Tampe, Björn

[["dc.bibliographiccitation.firstpage","136"],["dc.bibliographiccitation.journal","Neurobiology of Learning and Memory"],["dc.bibliographiccitation.lastpage","150"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Dere, Ekrem"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Arinrad, Sahab"],["dc.contributor.author","Schmidt, Manuela"],["dc.contributor.author","Zeisberg, Elisabeth"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2020-12-10T15:20:34Z"],["dc.date.available","2020-12-10T15:20:34Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.nlm.2018.02.023"],["dc.identifier.issn","1074-7427"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72715"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Cognitive, emotional and social phenotyping of mice in an observer-independent setting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","2072143"],["dc.bibliographiccitation.journal","Human Vaccines & Immunotherapeutics"],["dc.contributor.author","Plüß, Marlene"],["dc.contributor.author","Piantoni, Silvia"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Kim, Alfred H. J."],["dc.contributor.author","Korsten, Peter"],["dc.date.accessioned","2022-06-01T09:39:18Z"],["dc.date.available","2022-06-01T09:39:18Z"],["dc.date.issued","2022"],["dc.description.abstract","In recent years, advances in the treatment and management of patients with systemic lupus erythematosus (SLE) have improved their life expectancy and quality of life. However, lupus nephritis (LN) still represents a major life-threatening complication of the disease. Belimumab (BEL), a fully human monoclonal IgG1λ antibody neutralizing soluble B cell activating factor, was approved more than ten years ago as add-on therapy in adults and pediatric patients with a highly active, autoantibody-positive disease despite standard of care (SoC). Recently, the superiority of the addition of BEL to SoC was also demonstrated in LN. In this review, we provide a comprehensive overview of the study landscape, available therapeutic options for SLE (focusing on BEL in renal and non-renal SLE), and new perspectives in the treatment field of this disease. A personalized treatment approach will likely become available with the advent of novel therapeutic agents for SLE and LN."],["dc.identifier.doi","10.1080/21645515.2022.2072143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108436"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","2164-554X"],["dc.relation.issn","2164-5515"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Belimumab for systemic lupus erythematosus – Focus on lupus nephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["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.journal","Journal of Nephrology"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-01-11T14:05:40Z"],["dc.date.available","2022-01-11T14:05:40Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Background Renal involvement is a common and severe complication of ANCA (antineutrophil cytoplasmic antibody) associated vasculitis (AAV) potentially resulting in a pauci-immune necrotizing and crescentic antineutrophil cytoplasmic antibody (ANCA) glomerulonephritis (GN) with acute kidney injury (AKI), end-stage renal disease (ESRD) or death. We recently described that Bowman’s capsule rupture links glomerular damage to tubulointerstitial inflammation in ANCA-associated glomerulonephritis. Herein we provide a comprehensive histological subtyping of immune cell infiltrates in association with Bowman’s capsule rupture in ANCA GN. Methods A total of 44 kidney biopsies with ANCA GN were retrospectively included in a single-center observational study. Within a renal biopsy specimen, each glomerulus was scored separately for the presence of extensive and focal Bowman’s capsule rupture in injured glomeruli. Infiltrates of neutrophils, eosinophils, plasma cells, and mononucleated cells (macrophages, lymphocytes) were quantified as a fraction of the area of total cortical inflammation. Results Extensive Bowman’s capsule rupture was associated with tubulointerstitial inflammation containing infiltrates of neutrophils, eosinophils and plasma cells. A similar association was observed for the presence of focal Bowman’s capsule rupture, correlating with tubulointerstitial inflammation containing neutrophils, eosinophils and plasma cells. Multiple logistic regression confirmed that extensive Bowman’s capsule rupture correlated with tubulointerstitial inflammation containing neutrophils, and focal Bowman’s capsule rupture correlated with neutrophil and plasma cell infiltration. Furthermore, this association was specifically observed in PR3-ANCA GN. Conclusion To our knowledge, this is the first report linking Bowman’s capsule rupture directly to tubulointerstitial inflammation by immune cell subtypes. This underscores a pathomechanistic link between tubulointerstitial and glomerular lesions in ANCA GN and needs further investigation. Graphical abstract"],["dc.description.abstract","Abstract Background Renal involvement is a common and severe complication of ANCA (antineutrophil cytoplasmic antibody) associated vasculitis (AAV) potentially resulting in a pauci-immune necrotizing and crescentic antineutrophil cytoplasmic antibody (ANCA) glomerulonephritis (GN) with acute kidney injury (AKI), end-stage renal disease (ESRD) or death. We recently described that Bowman’s capsule rupture links glomerular damage to tubulointerstitial inflammation in ANCA-associated glomerulonephritis. Herein we provide a comprehensive histological subtyping of immune cell infiltrates in association with Bowman’s capsule rupture in ANCA GN. Methods A total of 44 kidney biopsies with ANCA GN were retrospectively included in a single-center observational study. Within a renal biopsy specimen, each glomerulus was scored separately for the presence of extensive and focal Bowman’s capsule rupture in injured glomeruli. Infiltrates of neutrophils, eosinophils, plasma cells, and mononucleated cells (macrophages, lymphocytes) were quantified as a fraction of the area of total cortical inflammation. Results Extensive Bowman’s capsule rupture was associated with tubulointerstitial inflammation containing infiltrates of neutrophils, eosinophils and plasma cells. A similar association was observed for the presence of focal Bowman’s capsule rupture, correlating with tubulointerstitial inflammation containing neutrophils, eosinophils and plasma cells. Multiple logistic regression confirmed that extensive