Anker, Stefan Dietmar

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","9"],["dc.contributor.author","Mordi, Ify R."],["dc.contributor.author","Santema, Bernadet T."],["dc.contributor.author","Kloosterman, Mariëlle"],["dc.contributor.author","Choy, Anna-Maria"],["dc.contributor.author","Rienstra, Michiel"],["dc.contributor.author","van Gelder, Isabelle"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Cleland, John G."],["dc.contributor.author","Dickstein, Kenneth"],["dc.contributor.author","Filippatos, Gerasimos"],["dc.contributor.author","van der Harst, Pim"],["dc.contributor.author","Hillege, Hans L."],["dc.contributor.author","Metra, Marco"],["dc.contributor.author","Ng, Leong L."],["dc.contributor.author","Ouwerkerk, Wouter"],["dc.contributor.author","Ponikowski, Piotr"],["dc.contributor.author","Samani, Nilesh J."],["dc.contributor.author","van Veldhuisen, Dirk J."],["dc.contributor.author","Zwinderman, Aeilko H."],["dc.contributor.author","Zannad, Faiez"],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","Lang, Chim C."],["dc.date.accessioned","2019-07-09T11:51:01Z"],["dc.date.available","2019-07-09T11:51:01Z"],["dc.date.issued","2019"],["dc.description.abstract","BACKGROUND: In patients with heart failure with reduced ejection fraction (HFrEF) on sub-optimal doses of beta-blockers, it is conceivable that changes in heart rate following treatment intensification might be important regardless of underlying heart rhythm. We aimed to compare the prognostic significance of both achieved heart rate and change in heart rate following beta-blocker uptitration in patients with HFrEF either in sinus rhythm (SR) or atrial fibrillation (AF). METHODS: We performed a post hoc analysis of the BIOSTAT-CHF study. We evaluated 1548 patients with HFrEF (mean age 67 years, 35% AF). Median follow-up was 21 months. Patients were evaluated at baseline and at 9 months. The combined primary outcome was all-cause mortality and heart failure hospitalisation stratified by heart rhythm and heart rate at baseline. RESULTS: Despite similar changes in heart rate and beta-blocker dose, a decrease in heart rate at 9 months was associated with reduced incidence of the primary outcome in both SR and AF patients [HR per 10 bpm decrease-SR: 0.83 (0.75-0.91), p < 0.001; AF: 0.89 (0.81-0.98), p = 0.018], whereas the relationship was less strong for achieved heart rate in AF [HR per 10 bpm higher-SR: 1.26 (1.10-1.46), p = 0.001; AF: 1.08 (0.94-1.23), p = 0.18]. Achieved heart rate at 9 months was only prognostically significant in AF patients with high baseline heart rates (p for interaction 0.017 vs. low). CONCLUSIONS: Following beta-blocker uptitration, both achieved and change in heart rate were prognostically significant regardless of starting heart rate in SR, however, they were only significant in AF patients with high baseline heart rate."],["dc.identifier.doi","10.1007/s00392-018-1409-x"],["dc.identifier.pmid","30610382"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59857"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/242209/EU//BIOSTAT-CHF"],["dc.relation.issn","1861-0692"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Prognostic significance of changes in heart rate following uptitration of beta-blockers in patients with sub-optimally treated heart failure with reduced ejection fraction in sinus rhythm versus atrial fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2102"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","2111"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Hoes, Martijn F."],["dc.contributor.author","Tromp, Jasper"],["dc.contributor.author","Ouwerkerk, Wouter"],["dc.contributor.author","Bomer, Nils"],["dc.contributor.author","Oberdorf‐Maass, Silke U."],["dc.contributor.author","Samani, Nilesh J."],["dc.contributor.author","Ng, Leong L."],["dc.contributor.author","Lang, Chim C."],["dc.contributor.author","van der Harst, Pim"],["dc.contributor.author","Hillege, Hans"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Metra, Marco"],["dc.contributor.author","van Veldhuisen, Dirk J."],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","van der Meer, Peter"],["dc.date.accessioned","2019-12-16T11:32:41Z"],["dc.date.accessioned","2021-10-27T13:21:56Z"],["dc.date.available","2019-12-16T11:32:41Z"],["dc.date.available","2021-10-27T13:21:56Z"],["dc.date.issued","2019"],["dc.description.abstract","AIMS: Cathepsin D is a ubiquitous lysosomal protease that is primarily secreted due to oxidative stress. The role of circulating cathepsin D in heart failure (HF) is unknown. The aim of this study is to determine the association between circulating cathepsin D levels and clinical outcomes in patients with HF and to investigate the biological settings that induce the release of cathepsin D in HF. METHODS AND