Patschan, Susann Andrea

[["dc.bibliographiccitation.artnumber","45"],["dc.bibliographiccitation.journal","Arthritis Research & Therapy"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Blaschke, Sabine"],["dc.contributor.author","Rinke, Kathinka"],["dc.contributor.author","Maring, Michael"],["dc.contributor.author","Flad, Thomas"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Mueller, Claudia A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Dihazi, Hassan"],["dc.date.accessioned","2018-11-07T09:59:46Z"],["dc.date.available","2018-11-07T09:59:46Z"],["dc.date.issued","2015"],["dc.description.abstract","Introduction: The introduction of tumor necrosis factor-alpha (TNF-alpha) antagonists has substantially improved patient's clinical outcome in rheumatoid arthritis (RA). However, nearly 20% to 40% of RA patients do not respond to anti-TNF-alpha treatment strategies. To identify valid predictors of TNF-alpha antagonist response in RA, serum proteome profiles from responders (R) and non-responders (NR) to etanercept, a soluble recombinant TNF-alpha receptor/IgG Fc fusion protein receptor, were compared in a prospective cohort study. Methods: In this clinical study 50 RA patients with inadequate response to conventional DMARDs were included and treated with etanercept. The primary efficacy endpoint was response according to the European League against Rheumatism (EULAR) improvement criteria. Serum samples collected prior to initiation and after six months of etanercept therapy were cleared of the most abundant major proteins by immunoaffinity chromatography. After separation by two-dimensional differential gel electrophoresis (2D-DIGE) and identification by mass spectrometry (MS) data were validated by Western blot analysis. Results: After six months of etanercept treatment 62% (n = 31) of RA patients achieved response. Haptoglobin-alpha 1 (Hp-alpha 1) and -alpha 2 (Hp-alpha 2) and vitamin D-binding protein (VDBP) were found to be significantly upregulated in responder sera (P <= 0.02) at study entry. In contrast, apolipoprotein C-III (ApoC-III) showed significantly higher levels in non-responders (P = 0.0162). At study end ApoA-II, Hp-alpha 1, Hp-alpha 2 and VDBP were identified to be expressed at significantly higher levels (P < 0.05) in responder sera. Conclusions: By application of clinical proteomics in immunodepleted sera we could identify and validate for the first time Hp-alpha 1, -alpha 2, VDBP and ApoC-III as potential biomarkers for prediction of etanercept drug response in RA."],["dc.description.sponsorship","Pfizer Research Initiative"],["dc.identifier.doi","10.1186/s13075-015-0553-1"],["dc.identifier.isi","000352187400001"],["dc.identifier.pmid","25884688"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13467"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37661"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1478-6362"],["dc.relation.issn","1478-6354"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Haptoglobin-alpha 1, -alpha 2, vitamin D-binding protein and apolipoprotein C-III as predictors of etanercept drug response in rheumatoid arthritis"],["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.artnumber","R94"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Johanna, Temme"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:01:04Z"],["dc.date.available","2018-11-07T09:01:04Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction: Sepsis is characterized by systemic microvascular dysfunction. Endothelial progenitor cells (EPCs) are critically involved in maintaining vascular homeostasis under both physiological and pathological conditions. The aim of the present study was to analyze the endothelial progenitor cell system in patients suffering from sepsis with acute renal dysfunction. Methods: Patients with newly diagnosed sepsis were recruited from the ICU in a nonrandomized prospective manner. Blood samples were obtained within the first 12 hours after the diagnosis of sepsis. For quantifying endothelial progenitor cells (EPCs), CD133(+)/Flk-1(+) cells were enumerated by cytometric analysis. Analysis of EPC proliferation was performed by a colony-forming units (CFU) assay. Blood concentrations of proangiogenic mediators were measured by ELISA. Acute renal dysfunction was diagnosed according to the Acute Kidney Injury Network (AKIN) criteria. Depending on the overall mean creatinine concentration during the stay at the ICU, patients were either assigned to a 'normal creatinine group' or to a 'high creatinine group'. Survival rates, frequency of dialysis, the simplified acute physiology score (SAPS) II scores, and different laboratory parameters were collected/used for further clinical characterization Results: Circulating EPCs were significantly higher in all sepsis patients included in the study as opposed to healthy controls. Patients within the 'high creatinine group' showed an even more pronounced EPC increase. In contrast, EPC proliferation was severely affected in sepsis. Neither total circulating EPCs nor EPC proliferation differed between patients requiring dialysis and patients without renal replacement therapy. Cell numbers and cell proliferation also did not differ between surviving patients and patients with sepsis-related death. Serum levels of vascular endothelial growth factor (VEGF), stromal derived factor-1 (SDF-1), and Angiopoietin-2 were higher in sepsis than in healthy controls. Sepsis patients within the 'high creatinine group' showed significantly higher mean serum levels of uric acid. Conclusions: Sepsis significantly affects the endothelial progenitor cell system, as