Tampe, Désirée

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-12-01T08:30:57Z"],["dc.date.available","2022-12-01T08:30:57Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a small vessel vasculitis often leading to critical illness by multi-organ failure. Data for patients with specifically ANCA-associated renal vasculitis requiring intensive care unit (ICU) supportive care are limited and have mainly focused on long-term renal and overall outcome. Particularly, data on critical illness during the initial course of disease are scarce and remain poorly determined. Therefore, the purpose of this retrospective study was to identify predictors of critical illness in a cohort of patients with ANCA-associated renal vasculitis. We retrospectively included a total number of 53 cases with confirmed ANCA-associated renal vasculitis between 2015 till 2020 in a single-center cohort study. We here identified an association between low hemoglobin levels and requirement of ICU supportive care in patients with ANCA-associated renal vasculitis. Furthermore, levels of hemoglobin below 9.8 g/dL at admission independently predicted prolonged requirement of ICU supportive care in critically ill patients with ANCA-associated renal vasculitis. These findings confirm that low levels of hemoglobin negatively affect short-term outcome and could further improve our current understanding for the role of anemia in ANCA-associated renal vasculitis."],["dc.description.sponsorship","Else-Kröner research program"],["dc.description.sponsorship","Research program, University Medical Center, University of Göttingen"],["dc.description.sponsorship"," Georg-August-Universität Göttingen 501100003385"],["dc.identifier.doi","10.1038/s41598-022-23313-7"],["dc.identifier.pii","23313"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118027"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","2045-2322"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Low levels of hemoglobin associate with critical illness and predict disease course in patients with ANCA-associated renal vasculitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","818"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cancer Cell"],["dc.bibliographiccitation.lastpage","834.e9"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Chen, Yang"],["dc.contributor.author","Yang, Sujuan"],["dc.contributor.author","Tavormina, Jena"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Wang, Huamin"],["dc.contributor.author","Mahadevan, Krishnan K."],["dc.contributor.author","Wu, Chang-Jiun"],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Chang, Chia-Chi"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2022-09-01T09:49:30Z"],["dc.date.available","2022-09-01T09:49:30Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/j.ccell.2022.06.011"],["dc.identifier.pii","S1535610822002756"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113442"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.issn","1535-6108"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Oncogenic collagen I homotrimers from cancer cells bind to α3β1 integrin and impact tumor microbiome and immunity to promote pancreatic cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2687"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","American Journal Of Pathology"],["dc.bibliographiccitation.lastpage","2698"],["dc.bibliographiccitation.volume","184"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Tampe, Bjoern"],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2018-11-07T09:34:44Z"],["dc.date.available","2018-11-07T09:34:44Z"],["dc.date.issued","2014"],["dc.description.abstract","Thrombospondin-1 (TSP1) is a multifunctional matricellular protein known to promote progression of chronic kidney disease. To gain insight into the underlying mechanisms through which TSP1 accelerates chronic kidney disease, we compared disease progression in Col4a3 knockout (K0) mice, which develop spontaneous kidney failure, with that of Col4a3;Tsp1 double-knockout (DK0) mice. Decline of excretory renal function was significantly delayed in the absence of TSP1. Although Col4a3;Tsp1 DK0 mice did progress toward end-stage renal failure, their kidneys exhibited distinct histopathological lesions, compared with creatinine level- matched Col4a3 K0 mice. Although kidneys of both Col4a3 K0 and Col4a3;Tsp1 DK0 mice exhibited a widened tubulointerstitium, predominant lesions in Col4a3 K0 kidneys were collagen deposition and fibroblast accumulation, whereas in Col4a3;Tsp1 DK0 kidney inflammation was predominant, with less collagen deposition. Altered disease progression correlated with impaired activation of transforming growth factor-beta 1 (TGF-beta 1) in vivo and in vitro in the absence of TSP1. In summary, our findings suggest that TSP1 contributes to progression of chronic kidney disease by catalyzing activation of latent TGF-beta 1, resulting in promotion of a fibroproliferative response over an inflammatory