Reinert, Marie-Christine

[["dc.bibliographiccitation.firstpage","930"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Muscle & Nerve"],["dc.bibliographiccitation.lastpage","936"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Hesse, Stefan"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T08:49:18Z"],["dc.date.available","2018-11-07T08:49:18Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction: To test the hypothesis that the efficacy of botulinum toxin depends on the activity of the neuromuscular junction, we developed an in vivo paradigm to determine the degree and duration of low-dose botulinum toxin-induced focal paresis in mice. Methods: We combined an automated wheel-running paradigm with low-dose botulinum toxin injections into the calf muscles of wild-type mice. Half of the mice were injected either before the nightly running or before the daily resting period. Results: After botulinum toxin injections, running distance and maximum velocity decreased dose-dependently. The degree and duration of decrease between the respective groups with regard to the time-points of injection were identical. Conclusions: This in vivo paradigm quantifies the degree of otherwise clinically inapparent botulinum toxin-induced focal calf muscle paresis. Increased muscle activity after low-dose injections does not influence the efficacy of botulinum toxin in normal muscles. Muscle Nerve 44: 930-936, 2011"],["dc.identifier.doi","10.1002/mus.22210"],["dc.identifier.isi","000297938800015"],["dc.identifier.pmid","22102464"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21429"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0148-639X"],["dc.title","BOTULINUM TOXIN-INDUCED FOCAL PARESIS IN MICE IS UNAFFECTED BY MUSCLE ACTIVITY"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","89"],["dc.bibliographiccitation.journal","Toxicon"],["dc.bibliographiccitation.lastpage","90"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Reinert, M. C."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Hesse, Stefan"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T09:23:39Z"],["dc.date.available","2018-11-07T09:23:39Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1016/j.toxicon.2012.07.089"],["dc.identifier.isi","000320075500077"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29632"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Santa Fe, NM"],["dc.relation.issn","0041-0101"],["dc.title","Novel in vivo test shows low-dosage botulinum toxin-induced focal calf muscle paresis is independent of increased muscle activity in wild-type mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","374"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","379"],["dc.bibliographiccitation.volume","235"],["dc.contributor.author","Schmitz, Thomas"],["dc.contributor.author","Endesfelder, Stefanie"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Müller, Susann"],["dc.contributor.author","Bührer, Christoph"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T09:10:49Z"],["dc.date.available","2018-11-07T09:10:49Z"],["dc.date.issued","2012"],["dc.description.abstract","In preterm infants, the risk to develop attention-deficit/hyperactivity disorder is 3 to 4-fold higher than in term infants. Moreover, preterm infants exhibit deficits in motor coordination and balance. Based on clinical data, higher oxygen levels in preterm infants lead to worse neurological outcome, and experimental hyperoxia causes wide-ranging cerebral changes in neonatal rodents. We hypothesize that hyperoxia in the immature brain may affect motor activity in preterm infants. We subjected newborn mice from P6 to P8 to 48 h of hyperoxia (80% O-2) and tested motor activity in running wheels starting at adolescent age P30. Subsequently, from P44 to P53, regular wheels were replaced by complex wheels with variable crossbar positions to assess motor coordination deficits. MRI with diffusion tensor imaging was performed in the corpus callosum to determine white matter diffusivity in mice after hyperoxia at ages P30 and P53 in comparison to control animals. Adolescent mice after neonatal hyperoxia revealed significantly higher values for maximum velocity and mean velocity in regular wheels than controls (P<0.05). In the complex running wheels, however, maximum velocity was decreased in animals after hyperoxia, as compared to controls (P<0.05). Decreased fractional anisotropy and increased radial diffusion coefficient were observed in the corpus callosum of P30 and P53 mice after neonatal hyperoxia compared to control mice. Hyperoxia in the immature brain causes hyperactivity, motor coordination deficits, and impaired white matter diffusivity in adolescent and young adult mice. (C) 2012 Elsevier Inc. All rights reserved."],["dc.description.sponsorship","Medical Faculty, University of Gottingen"],["dc.identifier.doi","10.1016/j.expneurol.2012.03.002"],["dc.identifier.isi","000303430400039"],["dc.identifier.pmid","22449476"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26581"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation.issn","0014-4886"],["dc.title","Adolescent hyperactivity and impaired coordination after neonatal hyperoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","NeuroToxicology"],["dc.bibliographiccitation.lastpage","8"],["dc.bibliographiccitation.volume","59"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Krez, Nadja"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Rummel, Andreas"],["dc.date.accessioned","2018-11-07T10:26:22Z"],["dc.date.available","2018-11-07T10:26:22Z"],["dc.date.issued","2017"],["dc.description.abstract","The highly potent Botulinum neurotoxins (BoNT) are successful drugs to treat neuromuscular disorders. Efforts are being made to further reduce the injected BoNT dose and to lengthen the interval between treatments. Detailed knowledge of the BoNT structure-activity relationship (SAR) allows combining the best features of the different BoNT serotypes. Of all seven BoNT serotypes A-G, BoNT/A displays the highest potency despite low neuronal binding affinity, while BoNT/B exhibits much higher affinity. Recently, a new BoNT/AB hybrid (AABB) was constructed comprising the catalytic and translocation domain of BoNT/A and the 50 kDa cell binding domain of BoNT/B. Here, we compared BoNT/A wild-type (AAAA) and AABB with regard to ex vivo potency and in vivo potency, efficacy and duration of action using the mouse phrenic nerve hemidiaphragm assay and the murine running wheel assay, respectively. The ex vivo potency of AABB was found to be 8.4-fold higher than that of AAAA. For the latter, two and 5 pg each of AAAA and AABB, respectively, were bilaterally injected into the calf muscles and mouse running wheel performance was automatically monitored during the following weeks to determine potency, efficacy and duration. Mice displayed a dose-dependent impairment of running performance. AABB showed potency, efficacy and duration equal to AAAA demonstrating successful exchange of the cell binding domain. AABB might combine the higher potency and longer duration of BoNT/A with the target specificity for the autonomic nervous system of BoNT/B. AABB might therefore constitute an improved treatment option for acetylcholine-mediated autonomic disorders such as hypersalivation or hyperhidrosis. (C) 2016 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.neuro.2016.12.008"],["dc.identifier.isi","000399061900001"],["dc.identifier.pmid","28043867"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43028"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1872-9711"],["dc.relation.issn","0161-813X"],["dc.title","BoNT/AB hybrid maintains similar duration of paresis as BoNT/A wild-type in murine running wheel assay"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroscience Methods"],["dc.bibliographiccitation.lastpage","48"],["dc.bibliographiccitation.volume","205"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Hesse, Stefan"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T09:12:06Z"],["dc.date.available","2018-11-07T09:12:06Z"],["dc.date.issued","2012"],["dc.description.abstract","Tetanus neurotoxin (TeNT) enhances activity of motoneurons by blocking spinal inhibitory interneurons. Based on this pathomechanism, we propose that low-dosage intramuscular injections of TeNT could serve as a specific treatment for central paretic muscles. However in vivo TeNT research is restricted because of the fear of triggering widespread muscle spasms. In addition, no reliable test to measure the in vivo toxicity of low-dosage TeNT is available. We introduce a novel wheel running-based paradigm with mice to quantify functional effects and thus the toxicity of low-dosage TeNT in vivo. We accustomed three groups of wildtype mice (n=14) to using a complex running wheel with irregularly spaced crossbars. Each group received an injection with a different low-dosage of TeNT (0.15 ng, 0.1 ng or 0.05 ng TeNT) into both tibialis anterior muscles. The maximum running velocity and accumulative running time of the groups were recorded during the following weeks. Three days after TeNT injections, the mice exhibited an increase in muscle tone of the injected tibialis anterior muscles but no generalized symptoms. However, we found that normal running in the complex wheel set-up was disturbed such that the maximum running velocity and running time of the mice decreased with the size of the dose. This effect peaked on the fifth and sixth nights after injection and returned to baseline level again within the next two weeks. With this novel in vivo automated paradigm we can accurately and objectively quantify the duration and degree of TeNT-induced focal increase in muscle tone. (C) 2012 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneumeth.2011.12.019"],["dc.identifier.isi","000301688600006"],["dc.identifier.pmid","22227534"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26874"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-0270"],["dc.title","Accurate quantification of tetanus neurotoxin-induced focal spasticity in mice using complex running wheels"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","216"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","221"],["dc.bibliographiccitation.volume","627"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Moennich, Angelika"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T10:10:20Z"],["dc.date.available","2018-11-07T10:10:20Z"],["dc.date.issued","2016"],["dc.description.abstract","Three botulinum neurotoxin type A (BoNT/A) products, incobotulinumtoxinA, onabotulinumtoxinA, and abobotulinumtoxinA, all manufactured by different methods, are employed in clinical practice. Comparing the three BoNT/A