Bramlage, Carsten

[["dc.bibliographiccitation.firstpage","A100"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","MEDIZINISCHE KLINIK"],["dc.bibliographiccitation.lastpage","A101"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Scheel, A."],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Grone, H. J."],["dc.contributor.author","Mueller, Gerhard A."],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T09:59:01Z"],["dc.date.available","2018-11-07T09:59:01Z"],["dc.date.issued","2006"],["dc.identifier.isi","000237562000323"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37491"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Urban & Vogel"],["dc.publisher.place","Munich"],["dc.relation.issn","0723-5003"],["dc.title","Effective therapy of a hepatitis-C-associated immunocomplex nephritis by means of cryoprecipitate apheresis and interferon-alpha"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1215"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Mini Reviews in Medicinal Chemistry"],["dc.bibliographiccitation.lastpage","1228"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Koziolek, M."],["dc.contributor.author","Vasko, R."],["dc.contributor.author","Bramlage, C."],["dc.contributor.author","Muller, G."],["dc.contributor.author","Strutz, F."],["dc.date.accessioned","2021-06-01T10:48:35Z"],["dc.date.available","2021-06-01T10:48:35Z"],["dc.date.issued","2009"],["dc.description.abstract","The chemokine CX3C-L/FKN is expressed in both soluble and transmembrane/mucin hybrid forms, thus combining chemoattractant functions together with receptor/adhesion molecule properties. In contrast to other chemokine receptors, CX3C-R is expressed not only on lymphoid cell populations, but also on several intrinsic cells including tubular epithelial cells and renal fibroblasts where it regulates various aspects of cell viability, matrix synthesis and degradation, migration, inflammation as well as oxidative stress. In the kidney, the chemokines/receptor pair has been shown to play a role in nephrogenesis as well as in the pathogenesis primary and secondary nephropathies. In several animal models and human specimens with acute and chronic renal failure including allograft nephropathy, CX3C-L/CX3C-R has been shown to exert immune and non-immune mediated renal damages. A blockade of this chemokine system ameliorated acute and chronic renal damages, though the latter to a more robust extent. There seems to a role of the CX3C-L/CX3C-R pair in mediating acute renal inflammation as well as in progressive chronic renal failure. However, functional studies are lacking for many aspects and further studies are necessary to better define the functional properties of CX3 C-L/FKN and its receptor."],["dc.identifier.doi","10.2174/138955709789055252"],["dc.identifier.isi","000271619500007"],["dc.identifier.pmid","19817712"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85989"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bentham Science Publ Ltd"],["dc.relation.issn","1389-5575"],["dc.title","The CX3C-Chemokine Fractalkine in Kidney Diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S8"],["dc.bibliographiccitation.issue","46"],["dc.bibliographiccitation.journal","DMW - Deutsche Medizinische Wochenschrift"],["dc.bibliographiccitation.lastpage","S9"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Bevandaf, J."],["dc.contributor.author","Maatouk, I."],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Lauterberg, Christina"],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T10:52:57Z"],["dc.date.available","2018-11-07T10:52:57Z"],["dc.date.issued","2007"],["dc.identifier.isi","000251423500025"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49234"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.issn","0012-0472"],["dc.title","BMP-5 is expressed in renal interstitial fibroblasts and has TGF-beta neutralizing effect in vitro"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","401"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Scandinavian Journal of Rheumatology"],["dc.bibliographiccitation.lastpage","409"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Kaps, C."],["dc.contributor.author","Ungethuem, U."],["dc.contributor.author","Bramlage, Peter"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Krenn, V."],["dc.contributor.author","Pruss, Axel"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Strutz, Frank M."],["dc.contributor.author","Burmester, Gerd-Ruediger"],["dc.contributor.author","Haeupl, T."],["dc.date.accessioned","2018-11-07T11:20:44Z"],["dc.date.available","2018-11-07T11:20:44Z"],["dc.date.issued","2008"],["dc.description.abstract","Objective: Growth differentiation factor-5 (GDF-5), a member of the transforming growth factor (TGF)-beta family, is involved in joint development during