Zschüntzsch, Jana

[["dc.bibliographiccitation.firstpage","224"],["dc.bibliographiccitation.journal","Acta Physiologica"],["dc.bibliographiccitation.lastpage","226"],["dc.bibliographiccitation.volume","210"],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Schmidt, J."],["dc.contributor.author","Brinkmeier, Heinrich"],["dc.date.accessioned","2018-11-07T09:42:49Z"],["dc.date.available","2018-11-07T09:42:49Z"],["dc.date.issued","2014"],["dc.identifier.isi","000332259900586"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34043"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1748-1716"],["dc.relation.issn","1748-1708"],["dc.title","Dystrophin deficiency leads to drastic weakness of mdx diaphragm muscle, but has little influence on soleus muscle force"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9-10"],["dc.bibliographiccitation.journal","Neuromuscular Disorders"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Makosch, Gregor"],["dc.contributor.author","Klinge, Lars"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Brinkmeier, Heinrich"],["dc.contributor.author","Liebetan, D."],["dc.contributor.author","Schmidt, J."],["dc.date.accessioned","2018-11-07T08:51:10Z"],["dc.date.available","2018-11-07T08:51:10Z"],["dc.date.issued","2011"],["dc.format.extent","710"],["dc.identifier.doi","10.1016/j.nmd.2011.06.984"],["dc.identifier.isi","000295955900233"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21866"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","16th International Congress of the World-Muscle-Society"],["dc.relation.eventlocation","Algarve, PORTUGAL"],["dc.relation.issn","0960-8966"],["dc.title","Human IgG improves the performance of mdx mice in voluntary wheel running"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1018"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","1031"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Zschüntzsch, Jana"],["dc.contributor.author","Jouvenal, Pia Vanessa"],["dc.contributor.author","Zhang, Yaxin"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Brinkmeier, Heinrich"],["dc.contributor.author","Schmidt, Jens"],["dc.date.accessioned","2021-04-14T08:26:53Z"],["dc.date.available","2021-04-14T08:26:53Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Background Duchenne muscular dystrophy (DMD) is a progressive muscle‐wasting disease caused by mutations in the dystrophin gene, which leads to structural instability of the dystrophin–glycoprotein‐complex with subsequent muscle degeneration. In addition, muscle inflammation has been implicated in disease progression and therapeutically addressed with glucocorticosteroids. These have numerous adverse effects. Treatment with human immunoglobulin G (IgG) improved clinical and para‐clinical parameters in the early disease phase in the well‐established mdx mouse model. The aim of the present study was to confirm the efficacy of IgG in a long‐term pre‐clinical study in mdx mice. Methods IgG (2 g/kg body weight) or NaCl solution as control was administered monthly over 18 months by intraperitoneal injection in mdx mice beginning at 3 weeks of age. Several clinical outcome measures including endurance, muscle strength, and echocardiography were assessed. After 18 months, the animals were sacrificed, blood was collected for analysis, and muscle samples were obtained for ex vivo muscle contraction tests, quantitative PCR, and histology. Results IgG significantly improved the daily voluntary running performance (1.9 m more total daily running distance, P \\u0026lt; 0.0001) and slowed the decrease in grip strength by 0.1 mN, (P = 0.018). IgG reduced fatigability of the diaphragm (improved ratio to maximum force by 0.09 ± 0.04, P = 0.044), but specific tetanic force remained unchanged in the ex vivo muscle contraction test. Cardiac function was significantly better after IgG, especially fractional area shortening (P = 0.012). These results were accompanied by a reduction in cardiac fibrosis and the infiltration of T cells (P = 0.0002) and macrophages (P = 0.0027). In addition, treatment with IgG resulted in a significant reduction of the infiltration of T cells (P ≤ 0.036) in the diaphragm, gastrocnemius, quadriceps, and a similar trend in tibialis anterior and macrophages (P ≤ 0.045) in gastrocnemius, quadriceps, tibialis anterior, and a similar trend in the diaphragm, as well as a decrease in myopathic changes as reflected by a reduced central nuclear index in the diaphragm, tibialis anterior, and quadriceps (P ≤ 0.002 in all). Conclusions The present study underscores the importance of an inflammatory contribution to the disease progression of DMD. The data demonstrate the long‐term efficacy of IgG in the mdx mouse. IgG is well tolerated by humans and could preferentially complement gene therapy in DMD. The data call for a clinical trial with IgG in DMD."],["dc.description.sponsorship","CSL Behring http://dx.doi.org/10.13039/100008322"],["dc.identifier.doi","10.1002/jcsm.12569"],["dc.identifier.pmid","32436338"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17353"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82110"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/355"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | S01: In vivo und in vitro Krankheitsmodelle"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.relation.workinggroup","RG Tiburcy (Stem Cell Disease Modeling)"],["dc.relation.workinggroup","RG Zimmermann (Engineered Human Myocardium)"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Long‐term human IgG treatment improves heart and muscle function in a mouse model of Duchenne muscular dystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","351"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","362"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Makosch, Gregor"],["dc.contributor.author","Klinge, Lars"],["dc.contributor.author","Malzahn, Doerthe"],["dc.contributor.author","Brinkmeier, Heinrich"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Schmidt, Jens"],["dc.date.accessioned","2018-11-07T10:21:27Z"],["dc.date.available","2018-11-07T10:21:27Z"],["dc.date.issued","2016"],["dc.description.abstract","Duchenne muscular dystrophy (DMD) is a severe hereditary myopathy. Standard treatment by glucocorticosteroids is limited because of numerous side effects. The aim of this study was to test immunomodulation by human immunoglobulin G (IgG) as treatment in the experimental mouse model (mdx) of DMD. 2g/kg human IgG compared to human albumin was injected intraperitoneally in mdx mice at the age of 3 and 7weeks. Advanced voluntary wheel running parameters were recorded continuously. At the age of 11 weeks, animals were killed so that blood, diaphragm, and lower limb muscles could be removed for quantitative PCR, histological analysis and exvivo muscle contraction tests. IgG compared to albumin significantly improved the voluntary running performance and reduced muscle fatigability in an exvivo muscle contraction test. Upon IgG treatment, serum creatine kinase values were diminished and mRNA expression levels of relevant inflammatory markers were reduced in the diaphragm and limb muscles. Macrophage infiltration and myopathic damage were significantly ameliorated in the quadriceps muscle. Collectively, this study demonstrates that, in the early disease course of mdx mice, human IgG improves the running performance and diminishes myopathic damage and inflammation in the muscle. Therefore, IgG may be a promising approach for treatment of DMD."],["dc.identifier.doi","10.1111/jnc.13269"],["dc.identifier.isi","000367956800015"],["dc.identifier.pmid","26230042"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42093"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","Treatment with human immunoglobulin G improves the early disease course in a mouse model of Duchenne muscular dystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9-10"],["dc.bibliographiccitation.journal","Neuromuscular Disorders"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Jouvenal, P."],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Brinkmeier, Heinrich"],["dc.contributor.author","Schmidt, J."],["dc.date.accessioned","2018-11-07T09:34:35Z"],["dc.date.available","2018-11-07T09:34:35Z"],["dc.date.issued","2014"],["dc.format.extent","819"],["dc.identifier.doi","10.1016/j.nmd.2014.06.097"],["dc.identifier.isi","000342870200094"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32201"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","19th International Congress of the World-Muscle-Society"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","1873-2364"],["dc.relation.issn","0960-8966"],["dc.title","Assessment of outcome measures for dystrophin deficient mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","177"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","178"],["dc.bibliographiccitation.volume","253"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Weller, Charlotte"],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Makosch, Gregor"],["dc.contributor.author","Klinge, Lars"],["dc.contributor.author","Metselaar, Josbert M."],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Brinkmeier, Heinrich"],["dc.contributor.author","Schmidt, Jens"],["dc.date.accessioned","2018-11-07T09:02:18Z"],["dc.date.available","2018-11-07T09:02:18Z"],["dc.date.issued","2012"],["dc.identifier.isi","000312764800478"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24650"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","11th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Boston, MA"],["dc.relation.issn","0165-5728"],["dc.title","Human IgG but not liposomal prednisolone improves the early clinical course of mdx mice as model for Duchenne muscular dystrophy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","132"],["dc.bibliographiccitation.journal","Clinical & Experimental Immunology"],["dc.bibliographiccitation.lastpage","133"],["dc.bibliographiccitation.volume","178"],["dc.contributor.author","Zschuentzsch, Jana"],["dc.contributor.author","Jouvenal, P."],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Tiburcy, Malte"],["dc.contributor.author","Malzahn, D."],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Brinkmeier, Heinrich"],["dc.contributor.author","Schmidt, J."],["dc.date.accessioned","2018-11-07T09:31:49Z"],["dc.date.available","2018-11-07T09:31:49Z"],["dc.date.issued","2014"],["dc.description.sponsorship","CSL Behring; Aktion Benni Co."],["dc.identifier.doi","10.1111/cei.12541"],["dc.identifier.isi","000346976700053"],["dc.identifier.pmid","25546792"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31616"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1365-2249"],["dc.relation.issn","0009-9104"],["dc.title","Human immunoglobulin G for experimental treatment of Duchenne muscular dystrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]