Michel, Uwe

[["dc.bibliographiccitation.firstpage","559"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Journal of Endocrinology"],["dc.bibliographiccitation.lastpage","564"],["dc.bibliographiccitation.volume","148"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Phillips, D."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2018-11-07T10:39:07Z"],["dc.date.available","2018-11-07T10:39:07Z"],["dc.date.issued","2003"],["dc.description.abstract","Objective: Activin is a growth and differentiation factor of many cell types, and has recently been implicated in inflammatory processes. Clinical data linking activin and its binding protein, follistatin (FS), are lacking. We measured serum levels of activin and FS in patients diagnosed with septicemia. Patients and measurements: Eight male and seven female patients of different ages, various forms of septicemia and different clinical outcome were investigated and compared with age- and sex-matched healthy controls. Serum concentrations of FS, activin, C-reactive protein (CRP) and blood leukocyte counts were determined during septicemia. Results: The median of the maximum activin concentrations of septicemic patients was 3.9-fold higher than in age- and sex-matched healthy control subjects (P < 0.01); the median of the maximum FS concentrations was 2.6-fold higher (P < 0.01). The highest increase of activin in septicemic patients was approximately 15.8-fold, whereas FS increased by up to 13.2-fold above normal. FS, activin and CRP serum levels generally paralleled each other, but were not correlated with leukocyte counts or clinical outcome. Conclusions: Circulatory concentrations of activin and FS are elevated in patients diagnosed with septicemia, consistent with potential roles in the systemic inflammatory response."],["dc.identifier.doi","10.1530/eje.0.1480559"],["dc.identifier.isi","000182915600012"],["dc.identifier.pmid","12720540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45971"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bio Scientifica Ltd"],["dc.relation.issn","0804-4643"],["dc.title","Serum concentrations of activin and follistatin are elevated and run in parallel in patients with septicemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","307"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","312"],["dc.bibliographiccitation.volume","326"],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Malik, I."],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kugler, S."],["dc.date.accessioned","2017-09-07T11:43:04Z"],["dc.date.available","2017-09-07T11:43:04Z"],["dc.date.issued","2005"],["dc.description.abstract","Viral vector-based expression of small interfering RNAs is a promising tool for gene regulation, both in cultured cells and in animal models. In this study, we analysed the ability of adeno-associated virus-2 to function as an RNAi vector in cultured primary hippocampal neurons in vitro and in retinal ganglion cells in vivo. We demonstrate a long-lasting, highly efficient, and specific down-regulation of gene expression in vivo and in vitro by the use of bicistronic vectors. This is the first evidence of a cell type-specific long-term (more than three-month-long) RNAi in the eye. Furthermore, our results constitute the prerequisite for the use of this technique in models of neurodegeneration and neuroregeneration in vivo and in vitro. (C) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.bbrc.2004.11.029"],["dc.identifier.gro","3143904"],["dc.identifier.isi","000225997300007"],["dc.identifier.pmid","15582578"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1470"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0006-291X"],["dc.title","Long-term in vivo and in vitro AAV-2-mediated RNA interference in rat retinal ganglion cells and cultured primary neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","241"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","244"],["dc.bibliographiccitation.volume","413"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Zeretzke, Moritz"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Michel, Uwe"],["dc.date.accessioned","2018-11-07T11:04:54Z"],["dc.date.available","2018-11-07T11:04:54Z"],["dc.date.issued","2007"],["dc.description.abstract","Activin A levels are elevated in the cerebrospinal fluid (CSF) of patients with meningitis and in the sera of patients with sepsis. The source(s) of the elevated concentrations of activin A in CSF and serum have not yet been discovered. Here we demonstrate that primary mouse microglial cells and peritoneal macrophages release activin A after treatment with agonists of Toll-like receptor (TLR) 2, 4, and 9. These findings provide further evidence for a role of activin in the innate immune response and suggest that microglial cells and macrophages are a source of elevated activin A concentrations observed in the CSF during bacterial meningitis and in the systemic circulation during sepsis. (c) 2006 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2006.11.065"],["dc.identifier.isi","000244763800013"],["dc.identifier.pmid","17194540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51950"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Microglial cells and peritoneal macrophages release activin A upon stimulation with Toll-like receptor agonists"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","673"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Immunotherapy"],["dc.bibliographiccitation.lastpage","684"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Michel, Uwe"],["dc.date.accessioned","2018-11-07T08:39:43Z"],["dc.date.available","2018-11-07T08:39:43Z"],["dc.date.issued","2010"],["dc.description.abstract","Severe bacterial infections such as sepsis and meningitis still kill or severely injure people despite the use of bactericidal antibiotics. Therefore, new strategies for a better therapy are needed. Activin A, a member of the TGF-beta superfamily and its binding protein follistatin (FS) are released by various cell types during acute and chronic inflammatory processes. Until now, a clear definition of conditions in which activin A exerts either its pro- or anti-inflammatory functions is lacking. The activin/FS-system participates in the fine-tuning of the host's inflammatory response upon infectious stimuli. This response is on the one hand necessary for fighting pathogens, but on the other hand can negatively affect the host. This article focuses on the role of activin A and FS in infection and after acute inflammatory stimuli. The therapeutic potentials of blocking or promoting activin actions are discussed."],["dc.identifier.doi","10.2217/IMT.10.64"],["dc.identifier.isi","000282617100013"],["dc.identifier.pmid","20874651"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19066"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Future Medicine Ltd"],["dc.relation.issn","1750-743X"],["dc.title","Role of activin in bacterial infections: a potential target for immunointervention?