embryogenesis and has the potential to regenerate cartilage in adult animals. As progression of chronic joint diseases is influenced by cytokines of the synovial tissue, we examined the expression and effects of GDF-5 in this tissue. Methods: Microarray experiments were investigated for differential expression of GDF-5 in synovial tissues, synovial fibroblasts, and peripheral blood cells. GDF-5 expression was validated by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemistry, double immunofluorescence, and in situ hybridization in synovial tissue of normal donors (ND) and patients with osteoarthritis (OA) and rheumatoid arthritis (RA). Effects of inflammation and therapy were investigated in RA and OA fibroblasts after stimulation with interleukin (IL)-1 beta, tumour necrosis factor (TNF)-alpha, methotrexate (MTX), and prednisolone. The influence of GDF-5 on macophages was studied by chemotaxis assay. Results: Microarray analysis and immunostaining revealed expression predominantly in synovial fibroblasts. Compared to patients without immunomodulating drugs, expression of GDF-5 was decreased significantly in patients receiving glucocorticoids and/or disease-modifying antirheumatic drugs (DMARDs) (p=0.007), but did not differ between the total group of ND, OA, and RA. Stimulation with prednisolone and TNF alpha reduced GDF-5 expression in OA and RA fibroblasts, whereas MTX and IL-1 beta revealed minor or no relevant change. GDF-5 also reduced cell migration of macrophages (p<0.001). Conclusion: GDF-5 is expressed in synovial fibroblasts and may counteract macrophage infiltration. Its modulation by inflammation and therapy suggests that glucocorticoids play a conflicting role by suppressing not only inflammation but also putative mechanisms of repair."],["dc.identifier.doi","10.1080/03009740802120010"],["dc.identifier.isi","000262270200001"],["dc.identifier.pmid","18830904"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55613"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis As"],["dc.relation.issn","0300-9742"],["dc.title","Modulatory effects of inflammation and therapy on GDF-5 expression in rheumatoid arthritis synovium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","142"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Transplantation Proceedings"],["dc.bibliographiccitation.lastpage","147"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Heeg, Malte"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Homayounfar, Kia"],["dc.contributor.author","Muehlhausen, Johannes"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.date.accessioned","2018-11-07T09:30:22Z"],["dc.date.available","2018-11-07T09:30:22Z"],["dc.date.issued","2013"],["dc.description.abstract","Background. The most common immunosuppressive regimens after renal transplantation include calcineurin inhibitors (CNI). However, due to renal toxicity long-term graft survival does not seem to be positively affected by CNIs. Methods. In the present study, we investigated 17 patients, in which the CM immunosuppression was converted to a CM-free, mycophenolate sodium (MPS) regimen. Conversion was performed due to progressive impairment of the graft function from suspected CM toxicity. We retrospectively analyzed graft function as well as toxicity and surrogate markers for 4 years before and 4 years after conversion using a repeated-measures mixed model data analysis and/or a paired sample t-test. Results. The mean time point of therapy conversion was 11.2 +/- 4.6 years after transplantation. Within 1 month of CNI discontinuation, allograft function improved significantly, remaining at a significant level for 2 years. The estimated glomerular filtration rate increased from 43.4 +/- 14.8 to a maximum of 55.7 +/- 21.7 mL/min at 1 year after conversion (P = .0027). After 4 years, the end of the observation period, renal function was similar to the baseline. There were no significant side effects. Conclusion. These data suggested that, when chronic CM-toxicity is suspected, renal allograft recipients may benefit from CM withdrawal in favor of a MPS-including immunosuppressive regimen."],["dc.identifier.doi","10.1016/j.transproceed.2012.10.028"],["dc.identifier.isi","000315007200025"],["dc.identifier.pmid","23375288"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31288"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1873-2623"],["dc.relation.issn","0041-1345"],["dc.title","Improvement of Renal Graft Function After Conversion From a Calcineurin Inhibitor Including Immunosuppression to a Mycophenolate Sodium Including Regimen: A 4-year Follow-up"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","747"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Evaluation in Clinical