Siebert, Heike

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","106"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T10:35:31Z"],["dc.date.available","2018-11-07T10:35:31Z"],["dc.date.issued","2003"],["dc.format.extent","389"],["dc.identifier.isi","000185600700017"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45118"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.conference","48th Annual Meeting of the German-Society-for-Neuropathology-and-Neuroanatomy"],["dc.relation.eventlocation","BERLIN, GERMANY"],["dc.relation.issn","0001-6322"],["dc.title","Permanent axonal loss in EAE in WLDs mice occurs independently of Wallerian degeneration"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","967"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Der Unfallchirurg"],["dc.bibliographiccitation.lastpage","988"],["dc.bibliographiccitation.volume","107"],["dc.contributor.author","Stengel, Dirk"],["dc.contributor.author","Ekkernkamp, A."],["dc.contributor.author","Dettori, J."],["dc.contributor.author","Hanson, B."],["dc.contributor.author","Sturmer, K. M."],["dc.contributor.author","Siebert, Heike"],["dc.date.accessioned","2018-11-07T10:45:27Z"],["dc.date.available","2018-11-07T10:45:27Z"],["dc.date.issued","2004"],["dc.description.abstract","We set out to clarify whether in hospitals with a large volume morbidity and mortality rates after total knee arthroplasty (TKA) can be improved, whether the effects are consistent, and whether minimum recommendable caseloads can be inferred. We conducted a systematic review using MEDLINE, EMBASE, CENTRAL, and CINAHL and performed a hand search without restrictions on language or publication types. We identified 1406 citations, of which 13 studies including 1,110,962 patients met our inclusion criteria. Of these, six studies explored the same administrative data source. Five studies enrolling 448,897 were eligible for quantitative analysis. All studies corresponded to evidence level 2b (prospective or retrospective cohort study with >80% follow-up). We found homogeneous results about hospital mortality. Between 2551 and 821 TKA must be performed by high-volume rather than by low-volume providers to prevent 1 extra death. Absolute event rates are notably small."],["dc.identifier.doi","10.1007/s00113-004-0850-7"],["dc.identifier.isi","000224891100016"],["dc.identifier.pmid","15452657"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47507"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0177-5537"],["dc.title","A rapid review of associations between provider volume and outcome of total knee arthroplasty. Where do the magical threshold values come from?"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8866"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","8875"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Herms, J."],["dc.contributor.author","Tings, T"],["dc.contributor.author","Gall, S."],["dc.contributor.author","Madlung, A."],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Siebert, H."],["dc.contributor.author","Schurmann, P."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Kretzschmar, Hans"],["dc.date.accessioned","2017-09-07T11:47:27Z"],["dc.date.available","2017-09-07T11:47:27Z"],["dc.date.issued","1999"],["dc.description.abstract","The prion protein (PrPC) is a copper-binding protein of unknown function that plays an important role in the etiology of transmissible spongiform encephalopathies. Using morphological techniques and synaptosomal fractionation methods, we show that PrPC is predominantly localized to synaptic membranes. Atomic absorption spectroscopy was used to identify PrPC-related changes in the synaptosomal copper concentration in transgenic mouse lines. The synaptic transmission in the presence of H2O2, which is known to be decomposed to highly reactive hydroxyl radicals in the presence of iron or copper and to alter synaptic activity, was studied in these animals. The response of synaptic activity to H2O2 was found to correlate with the amount of PrPC expression in the presynaptic neuron in cerebellar slice preparations from wild-type, Prnp(0/0), and PrP gene-reconstituted transgenic mice. Thus, our data gives strong evidence for the predominantly synaptic location of PrPC, its involvement in the regulation of the presynaptic copper concentration, and synaptic activity in defined conditions."],["dc.identifier.doi","10.1523/JNEUROSCI.19-20-08866.1999"],["dc.identifier.gro","3144439"],["dc.identifier.isi","000083072500020"],["dc.identifier.pmid","10516306"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2063"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Evidence of presynaptic location and function of the prion protein"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Kahle, Philipp J."],["dc.contributor.author","Kramer, Michael L."],["dc.contributor.author","Isik, Thomas"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T08:28:16Z"],["dc.date.available","2018-11-07T08:28:16Z"],["dc.date.issued","2009"],["dc.format.extent","43"],["dc.identifier.isi","000266400900112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16384"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","Leipzig, GERMANY"],["dc.relation.issn","0022-3042"],["dc.title","Over-expression of alpha-synuclein in the nervous system enhances axonal degeneration after peripheral nerve lesion in a transgenic mouse strain"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Neuroscience"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Dippel, N."],["dc.contributor.author","Liefner, M."