Trendelenburg, George

[["dc.bibliographiccitation.artnumber","e0148428"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Andresen, Lena"],["dc.contributor.author","Theodorou, Konstantina"],["dc.contributor.author","Gruenewald, Sarah"],["dc.contributor.author","Czech-Zechmeister, Bozena"],["dc.contributor.author","Koennecke, Birte"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T10:18:18Z"],["dc.date.available","2018-11-07T10:18:18Z"],["dc.date.issued","2016"],["dc.description.abstract","Toll-like receptors (TLRs) are central sensors for the inflammatory response in ischemia-reperfusion injury. We therefore investigated whether TLR4 inhibition could be used to treat stroke in a standard model of focal cerebral ischemia. Anti-TLR4/MD2-antibody (mAb clone MTS510) blocked TLR4-induced cell activation in vitro, as reported previously. Here, different routes of MTS510 application in vivo were used to study the effects on stroke outcome up to 2d after occlusion of the middle cerebral artery (MCAO) for 45min in adult male C57Bl/6 wild-type mice. Improved neurological performance, reduced infarct volumes, and reduced brain swelling showed that intravascular application of MTS510 had a protective effect in the model of 45min MCAO. Evaluation of potential long-term adverse effects of anti-TLR4-mAb-treament revealed no significant deleterious effect on infarct volumes nor neurological deficit after 14d of reperfusion in a mild model of stroke (15min MCAO). Interestingly, inhibition of TLR4 resulted in an altered adaptive immune response at 48 hours after reperfusion. We conclude that blocking TLR4 by the use of specific mAb is a promising strategy for stroke therapy. However, long-term studies with increased functional sensitivity, larger sampling sizes and use of other species are required before a clinical use could be envisaged."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pone.0148428"],["dc.identifier.isi","000369554000092"],["dc.identifier.pmid","26849209"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12842"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41412"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Evaluation of the Therapeutic Potential of Anti-TLR4-Antibody MTS510 in Experimental Stroke and Significance of Different Routes of Application"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","923"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","924"],["dc.bibliographiccitation.volume","260"],["dc.contributor.author","Witsch, Jens"],["dc.contributor.author","Bohner, Georg"],["dc.contributor.author","Rech, Juergen"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T09:27:40Z"],["dc.date.available","2018-11-07T09:27:40Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1007/s00415-012-6813-y"],["dc.identifier.isi","000316071400029"],["dc.identifier.pmid","23292206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30591"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.title","Perivascular white matter lesion pattern in a patient with steroid-responsive encephalopathy"],["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","2080"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow & Metabolism"],["dc.bibliographiccitation.lastpage","2088"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Krey, Lea"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Czech-Zechmeister, Bozena"],["dc.contributor.author","Koennecke, Birte"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T09:48:30Z"],["dc.date.available","2018-11-07T09:48:30Z"],["dc.date.issued","2015"],["dc.description.abstract","Sirtuin-2 (Sirt2) is a member of the NAD+-dependent protein deacetylase family. Various members of the sirtuin class have been found to be involved in processes related to longevity, regulation of inflammation, and neuroprotection. Induction of Sirt2 mRNA was found in the whole hemisphere after experimental stroke in a recent screening approach. Moreover, Sirt2 protein is highly expressed in myelin-rich brain regions after stroke. To examine the effects of Sirt2 on ischemic stroke, we induced transient focal cerebral ischemia in adult male Sirt2-knockout and wild-type mice. Two stroke models with different occlusion times were applied: a severe ischemia (45 minutes of middle cerebral artery occlusion (MCAO)) and a mild one (15 minutes of MCAO), which was used to focus on subcortical infarcts. Neurological deficit was determined at 48 hours after 45 minutes of MCAO, and up to 7 days after induction of 15 minutes of cerebral ischemia. In contrast to recent data on Sirt1, Sirt2(-/-) mice showed less neurological deficits in both models of experimental stroke, with the strongest manifestation after 48 hours of reperfusion. However, we did not observe a significant difference of stroke volumes or inflammatory cell count between Sirt2-deficient and wild-type mice. Thus we postulate that Sirt2 mediates myelin-dependent neuronal dysfunction during the early phase after ischemic stroke."],["dc.identifier.doi","10.1038/jcbfm.2015.178"],["dc.identifier.isi","000365891300020"],["dc.identifier.pmid","26219598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35322"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1559-7016"],["dc.relation.issn","0271-678X"],["dc.title","Knockout of silent information regulator 2 (SIRT2) preserves neurological function after experimental stroke in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","908"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Archives of Neurology"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Trendelenburg, George"],["dc.contributor.author","Zimmer, Claus"],["dc.contributor.author","Forschler, Annette"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Zschenderlein, Rolf"],["dc.date.accessioned","2022-03-01T11:43:38Z"],["dc.date.available","2022-03-01T11:43:38Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1001/archneur.63.6.908"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102798"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0003-9942"],["dc.title","Atypical