response. Furthermore, the findings suggest that fibro-proliferative and inflammatory lesions are independent entities, both of which contribute to decline of renal function."],["dc.identifier.doi","10.1016/j.ajpath.2014.06.014"],["dc.identifier.isi","000342276800010"],["dc.identifier.pmid","25111226"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32238"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/79"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","1525-2191"],["dc.relation.issn","0002-9440"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Thrombospondin-1 Deficiency Causes a Shift from Fibroproliferative to Inflammatory Kidney Disease and Delays Onset of Renal Failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Kluge, Ingmar Alexander"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-05-02T08:09:46Z"],["dc.date.available","2022-05-02T08:09:46Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s40620-022-01320-1"],["dc.identifier.pii","1320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107458"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1724-6059"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","pANCA autoantibody testing by indirect immunofluorescence indicates interstitial arteritis independent of MPO-ANCA immunoassays in ANCA-associated glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","810"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","811"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Bosukonda, Dattatreyamurty"],["dc.contributor.author","Keck, Peter"],["dc.contributor.author","Taduri, Gangadhar"],["dc.contributor.author","Bechtel, Wibke"],["dc.contributor.author","Okada, Hirokazu"],["dc.contributor.author","Carlson, William"],["dc.contributor.author","Bey, Philippe"],["dc.contributor.author","Rusckowski, Mary"],["dc.contributor.author","Tampe, Bjoern"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Kanasaki, Keizo"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2018-11-07T09:23:08Z"],["dc.date.available","2018-11-07T09:23:08Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1038/nm.3081"],["dc.identifier.isi","000321557700014"],["dc.identifier.pmid","23836214"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29512"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Regarding the mechanism of action of a proposed peptide agonist of the bone morphogenetic protein receptor activin-like kinase 3 Reply"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","157"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","176"],["dc.bibliographiccitation.volume","91"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Steinle, Ulrike"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Carstens, Julienne L."],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2020-05-04T07:22:12Z"],["dc.date.available","2020-05-04T07:22:12Z"],["dc.date.issued","2017"],["dc.description.abstract","Acute kidney injury (AKI) and progressive chronic kidney disease (CKD) are intrinsically tied syndromes. In this regard, the acutely injured kidney often does not achieve its full regenerative capacity and AKI directly transitions into progressive CKD associated with tubulointerstitial fibrosis. Underlying mechanisms of such AKI-to-CKD progression are still incompletely understood and specific therapeutic interventions are still elusive. Because epigenetic modifications play a role in maintaining tissue fibrosis, we used a murine model of ischemia-reperfusion injury to determine whether aberrant promoter methylation of RASAL1 contributes causally to the switch between physiological regeneration and tubulointerstitial fibrogenesis, a hallmark of AKI-to-CKD progression. It is known that the antihypertensive drug hydralazine has demethylating activity, and that its optimum demethylating activity occurs at concentrations below blood pressure-lowering doses. Administration of low-dose hydralazine effectively induced expression of hydroxylase TET3, which catalyzed RASAL1 hydroxymethylation and subsequent RASAL1 promoter demethylation. Hydralazine-induced CpG promoter demethylation subsequently attenuated renal fibrosis and preserved excretory renal function independent of its blood pressure-lowering effects. In comparison, RASAL1 demethylation and inhibition of tubulointerstitial fibrosis was not detected upon administration of the angiotensin-converting enzyme inhibitor Ramipril in this model. Thus, RASAL1 promoter methylation and subsequent transcriptional RASAL1 suppression plays a causal role in AKI-to-CKD progression."],["dc.identifier.doi","10.1016/j.kint.2016.07.042"],["dc.identifier.pmid","27692563"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/64543"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/307"],["dc.language.iso","en"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | D03: ENPP3-vermittelter Phosphat-Metabolismus bei der Herzfibrose"],["dc.relation.eissn","1523-1755"],["dc.relation.issn","0085-2538"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.title","Low-dose