FOV / Matrix) = (30 mm / 256) = 0,0117 mm2; Schichtdicke = 1,0 mm, Aufl{\"o}sung von 0,0137 mm3. Die Resultate wurden verglichen mit 9 Wildtyp-M{\"a}usen vom Stamm C57BL/6J, und mittels der Auswerte-Software Interactive Data Language (IDL) prozessiert. Es zeigten sich gewisse positive Effekte hinsichtlich Compliance der Aorta ascendens durch Sport, die Ergebnisse waren f{\"u}r ApoE-/--M{\"a}use ohne WTD jedoch wesentlich konsistenter als f{\"u}r ApoE-/--M{\"a}use mit WTD, wo die Ergebnisse teilweise widerspr{\"u}chlich erscheinen. Dasselbe gilt f{\"u}r die Aorta abdominalis, die sich zudem in vielen MR-Untersuchungen nicht auswerten ließ, was zu nicht interpretierbaren Ergebnissen f{\"u}hrte. Bez{\"u}glich der Validit{\"a}t zeigte sich eine sehr hohe Intra-Observer- und Inter-Observer-{\"U}bereinstimmung der Ergebnisse, dies zeigte sich auch f{\"u}r Messungen zu zwei Zeitpunkten. Schlussfolgerung: Die Ergebnisse erscheinen insgesamt kritisch beleuchtet nicht signifikant und zeigen allenfalls Besserungs-Tendenzen f{\"u}r die Compliance der Aorta ascendens und abdominalis bei ApoE-/--M{\"a}usen durch Sport. Weitere MRT-Studien mit h{\"o}heren Feldst{\"a}rken und weiterentwickelten MR-Protokollen sind notwendig, um die Aussage dieser Doktorarbeit, dass Atherosklerose bei ApoE-/--M{\"a}usen durch Sport teilweise reversibel ist, zu best{\"a}tigen.},
  subject      = {Magnetresonanztomographie},
  language  = {de}
}