Appearance of a Primary Central Nervous System Lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","721"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neural Regeneration Research"],["dc.bibliographiccitation.lastpage","722"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Eidizadeh, Abass"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T10:14:37Z"],["dc.date.available","2018-11-07T10:14:37Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.4103/1673-5374.182689"],["dc.identifier.isi","000378537700010"],["dc.identifier.pmid","27335546"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13731"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40649"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Medknow Publications & Media Pvt Ltd"],["dc.relation.issn","1876-7958"],["dc.relation.issn","1673-5374"],["dc.rights","CC BY-NC-SA 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/3.0"],["dc.title","Focusing on the protective effects of metallothionein-I/II in cerebral ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1547"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","1548"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Osthoff, Michael"],["dc.contributor.author","Trendelenburg, George"],["dc.contributor.author","Eisen, Damon P."],["dc.contributor.author","Trendelenburg, Marten"],["dc.date.accessioned","2018-11-07T08:49:25Z"],["dc.date.available","2018-11-07T08:49:25Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1038/nm.2588"],["dc.identifier.isi","000297978000015"],["dc.identifier.pmid","22146452"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21453"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1078-8956"],["dc.title","Mannose-binding lectin-the forgotten molecule?"],["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","4504"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","4516"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Langenkamp, Elise"],["dc.contributor.author","Zhang, Lei"],["dc.contributor.author","Lugano, Roberta"],["dc.contributor.author","Huang, Hua"],["dc.contributor.author","Elhassan, Tamador Elsir Abu"],["dc.contributor.author","Georganaki, Maria"],["dc.contributor.author","Bazzar, Wesam"],["dc.contributor.author","Lööf, Johan"],["dc.contributor.author","Trendelenburg, George"],["dc.contributor.author","Dimberg, Anna"],["dc.date.accessioned","2021-06-01T10:47:45Z"],["dc.date.available","2021-06-01T10:47:45Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1158/0008-5472.CAN-14-3636"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85704"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Elevated Expression of the C-Type Lectin CD93 in the Glioblastoma Vasculature Regulates Cytoskeletal Rearrangements That Enhance Vessel Function and Reduce Host Survival"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0144035"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Eidizadeh, Abass"],["dc.contributor.author","Khajehalichalehshtari, Manuel"],["dc.contributor.author","Freyer, Dorette"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T09:47:32Z"],["dc.date.available","2018-11-07T09:47:32Z"],["dc.date.issued","2015"],["dc.description.abstract","Metallothionein-II (MT-II) is an ubiquitously expressed small-molecular-weight protein and highly induced in various species and tissues upon stress, inflammation, and ischemia. MT-deficiency exacerbates ischemic injury in rodent stroke models in vitro and in vivo. However, there is conflicting data on the potential neuroprotective effect of exogenously applied metallothionein. Thus, we applied MT-II in an in vitro stroke model and intraperitoneally (i.p.) in two in vivo standard models of transient middle cerebral artery occlusion (MCAO) (a 'stringent' one [ 60min MCAO/48h reperfusion] and a 'mild' one [30min MCAO/72h reperfusion]), as well as i.v. together with recombinant tissue plasminogen activator (rtPA) to evaluate if exogenous MT-II-application protects against ischemic stroke. Whereas MT-II did not protect against 60min MCAO, there was a significant reduction of direct and indirect infarct volumes and neurological deficit in the MT-II (i.p.) treated animals in the 'mild' model at 3d after MCAO. Furthermore, MT-II also improved survival of the mice after MCAO, suppressed TNF-alpha mRNA induction in ischemic brain tissue, and protected primary neuronal cells against oxygen-glucose-deprivation in vitro. Thus, exogenous application of MT-II protects against ischemic injury in vitro and in vivo. However, long-term studies with different species and larger sampling sizes are required before a clinical use can be envisaged."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1371/journal.pone.0144035"],["dc.identifier.isi","000366715900023"],["dc.identifier.pmid","26658636"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35134"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Assessment of the Therapeutic Potential of Metallothionein-II Application in Focal Cerebral Ischemia In Vitro and In Vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1857"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow & Metabolism"],["dc.bibliographiccitation.lastpage","1867"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T09:32:09Z"],["dc.date.available","2018-11-07T09:32:09Z"],["dc.date.issued","2014"],["dc.description.abstract","Analogous to Toll-like receptors, NOD-like receptors represent a class of pattern recognition receptors, which are cytosolic and constitute part of different inflammasomes. These large protein complexes are activated not only by different