RESULTS: Cathepsin D levels were studied in 2174 patients with HF from the BIOSTAT-CHF index study. Results were validated in 1700 HF patients from the BIOSTAT-CHF validation cohort. The primary combined outcome was all-cause mortality and/or HF hospitalizations. Human pluripotent stem cell-derived cardiomyocytes were subjected to hypoxic, pro-inflammatory signalling and stretch conditions. Additionally, cathepsin D expression was inhibited by targeted short hairpin RNAs (shRNA). Higher levels of cathepsin D were independently associated with diabetes mellitus, renal failure and higher levels of interleukin-6 and N-terminal pro-B-type natriuretic peptide (P < 0.001 for all). Cathepsin D levels were independently associated with the primary combined outcome [hazard ratio (HR) per standard deviation (SD): 1.12; 95% confidence interval (CI) 1.02-1.23], which was validated in an independent cohort (HR per SD: 1.23, 95% CI 1.09-1.40). In vitro experiments demonstrated that human stem cell-derived cardiomyocytes released cathepsin D and troponin T in response to mechanical stretch. ShRNA-mediated silencing of cathepsin D resulted in increased necrosis, abrogated autophagy, increased stress-induced metabolism, and increased release of troponin T from human stem cell-derived cardiomyocytes under stress. CONCLUSIONS: Circulating cathepsin D levels are associated with HF severity and poorer outcome, and reduced levels of cathepsin D may have detrimental effects with therapeutic potential in"],["dc.identifier.doi","10.1002/ejhf.1674"],["dc.identifier.eissn","1879-0844"],["dc.identifier.issn","1388-9842"],["dc.identifier.pmid","31797504"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16943"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92055"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1879-0844"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.subject.ddc","610"],["dc.title","The role of cathepsin D in the pathophysiology of heart failure and its potentially beneficial properties: a translational approach"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","903"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","908"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Papp, Zoltan"],["dc.date.accessioned","2019-11-19T08:40:42Z"],["dc.date.accessioned","2021-10-27T13:21:29Z"],["dc.date.available","2019-11-19T08:40:42Z"],["dc.date.available","2021-10-27T13:21:29Z"],["dc.date.issued","2019"],["dc.description.abstract","In 2014, the Heart Failure Association (HFA) of the European Society of Cardiology (ESC) founded the first open access journal focusing on heart failure, called ESC Heart Failure (ESC-HF). In the first 5 years, in ESC-HF we published more than 450 articles. Through ESC-HF, the HFA gives room for heart failure research output from around the world. A transfer process from the European Journal of Heart Failure to ESC-HF has also been installed. As a consequence, in 2018 ESC-HF received 289 submissions, and published 148 items (acceptance rate 51%). The journal is listed in Scopus since 2014 and on the PubMed website since 2015. In 2019, we received our first impact factor from ISI Web of Knowledge / Thomson-Reuters, which is 3.407 for 2018. This report reviews which papers get best cited. Not surprisingly, many of the best cited papers are reviews and facts & numbers mini reviews, but original research is also well cited."],["dc.identifier.doi","10.1002/ehf2.12540"],["dc.identifier.eissn","2055-5822"],["dc.identifier.isbn","31657535"],["dc.identifier.issn","2055-5822"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92026"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2055-5822"],["dc.relation.issn","2055-5822"],["dc.relation.issn","2055-5822"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Open access efforts begin to bloom: ESC Heart Failure gets full attention and first impact factor"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","448"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC heart failure"],["dc.bibliographiccitation.lastpage","457"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Dos Santos, Marcelo R."],["dc.contributor.author","Emami, Amir"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Bekfani, Tarek"],["dc.contributor.author","Sandek, Anja"],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","von Haehling, Stephan"],["dc.date.accessioned","2019-07-09T11:44:42Z"],["dc.date.available","2019-07-09T11:44:42Z"],["dc.date.issued","2017-11"],["dc.description.abstract","AIMS: We aimed to assess determinants of anorexia, that is loss of appetite in patients with heart failure (HF) and aimed to further elucidate the association between anorexia, functional capacity, and outcomes in affected patients. METHODS AND RESULTS: We assessed anorexia status among 166 