Diem, Ricarda

[["dc.bibliographiccitation.firstpage","1770"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","1781"],["dc.bibliographiccitation.volume","178"],["dc.contributor.author","Rau, C. R."],["dc.contributor.author","Hein, K."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Kretzschmar, B."],["dc.contributor.author","Hillgruber, C."],["dc.contributor.author","Mcrae, B. L."],["dc.contributor.author","Diem, R."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:44:17Z"],["dc.date.available","2017-09-07T11:44:17Z"],["dc.date.issued","2011"],["dc.description.abstract","In multiple sclerosis, long-term disability is caused by axonal and neuronal damage. Established therapies target primarily the inflammatory component of the disease, but fail to prevent neurodegeneration. Fingolimod (codenamed FTY720) is an oral sphingosine 1-phosphate (S1P) receptor modulator with promising results in phase II trials in multiple sclerosis patients and is under further development as a novel treatment for multiple sclerosis. To evaluate whether FTY720 has neuroprotective properties, we tested this drug in a rat model of myelin oligodendrocyte glycoprotein-induced optic neuritis. FTY720 exerted significant anti-inflammatory effects during optic neuritis and reduced inflammation, demyelination, and axonal damage; however, FTY720 treatment did not prevent apoptosis of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve. Consistent with this lack of effect on RGC survival, FTY720 treatment did not improve visual function, nor did it prevent apoptosis of RGCs in vitro. We observed a persistent activation of apoptotic signaling pathways in RGCs under FTY720 treatment, a possible underlying mechanism for the lack of neuroprotection in the presence of strong anti-inflammatory effects, Furthermore, FTY720 shifted the remaining inflammation in the optic nerve toward neurotoxicity by modest up-regulation of potential neurotoxic cytokines. We conclude that FTY720-induced anti-inflammation and axon protection did not of itself protect neurons from apoptotic cell death. (Am J Pathol 2011, 178:1770-1781; DOI: 10.1016/j.ajpath.2011.01.003)"],["dc.identifier.doi","10.1016/j.ajpath.2011.01.003"],["dc.identifier.gro","3142743"],["dc.identifier.isi","000298306700034"],["dc.identifier.pmid","21406175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/181"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: European Union [LSHM-CT-2005-018637]; Abbott USA"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0002-9440"],["dc.title","Anti-Inflammatory Effects of FTY720 Do Not Prevent Neuronal Cell Loss in a Rat Model of Optic Neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Hein, Katharina"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Saettler, Muriel B."],["dc.contributor.author","Kretzschmar, Benedikt"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Baehr, Mathias"],["dc.date.accessioned","2018-11-07T08:36:54Z"],["dc.date.available","2018-11-07T08:36:54Z"],["dc.date.issued","2010"],["dc.identifier.isi","000283694400499"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18417"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Sitges, SPAIN"],["dc.title","Monitoring of degeneration of the retinal nerve fiber layer by optical coherence tomography in rats with autoimmune optic neuritis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","715"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Fortschritte der Neurologie · Psychiatrie"],["dc.bibliographiccitation.lastpage","727"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Linker, R. A."],["dc.contributor.author","Stadelmann, C."],["dc.contributor.author","Diem, R."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Brück, W."],["dc.contributor.author","Gold, R."],["dc.date.accessioned","2017-09-07T11:53:40Z"],["dc.date.available","2017-09-07T11:53:40Z"],["dc.date.issued","2005"],["dc.description.abstract","In this article, recent advances in the research on pathogenesis and therapy of multiple sclerosis (MS) will be summarized. New evidence from clinical studies, imaging, histopathology and experimental models are discussed with a focus on neurodegenerative aspects and evidence from recent therapeutic studies. During the last decade, important advances in immunotherapy have been achieved, which proved especially useful for patients with relapsing remitting MS. The introduction of interferons and glatiramer acetate into MS therapy often leads to a stabilization of the disease course if administered adequately and early. The pathogenetic insights presented here may open new avenues for innovative immunodulatory approaches and lead to an individualized MS therapy in the future. Neuroprotective treatment strategies aim at the protection of glial and neuronal cells."],["dc.description.abstract","In dieser Übersichtsarbeit stellen wir die in den letzten Jahren erzielten Fortschritte bei der Erforschung der Multiplen Sklerose dar und