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S198"],["dc.bibliographiccitation.journal","Inflammation Research"],["dc.bibliographiccitation.lastpage","S199"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Phillips, David J."],["dc.contributor.author","Jenzewski, Peter"],["dc.contributor.author","O'Connor, Anne E."],["dc.contributor.author","Michel, Uwe"],["dc.date.accessioned","2018-11-07T09:42:20Z"],["dc.date.available","2018-11-07T09:42:20Z"],["dc.date.issued","2005"],["dc.identifier.isi","000205501600369"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33934"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Birkhauser Verlag Ag"],["dc.publisher.place","Basel"],["dc.relation.issn","1023-3830"],["dc.title","Activin A in cerebrospinal fluid is elevated in patients with meningitis or cerebral haemorrhages"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","178"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Nau, R."],["dc.contributor.author","Michel, Uwe"],["dc.date.accessioned","2018-11-07T09:21:09Z"],["dc.date.available","2018-11-07T09:21:09Z"],["dc.date.issued","2006"],["dc.format.extent","134"],["dc.identifier.isi","000241633101005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29047"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","8th International Conference of Neuroimmunology"],["dc.relation.eventlocation","Nagoya, JAPAN"],["dc.relation.issn","0165-5728"],["dc.title","Release of activin A by microglial cells upon stimulation with bacterial TLR-agonists"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","349"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","353"],["dc.bibliographiccitation.volume","384"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Dietz, Gunnar P. H."],["dc.contributor.author","Mitchell, T. J."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2017-09-07T11:54:17Z"],["dc.date.available","2017-09-07T11:54:17Z"],["dc.date.issued","2005"],["dc.description.abstract","Severe brain damage in patients with pneumococcal meninigits is in part caused by the cytosolic pneumococcal protein pneumolysin. The devastating effect of this neurotoxin might be alleviated by interfering with the cell death pathways that it sets in motion. An important player in these pathways is Bcl-X-L, an antiapoptotic protein of the Bcl-2 family, which is neuroprotective in various in vitro and in vivo models of cell death. We investigated whether its membrane-permeable form, the TAT-Bcl-X-L fusion protein, is capable of protecting human SH-SY5Y neuroblastoma cells against pneumolysin-induced cell death. Under mild pneumolysin-induced neuronal injury, TAT-Bcl-X-L increased cell viability significantly by approximately 40% (82.7 +/- 16.1% versus 70.0 +/- 8.2%; p = 0.04). When the cells were exposed to a more rigorous pneumolysin treatment, TAT-Bcl-X-L had no protective effects. This suggests the involvement of additional neuronal death pathways in pneumolysin-induced cell death, which are not controlled by Bcl-X-L. Therefore, BCI-X-L, a promising therapeutic candidate for ischemia and neurodegenerative diseases, is only of partial efficacy in preventing the direct neurotoxicity of pneumolysin. (c) 2005 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2005.05.027"],["dc.identifier.gro","3143814"],["dc.identifier.isi","000230463700028"],["dc.identifier.pmid","15961228"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1370"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0304-3940"],["dc.title","Limited protection of TAT-Bcl-X-L against pneumolysin-induced neuronal cell death"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","50"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","57"],["dc.bibliographiccitation.volume","250"],["dc.contributor.author","Ebert, Sandra"],["dc.contributor.author","Phillips, David J."],["dc.contributor.author","Jenzewski, Peter"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","O'Connor, Anne E."],["dc.contributor.author","Michel, Uwe"],["dc.date.accessioned","2018-11-07T08:54:46Z"],["dc.date.available","2018-11-07T08:54:46Z"],["dc.date.issued","2006"],["dc.description.abstract","Objective: Activin A, and its binding protein, follistatin (FS), are expressed in the central nervous system (CNS). We have previously shown elevated concentrations of FS in the cerebrospinal fluid (CSF) of patients with meningitis and increased concentrations of activin A in the CSF of rabbits with bacterial meningitis. Methods: We measured CSF and serum concentrations of activin A and FS in normal subjects and in patients with various neurological diseases using previously validated immunoassays specific for activin A or FS. Results: In healthy persons, serum concentrations of both activin A and FS were age-dependent. In CSF, concentrations of activin A ranged from 0.03 to 0.33 ng/ml and were strongly correlated with age in both sexes, whereas FS CSF concentrations were below the assay detection limit in most of the patients. Activin A concentrations in CSF of patients with various neurological diseases, including meningitis, chronic inflammatory CNS diseases, neurodegenerative diseases, tumors in the CNS, cerebral ischemia, intracerebral/subarachnoid hemorrhages, subdural hemorrhages and epileptic seizures, were compared with age- and sex-matched control patients. The comparisons revealed significantly elevated concentrations of activin A in patients with meningitis (P=0.017). Serum concentrations of activin A or FS were not affected by any of the neurological diseases examined. Conclusions: Our results show for the first time that in normal subjects concentrations of activin A in CSF are correlated with age, and furthermore, that activin A CSF concentrations are elevated in patients with meningitis. The latter underlines a role for activin A in acute inflammatory processes within the CNS. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2006.06.026"],["dc.identifier.isi","000242471500009"],["dc.identifier.pmid","16920154"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22746"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0022-510X"],["dc.title","Activin A concentrations in human cerebrospinal fluid are age-dependent and elevated in meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]