products is difficult because their concentrations and volumes differ and the precise dose equivalence ratio is not known. We aimed to compare the neurotoxic potencies by a systematic analysis of injected volume and dose. The potency of BoNT in inducing hind limb paresis was assessed by analyzing the wheel-running performance of mice. To standardize the volume, the effect of an identical dose of incobotulinumtoxinA dissolved in different volumes of saline (15,10, 5, and 2 mu l) was studied in four groups of mice (n = 13-15). The potencies of the BoNT products were then compared by injecting identical volumes (10 mu l) containing different doses into both hind leg muscles. Mice injected with incobotulinumtoxinA showed a volume-dependent reduction in wheel-running, with larger volumes inducing more intense paresis. A standardized volume containing the same number of mouse units of the BoNT/A products produced different degrees of paresis. The conversion ratio of incobotulinumtoxinA and onabotulinumtoxinA is estimated to be between 1:0.75 and 1:0.5. OnabotulinumtoxinA displayed a two-fold greater potency than abobotulinumtoxinA. Doses of onabotulinumtoxinA and abobotulinumtoxinA that produce an identical severity of pareses even result in the same duration of pareses. This wheel-running assay allows one to compare the neurotoxic potency of different volumes and doses of the BoNT products in vivo. Our results argue against common clinical practice because incobotulinumtoxinA and onabotulinumtoxinA are not readily interchangeable and a two-fold dose of abobotulinumtoxinA is needed to induce an effect identical to onabotulinumtoxinA. In addition, this emphasizes that the duration of BoNT-induced effect is the same as long as equipotent doses of BoNT are injected. (C) 2016 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2016.06.001"],["dc.identifier.isi","000380418400033"],["dc.identifier.pmid","27268041"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39832"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1872-7972"],["dc.relation.issn","0304-3940"],["dc.title","In-vivo comparison of the neurotoxic potencies of incobotulinumtoxinA, onabotulinumtoxinA, and abobotulinumtoxinA"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","34"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Lagumersindez-Denis, Nielsen"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Hollasch, Heiko"],["dc.contributor.author","Flach, Anne"],["dc.contributor.author","Bruehl, Hilke"],["dc.contributor.author","Cullen, Eilish"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Linington, Christopher"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nessler, Stefan"],["dc.date.accessioned","2018-11-07T10:22:07Z"],["dc.date.available","2018-11-07T10:22:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Cortical demyelination is a widely recognized hallmark of multiple sclerosis (MS) and correlate of disease progression and cognitive decline. The pathomechanisms initiating and driving gray matter damage are only incompletely understood. Here, we determined the infiltrating leukocyte subpopulations in 26 cortical demyelinated lesions of biopsied MS patients and assessed their contribution to cortical lesion formation in a newly developed mouse model. We find that conformation-specific anti-myelin antibodies contribute to cortical demyelination even in the absence of the classical complement pathway. T cells and natural killer cells are relevant for intracortical type 2 but dispensable for subpial type 3 lesions, whereas CCR2(+) monocytes are required for both. Depleting CCR2(+) monocytes in marmoset monkeys with experimental autoimmune encephalomyelitis using a novel humanized CCR2 targeting antibody translates into significantly less cortical demyelination and disease severity. We conclude that biologics depleting CCR2(+) monocytes might be attractive candidates for preventing cortical lesion formation and ameliorating disease progression in MS."],["dc.identifier.doi","10.1007/s00401-017-1706-x"],["dc.identifier.isi","000403235900002"],["dc.identifier.pmid","28386765"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14713"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42218"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Differential contribution of immune effector mechanisms to cortical demyelination in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Toxicon"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Kutschenko, Anna"],["dc.contributor.author","Reinert, M. C."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Hesse, Stefan"],["dc.contributor.author","Liebetanz, David"],["dc.date.accessioned","2018-11-07T09:23:40Z"],["dc.date.available","2018-11-07T09:23:40Z"],["dc.date.issued","2013"],["dc.format.extent","90"],["dc.identifier.doi","10.1016/j.toxicon.2012.07.090"],["dc.identifier.isi","000320075500078"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29633"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.conference","7th International Conference on Basic and Therapeutic Aspects of Botulinum and Tetanus Toxins (TOXINS)"],["dc.relation.eventlocation","Santa Fe, NM"],["dc.relation.issn","0041-0101"],["dc.title","Low-dosage tetanus neurotoxin induces focal, temporarily increased muscle tone in wild-type mice"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]