diskutieren sie kritisch. Aus klinischen, bildgebenden, pathologischen, immunologischen und tierexperimentellen Studien resultierten neue Erkenntnisse zur Pathogenese und Therapie der MS. Schwerpunkte liegen insbesondere auf neurodegenerativen Aspekten der Erkrankung sowie auf therapierelevanten Befunden, die bereits zu einer deutlichen Verbesserung der Immuntherapie im letzten Jahrzehnt führten. Vor allem bei der schubförmig verlaufenden MS kann seit der Einführung der Immunmodulation mit Interferonen und Glatiramerazetat in vielen Fällen die Krankheit durch adäquate und frühe Behandlung langfristig stabilisiert werden. In naher Zukunft sind neue Immuntherapeutika, aber wahrscheinlich auch individualisierte Behandlungsansätze zu erwarten. Die weitere Entwicklung neurobiologisch-protektiver Strategien soll gezielt das Überleben von Glia- und Nervenzellen fördern."],["dc.identifier.doi","10.1055/s-2004-830256"],["dc.identifier.gro","3143783"],["dc.identifier.isi","000234046600002"],["dc.identifier.pmid","16355314"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1335"],["dc.language.iso","de"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0720-4299"],["dc.title","Recent advances in pathogenesis and therapy of multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","163"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","171"],["dc.bibliographiccitation.volume","193"],["dc.contributor.author","Sattler, Michael"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Boger, I."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:54:30Z"],["dc.date.available","2017-09-07T11:54:30Z"],["dc.date.issued","2005"],["dc.description.abstract","In patients with multiple sclerosis (MS), non-remitting deficits are mainly caused by axonal and neuronal damage. We demonstrated previously that myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis in rats provokes severe axonal and neuronal injury even before clinical manifestation of the disease. In our present study, we investigated effects of simvastatin treatment on degeneration of retinal ganglion cell (RGC) bodies as well as their axons during MOG-induced optic neuritis. Electrophysiological functions of optic nerves and RGCs were analyzed in vivo. Although neuroprotective effects of simvastatin have been demonstrated before in other experimental settings, we did not observe an increase in RGC survival nor an improvement of visual functions. As we could not reproduce the anti-inflammatory effects that were observed under statin therapy in other EAE models, we hypothesize that patients suffering from optic neuritis might not take advantage of simvastatin applications. (c) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2004.12.010"],["dc.identifier.gro","3143859"],["dc.identifier.isi","000228413300016"],["dc.identifier.pmid","15817275"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1419"],["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","0014-4886"],["dc.title","Simvastatin treatment does not protect retinal ganglion cells from degeneration in a rat model of autoimmune optic neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6993"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","7000"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Hobom, M."],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Weissert, Robert"],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Meyer, Ralf"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:44:18Z"],["dc.date.available","2017-09-07T11:44:18Z"],["dc.date.issued","2003"],["dc.description.abstract","Optic neuritis is one of the most common clinical manifestations of multiple sclerosis ( MS), a chronic inflammatory disease of the CNS. High-dosage methylprednisolone treatment has been established as the standard therapy of acute inflammation of the optic nerve ( ON). The rationale for corticosteroid treatment lies in the antiinflammatory and immunosuppressive properties of these drugs, as shown in experimental autoimmune encephalomyelitis (EAE), the animal model of MS. To investigate the influence of methylprednisolone therapy on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the ON, we used a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced EAE. Optic neuritis was diagnosed by recording visual evoked potentials, and RGC function was monitored by measuring electroretinograms. Methylprednisolone treatment significantly increased RGC apoptosis during MOG-EAE. By Western blot analysis, we identified the underlying molecular mechanism: a suppression of mitogen-activated protein kinase ( MAPK) phosphorylation, which is a key event in an endogenous neuroprotective pathway. The methylprednisolone-induced inhibition of MAPK phosphorylation was calcium dependent. Hence, we provide evidence for negative effects of steroid treatment on neuronal survival during chronic inflammatory autoimmune disease of the CNS, which should result in a reevaluation of the current therapy