patients with HF (25 female, 66 ± 12 years) who participated in the Studies Investigating Co-morbidities Aggravating HF. Anorexia was assessed by a 6-point Likert scale (ranging from 0 to 5), wherein values ≥1 indicate anorexia. Functional capacity was assessed as peak oxygen uptake (peak VO2 ), 6 min walk test, and short physical performance battery test. A total of 57 patients (34%) reported any anorexia, and these patients showed lower values of peak VO2 , 6 min walk distance, and short physical performance battery score (all P < 0.05). Using multivariate analysis adjusting for clinically important factors, only high-sensitivity C-reactive protein [odds ratio (OR) 1.24, P = 0.04], use of loop diuretics (OR 5.76, P = 0.03), and the presence of cachexia (OR 2.53, P = 0.04) remained independent predictors of anorexia. A total of 22 patients (13%) died during a mean follow-up of 22.5 ± 5.1 months. Kaplan-Meier curves for cumulative survival showed that those patients with anorexia presented higher mortality (Log-rank test P = 0.03). CONCLUSIONS: Inflammation, use of loop diuretics, and cachexia are associated with an increased likelihood of anorexia in patients with HF, and patients with anorexia showed impaired functional capacity and poor outcomes."],["dc.identifier.doi","10.1002/ehf2.12209"],["dc.identifier.pmid","28960880"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14870"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59070"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241558/EU//SICA-HF"],["dc.relation.issn","2055-5822"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Anorexia, functional capacity, and clinical outcome in patients with chronic heart failure: results from the Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF)."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e00037"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle ‐ Clinical Reports"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Saitoh, Masakazu"],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Springer, Jochen"],["dc.contributor.author","Haehling, Stephan von"],["dc.date.accessioned","2019-07-10T08:12:05Z"],["dc.date.available","2019-07-10T08:12:05Z"],["dc.date.issued","2017"],["dc.description.abstract","Myostatin, a member of the transforming growth factor beta (TGF‐β) superfamily that is highly expressed in skeletal muscle, was first described in 1997. It has been known that loss of myostatin function induces an increase in muscle mass in mice, cow, dogs and humans. Therefore, myostatin and its receptor have emerged as a therapeutic target for loss of skeletal muscle such as sarcopenia and cachexia, as well as muscular dystrophies. At the molecular level, myostatin binds to and activates the activin receptor IIB (ActRIIB)/Alk 4/5 complex. Therapeutic approaches therefore are being taken both pre‐clinically and clinically to inhibit the myostatin signaling pathway. Several myostatin inhibitors , including myostatin antibodies, anti‐myostatin peptibody, activin A antibody, soluble (decoy) forms of ActRIIB (ActRⅡB‐Fc), anti‐myostatin adnectin, ActRⅡB antibody have been tested in the last decade. The aim of this review is to present the current knowledge of several myostatin inhibitors as a therapeutic approach for patients with loss of skeletal muscle."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14833"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60859"],["dc.language.iso","de"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.issn","2190-6009"],["dc.rights","CC BY 4.0"],["dc.rights.access","openAccess"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.subject","Myostatin; Myostatin inhibitor; Muscle wasting; Sarcopenia; Cachexia;Neuromuscular dystrophy"],["dc.subject.ddc","610"],["dc.title","Myostatin inhibitors as pharmacological treatment for muscle wasting and muscular dystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","715"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","720"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2019-09-24T12:49:14Z"],["dc.date.accessioned","2021-10-27T13:21:19Z"],["dc.date.available","2019-09-24T12:49:14Z"],["dc.date.available","2021-10-27T13:21:19Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1002/jcsm.12482"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.pmid","31454183"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16407"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92012"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The Journal of Cachexia, Sarcopenia and Muscle in 2019"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1415"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","1423"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Bomer, Nils"],["dc.contributor.author","Grote