Becker, Alexander

[["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Schuster, Manfred"],["dc.contributor.author","Loibner, Hans"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Kuba, Keiji"],["dc.contributor.author","Imai, Yumiko"],["dc.contributor.author","Penninger, Josef"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2018-11-07T11:09:55Z"],["dc.date.available","2018-11-07T11:09:55Z"],["dc.date.issued","2008"],["dc.format.extent","S947"],["dc.identifier.isi","000262104503504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53105"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","81st Annual Scientific Session of the American-Heart-Association"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0009-7322"],["dc.title","Angiotensin-Converting-Enzyme 2 (rhACE2) Potently Attenuates the Negative Hemodynamic Effects of Angiotensin II (ATII) and Improves Post-Myocardial Infarction (MI) Remodeling"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Rokita, Adam G."],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Grebe, Cornelia"],["dc.contributor.author","Preuss, Lena"],["dc.contributor.author","Gupta, Shamindra N."],["dc.contributor.author","Schmidt, Kathie"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Schäfer, Katrin"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Zhu, W."],["dc.contributor.author","Reuter, Sean P."],["dc.contributor.author","Field, Loren J."],["dc.contributor.author","Kararigas, Georgios"],["dc.contributor.author","Regitz-Zagrosek, Vera"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Krueger, Martina"],["dc.contributor.author","Linke, Wolfgang A."],["dc.contributor.author","Backs, Johannes"],["dc.date.accessioned","2018-11-07T08:56:56Z"],["dc.date.available","2018-11-07T08:56:56Z"],["dc.date.issued","2011"],["dc.format.extent","E421"],["dc.identifier.doi","10.1161/CIRCULATIONAHA.110.017566"],["dc.identifier.isi","000289833500003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23266"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0009-7322"],["dc.title","Response to Letter Regarding Article, \"Differential Cardiac Remodeling in Preload Versus Afterload\""],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","31"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Hellenkamp, Kristian"],["dc.contributor.author","Onimischewski, Sabrina"],["dc.contributor.author","Kruppa, Jochen"],["dc.contributor.author","Fasshauer, Martin"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Huenlich, Mark"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Wachter, Rolf"],["dc.date.accessioned","2017-09-07T11:54:41Z"],["dc.date.available","2017-09-07T11:54:41Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: While early pneumonia is common in patients after out-of-hospital cardiac arrest (OHCA), little is known about the impact of pneumonia and the optimal timing of antibiotic therapy after OHCA. Methods: We conducted a 5-year retrospective cohort study, including patients who suffered from OHCA and were treated with therapeutic hypothermia. ICU treatment was strictly standardized with defined treatment goals and procedures. Medical records, chest radiographic images and microbiological findings were reviewed. Results: Within the study period, 442 patients were admitted to our medical ICU after successfully resuscitated cardiac arrest. Of those, 174 patients fulfilled all inclusion and no exclusion criteria and were included into final analysis. Pneumonia within the first week could be confirmed in 39 patients (22.4 %) and was confirmed or probable in 100 patients (57.5 %), without a difference between survivors and non-survivors (37.8 % vs. 23.1 % confirmed pneumonia, p = 0.125). In patients with confirmed pneumonia a tracheotomy was performed more frequently (28.2 vs. 12.6 %, p = 0.026) compared to patients without confirmed pneumonia. Importantly, patients with confirmed pneumonia had a longer ICU-(14.0 [8.5-20.0] vs. 8.0 [5.0-14.0] days, p < 0.001) and hospital stay (23.0 [11.5-29.0] vs. 15.0 [6.5-25.0] days, p = 0.016). A positive end expiratory pressure (PEEP) > = 10.5 mbar on day 1 of the hospital stay was identified as early predictor of confirmed pneumonia (odds ratio 2.898, p = 0.006). No other reliable predictor could be identified. Median time to antibiotic therapy was 8.7 [5.4-22.8] hours, without a difference between patients with or without confirmed pneumonia (p = 0.381) and without a difference between survivors and non-survivors (p = 0.264). Patients receiving antibiotics within 12 hours after admission had a shorter ICU-(8.0 [4.0-14.0] vs. 10.5 [6.0-16.0] vs. 13.5 [8.0-20.0] days, p = 0.004) and hospital-stay (14.0 [6.0-25.0] vs. 16.5 [11.0-27.0] vs. 21.0 [17.0-28.0] days, p = 0.007) compared to patients receiving antibiotics after 12 to 36 or more than 36 hours, respectively. Conclusions: Early pneumonia may extend length of ICU- and hospital-stay after OHCA and its occurrence is difficult to predict. A delayed initiation of antibiotic therapy in OHCA patients may increase the duration of the ICU-and hospital-stay."