Pathogens, but also by sterile inflammation or by specific metabolic conditions. Mutations can cause hereditary autoinflammatory systemic diseases, and inflammasome activation has been linked to many multifactorial diseases, such as diabetes or cardiovascular diseases. Increasing data also support an important role in different central nervous diseases such as stroke. Thus, the current knowledge of the functional role of this intracellular 'master switch' of inflammation is discussed with a focus on its role in ischemic stroke, neurodegeneration, and also with regard to the recent data which argues for a relevant role in other organs or biologic systems which influence stroke incidence or prognosis."],["dc.identifier.doi","10.1038/jcbfm.2014.159"],["dc.identifier.isi","000345814200001"],["dc.identifier.pmid","25227604"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31683"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1559-7016"],["dc.relation.issn","0271-678X"],["dc.title","Molecular regulation of cell fate in cerebral ischemia: role of the inflammasome and connected pathways"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","672"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Pathogens"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Bannasch, Johannes H."],["dc.contributor.author","Berger, Benjamin"],["dc.contributor.author","Schwartkop, Claus-Peter"],["dc.contributor.author","Berning, Marco"],["dc.contributor.author","Goetze, Oliver"],["dc.contributor.author","Panning, Marcus"],["dc.contributor.author","Fritz-Weltin, Miriam"],["dc.contributor.author","Trendelenburg, George"],["dc.contributor.author","Gelderblom, Mathias"],["dc.contributor.author","Pischke, Sven"],["dc.date.accessioned","2021-08-12T07:46:03Z"],["dc.date.available","2021-08-12T07:46:03Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Neuralgic amyotrophy (NA) has been described as a possible extrahepatic manifestation of hepatitis E virus (HEV) infection. Usually, HEV-associated NA occurs bilaterally. The clinical characteristics determining the course of HEV-associated NA have still not been defined. Methods: In this retrospective multicentric case series, 16 patients with HEV-associated NA were studied and compared to 176 HEV patients without NA in terms of their age, sex, and ALT levels. Results: Neither gender distribution (75% vs. 67% male) nor age (47 vs. 48 years median) differed significantly between the NA patients and controls. Eight NA patients (50%) presented with bilateral involvement—seven of these had right-side dominance and one had left-side dominance. Thirteen cases (81%) were hospitalized. Eight of these patients stayed in hospital for five to seven days, and five patients stayed for up to two weeks. The time from the onset of NA to the HEV diagnosis, as well as the diagnostic and therapeutic proceedings, showed a large variability. In total, 13 (81%) patients received treatment: 1/13 (8%) received intravenous immunoglobulins, 8/13 (62%) received glucocorticoids, 3/13 (23%) received ribavirin, and 6/13 (46%) received pregabalin/gabapentin. Patients with ages above the median (47 years) were more likely to be treated (p = 0.001). Conclusion: HEV-associated NA causes a relevant morbidity. In our case series neither the type of treatment nor the time of initiation of therapy had a significant effect on the duration of hospitalization or the course of the disease. The clinical presentation, the common diagnostic and therapeutic procedures, and the patients’ characteristics showed large variability, demonstrating the necessity of standardized protocols for this rare but relevant disease."],["dc.description.abstract","Background: Neuralgic amyotrophy (NA) has been described as a possible extrahepatic manifestation of hepatitis E virus (HEV) infection. Usually, HEV-associated NA occurs bilaterally. The clinical characteristics determining the course of HEV-associated NA have still not been defined. Methods: In this retrospective multicentric case series, 16 patients with HEV-associated NA were studied and compared to 176 HEV patients without NA in terms of their age, sex, and ALT levels. Results: Neither gender distribution (75% vs. 67% male) nor age (47 vs. 48 years median) differed significantly between the NA patients and controls. Eight NA patients (50%) presented with bilateral involvement—seven of these had right-side dominance and one had left-side dominance. Thirteen cases (81%) were hospitalized. Eight of these patients stayed in hospital for five to seven days, and five patients stayed for up to two weeks. The time from the onset of NA to the HEV diagnosis, as well as the diagnostic and therapeutic proceedings, showed a large variability. In total, 13 (81%) patients received treatment: 1/13 (8%) received intravenous immunoglobulins, 8/13 (62%) received glucocorticoids, 3/13 (23%) received ribavirin, and 6/13 (46%) received pregabalin/gabapentin. Patients with ages above the median (47 years) were more likely to be treated (p = 0.001). Conclusion: HEV-associated NA causes a relevant morbidity. In our case series neither the type of treatment nor the time of initiation of therapy had a significant effect on the duration of hospitalization or the course of the disease. The clinical presentation, the common diagnostic and therapeutic procedures, and the patients’ characteristics showed large variability, demonstrating the necessity of standardized protocols for this rare but relevant disease."],["dc.identifier.doi","10.3390/pathogens10060672"],["dc.identifier.pii","pathogens10060672"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88608"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","2076-0817"],["dc.title","HEV-Associated Neuralgic Amyotrophy: A Multicentric Case Series"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]