Koziolek, Michael Johann

[["dc.bibliographiccitation.firstpage","222"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Therapeutic Apheresis and Dialysis"],["dc.bibliographiccitation.lastpage","225"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Fuezesi, Laszlo"],["dc.contributor.author","Koenig, Fatima"],["dc.contributor.author","Strutz, Frank M."],["dc.contributor.author","Mueller, Gerhard Anton"],["dc.date.accessioned","2018-11-07T08:44:57Z"],["dc.date.available","2018-11-07T08:44:57Z"],["dc.date.issued","2010"],["dc.description.abstract","We report a case of a 27-year-old female with thrombotic microangiopathy as an initial presentation of an unexpected disseminated gastric carcinoma. Based on clinical features and laboratory findings, thrombotic thrombocytopenic purpura (TTP) was diagnosed and plasma exchange started. However, she had responded poorly to plasmapheresis, developed multiorgan failure and died 72 h after admission. Autopsy revealed a disseminated gastric adenocarcinoma with metastatic infiltration of dura mater and disseminated tumor cell emboli in the microcirculation of the liver and lungs. Genetic analysis revealed amplification of KRAS oncogene and aberrations in DCC tumor suppressor gene, which can explain the young age and advanced disease at presentation. The role of plasmapheresis in cancer-associated TTP is uncertain. Plasmapheresis delivers fresh coagulation factors and may theoretically promote microthrombi formation and lead to worsening of the disease. Thrombotic thrombocytopenic purpura seems to be a late and prognostically poor manifestation of an underlying malignancy, with majority of patients dying soon after diagnosis. It is important to be aware of this possibility in thrombotic microangiopathy, especially with atypical features and poor response to standard treatment."],["dc.identifier.doi","10.1111/j.1744-9987.2009.00710.x"],["dc.identifier.isi","000276036600014"],["dc.identifier.pmid","20438546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20315"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","1744-9979"],["dc.title","Fulminant Plasmapheresis-refractory Thrombotic Microangiopathy Associated With Advanced Gastric Cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","314A"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","315A"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Blaschke, S."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T10:06:57Z"],["dc.date.available","2018-11-07T10:06:57Z"],["dc.date.issued","2002"],["dc.identifier.isi","000177757501553"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39194"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","1046-6673"],["dc.title","Role of fractalkine (CX3C-L) and its receptor (CX3C-R) in renal fibrogenesis."],["dc.type","conference_abstract"],["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.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Strutz, Frank M."],["dc.contributor.author","Sisic, Z."],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Kretzler, M."],["dc.date.accessioned","2018-11-07T10:07:16Z"],["dc.date.available","2018-11-07T10:07:16Z"],["dc.date.issued","2002"],["dc.format.extent","543A"],["dc.identifier.isi","000177757502666"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39243"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","1046-6673"],["dc.title","Integrin linked kinase (ILK) mediates epithelial-mesenchymal transformation in tubular epithelial cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","384"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","388"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Zipfel, Peter F."],["dc.contributor.author","Skerka, Christine"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Groene, Elisabeth F."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T11:12:37Z"],["dc.date.available","2018-11-07T11:12:37Z"],["dc.date.issued","2008"],["dc.description.abstract","A 36-year-old patient complained of progressing fatigue, lack of appetite, and weakness for a few weeks, for which he had been using paracetamol (acetaminophen) intermittently. He was referred to our center from another hospital with hemolysis, thrombocytopenia, and acute renal failure (ARF). On admission, the patient did not complain of any specific additional symptoms. Besides paracetamol, he had not received any other medication. The patient reported flu-like symptoms 3 months before admission. The family history was unremarkable. Physical examination revealed a pale-looking patient (180 cm; 81 kg) with icteric sclerae. He was tachycardic (110 heart beats per min) and had elevated blood pressure (155/90mmHg). No other physical abnormalities were detectable. Laboratory investigations are depicted in Table 1. Specific analyses: von Willebrand factor cleavage protease activity 31% (40-120%), von Willebrand Factor Multimere negative, antibodies to von Willebrand Factor cleavage protease negative, factor H 614 mgl(-1) (345-590 mgl(-1)). Western blot analyses with patient's serum revealed the presence of complement factor H (CFH) and complement factor H-like protein 1 (CFHL1), but no detectable levels of complement factor H-related proteins 1 and 3 (CFHR1 and CFHR3) (Figure 1a). Antibodies to CFHR1 were negative. Genetic analyses 1 showed no CFH mutation, but revealed homozygous deletion of a 83 kb genomic fragment representing CFHR3 and CFHR1 (Figure 1b). Kidneys were of normal size with increased density by ultrasound examination. Electrocardiography revealed ischemic changes posteroseptally, and hypertrophy of the left ventricle was diagnosed by echocardiography."],["dc.identifier.doi","10.1038/ki.2008.133"],["dc.identifier.isi","000257622900018"],["dc.identifier.pmid","18449173"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53705"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0085-2538"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Chronic