hydralazine prevents fibrosis in a murine model of acute kidney injury-to-chronic kidney disease progression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","112972982210887"],["dc.bibliographiccitation.journal","The Journal of Vascular Access : JVA"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Plüß, Marlene"],["dc.contributor.author","Kuczera, Tim"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-05-02T08:09:23Z"],["dc.date.available","2022-05-02T08:09:23Z"],["dc.date.issued","2022"],["dc.description.abstract","Background: We have previously reported that the rapid atrial swirl sign (RASS) is an accurate and safe procedure for ultrasound (US)-guided tip positioning of retrograde-tunneled hemodialysis catheters (HDCs). However, application of RASS for placement of antegrade HDCs has not been investigated yet. Therefore, we here report our first experience of applying RASS for US-guided tip positioning of antegrade-tunneled HDCs. Methods: We performed a cross-sectional study to assess the feasibility of applying the RASS for US-guided tip positioning of antegrade-tunneled HDCs. We included a total number of 15 antegrade-tunneled HDC insertions in 13 patients requiring placement of a HDC for the temporary or permanent treatment of ESKD in a single-center, cross-sectional pilot study. Results: The overall success rate of applying the RASS for US-guided tip positioning of antegrade-tunneled HDCs was 15/15 (100%) confirmed by portable anterior-posterior chest radiography, with no major adverse events after HDC insertions. In addition, this insertion technique demonstrated optimal HDC flow without any observed malfunction. Conclusion: This study investigated the efficacy of the RASS for US-guided tip positioning of antegrade-tunneled HDCs in patients with ESKD. Application of the RASS for US-guided tip positioning is an accurate and safe procedure for proper placement of antegrade-tunneled HDCs."],["dc.identifier.doi","10.1177/11297298221088763"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107369"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1724-6032"],["dc.relation.issn","1129-7298"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.relation.orgunit","Klinik für Nephrologie und Rheumatologie"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0/"],["dc.title","The rapid atrial swirl sign for ultrasound-guided tip positioning of antegrade-tunneled hemodialysis catheters: A cross-sectional pilot study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","24075"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Nyamsuren, Gunsmaa"],["dc.contributor.author","Rapp, Gregor"],["dc.contributor.author","Dihazi, Hassan"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2022-01-11T14:06:04Z"],["dc.date.available","2022-01-11T14:06:04Z"],["dc.date.issued","2021"],["dc.description.abstract","Aryl hydrocarbon receptor nuclear translocator (ARNT) mediates anti-fibrotic activity in kidney and liver through induction of ALK3-receptor expression and subsequently increased Smad1/5/8 signaling. While expression of ARNT can be pharmacologically induced by sub-immunosuppressive doses of FK506 or by GPI1046, its anti-fibrotic activity is only realized when ARNT-ARNT homodimers form, as opposed to formation of ARNT-AHR or ARNT-HIF1α heterodimers. Mechanisms underlying ARNTs dimerization decision to specifically form ARNT–ARNT homodimers and possible cues to specifically induce ARNT homodimerization have been previously unknown. Here, we demonstrate that phosphorylation of the Ser77 residue is critical for ARNT–ARNT homodimer formation and stabilization. We further demonstrate that inhibition of PP2A phosphatase activity by LB100 enhances ARNT–ARNT homodimers both in vivo and in vitro (mouse tubular epithelial cells and human embryonic kidney cells). In murine models of kidney fibrosis, and also of liver fibrosis, combinations of FK506 or GPI1046 (to induce ARNT expression) with LB100 (to enhance ARNT homodimerization) elicit additive anti-fibrotic activities. Our study provides additional evidence for the anti-fibrotic activity of ARNT–ARNT homodimers and reveals Ser77 phosphorylation as a novel pharmacological target to realize the therapeutic potential of increased ARNT transactivation activity."