Patschan, Daniel

[["dc.bibliographiccitation.artnumber","952699"],["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Lemmer, D.; 1Department of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Schmidt, J.; 3Department of Neurology and Pain Treatment, Immanuel Klinik Rüdersdorf, University Hospital of the Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany"],["dc.contributor.affiliation","Kummer, K.; 5Department of Neurology, Neuromuscular Center, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Lemmer, B.; 6Department of Physics, Georg-August-University Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Wrede, A.; 7Department of Neuropathology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Seitz, C.; 8Department of Dermatology, Allergology and Venereology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Balcarek, P.; 9Department of Trauma Surgery, Orthopedics and Plastic Surgery, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Schwarze, K.; 1Department of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Müller, G. A.; 1Department of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Patschan, D.; 4Faculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany"],["dc.contributor.affiliation","Patschan, S.; 4Faculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany"],["dc.contributor.author","Lemmer, D."],["dc.contributor.author","Schmidt, J."],["dc.contributor.author","Kummer, K."],["dc.contributor.author","Lemmer, B."],["dc.contributor.author","Wrede, A."],["dc.contributor.author","Seitz, C."],["dc.contributor.author","Balcarek, P."],["dc.contributor.author","Schwarze, K."],["dc.contributor.author","Müller, G. A."],["dc.contributor.author","Patschan, D."],["dc.contributor.author","Patschan, S."],["dc.date.accessioned","2022-12-01T08:31:33Z"],["dc.date.available","2022-12-01T08:31:33Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:12:29Z"],["dc.description.abstract","Background and aim\r\n Inflammatory myopathies are heterogeneous in terms of etiology, (immuno)pathology, and clinical findings. Endothelial cell injury, as it occurs in DM, is a common feature of numerous inflammatory and non-inflammatory vascular diseases. Vascular regeneration is mediated by both local and blood-derived mechanisms, such as the mobilization and activation of so-called proangiogenic cells (PACs) or early endothelial progenitor cells (eEPCs). The current study aimed to evaluate parameters of eEPC integrity in dermatomyositis (DM), compared to necrotizing myopathy (NM) and to non-myopathic controls.\r\n \r\n \r\n Methods\r\n \r\n Blood samples from DM and NM patients were compared to non-myositis controls and analyzed for the following parameters: circulating CD133\r\n +\r\n /VEGFR-2\r\n +\r\n cells, number of colony-forming unit endothelial cells (CFU-ECs), concentrations of angiopoietin 1, vascular endothelial growth factor (VEGF), and CXCL-16. Muscle biopsies from DM and NM subjects underwent immunofluorescence analysis for CXCR6, nestin, and CD31 (PECAM-1). Finally, myotubes, derived from healthy donors, were stimulated with serum samples from DM and NM patients, subsequently followed by RT-PCR for the following candidates: IL-1β, IL-6, nestin, and CD31.\r\n \r\n \r\n \r\n Results\r\n \r\n Seventeen (17) DM patients, 7 NM patients, and 40 non-myositis controls were included. CD133\r\n +\r\n /VEGFR-2\r\n +\r\n cells did not differ between the groups. Both DM and NM patients showed lower CFU-ECs than controls. In DM, intramuscular CD31 abundances were significantly reduced, which indicated vascular rarefaction. Muscular CXCR6 was elevated in both diseases. Circulating CXCL-16 was higher in DM and NM in contrast, compared to controls. Serum from patients with DM but not NM induced a profound upregulation of mRNS expression of CD31 and IL-6 in cultured myotubes.\r\n \r\n \r\n \r\n Conclusion\r\n Our study demonstrates the loss of intramuscular microvessels in DM, accompanied by endothelial activation in DM and NM. Vascular regeneration was impaired in DM and NM. The findings suggest a role for inflammation-associated vascular damage in the pathogenesis of DM."],["dc.identifier.doi","10.3389/fneur.2022.952699"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118201"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1664-2295"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Impairment of muscular endothelial cell regeneration in dermatomyositis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","19"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of injury & violence