course of a hemolytic uremic syndrome caused by a deficiency of factor H-related proteins (CFHR1 and CFHR3)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","96"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","109"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Heeg, MHJ"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Schaefer, L."],["dc.contributor.author","Sharma, K."],["dc.contributor.author","Mueller, Gerhard A."],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T09:23:04Z"],["dc.date.available","2018-11-07T09:23:04Z"],["dc.date.issued","2005"],["dc.description.abstract","Background. The peptide hormone relaxin has been demonstrated to exert antifibrotic effects in renal and extrarenal tissues. The aims of this study were to identify potential anti-fibrotic effects of relaxin on human renal fibroblasts in vitro and to analyze their mechanisms. Methods. All experiments were performed in established renal fibroblast cell lines and in primary cortical fibroblasts. Effects of relaxin were analyzed on cell proliferation, apoptosis, activation of renal fibroblasts, synthesis and secretion of collagen type I and fibronectin, as well as on the secretion of matrix metalloproteinases (MMPs). Effects on transforming growth factor-beta 1 (TGF-beta 1) receptor binding were analyzed by flow cytometry and on TGF-beta 1 signal transduction by immunoblot analyses for Smad4 and 7, translocation from cytosol to nucleus for Smad2 and 3 as well as for phosphorylated and unphosphorylated forms of p38, c-Jun NH2 terminal kinase (JNK) and extracellular-regulated protein kinase (ERK). Finally, specific siRNAs for Smad2 and 3 were applied to assess the signal transduction pathway. Results. After stimulation with relaxin, tyrosine phosphorylation of a 220 kD protein was demonstrated, indicating interaction with the receptor. Relaxin had only modest inhibitory effects on cell proliferation, and no effects on apoptosis. Conversely, relaxin exerted robust effects on TGF-beta 1-induced fibroblast to myofibroblast transformation as well as on matrix synthesis and secretion even at the smallest dose tested. The secretion of MMP-2 and MMP-9 was induced noticeably by all investigated relaxin concentrations. TGF-beta 1 receptor binding was not influenced by relaxin; however, it prevented Smad2 phosphorylation, translocation to nucleus, and complex formation between Smad2 and 3 indicating a possible interaction with TGF-beta 1 signaling. These findings were corroborated by studies using siRNAs to Smad2 and 3 where siRNA to Smad2 but not to Smad3 inhibited the TGF-beta 1 induction of fibronectin synthesis. There was no influence of relaxin on intracellular Smad3, Smad4, and Smad7 translocation or phosphorylation of mitogen-activated protein (MAP) kinases. Conclusion. Relaxin is a potent inhibitor of TGF-beta 1-induced extracellular matrix (ECM) synthesis and secretion as well as fibroblast activation. Furthermore, it induces ECM degradation by induction of MMP-2 and MMP-9. These effects are mediated, at least in part, by inhibition of TGF-beta 1 signaling."],["dc.identifier.doi","10.1111/j.1523-1755.2005.00384.x"],["dc.identifier.isi","000229636800009"],["dc.identifier.pmid","15954899"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29491"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing Inc"],["dc.relation.issn","0085-2538"],["dc.title","The antifibrotic effects of relaxin in human renal fibroblasts are mediated in part by inhibition of the Smad2 pathway"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","51"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","52"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Kurz, Bernd"],["dc.contributor.author","Mueller, Gerhard Anton"],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T09:38:39Z"],["dc.date.available","2018-11-07T09:38:39Z"],["dc.date.issued","2006"],["dc.identifier.isi","000239919000138"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33113"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Glasgow, SCOTLAND"],["dc.relation.issn","0931-0509"],["dc.title","Hyperglycemia induces the expression of basic fibroblast growth factor (FGF-2) through activation of the protein kinase C beta-1 and p65 nf-kappa b in human renal fibroblasts"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1575"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","1578"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Strutz, Frank M."],["dc.contributor.author","Scheel, A."],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Kochsiek, T."],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Mueller, Gerhard A."],["dc.date.accessioned","2018-11-07T10:34:23Z"],["dc.date.available","2018-11-07T10:34:23Z"],["dc.date.issued","2003"],["dc.description.abstract","When confronted by the combination of initial high fever associated with intense malaise, splenomegaly, elevated levels of transaminases, and acute renal failure, consideration must be given to the differential diagnosis of leptospirosis even in Germany. As a rule, the diagnosis is confirmed by serological testing based on the titer curve. Renal involvement is frequent, but usually has a good prognosis, especially if jaundice has not developed. Treatment with doxycycline or penicillin can shorten the disease course and exudation, possibly also the nephritis, or hinder it."],["dc.identifier.doi","10.1007/s00108-003-1090-6"],["dc.identifier.isi","000186903900012"],["dc.identifier.pmid","14689199"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44860"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0020-9554"],["dc.title","\"Idiosyncratic infection\" accompanied by fever, splenomegaly, and acute renal failure in a 24-year-old forestry student"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]