reflected by increased EPC numbers, increased concentrations of proangiogenic mediators, and reduced proliferative capacity of the cells. This occurs independently from the frequency of dialysis and from patient survival. Increased serum levels of uric acid are possibly responsible for stronger EPC mobilization in sepsis patients with higher average creatinine levels."],["dc.identifier.doi","10.1186/cc10100"],["dc.identifier.isi","000292506000018"],["dc.identifier.pmid","21396100"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24323"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15283 but duplicate"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1466-609X"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.holder","Patschan et al.; licensee BioMed Central Ltd."],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Endothelial progenitor cells (EPC) in sepsis with acute renal dysfunction (ARD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","227"],["dc.bibliographiccitation.journal","BMC Nephrology"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Rinneburger, Joerg"],["dc.contributor.author","Idrizi, Nazif"],["dc.contributor.author","Backhaus, Rico"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:18:33Z"],["dc.date.available","2018-11-07T09:18:33Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Acute kidney injury (AKI) severely worsens prognosis of hospitalized patients. Early Endothelial Outgrowth Cells act protective in murine acute ischemic renal failure and renoprotective actions of eEOCs have been documented to increase after cell pretreatment with 8-O-cAMP and Melatonin. Angiopoietin-1 is critically involved in maintaining vascular integrity and regeneration. Aim of the study was to analyze the consequences of eEOC treatment with Ang-1 in murine AKI. Methods: After 40 minutes of unilateral renal artery clamping with contralateral nephrectomy, male C57/Bl6N mice were injected with either untreated or pretreated (Ang-1) syngeneic murine eEOCs. Two days later serum creatinine levels and morphology were evaluated. Cultured, Ang-1 treated murine eEOCs were analyzed for production/release of proangiogenic and proinflammatory mediators, migratory activity, and cell survival, respectively. Results: Angiopoietin-1 pretreatment of eEOCs significantly reduced serum creatinine in cell-injected mice. In vitro analysis showed increased migration of Ang-1 treated eEOCs and supernatant from Ang-1 treated eEOCs stimulated migration of cultured mature endothelial cells. In addition, Ang-1 reduced percentages of Annexin V+/PI+ eEOCs. Intrarenal numbers of eEOCs remained unaffected by Ang-1 and eEOCs did not produce more or less proangiogenic/proinflammatory mediators after being stimulated with Ang-1. Conclusions: Angiopoietin-1 pretreatment of eEOCs increases the cells' renoprotective competence in ischemic AKI. Thus, the armentarium of eEOC agonists in AKI is increasingly being expanded and the treatment of AKI with eEOCs becomes a promising future option."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.doi","10.1186/1471-2369-14-227"],["dc.identifier.isi","000327482300001"],["dc.identifier.pmid","24144241"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28432"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2369"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Angiopoietin-1 treated early endothelial outgrowth cells (eEOCs) are activated in vitro and reduce renal damage in murine acute ischemic kidney injury (iAKI)"],["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","1523"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Lupus"],["dc.bibliographiccitation.lastpage","1525"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Fliesser, E. E."],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Niewold, T. B."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Patschan, Susann Andrea"],["dc.date.accessioned","2018-11-07T09:16:51Z"],["dc.date.available","2018-11-07T09:16:51Z"],["dc.date.issued","2013"],["dc.description.abstract","We report the case of a 19-year-old woman with progressive proliferative lupus nephritis (LN) class III after induction and maintenance therapy with mycophenolate mofetil (MMF). Despite a satisfying clinical improvement proteinuria progressed under this medication. We treated the patient with additional belimumab after discussing other options. Following treatment with belimumab, proteinuria rapidly improved to almost normal levels and clinical remission lasted. Belimumab might hold promise for this indication."],["dc.description.sponsorship","GlaxoSmithKline"],["dc.identifier.doi","10.1177/0961203313504145"],["dc.identifier.isi","000329545400012"],["dc.identifier.pmid","24014569"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28030"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.eissn","0961-2033"],["dc.relation.issn","1477-0962"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Successful treatment of a mycophenolate mofetil-refractory proliferative lupus nephritis with Belimumab in a 19-year-old woman"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","53"],["dc.bibliographiccitation.journal","BMC Nephrology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Tampe, Bjoern"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T10:27:33Z"],["dc.date.available","2018-11-07T10:27:33Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: In recent years, early Endothelial Progenitor Cells (eEPCs) have been proven as effective tool in murine ischemic AKI and in diabetic nephropathy. The mechanisms of eEPC-mediated vasoprotection have been elucidated in detail. Besides