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T11:04:29Z"],["dc.date.available","2018-11-07T11:04:29Z"],["dc.date.issued","2000"],["dc.format.extent","362"],["dc.identifier.isi","000088236602062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51852"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Science Ltd"],["dc.publisher.place","Oxford"],["dc.relation.issn","0953-816X"],["dc.title","The role of matrix metalloproteinases and TNF-alpha during Wallerian degeneration in the mouse sciatic nerve"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","159"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","164"],["dc.bibliographiccitation.volume","916"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Engelke, Sebastian"],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T08:32:21Z"],["dc.date.available","2018-11-07T08:32:21Z"],["dc.date.issued","2001"],["dc.description.abstract","Wallerian degeneration of a peripheral nerve is mainly characterized by axon and myelin degradation and is paralleled by a massive invasion of peripheral macrophages into the nerve. These cells enter the nerve attracted by a cascade of chemokines and cytokines but require proteolytic and enzymatic factors which enables them to cross the blood-nerve barrier. Here we investigated whether U-naphthyl (alpha -NA) esterases - which have been shown to be exclusively expressed in human monocytes - play a role during Wallerian degeneration. These enzymes were blocked by the specific inhibitor bis(4-nitrophenyl)-phosphate (BNPP) in an established in vitro model of Wallerian degeneration. Sciatic nerve segments of mice were co-cultured with peritoneal macrophages and BNPP was added to the cultures in various concentrations and at different timepoints. The macrophage numbers and myelin density in the nerve segments and the myelin load of macrophages were evaluated. After BNPP treatment the macrophage number within the nerve was significantly diminished and the myelin load within the macrophages was decreased, resulting in elevated levels of preserved myelin within the nerves. These experiments clearly showed a double effect of the UNA esterase inhibitor BNPP on macrophages, First, it suggests a role for UNA esterases on the migratory potential of macrophages since their invasion into the nerves was diminished. Second, the reduced myelin uptake is due to the inhibition of phagocytic capacity of these cells by BNPP. The therapeutical use of this inhibitor for treatment of autoimmune diseases such as multiple sclerosis or Guillain-Barre syndrome remains to be investigated. (C) 2001 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0006-8993(01)02887-6"],["dc.identifier.isi","000171812300019"],["dc.identifier.pmid","11597603"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17322"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Concentration-dependent effects of the esterase inhibitor BNPP on macrophage migration and myelin phagocytosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3401"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","3408"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Kuhlmann, Tanja"],["dc.contributor.author","Bitsch, Andreas"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Brück, Wolfgang"],["dc.date.accessioned","2022-03-01T11:44:15Z"],["dc.date.available","2022-03-01T11:44:15Z"],["dc.date.issued","2001"],["dc.description.abstract","The present study investigated the fate of macrophages in peripheral nerves undergoing Wallerian degeneration, especially their disappearance from the injured nerves after phagocytosis of axonal and myelin debris. Wallerian degeneration was induced in adult male C57Bl/6 mice by transecting the right sciatic nerve. Five days after transection, the male sciatic nerves were transplanted into female recipient mice by placing them exactly parallel to the host sciatic nerves. Nerves of the female recipient mice were also transected to induce breakdown of the blood-nerve barrier in the host animal. Apoptosis was assessed by morphological, immunohistochemical (activated caspase-3), and molecular (DNA fragmentation) methods in transplanted, recipient, and in control nerves. A subpopulation of macrophages within the degenerating nerves died locally by apoptosis in each experiment. The fate of the male macrophages within the transplanted nerves and the host organism was investigated by in situ hybridization with a Y-chromosome-specific DNA probe (145SC5). In situ hybridization specifically stained cells within the transplanted male nerve. Y-chromosome-positive cells were detected not only inside the transplanted nerve, but also inside the female host nerve, the perineurial tissue, the local perineurial blood vessels, draining lymph nodes and the spleen of the female host, suggesting hematogenous as well as lymphatic elimination of macrophages from the injured nerve. These data indicate that local apoptosis and systemic elimination via circulation to the local lymph nodes and the spleen are involved in the disappearance of macrophages from the injured peripheral nervous system."],["dc.identifier.doi","10.1523/JNEUROSCI.21-10-03401.2001"],["dc.identifier.isi","000168409400016"],["dc.identifier.pmid","11331370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102973"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Macrophages Are Eliminated from the Injured Peripheral Nerve via Local Apoptosis and Circulation to Regional Lymph Nodes and the Spleen"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3219"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Atmospheric Measurement Techniques"],["dc.bibliographiccitation.lastpage","3228"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Siebert, H."],["dc.contributor.author","Shaw, R. A."],["dc.contributor.author","Ditas, J."],["dc.contributor.author","Schmeissner, T."],["dc.contributor.author","Malinowski, S. P."],["dc.contributor.author","Bodenschatz, E."],["dc.contributor.author","Xu, H."],["dc.date.accessioned","2022-06-08T07:57:37Z"],["dc.date.available","2022-06-08T07:57:37Z"],["dc.date.issued","2015"],["dc.description.abstract","Abstract. Mountain research stations are advantageous not only for long-term sampling of cloud properties but also for measurements that are prohibitively difficult to perform on airborne platforms due to the large true air speed or adverse factors such as weight and complexity of the equipment necessary. Some