Practice"],["dc.bibliographiccitation.lastpage","754"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Kröplin, Juliane"],["dc.contributor.author","Wallbach, Manuel"],["dc.contributor.author","Minguet, Joan"],["dc.contributor.author","Smith, Katherine Helen"],["dc.contributor.author","Lüders, Stephan"],["dc.contributor.author","Schrader, Joachim"],["dc.contributor.author","Patschan, Susan"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Deutsch, Cornelia"],["dc.contributor.author","Bramlage, Peter"],["dc.contributor.author","Müller, Gerhard Anton"],["dc.contributor.author","Koziolek, Michael"],["dc.date.accessioned","2020-12-10T18:28:59Z"],["dc.date.available","2020-12-10T18:28:59Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1111/jep.12709"],["dc.identifier.issn","1356-1294"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76484"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Management of cardiovascular risk factors in patients with ANCA-associated vasculitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e0222102"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Grupp, Clemens"],["dc.contributor.author","Troche-Polzien, Ilka"],["dc.contributor.author","Stock, Johanna"],["dc.contributor.author","Bramlage, Carsten"],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.editor","Gonzalez Suarez, Maria Lourdes"],["dc.date.accessioned","2020-12-10T18:42:10Z"],["dc.date.available","2020-12-10T18:42:10Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1371/journal.pone.0222102"],["dc.identifier.eissn","1932-6203"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16604"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77833"],["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","Thrombophilic risk factors in hemodialysis: Association with early vascular access occlusion and patient survival in long-term follow-up"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","235"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Clinical Apheresis"],["dc.bibliographiccitation.lastpage","242"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Strauchmann, Julia"],["dc.contributor.author","Wallbach, Manuel"],["dc.contributor.author","Bramlage, Carsten"],["dc.contributor.author","Puls, Miriam"],["dc.contributor.author","Konstantinides, Stavros V."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.date.accessioned","2018-11-07T09:34:08Z"],["dc.date.available","2018-11-07T09:34:08Z"],["dc.date.issued","2014"],["dc.description.abstract","Lipoprotein apheresis (LA) is believed to exert anti-atherosclerotic effects beyond LDL-cholesterol reduction. We investigated 22 patients undergoing regular LA on a weekly basis (group A) before (AP) and after LA procedure (EP), 15 healthy individuals (group B), and 22 hyperlipoproteinemic patients with concomitant cardiovascular end organ damage treated without LA therapy (group C). Biomarkers of endothelial inflammation (hsCRP), plaque destabilization, and rupture (sVCAM, MMP-9, PAPP-A, ADMA) were quantified. Intergroup comparison revealed a statistically significant lower MMP-9 level in group A (AP and EP) compared with group C (P<0.01), whereas PAPP-A levels were lower in group B compared with group A and C (P=0.04). EP ADMA-levels and EP sVCAM levels in group A were statistically lower compared with group B and C. AP and EP values comparison revealed a significant reduction for hsCRP (mean 41.0 +/- 16.7%, P<0.01), sVCAM (mean 69.6 +/- 14.0%, P<0.01), PAPP-A (mean 88.7 +/- 20.4%, P<0.01), ADMA (mean 69.7 +/- 18.4% P<0.01). In conclusion, we observed a transient decrease in the plasma concentrations of several biomarkers expressed during plaque destabilization and elevated cardiovascular risk after a single LA treatment. J. Clin. Apheresis 29:235-242, 2014. (c) 2013 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/jca.21311"],["dc.identifier.isi","000343831500001"],["dc.identifier.pmid","24281903"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32112"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1101"],["dc.relation.issn","0733-2459"],["dc.title","Lipoprotein Apheresis Reduces Biomarkers of Plaque Destabilization and Cardiovascular Risk"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2939"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Clinical Rheumatology"],["dc.bibliographiccitation.lastpage","2946"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Froelich, Britta"],["dc.contributor.author","Wallbach, Manuel"],["dc.contributor.author","Minguet, Joan"],["dc.contributor.author","Grupp, Clemens"],["dc.contributor.author","Deutsch, Cornelia"],["dc.contributor.author","Bramlage, Peter"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Mueller, Gerhard Anton"],["dc.date.accessioned","2018-11-07T10:05:16Z"],["dc.date.available","2018-11-07T10:05:16Z"],["dc.date.issued","2016"],["dc.description.abstract","In patients with