producing a diverse range of humoral factors, the cells also act by secreting vasomodulatory microvesicles. Only few data in contrast have been published about the role of so-called Endothelial Colony Forming Cells (ECFCs - late EPCs) in ischemic AKI. We thus aimed to investigate ECFC effects on postischemic kidney function over several weeks. Our special interest focused on endothelial-to-mesenchymal transition (EndoMT), peritubular capillary density (PTCD), endothelial alpha-Tubulin (aT - cytoskeletal integrity), and endothelial p62 (marker of autophagocytic flux). Methods: Eight to twelve weeks old male C57Bl/6 N mice were subjected to bilateral renal pedicle clamping for 35 or 45 min, respectively. Donor-derived syngeneic ECFCs (0.5 x 10(6)) were i.v. injected at the end of ischemia. Animals were analyzed 1, 4 and 6 weeks later. Results: Cell therapy improved kidney function exclusively at week 1 (35 and 45 min). Ischemia-induced fibrosis was diminished in all experimental groups by ECFCs, while PTCD loss remained unaffected. Significant EndoMT was detected in only two of 6 groups (35 min, week 4 and 45 min, week 6), ECFCs reduced EndoMT only in the latter. Endothelial aT declined under almost all experimental conditions and these effects were further aggravated by ECFCs. p62 was elevated in endothelial cells, more so after 45 than after 35 min of ischemia. Cell therapy did not modulate p62 abundances at any time point. Conclusion: A single dose of ECFCs administered shortly post-ischemia is capable to reduce interstitial fibrosis in the mid-to long-term whereas excretory dysfunction is improved only in a transient manner. There are certain differences in renal outcome parameters between eEPCs and ECFC. The latter do not prevent animals from peritubular capillary loss and they also do not further elevate endothelial p62. We conclude that differences between eEPCs and ECFCs result from certain mechanisms by which the cells act around and within vessels. Overall, ECFC treatment was not as efficient as eEPC therapy in preventing mice from ischemia-induced mid-to long-term damage."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft(INST) [DFG-PA 1530/7-1, 1525/16-1]"],["dc.identifier.doi","10.1186/s12882-017-0471-3"],["dc.identifier.isi","000397680100004"],["dc.identifier.pmid","28166726"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14227"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43255"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2369"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Endothelial Colony Forming Cells (ECFCs) in murine AKI - implications for future cell-based therapies"],["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.artnumber","339"],["dc.bibliographiccitation.journal","BMC Musculoskeletal Disorders"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Mueller, C."],["dc.contributor.author","Seitz, C."],["dc.contributor.author","Herink, Claudia"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Patschan, Daniel"],["dc.date.accessioned","2018-11-07T10:10:11Z"],["dc.date.available","2018-11-07T10:10:11Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Patients with systemic sclerosis (SSc) are endagered by tissue fibrosis and by microvasculopathy, with the latter caused by endothelial cell expansion/proliferation. SSc-associated fibrosis potentially results from mesenchymal transdifferentiation of endothelial cells. Early Endothelial Progenitor Cells (eEPCs) act proangiogenic under diverse conditions. Aim of the study was to analyze eEPC regeneration and mesenchymal transdifferentiation in patients with limited and diffuse SSs (lSSc and dSSc). Methods: Patients with both, lSSc and dSSc were included into the study. The following parameters were evaluated: eEPC numbers and regeneration, concentrations of vasomodulatory mediators, mesenchymal properties of blood-derived eEPC. Serum samples of healthy subjects and SS patients were used for stimulation of cultured human eEPC, subsequently followed by analysis of mesenchymal cell characteristics and mobility. Results: Twenty-nine patients were included into the study. Regenerative activity of blood-derived eEPCs did not differ between Controls and patients. Circulating eEPC were significantly lower in all patients with SSc, and in limited and diffuse SSc (lSSc/dSSc). Serum concentrations of promesenchymal TGF-b was elevated in all patients with SSc. Cultured mononuclear cells from SS patients displayed higher abundances of CD31 and of CD31 and aSMA combined. Finally, serum from SSc patients inhibited migration of cultured eEPCs and the cells showed lower sensitivity towards the endothelin antagonist Bosentan. Conclusions: The eEPC system, which represents an essential element of the endogenous vascular repair machinery is affected in SSc. The increased appearance of mesenchymal properties in eEPC may indicate that alterations of the cells potentially contribute to the accumulation of connective tissue and to vascular malfunction."],["dc.description.sponsorship","Heidenreich von-Siebold Programm"],["dc.identifier.doi","10.1186/s12891-016-1197-2"],["dc.identifier.isi","000395017600003"],["dc.identifier.pmid","27519706"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13866"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39808"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2474"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Early Endothelial Progenitor Cells (eEPCs) in systemic sclerosis (SSc) - dynamics of cellular regeneration and mesenchymal transdifferentiation"],["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"]]