cloud–turbulence measurements, especially Lagrangian in nature, fall into this category. We report results from simultaneous, high-resolution and collocated measurements of cloud microphysical and turbulence properties during several warm cloud events at the Umweltforschungsstation Schneefernerhaus (UFS) on Zugspitze in the German Alps. The data gathered were found to be representative of observations made with similar instrumentation in free clouds. The observed turbulence shared all features known for high-Reynolds-number flows: it exhibited approximately Gaussian fluctuations for all three velocity components, a clearly defined inertial subrange following Kolmogorov scaling (power spectrum, and second- and third-order Eulerian structure functions), and highly intermittent velocity gradients, as well as approximately lognormal kinetic energy dissipation rates. The clouds were observed to have liquid water contents on the order of 1 g m−3 and size distributions typical of continental clouds, sometimes exhibiting long positive tails indicative of large drop production through turbulent mixing or coalescence growth. Dimensionless parameters relevant to cloud–turbulence interactions, the Stokes number and settling parameter are in the range typically observed in atmospheric clouds. Observed fluctuations in droplet number concentration and diameter suggest a preference for inhomogeneous mixing. Finally, enhanced variance in liquid water content fluctuations is observed at high frequencies, and the scale break occurs at a value consistent with the independently estimated phase relaxation time from microphysical measurements."],["dc.identifier.doi","10.5194/amt-8-3219-2015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/110152"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-575"],["dc.relation.eissn","1867-8548"],["dc.title","High-resolution measurement of cloud microphysics and turbulence at a mountaintop station"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Bitsch, Annette"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.date.accessioned","2018-11-07T11:24:45Z"],["dc.date.available","2018-11-07T11:24:45Z"],["dc.date.issued","2001"],["dc.format.extent","532"],["dc.identifier.isi","000171662200082"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56477"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","0001-6322"],["dc.title","Evidence for local and systemic elimination of macrophages from the injured peripheral nervous system"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","57"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Singh, Shailender"],["dc.contributor.author","Dallenga, Tobias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","Roemer, Shanu"],["dc.contributor.author","Maruschak, Brigitte"],["dc.contributor.author","Siebert, Heike"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.date.accessioned","2018-11-07T10:26:08Z"],["dc.date.available","2018-11-07T10:26:08Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Axonal damage and loss substantially contribute to the incremental accumulation of clinical disability in progressive multiple sclerosis. Here, we assessed the amount of Wallerian degeneration in brain tissue of multiple sclerosis patients in relation to demyelinating lesion activity and asked whether a transient blockade of Wallerian degeneration decreases axonal loss and clinical disability in a mouse model of inflammatory demyelination. Methods: Wallerian degeneration and acute axonal damage were determined immunohistochemically in the periplaque white matter of multiple sclerosis patients with early actively demyelinating lesions, chronic active lesions, and inactive lesions. Furthermore, we studied the effects of Wallerian degeneration blockage on clinical severity, inflammatory pathology, acute axonal damage, and long-term axonal loss in experimental autoimmune encephalomyelitis using Wallerian degeneration slow (WldS) mutant mice. Results: The highest numbers of axons undergoing Wallerian degeneration were found in the perilesional white matter of multiple sclerosis patients early in the disease course and with actively demyelinating lesions. Furthermore, Wallerian degeneration was more abundant in patients harboring chronic active as compared to chronic inactive lesions. No co-localization of neuropeptide Y-Y1 receptor, a bona fide immunohistochemical marker of Wallerian degeneration, with amyloid precursor protein, frequently used as an indicator of acute axonal transport disturbance, was observed in human and mouse tissue, indicating distinct axon-degenerative processes. Experimentally, a delay of Wallerian degeneration, as observed in WldS mice, did not result in a reduction of clinical disability or acute axonal damage in experimental autoimmune encephalomyelitis, further supporting that acute axonal damage as reflected by axonal transport disturbances does not share common molecular mechanisms with Wallerian degeneration. Furthermore, delaying Wallerian degeneration did not result in a net rescue of axons in late lesion stages of experimental autoimmune encephalomyelitis. Conclusions: Our data indicate that in multiple sclerosis, ongoing demyelination in focal lesions is associated with axonal degeneration in the perilesional white matter, supporting a role for focal pathology in diffuse white matter damage. Also, our results suggest that interfering with Wallerian degeneration in inflammatory demyelination does not suffice to prevent acute axonal damage and finally axonal loss."],["dc.identifier.doi","10.1186/s12974-017-0831-8"],["dc.identifier.isi","000397153100002"],["dc.identifier.pmid","28302146"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14381"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42975"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Relationship of acute axonal damage, Wallerian degeneration, and clinical disability in multiple sclerosis"],["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"]]