research"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Müller, Gerhard Anton"],["dc.date.accessioned","2019-07-09T11:42:34Z"],["dc.date.available","2019-07-09T11:42:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Acute kidney injury is a frequent and serious complication in hospitalized patients. Mortality rates have not substantially been decreased during the last 20 years. In most patients AKI results from transient renal hypoperfusion or ischemia. The consequences include tubular cell dysfunction/damage, inflammation of the organ, and post-ischemic microvasculopathy. The two latter events perpetuate kidney damage in AKI. Clinical manifestations result from diminished excretion of water, electrolytes, and endogenous / exogenous waste products. Patients are endangered by cardiovascular complications such as hypertension, heart failure, and arrhythmia. In addition, the whole organism may be affected by systemic toxification (uremia). The diagnostic approach in AKI involves several steps with renal biopsy inevitable in some patients. The current therapy focuses on preventing further kidney damage and on treatment of complications. Different pharmacological strategies have failed to significantly improve prognosis in AKI. If dialysis treatment becomes mandatory, intermittent and continuous renal replacement therapies are equally effective. Thus, new therapies are urgently needed in order to reduce short- and long-term outcome in AKI. In this respect, stem cell-based regimens may offer promising perspectives."],["dc.identifier.doi","10.5249/jivr.v7i1.604"],["dc.identifier.fs","609121"],["dc.identifier.pmid","25618438"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13574"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58696"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2008-4072"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.subject.mesh","Acute Kidney Injury"],["dc.subject.mesh","Causality"],["dc.subject.mesh","Chronic Disease"],["dc.subject.mesh","Comorbidity"],["dc.subject.mesh","Female"],["dc.subject.mesh","Germany"],["dc.subject.mesh","Health Status"],["dc.subject.mesh","Hospitalization"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Inpatients"],["dc.subject.mesh","Male"],["dc.subject.mesh","Primary Prevention"],["dc.subject.mesh","Renal Dialysis"],["dc.subject.mesh","Risk Factors"],["dc.title","Acute kidney injury."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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.firstpage","637"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.bibliographiccitation.lastpage","644"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Mueller, Gerhard Anton"],["dc.date.accessioned","2018-11-07T10:08:10Z"],["dc.date.available","2018-11-07T10:08:10Z"],["dc.date.issued","2016"],["dc.description.abstract","Autophagy enables cells to digest endogenous/exogenous waste products, thus potentially prolonging the cellular lifespan. Early endothelial progenitor cells (eEPCs) protect mice from ischemic acute kidney injury (AKI). The mid-term prognosis in AKI critically depends on vascular rarefication and interstitial fibrosis with the latter partly being induced by mesenchymal transdifferentiation of endothelial cells (EndoMT). This study aimed to determine the impact of eEPC preconditioning with different autophagy inducing agents [suberoylanilide hydroxamic acid (SAHA)/temsirolimus] in ischemic AKI. Male C57/Bl6 N mice were subjected to bilateral renal ischemia (40 min). Animals were injected with either untreated, or SAHA- or temsirolimus-pretreated syngeneic murine eEPCs at the time of reperfusion. Mice were analyzed 48 h and 4 weeks later. In addition, cultured eEPCs were treated with transforming growth factor (TGF)-beta +/- SAHA, autophagy (perinuclear LC3-II), and stress-induced premature senescence (SIPS-senescence-associated beta-galactosidase, SA-beta-Gal), and were evaluated 96 h later. Cultured eEPCs showed reduced perinuclear density of LC3-II + vesicles and elevated levels of SA-beta-Gal after treatment with TGF-beta alone, indicating impaired autophagy and aggravated SIPS. These effects were completely abrogated by SAHA. Systemic administration of either SAHA or tems pretreated eEPCs resulted in elevated intrarenal endothelial p62 at 48 h and 4 weeks, indicating stimulated endothelial autophagy. This effect was most pronounced after injection of SAHA-treated eEPCs. At 4 weeks endothelial expression of mesenchymal alpha-smooth muscle actin (alpha SMA) was reduced in animals receiving untreated and SAHA-pretreated cells. In addition, SAHA-treated cells reduced fibrosis