Bowman’s capsule rupture correlated with tubulointerstitial inflammation containing neutrophils, and focal Bowman’s capsule rupture correlated with neutrophil and plasma cell infiltration. Furthermore, this association was specifically observed in PR3-ANCA GN. Conclusion To our knowledge, this is the first report linking Bowman’s capsule rupture directly to tubulointerstitial inflammation by immune cell subtypes. This underscores a pathomechanistic link between tubulointerstitial and glomerular lesions in ANCA GN and needs further investigation. Graphical abstract"],["dc.identifier.doi","10.1007/s40620-021-01208-6"],["dc.identifier.pii","1208"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97717"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","1724-6059"],["dc.relation.issn","1121-8428"],["dc.title","Neutrophils associate with Bowman’s capsule rupture specifically in PR3-ANCA glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","annrheumdis-2020-218491"],["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Larsen, Jörg"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T10:47:36Z"],["dc.date.available","2021-06-01T10:47:36Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1136/annrheumdis-2020-218491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85655"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1468-2060"],["dc.relation.issn","0003-4967"],["dc.title","Repeated false-negative tests delayed diagnosis of COVID-19 in a case with granulomatosis with polyangiitis under maintenance therapy with rituximab and concomitant influenza pneumonia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","998"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Lovisa, Sara"],["dc.contributor.author","LeBleu, Valerie S."],["dc.contributor.author","Tampe, Bjorn"],["dc.contributor.author","Sugimoto, Hikaru"],["dc.contributor.author","Vadnagara, Komal"],["dc.contributor.author","Carstens, Julienne L."],["dc.contributor.author","Wu, Chia-Chin"],["dc.contributor.author","Hagos, Yohannes"],["dc.contributor.author","Burckhardt, Birgitta-Christina"],["dc.contributor.author","Pentcheva-Hoang, Tsvetelina"],["dc.contributor.author","Nischal, Hersharan"],["dc.contributor.author","Allison, James P."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.date.accessioned","2018-11-07T09:52:34Z"],["dc.date.available","2018-11-07T09:52:34Z"],["dc.date.issued","2015"],["dc.description.abstract","Kidney fibrosis is marked by an epithelial-to-mesenchymal transition (EMT) of tubular epithelial cells (TECs). Here we find that, during renal fibrosis, TECs acquire a partial EMT program during which they remain associated with their basement membrane and express markers of both epithelial and mesenchymal cells. The functional consequence of the EMT program during fibrotic injury is an arrest in the G2 phase of the cell cycle and lower expression of several solute and solvent transporters in TECs. We also found that transgenic expression of either Twist1 (encoding twist family bHLH transcription factor 1, known as Twist) or Snai1 (encoding snail family zinc finger 1, known as Snail) expression is sufficient to promote prolonged TGF-beta 1-induced G2 arrest of TECs, limiting the cells' potential for repair and regeneration. In mouse models of experimentally induced renal fibrosis, conditional deletion of Twist1 or Snai1 in proximal TECs resulted in inhibition of the EMT program and the maintenance of TEC integrity, while also restoring cell proliferation, dedifferentiation-associated repair and regeneration of the kidney parenchyma and attenuating interstitial fibrosis. Thus, inhibition of the EMT program in TECs during chronic renal injury represents a potential anti-fibrosis therapy."],["dc.identifier.doi","10.1038/nm.3902"],["dc.identifier.isi","000360961300012"],["dc.identifier.pmid","26236991"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36152"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1546-170X"],["dc.relation.issn","1078-8956"],["dc.title","Epithelial-to-mesenchymal transition induces cell cycle arrest and parenchymal damage in renal fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","The Lancet Infectious Diseases"],["dc.contributor.author","Arora, Prerna"],["dc.contributor.author","Nehlmeier, Inga"],["dc.contributor.author","Kempf, Amy"],["dc.contributor.author","Cossmann, Anne"],["dc.contributor.author","Schulz, Sebastian R"],["dc.contributor.author","Dopfer-Jablonka, Alexandra"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Dickel, Steffen"],["dc.contributor.author","Hoffmann, Markus"],["dc.date.accessioned","2022-10-04T10:21:46Z"],["dc.date.available","2022-10-04T10:21:46Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1016/S1473-3099(22)00591-6"],["dc.identifier.pii","S1473309922005916"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114495"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.issn","1473-3099"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Lung cell entry, cell–cell fusion capacity, and neutralisation sensitivity of omicron sublineage BA.2.75"],["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.firstpage","578"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","586"],["dc.bibliographiccitation.volume","60"],["dc.contributor.author","Wallbach, M."],["dc.contributor.author","Tampe, B."],["dc.contributor.author","Dihazi, H."],["dc.contributor.author","Koziolek, M. J."],["dc.date.accessioned","2020-12-10T14:08:25Z"],["dc.date.available","2020-12-10T14:08:25Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00108-019-0602-y"],["dc.identifier.eissn","1432-1289"],["dc.identifier.issn","0020-9554"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70458"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Akute Nierenschädigung: von Kreatinin zu KIM‑1?"],["dc.title.alternative","Acute kidney injury: from creatinine to KIM‑1?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","annrheumdis-2021-219970"],["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T10:47:36Z"],["dc.date.available","2021-06-01T10:47:36Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1136/annrheumdis-2021-219970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85659"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1468-2060"],["dc.relation.issn","0003-4967"],["dc.title","Correspondence on ‘Bowman’s capsule rupture on renal biopsy improves the outcome prediction of ANCA-associated glomerulonephritis classifications’"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]