regimen."],["dc.identifier.gro","3144072"],["dc.identifier.isi","000184587100004"],["dc.identifier.pmid","12904460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1655"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Methylprednisolone increases neuronal apoptosis during autoimmune CNS inflammation by inhibition of an endogenous neuroprotective pathway"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","154"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Hobom, M."],["dc.contributor.author","Bahr, M."],["dc.date.accessioned","2018-11-07T10:46:04Z"],["dc.date.available","2018-11-07T10:46:04Z"],["dc.date.issued","2004"],["dc.format.extent","200"],["dc.identifier.isi","000224003200663"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47660"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","7th International Congress of the International-Society-of-Neuroimmunology"],["dc.relation.eventlocation","Venice, ITALY"],["dc.relation.issn","0165-5728"],["dc.title","Neuroprotection in multiple sclerosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","199"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","210"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Sühs, K.-W."],["dc.contributor.author","Hein, K."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Görlitz, A."],["dc.contributor.author","Ciupka, C."],["dc.contributor.author","Scholz, K."],["dc.contributor.author","Käsmann-Kellner, B."],["dc.contributor.author","Papanagiotou, P."],["dc.contributor.author","Schäffler, N."],["dc.contributor.author","Restemeyer, C."],["dc.contributor.author","Bittersohl, D."],["dc.contributor.author","Hassenstein, A."],["dc.contributor.author","Seitz, B."],["dc.contributor.author","Reith, W."],["dc.contributor.author","Fassbender, K."],["dc.contributor.author","Hilgers, R."],["dc.contributor.author","Heesen, C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Diem, R."],["dc.date.accessioned","2017-09-07T11:48:29Z"],["dc.date.available","2017-09-07T11:48:29Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective: Based on findings in animal models of autoimmune optic nerve inflammation, we have assessed the safety and efficacy of erythropoietin in patients presenting with a first episode of optic neuritis. Methods: Patients with optic neuritis who attended the University Hospitals of Homburg/Saar, Gottingen, or Hamburg (Germany) were included in this double-blind, placebo-controlled, phase 2 study (ClinicalTrials.gov, NCT00355095). They were randomly assigned to groups receiving either 33,000IU recombinant human erythropoietin intravenously daily for 3 days or placebo as an add-on therapy to methylprednisolone. The primary outcome parameter was change in retinal nerve fiber layer (RNFL) thickness after 16 weeks. Secondary outcome parameters included optic nerve atrophy as assessed by magnetic resonance imaging, and changes in visual acuity, visual field, and visual evoked potentials (VEPs). Results: Forty patients were assigned to the treatment groups (21/19 erythropoietin/placebo). Safety monitoring revealed no relevant issues. Thirty-seven patients (20/17 erythropoietin/placebo) were analyzed for the primary endpoint according to the intention-to-treat protocol. RNFL thinning was less apparent after erythropoietin treatment. Thickness of the RNFL decreased by a median of 7.5 mu m by week 16 (mean +/- standard deviation, 10.55 +/- 17.54 mu m) compared to a median of 16.0 mu m (22.65 +/- 29.18 mu m) in the placebo group (p = 0.0357). Decrease in retrobulbar diameter of the optic nerve was smaller in the erythropoietin group (p = 0.0112). VEP latencies at week 16 were shorter in erythropoietin-treated patients than in the placebo group (p = 0.0011). Testing of visual functions revealed trends toward an improved outcome after erythropoietin treatment. Interpretation: These results give the first indications that erythropoietin might be neuroprotective in optic neuritis. ANN NEUROL 2012;72:199210."],["dc.identifier.doi","10.1002/ana.23573"],["dc.identifier.gro","3142489"],["dc.identifier.isi","000307946000010"],["dc.identifier.pmid","22926853"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8846"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0364-5134"],["dc.title","A randomized, double-blind, phase 2 study of erythropoietin in optic neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","81"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Williams, Sarah K."