at week 4. Tems in contrast aggravated EndoMT. Postischemic renal function declined after renal ischemia and remained unaffected in all experimental cell treatment groups. In ischemic AKI, intrarenal endothelial autophagy may be stabilized by systemic administration of pharmacologically preconditioned eEPCs. Early EPCs can reduce postischemic EndoMT and fibrosis in the mid-term. Autophagy induction in eEPCs either increases or decreases the mesenchymal properties of intrarenal endothelial cells, depending on the substance being used. Thus, endothelial autophagy induction in ischemic AKI, mediated by eEPCs is not a renoprotective event per se."],["dc.description.sponsorship","Else Kroner-Fresenius-Stiftung"],["dc.identifier.doi","10.1007/s40620-015-0222-0"],["dc.identifier.isi","000383012600006"],["dc.identifier.pmid","26289253"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12095"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39417"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wichtig Publishing"],["dc.relation.issn","1724-6059"],["dc.relation.issn","1121-8428"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Endothelial autophagy and Endothelial-to-Mesenchymal Transition (EndoMT) in eEPC treatment of ischemic AKI"],["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","36"],["dc.bibliographiccitation.journal","BMC Anesthesiology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Heeg, Malte"],["dc.contributor.author","Mertens, Alexander"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Patschan, Daniel"],["dc.date.accessioned","2018-11-07T09:18:27Z"],["dc.date.available","2018-11-07T09:18:27Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: AKI significantly worsens prognosis of hospitalized patients. This is particularly the case in patients with sepsis. The risk for aquiring sepsis is significantly increased in malignant diseases. Aim of the present retrospective study was to analyze outcomes of tumor patients with sepsis and AKI. Methods: One-thousand and seventeen patients, treated at the ICU of the Department of Nephrology and Rheumatology of the University Hospital Gottingen from 2009 to 2011 were retrospectively analyzed for mortality, sepsis, AKI, need for renal replacement therapy (dialysis) and malignancies. Results: AKI occurred significantly more frequent in septic than in non-septic patients and in tumor as oposed to non-tumor patients. Mortaliy rates were higher in the respective latter groups. Mortality increased even further if patients suffered from a malignant disease with sepsis and AKI. Mortality rates peaked if dialysis treatment became mandatory. In non-solid tumors 100% of the patients died if they suffered drom sepsis and AKI. This was not the case in solid malignancies (mortality rate 56%). Conclusions: We conclude that prognosis of tumor patients with AKI and sepsis is very poor. Mortality increases to almost 70% if diaylsis therapy is initiated. Non-solid tumors are associated with a 100% mortality if sepsis and AKI conincide."],["dc.identifier.doi","10.1186/1471-2253-13-36"],["dc.identifier.isi","000328382700001"],["dc.identifier.pmid","24168374"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28413"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2253"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Prognosis of AKI in malignant diseases with and without sepsis"],["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","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"]]

[["dc.bibliographiccitation.firstpage","1907"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Rheumatology International"],["dc.bibliographiccitation.lastpage","1917"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Hoffmann, Johanna Charlotte"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Müller, Claudia"],["dc.contributor.author","Schwarze, Katrin"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Ritter, Oliver"],["dc.contributor.author","Müller, Gerhard Anton"],["dc.contributor.author","Patschan, Susann"],["dc.date.accessioned","2020-12-10T14:10:11Z"],["dc.date.available","2020-12-10T14:10:11Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00296-019-04364-y"],["dc.identifier.eissn","1437-160X"],["dc.identifier.issn","0172-8172"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16590"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70667"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cytokine profiling in anti neutrophil cytoplasmic antibody-associated vasculitis: a cross-sectional cohort study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]