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1038/s41598-021-03523-1"],["dc.identifier.pii","3523"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97817"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","2045-2322"],["dc.title","PP2A phosphatase inhibition is anti-fibrotic through Ser77 phosphorylation-mediated ARNT/ARNT homodimer formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Biggemann, Lorenz"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-05-02T08:09:46Z"],["dc.date.available","2022-05-02T08:09:46Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is characterized by small vessel inflammation and the presence of autoantibodies against cytoplasmic proteases, most often proteinase-3 and myeloperoxidase. Peripheral blood monocytes are an important source of local macrophage accumulation within parenchymal organs, as evidenced by their presence in early lesions in ANCA-associated glomerulonephritis. Major histocompatibility complex (MHC) II cell surface receptor human leukocyte antigen receptor (HLA-DR) allows antigen presentation to T cells and is crucial for the initiation of an immune response. We herein report HLA-DR abundance in AAV and the kinetics of HLA-DR + monocytes and T lymphocytes during remission induction therapy in AAV. Life-threatening AAV with pulmonary hemorrhage and renal involvement was associated with the presence of HLA-DR in a considerable population of peripheral blood monocytes and T lymphocytes, and relapsing disease manifested despite persistent B cell depletion after remission induction with rituximab. Moreover, remission induction in AAV with steroids, plasma exchange and intravenous cyclophosphamide, and improvement of clinical symptoms were associated with a decrease in HLA-DR + differing between monocytes and T lymphocytes. Particularly, persistent suppression of HLA-DR + monocytes was observed during remission induction, while an initial decrease in HLA-DR + T lymphocytes was followed by recovery of this population during the further course. Detailed insights into HLA-DR kinetics could pave the way towards an increased understanding of immunopathology and identify patients that could mostly benefit from distinct remission induction regimens."],["dc.description.abstract","Abstract Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is characterized by small vessel inflammation and the presence of autoantibodies against cytoplasmic proteases, most often proteinase-3 and myeloperoxidase. Peripheral blood monocytes are an important source of local macrophage accumulation within parenchymal organs, as evidenced by their presence in early lesions in ANCA-associated glomerulonephritis. Major histocompatibility complex (MHC) II cell surface receptor human leukocyte antigen receptor (HLA-DR) allows antigen presentation to T cells and is crucial for the initiation of an immune response. We herein report HLA-DR abundance in AAV and the kinetics of HLA-DR + monocytes and T lymphocytes during remission induction therapy in AAV. Life-threatening AAV with pulmonary hemorrhage and renal involvement was associated with the presence of HLA-DR in a considerable population of peripheral blood monocytes and T lymphocytes, and relapsing disease manifested despite persistent B cell depletion after remission induction with rituximab. Moreover, remission induction in AAV with steroids, plasma exchange and intravenous cyclophosphamide, and improvement of clinical symptoms were associated with a decrease in HLA-DR + differing between monocytes and T lymphocytes. Particularly, persistent suppression of HLA-DR + monocytes was observed during remission induction, while an initial decrease in HLA-DR + T lymphocytes was followed by recovery of this population during the further course. Detailed insights into HLA-DR kinetics could pave the way towards an increased understanding of immunopathology and identify patients that could mostly benefit from distinct remission induction regimens."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.identifier.doi","10.1007/s40620-022-01330-z"],["dc.identifier.pii","1330"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107459"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1724-6059"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Kinetics of human leukocyte antigen receptor HLA-DR+ monocytes and T lymphocytes during remission induction therapy in ANCA-associated vasculitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","102924"],["dc.bibliographiccitation.journal","Journal of Autoimmunity"],["dc.bibliographiccitation.volume","133"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Kluge, Ingmar Alexander"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-11-01T10:16:29Z"],["dc.date.available","2022-11-01T10:16:29Z"],["dc.date.issued","2022"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/501100003385 Georg-August-Universität Göttingen"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/100018165 Chandrakasem Rajabhat University"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/100019147 Universitätsmedizin Göttingen"],["dc.description.sponsorship"," http://dx.doi.org/10.13039/501100001659 Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.1016/j.jaut.2022.102924"],["dc.identifier.pii","S0896841122001329"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116576"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-605"],["dc.relation.issn","0896-8411"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Intrarenal synthesis of complement C3 localized to distinct vascular compartments in ANCA-associated renal vasculitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]