Palus, Sandra

[["dc.bibliographiccitation.firstpage","594"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","605"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Pötsch, Mareike S."],["dc.contributor.author","Ishida, Junichi"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2021-06-01T10:50:56Z"],["dc.date.available","2021-06-01T10:50:56Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1002/jcsm.12537"],["dc.identifier.eissn","2190-6009"],["dc.identifier.issn","2190-5991"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17186"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86832"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","MT‐102 prevents tissue wasting and improves survival in a rat model of severe cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","174"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Cachexia Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","180"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Konishi, Masaaki"],["dc.contributor.author","Pelgrim, Loes"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Baumgarten, Anna"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Anker, Stefan-D."],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2018-11-07T09:56:41Z"],["dc.date.available","2018-11-07T09:56:41Z"],["dc.date.issued","2015"],["dc.description.abstract","Background Activity of xanthine oxidase is induced in cancer cachexia, and its inhibition by allopurinol or oxypurinol improves survival and reduces wasting in the Yoshida hepatoma cancer cachexia model. Here, we tested the effects of the second-generation xanthine oxidase inhibitor febuxostat compared with placebo in the same model as used previously by our group. Methods Wistar rats (similar to 200g) were treated daily with febuxostat at 5mg/kg/day or placebo via gavage for a maximum of 17days. Weight change, quality of life, and body composition were analysed. After sacrifice, proteasome activity in the gastrocnemius muscle was measured. Muscle-specific proteins involved in metabolism were analysed by western blotting. Results Treatment of the tumour-bearing rats with febuxostat led to a significantly improved survival compared with placebo (hazard ratio: 0.45, 95% confidence interval: 0.22-0.93, P=0.03). Loss of body weight was reduced (-26.312.4g) compared with placebo (-50.2 +/- 2.1g, P<0.01). Wasting of lean mass was attenuated (-12.7 +/- 10.8g) vs. placebo (-31.9 +/- 2.1g, P<0.05). While we did not see an effect of febuxostat on proteasome activity at the end of the study, the pAkt/Akt ratio was improved by febuxostat (0.94 +/- 0.09) vs. placebo (0.41 +/- 0.05, P<0.01), suggesting an increase in protein synthesis. Conclusions Febuxostat attenuated cachexia progression and improved survival of tumour-bearing rats."],["dc.description.sponsorship","Sumitomo Life Welfare and Culture Foundation"],["dc.identifier.doi","10.1002/jcsm.12017"],["dc.identifier.isi","000355340500007"],["dc.identifier.pmid","26136193"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13567"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37010"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Febuxostat improves outcome in a rat model of cancer cachexia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","555"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","566"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Musolino, Vincenzo"],["dc.contributor.author","Palus, Sandra"],["dc.contributor.author","Tschirner, Anika"],["dc.contributor.author","Drescher, Cathleen"],["dc.contributor.author","Gliozzi, Micaela"],["dc.contributor.author","Carresi, Cristina"],["dc.contributor.author","Vitale, Cristiana"],["dc.contributor.author","Muscoli, Carolina"],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","von Haehling, Stephan"],["dc.contributor.author","Anker, Stefan D."],["dc.contributor.author","Mollace, Vincenzo"],["dc.contributor.author","Springer, Jochen"],["dc.date.accessioned","2019-07-09T11:42:54Z"],["dc.date.available","2019-07-09T11:42:54Z"],["dc.date.issued","2016"],["dc.description.abstract","Background Cachexia is a complex metabolic syndrome associated with cancer. One of the features of cachexia is the loss of muscle mass, characterized by an imbalance between protein synthesis and protein degradation. Muscle atrophy is caused by the hyperactivation of some of the main cellular catabolic pathways, including autophagy. Cachexia also affects the cardiac muscle. As a consequence of the atrophy of the heart, cardiac function is impaired and mortality is increased. Anticachectic therapy in patients with cancer cachexia is so far limited to nutritional support and anabolic steroids. The use of the appetite stimulant megestrol acetate (MA) has been discussed as a treatment for cachexia. Methods In this study the effects of MA were tested in cachectic tumour-bearing rats (Yoshida AH-130 ascites hepatoma). Rats were treated daily with 100 mg/kg of MA or placebo starting one day after tumour inoculation, and for a period of 16 days. Body weight and body composition were assessed at baseline and at the end of the study. Cardiac function was analysed by echocardiography at baseline and at day 11. Locomotor activity and food intake were assessed before tumour inoculation and at day 11. Autophagic markers were assessed in gastrocnemius muscle and heart by western blot analysis. Results Treatment with 100 mg/kg/day MA significantly attenuated the loss of body weight ( 9 ± 12%, P<0.05) and the wasting of lean and fat mass ( 7.0 ± 6% and 22.4 ± 3 %, P<0.001 and P<0.05, respectively). Administration of 100 mg/kg/day MA significantly protected the heart from general atrophy (633.8 ± 30mg vs. placebo 474 ± 13 mg, P<0.001). Tumour-bearing rats displayed cardiac dysfunction, as indicated by the significant impairment of the left ventricular ejection fraction, the left ventricular fractional shortening, the stroke volume, the end dyastolic volume, and the end systolic volume. In contrast, MA significantly improved left ventricular ejection fraction, left ventricular fractional shortening, and left ventricular end systolic volume. Western blotting analysis showed an upregulation of the autophagic pathway in the gastrocnemius and hearts of the placebo-treated tumour-bearing rats. Treatment with MA, however, was able to modulate the autophagic markers (e.g. Beclin-1, p62, TRAF6, and LC3) in the gastrocnemius and in the hearts of tumourbearing rats. Most importantly, 100 mg/kg/day MA reduced mortality [hazard ratio (HR): 0.44; 95%CI: 0.20–1.00; P = 0.0486]. Conclusions Megestrol acetate improved survival and reduced wasting through a marked downregulation of autophagy, occurring in both skeletal and heart muscle, the latter effect leading to a significant improvement of cardiac function. Our data suggest thatMA might represent a valuable strategy to counteract the development of cancer cachexia-induced cardiomyopathy."],["dc.identifier.doi","10.1002/jcsm.12116"],["dc.identifier.pmid","27239419"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13987"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58781"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2190-6009"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Megestrol acetate improves cardiac function in a model of cancer cachexia-induced cardiomyopathy by autophagic modulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]