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Knöferle, Johanna"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Fairless, Richard"],["dc.contributor.author","Hochmeister, Sonja"],["dc.contributor.author","Sühs, Kurt-Wolfram"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2019-07-09T11:52:52Z"],["dc.date.available","2019-07-09T11:52:52Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: The aim of this study was to investigate the role of voltage-dependent calcium channels (VDCCs) in axon degeneration during autoimmune optic neuritis. Methods: Calcium ion (Ca2 ) influx into the optic nerve (ON) through VDCCs was investigated in a rat model of optic neuritis using manganese-enhanced magnetic resonance imaging and in vivo calcium imaging. After having identified the most relevant channel subtype (N-type VDCCs), we correlated immunohistochemistry of channel expression with ON histopathology. In the confirmatory part of this work, we performed a treatment study using -conotoxin GVIA, an N-type specific blocker. Results: We observed that pathological Ca2 influx into ONs during optic neuritis is mediated via N-type VDCCs. By analyzing the expression of VDCCs in the inflamed ONs, we detected an upregulation of 1B, the pore-forming subunit of N-type VDCCs, in demyelinated axons. However, high expression levels were also found on macrophages/activated microglia, and lower levels were detected on astrocytes. The relevance of N-type VDCCs for inflammation-induced axonal degeneration and the severity of optic neuritis was corroborated by treatment with -conotoxin GVIA. This blocker led to decreased axon and myelin degeneration in the ONs together with a reduced number of macrophages/activated microglia. These protective effects were confirmed by analyzing the spinal cords of the same animals. Interpretation: We conclude that N-type VDCCs play an important role in inflammation-induced axon degeneration via two mechanisms: First, they directly mediate toxic Ca2 influx into the axons; and second, they contribute to macrophage/microglia function, thereby promoting secondary axonal damage."],["dc.identifier.doi","10.1002/ ana.21668"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6088"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60296"],["dc.language.iso","en"],["dc.subject.ddc","610"],["dc.title","Role of N-Type Voltage-Dependent Calcium Channels in Autoimmune Optic Neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","184"],["dc.contributor.author","Diem, R."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:49:51Z"],["dc.date.available","2017-09-07T11:49:51Z"],["dc.date.issued","2007"],["dc.description.abstract","Neurodegeneration in multiple sclerosis (MS) is the structural correlate of permanent neurological disability in patients. The histopathological features of neurodegeneration include destruction of axons as well as apoptotic cell death of neuronal cell bodies. Therapeutic efforts to control these clinically important aspects of MS pathology showed limited success so far. In this review article, we give an overview about the current knowledge concerning the molecular mechanisms of neurodegeneration in autoimmune inflammation that is mainly derived from animal models. Further, we critically discuss experimental neuroprotective strategies with respect to their functional relevance and differentiate between anti-apoptotic and axon protective treatment approaches. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2006.11.025"],["dc.identifier.gro","3143529"],["dc.identifier.isi","000245727400004"],["dc.identifier.pmid","17188756"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1053"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0165-5728"],["dc.title","Neurodegeneration and -protection in autoimmune CNS inflammation"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2058"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","2066"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Meyer, Ralf"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:46:40Z"],["dc.date.available","2017-09-07T11:46:40Z"],["dc.date.issued","2001"],["dc.description.abstract","Tumor-necrosis-factor-alpha (TNF-alpha) prevented secondary death of retinal ganglion cells (RGCs) after axotomy of the optic nerve in vivo. This RGC rescue was confirmed in vitro in a mixed retinal culture model. In accordance with our previous findings, TNF-alpha decreased outward potassium currents in RGCs. Antagonism of the TNF-alpha -induced decrease in outward potassium currents with the potassium channel opener minoxidilsulfate (as verified by electrophysiology) abolished neuroprotection. Western blot analysis revealed an upregulation of phospho-Akt as a consequence of TNF-alpha -induced potassium current reduction. Inhibition of the phosphatidylinositol 3-kinase-Akt pathway with wortmannin decreased TNF-alpha -promoted RGC survival. These data point to a functionally relevant cytokine-dependent neuroprotective signaling cascade in adult CNS neurons."],["dc.identifier.gro","3144297"],["dc.identifier.isi","000167422200027"],["dc.identifier.pmid","11245689"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1906"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Reduction of potassium currents and phosphatidylinositol 3-kinase-dependent Akt phosphorylation by tumor necrosis factor-alpha rescues axotomized retinal ganglion cells from retrograde cell death in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]