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1186/s13054-016-1191-y"],["dc.identifier.gro","3141734"],["dc.identifier.isi","000369498800001"],["dc.identifier.pmid","26831508"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12806"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/480"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Gottingen University"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.eissn","1364-8535"],["dc.relation.issn","1466-609X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Early pneumonia and timing of antibiotic therapy in patients after nontraumatic out-of-hospital cardiac arrest"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","58"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","63"],["dc.bibliographiccitation.volume","234"],["dc.contributor.author","Hellenkamp, Kristian"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Gabriel, Yannick D."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Hünlich, Mark"],["dc.contributor.author","Jacobshagen, Claudius"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Schroeter, Marco R."],["dc.date.accessioned","2018-04-23T11:48:16Z"],["dc.date.available","2018-04-23T11:48:16Z"],["dc.date.issued","2017"],["dc.description.abstract","Background Bioresorbable vascular scaffolds (BVS) are widely used in routine clinical practice. While previous studies reported acceptable short- to midterm outcome after BVS implantation, data on longer-term outcome are rare. Methods Patients treated with at least one Absorb®-BVS were consecutively enrolled. Follow-up data were assessed after 834.0 [769.0–1026.0] days. The primary device-oriented composite endpoint (DOCE) was defined as cardiovascular death, myocardial infarction (MI) and/or target lesion revascularization (TLR). Results Between 2012 and 2014, 195 patients were included into study analysis. Overall, 244 BVS were implanted. Mean patient age was 64.0[54.3–74.0] years. Three-quarter of patients had an ACS; of those 42.9% had ST-elevation-MI and 40.8% had non-ST-elevation-MI. DOCE occurred in 3.1%, 6.7%, 11.8% and 15.4% of patients during hospital stay, within 6-months, 18-months or during the complete follow-up period, respectively. In those patients, median time until DOCE was 211.5[43.25–567.25] days. In 11 (36.7%) patients DOCE occurred after > 12 months. Using univariable analysis, bifurcation stenting was associated with a hazard ratio (HR) of 11.8[2.38–58.57] for TLR (p = 0.002) and 2.1[1.02–4.49] for DOCE (p = 0.045). Similarly, in ACS patients, bifurcation stenting was associated with an increased risk for TLR (HR = 10.4[2.01–53.56]; p = 0.005) and for DOCE (HR = 2.4[1.09–5.32]; p = 0.029) and in multivariable analysis, it remained an independent predictor of DOCE (HR = 3.0; p = 0.018). Conclusions Although, the rates of (potentially) device-related complications following BVS implantation are acceptable, they are nonetheless not negligible. Interestingly, they did not decline over time. Bifurcation stenting could be found as relevant procedure-related predictor of DOCE, especially in ACS patients. Randomized trials are warranted to confirm these findings."],["dc.identifier.doi","10.1016/j.ijcard.2017.02.069"],["dc.identifier.gro","3142343"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13479"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0167-5273"],["dc.title","Mid- to long-term outcome of patients treated with everolimus-eluting bioresorbable vascular scaffolds: Data of the BVS registry Göttingen predominantly from ACS patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","767"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Child & Adolescent Psychiatry"],["dc.bibliographiccitation.lastpage","774"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Wang, B."],["dc.contributor.author","Brueni, L. G."],["dc.contributor.author","Isensee, C."],["dc.contributor.author","Meyer, T."],["dc.contributor.author","Bock, N."],["dc.contributor.author","Ravens-Sieberer, U."],["dc.contributor.author","Klasen, F."],["dc.contributor.author","Schlack, R."],["dc.contributor.author","Becker, A."],["dc.contributor.author","Rothenberger, A."],["dc.date.accessioned","2020-12-10T14:11:05Z"],["dc.date.available","2020-12-10T14:11:05Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1007/s00787-017-1059-y"],["dc.identifier.eissn","1435-165X"],["dc.identifier.issn","1018-8827"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70960"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Predictive value of dysregulation profile trajectories in childhood for symptoms of ADHD, anxiety and depression in late adolescence"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","928"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stem Cells"],["dc.bibliographiccitation.lastpage","940"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Renger, Anke"],["dc.contributor.author","Zafiriou, Maria-Patapia"],["dc.contributor.author","Noack, Claudia"],["dc.contributor.author","Pavlova, Elena"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Sharkova, Krasimira"],["dc.contributor.author","Bergmann, Martin W."