Beverborg, Niels"],["dc.contributor.author","Hoes, Martijn F."],["dc.contributor.author","Streng, Koen W."],["dc.contributor.author","Vermeer, Mathilde"],["dc.contributor.author","Dokter, Martin M."],["dc.contributor.author","IJmker, Jan"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Cleland, John G.F."],["dc.contributor.author","Hillege, Hans L."],["dc.contributor.author","Lang, Chim C."],["dc.contributor.author","Ng, Leong L."],["dc.contributor.author","Samani, Nilesh J."],["dc.contributor.author","Tromp, Jasper"],["dc.contributor.author","Veldhuisen, Dirk J."],["dc.contributor.author","Touw, Daan J."],["dc.contributor.author","Voors, Adriaan A."],["dc.contributor.author","Meer, Peter"],["dc.date.accessioned","2019-12-16T11:28:05Z"],["dc.date.accessioned","2021-10-27T13:21:55Z"],["dc.date.available","2019-12-16T11:28:05Z"],["dc.date.available","2021-10-27T13:21:55Z"],["dc.date.issued","2019"],["dc.description.abstract","AIMS: Severe deficiency of the essential trace element selenium can cause myocardial dysfunction although the mechanism at cellular level is uncertain. Whether, in clinical practice, moderate selenium deficiency is associated with worse symptoms and outcome in patients with heart failure is unknown. METHODS AND RESULTS: BIOSTAT-CHF is a multinational, prospective, observational cohort study that enrolled patients with worsening heart failure. Serum concentrations of selenium were measured by inductively coupled plasma mass spectrometry. Primary endpoint was a composite of all-cause mortality and hospitalization for heart failure; secondary endpoint was all-cause mortality. To investigate potential mechanisms by which selenium deficiency might affect prognosis, human cardiomyocytes were cultured in absence of selenium, and mitochondrial function and oxidative stress were assessed. Serum selenium concentration (deficiency) was <70 μg/L in 485 (20.4%) patients, who were older, more often women, had worse New York Heart Association class, more severe signs and symptoms of heart failure and poorer exercise capacity (6-min walking test) and quality of life (Kansas City Cardiomyopathy Questionnaire). Selenium deficiency was associated with higher rates of the primary endpoint [hazard ratio (HR) 1.23; 95% confidence interval (CI) 1.06-1.42] and all-cause mortality (HR 1.52; 95% CI 1.26-1.86). In cultured human cardiomyocytes, selenium deprivation impaired mitochondrial function and oxidative phosphorylation, and increased intracellular reactive oxygen species levels. CONCLUSIONS: Selenium deficiency in heart failure patients is independently associated with impaired exercise tolerance and a 50% higher mortality rate, and impaired mitochondrial function in vitro, in human cardiomyocytes. Clinical trials are needed to investigate the effect of selenium supplements in patients with heart failure, especially if they have low plasma concentrations of selenium."],["dc.identifier.doi","10.1002/ejhf.1644"],["dc.identifier.eissn","1879-0844"],["dc.identifier.issn","1388-9842"],["dc.identifier.pmid","31808274"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16942"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92054"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1879-0844"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Selenium and outcome in heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","50"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Werner, Claudia G."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Haehling, Stephan von"],["dc.date.accessioned","2019-07-09T11:50:04Z"],["dc.date.available","2019-07-09T11:50:04Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1007/s13539-012-0061-y"],["dc.identifier.pmid","22460618"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59693"],["dc.language.iso","en"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241558/EU//SICA-HF"],["dc.relation.issn","2190-6009"],["dc.subject.ddc","610"],["dc.title","Recent developments in the treatment of cachexia: highlights from the 6th Cachexia Conference."],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","675"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of cachexia, sarcopenia and muscle"],["dc.bibliographiccitation.lastpage","680"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2019-07-09T11:44:44Z"],["dc.date.available","2019-07-09T11:44:44Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1002/jcsm.12247"],["dc.identifier.pmid","29076661"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14884"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59082"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2190-6009"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Oodles of opportunities: the Journal of Cachexia, Sarcopenia and Muscle in 2017."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]