rheumatic diseases, reliable markers for determining disease activity are scarce. One potential parameter is the level of immunoglobulin free light chains (FLCs), which is known to be elevated in the blood of patients with certain rheumatic diseases. Few studies have quantified FLCs in urine, a convenient source of test sample, in patients with different rheumatic diseases. We carried out a retrospective analysis of patients with rheumatic disease attending the University hospital of Goettingen, Germany. Subjects were included if they had urine levels of both kappa and lambda FLCs available and did not have myeloma. Data regarding systemic inflammation and kidney function were recorded, and FLC levels were correlated with inflammatory markers. Of the 382 patients with rheumatic disease, 40.1 % had chronic polyarthritis, 21.2 % connective tissue disease, 18.6 % spondyloarthritis and 15.7 % vasculitis. Elevated levels of kappa FLCs were found for 84 % of patients and elevated lambda for 52.7 %. For the patients with rheumatoid arthritis, FLCs correlated with C-reactive protein (kappa, r = 0.368, p < 0.001; lambda, r = 0.398, p < 0.001) and erythrocyte sedimentation rate (kappa, r = 0.692, p < 0.001; lambda, r = 0.612, p < 0.001). Patients being treated with rituximab displayed FLC levels similar to those of the reference group. There were clear elevations in both kappa and lambda FLCs in patients with rheumatic disease, but not in kappa/lambda ratio. The correlation between FLCs and inflammatory markers in patients with rheumatoid arthritis demonstrates their potential for predicting disease activity."],["dc.identifier.doi","10.1007/s10067-016-3437-0"],["dc.identifier.isi","000388826200010"],["dc.identifier.pmid","27734231"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38865"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","London"],["dc.relation.issn","1434-9949"],["dc.relation.issn","0770-3198"],["dc.title","The significance and predictive value of free light chains in the urine of patients with chronic inflammatory rheumatic disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","684"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","698"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Mueller, Gerhard-Anton"],["dc.contributor.author","Zapf, Antonia"],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Schmid, Holger"],["dc.contributor.author","Cohen, Clemens D."],["dc.contributor.author","Koschnick, Stefan"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Bramlage, Carsten"],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T08:45:39Z"],["dc.date.available","2018-11-07T08:45:39Z"],["dc.date.issued","2010"],["dc.description.abstract","Methods. Functional data were analysed in folic acid nephropathy (FAN) at different time points (up to day 142 after induction). Immunostaining for CX3C-L, CD3, S100A4, collagen type I, fibronectin, alpha-smooth muscle actin, Tamm-horsfall protein, aquaporin 1 and 2 as well as quantitative real-time PCR (qRT-PCR) for CX3C-L, CX3C-R and fibroblast-specific protein 1 (FSP-1) were performed. Additionally, regulatory mechanisms and functional activity of CX3C-L in murine proximal and distal tubular epithelial cells as well as in fibroblasts were investigated. Results. CX3C-L/GAPDH ratio was upregulated in FAN 3.4-fold at day 7 further increasing up to 7.1-fold at day 106. The expression of mRNA CX3C-L correlated well with CX3C-R (R-2 = 0.96), the number of infiltrating CD3+ cells (R-2 = 0.60) and the degree of tubulointerstitial fibrosis (R-2 = 0.56) and moderately with FSP-1 (R-2 = 0.33). Interleukin-1 beta, tumour necrosis factor-alpha, transforming growth factor-beta as well as the reactive oxygen species (ROS) H2O2 were identified by qRT-PCR as inductors of CX3C-L/fractalkine (FKN) in tubular epithelial cells. Functionally, CX3C-L/FKN chemoattracts peripheral blood mononuclear cells, activates several aspects of fibrogenesis and induces the mitogen-activated protein kinases in renal fibroblasts. Conclusions. In FAN, there is a good correlation between the expression of CX3C-L with markers of interstitial inflammation and fibrosis which may result from upregulation by pro-inflammatory and pro-fibrotic cytokines as well as by ROS in tubular epithelial cells. The FKN system may promote renal inflammation and renal fibrogenesis."],["dc.description.sponsorship","Georg-August-University"],["dc.identifier.doi","10.1093/ndt/gfp602"],["dc.identifier.isi","000274987800011"],["dc.identifier.pmid","19934081"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20497"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0931-0509"],["dc.title","Role of CX3C-chemokine CX3C-L/fractalkine expression in a model of slowly progressive renal failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]