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.contributor.author","Zelarayán, Laura C."],["dc.date.accessioned","2017-09-07T11:47:43Z"],["dc.date.available","2017-09-07T11:47:43Z"],["dc.date.issued","2013"],["dc.description.abstract","The multiphasic regulation of the Wnt/beta-catenin canonical pathway is essential for cardiogenesis in vivo and in vitro. To achieve tight regulation of the Wnt/b-catenin signaling, tissue- and cell-specific coactivators and repressors need to be recruited. The identification of such factors may help to elucidate mechanisms leading to enhanced cardiac differentiation efficiency in vitro as well as promote regeneration in vivo. Using a yeast-two-hybrid screen, we identified four-and-a-half-LIM-domain 2 (FHL2) as a cardiac-specific beta-catenin interaction partner and activator of Wnt/beta-catenin-dependent transcription. We analyzed the role of this interaction for early cardiogenesis in an in vitro model by making use of embryoid body cultures from mouse embryonic stem cells (ESCs). In this model, stable FHL2 gain-of-function promoted mesodermal cell formation and cell proliferation while arresting cardiac differentiation in an early cardiogenic mesodermal progenitor state. Mechanistically, FHL2 overexpression enhanced nuclear accumulation of beta-catenin and activated Wnt/beta-catenin-dependent transcription leading to sustained upregulation of the early cardiogenic gene Igfbp5. In an alternative P19 cell model, transient FHL2 overexpression led to early activation of Wnt/beta-catenin-dependent transcription, but not sustained high-level of Igfbp5 expression. This resulted in enhanced cardiogenesis. We propose that early Wnt/beta-catenin-dependent transcriptional activation mediated by FHL2 is important for the transition to and expansion of early cardiogenic mesodermal cells. Collectively, our findings offer mechanistic insight into the early cardiogenic code and may be further exploited to enhance cardiac progenitor cell activity in vitro and in vivo. STEM CELLS 2013;31:928-940"],["dc.identifier.doi","10.1002/stem.1332"],["dc.identifier.gro","3142355"],["dc.identifier.isi","000318014100010"],["dc.identifier.pmid","23341242"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10650"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7364"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/49"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.issn","1066-5099"],["dc.relation.issn","1549-4918"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","The Four and a Half LIM-Domain 2 Controls Early Cardiac Cell Commitment and Expansion Via Regulating β-Catenin-Dependent Transcription"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","404"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Psychological Medicine"],["dc.bibliographiccitation.lastpage","415"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Kunze, B."],["dc.contributor.author","Wang, B."],["dc.contributor.author","Isensee, C."],["dc.contributor.author","Schlack, R."],["dc.contributor.author","Ravens-Sieberer, U."],["dc.contributor.author","Klasen, F."],["dc.contributor.author","Rothenberger, A."],["dc.contributor.author","Becker, A."],["dc.date.accessioned","2020-12-10T15:22:16Z"],["dc.date.available","2020-12-10T15:22:16Z"],["dc.date.issued","2018"],["dc.description.abstract","Severe mood dysregulation is common in childhood and can be highly impairing. The Dysregulation Profile (DP) can be considered as a broader phenotype of emotional dysregulation, including affect, cognition and behaviour. Since mood dysregulation may persist, but differently in boys and girls, the gender associated course needs to be considered longitudinally to gain a better insight in order to support the children more adequately. This study is focusing on gender associated subgroup trajectories of the Strengths and Difficulties Questionnaire-Dysregulation Profile (SDQ-DP) in middle childhood (9-13 years of age) and includes the potential impact of clinical and psychosocial characteristics."],["dc.identifier.doi","10.1017/S0033291717001714"],["dc.identifier.eissn","1469-8978"],["dc.identifier.issn","0033-2917"],["dc.identifier.pmid","28637519"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73335"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","final"],["dc.title","Gender associated developmental trajectories of SDQ-dysregulation profile and its predictors in children"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","51"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PSYCHOPHARMAKOTHERAPIE"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Degner, Detlef"],["dc.contributor.author","Ruether, Eckart"],["dc.contributor.author","Grohmann, Renate"],["dc.contributor.author","Becker, Alexander"],["dc.date.accessioned","2018-11-07T08:48:31Z"],["dc.date.available","2018-11-07T08:48:31Z"],["dc.date.issued","2010"],["dc.description.abstract","QTc interval prolongation associated with psychopharmacological treatment with amitriptyline and ziprasidone Cardiac adverse events during psychopharmacological treatment are a strong risk factor for patients, especially alterations of QTc time which can lead to serious and life- threatening complications. The authors report a case of a 41 years old woman suffering from a sehizoaffective disorder. She had risk factors, e.g. obesity, hypothyroidism and increased cholesterine levels. During the treatment with amitriptyline in combination with ziprasidone we observed QTc interval prolongations without clinical signs. After discontinuation of both drugs the QTc time normalised. This case report demonstrates the clinical relevance of QTc interval alterations associated with drug therapy and shows specific risk factors."],["dc.identifier.isi","000294082300010"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21231"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wissenschaftliche Verlagsgesellschaft Stuttgart"],["dc.relation.issn","0944-6877"],["dc.title","QTc interval prolongation associated with psychopharmacological treatment with amitriptyline and ziprasidone"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1285"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","1298"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Didie, Michael"],["dc.contributor.author","Christalla, Peter"],["dc.contributor.author","Rubart, Michael"],["dc.contributor.author","Muppala, Vijayakumar"],["dc.contributor.author","Doeker, Stephan"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","El-Armouche, Ali"],["dc.contributor.author","Rau, Thomas"],["dc.contributor.author","Eschenhagen, Thomas"],["dc.contributor.author","Schwoerer, Alexander Peter"],["dc.contributor.author","Ehmke, Heimo"],["dc.contributor.author","Schumacher, Udo"],["dc.contributor.author","Fuchs, Sigrid"],["dc.contributor.author","Lange, Claudia"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Tao, Wen"],["dc.contributor.author","Scherschel, John A."],["dc.contributor.author","Soonpaa, Mark H."],["dc.contributor.author","Yang, Tao"],["dc.contributor.author","Lin, Qiong"],["dc.contributor.author","Zenke, Martin"],["dc.contributor.author","Han, Dong-Wook"],["dc.contributor.author","Schoeler, Hans R."],["dc.contributor.author","Rudolph, Cornelia"],["dc.contributor.author","Steinemann, Doris"],["dc.contributor.author","Schlegelberger, Brigitte"],["dc.contributor.author","Kattman, Steve"],["dc.contributor.author","Witty, Alec"],["dc.contributor.author","Keller, Gordon"],["dc.contributor.author","Field, Loren J."],["dc.contributor.author","Zimmermann, Wolfram-Hubertus"],["dc.date.accessioned","2017-09-07T11:47:47Z"],["dc.date.available","2017-09-07T11:47:47Z"],["dc.date.issued","2013"],["dc.description.abstract","Uniparental parthenotes are considered an unwanted byproduct of in vitro fertilization. In utero parthenote development is severely compromised by defective organogenesis and in particular by defective cardiogenesis. Although developmentally compromised, apparently pluripotent stem cells can be derived from parthenogenetic blastocysts. Here we hypothesized that nonembryonic parthenogenetic stem cells (PSCs) can be directed toward the cardiac lineage and applied to tissue-engineered heart repair. We first confirmed similar fundamental properties in murine PSCs and embryonic stem cells (ESCs), despite notable differences in genetic (allelic variability) and epigenetic (differential imprinting) characteristics. Haploidentity of major histocompatibility complexes (MHCs) in PSCs is particularly attractive for allogeneic cell-based therapies. Accordingly, we confirmed acceptance of PSCs in MHC-matched allotransplantation. Cardiomyocyte derivation from PSCs and ESCs was equally effective. The use of cardiomyocyte-restricted GFP enabled cell sorting and documentation of advanced structural and functional maturation in vitro and in vivo. This included seamless electrical integration of PSC-derived cardiomyocytes into recipient myocardium. Finally, we enriched cardiomyocytes to facilitate engineering of force-generating myocardium and demonstrated the utility of this technique in enhancing regional myocardial function after myocardial infarction. Collectively, our data demonstrate pluripotency, with unrestricted cardiogenicity in PSCs, and introduce this unique cell type as an attractive source for tissue-engineered heart repair."],["dc.identifier.doi","10.1172/JCI66854"],["dc.identifier.gro","3142382"],["dc.identifier.isi","000315749400038"],["dc.identifier.pmid","23434590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7663"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/10"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A02: Bedeutung des Phosphatase-Inhibitors-1 für die SR-spezifische Modulation der Beta- adrenozeptor-Signalkaskade"],["dc.relation","SFB 1002 | C04: Fibroblasten-Kardiomyozyten Interaktion im gesunden und erkrankten Herzen: Mechanismen und therapeutische Interventionen bei Kardiofibroblastopathien"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG El-Armouche"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.title","Parthenogenetic stem cells for tissue-engineered heart repair"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","40"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Becker, Alexander"],["dc.contributor.author","Friedrich, Martin"],["dc.contributor.author","Behnes, Carl Ludwig"],["dc.contributor.author","Seidler, Tim"],["dc.date.accessioned","2018-11-07T10:07:25Z"],["dc.date.available","2018-11-07T10:07:25Z"],["dc.date.issued","2016"],["dc.format.extent","3115"],["dc.identifier.doi","10.1093/eurheartj/ehw195"],["dc.identifier.isi","000388522900014"],["dc.identifier.pmid","27233947"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39274"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","Near-catastrophic event from a benign cause"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]