Lange, Peter

[["dc.bibliographiccitation.firstpage","126"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","134"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Fronek, Kathrin"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Eiffert, Helmut"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Lange, Peter"],["dc.date.accessioned","2018-11-07T08:51:09Z"],["dc.date.available","2018-11-07T08:51:09Z"],["dc.date.issued","2011"],["dc.description.abstract","Background/Aims: Determination of marker proteins of neuronal degeneration in cerebrospinal fluid (CSF) is of increasing importance. However, preanalytical problems may compromise the results. Methods: We studied the influence of the transport tube material and shaking at room temperature on the CSF concentrations of beta-amyloid and tau protein determined by enzyme immunoassays. Results: The materials of the transport tube moderately influenced the CSF concentrations of beta-amyloid and tau protein. Polyethylene and polypropylene tubes were well suited, but glass, polycarbonate and polystyrene tubes caused a decrease in the CSF beta-amyloid and tau protein concentrations. The strongest impact, however, was caused by bacterial contamination of samples. Contamination with high concentrations of Pseudomonas aeruginosa and related species rendered beta-amyloid undetectable and strongly diminished tau protein concentrations. The effects of several Gram-positive bacteria were less pronounced. Addition of 0.1% sodium azide prior to bacterial contamination increased the interval at which CSF could be kept at room temperature without a substantial reduction of the beta-amyloid or tau protein concentration. Conclusion: Polyethylene or polypropylene tubes are suitable transport vessels for CSF samples. Bacterial contamination during sampling and portioning must be avoided. Addition of sodium azide may be an option when transport of the sample is delayed. Copyright (C) 2011 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000330912"],["dc.identifier.fs","580959"],["dc.identifier.isi","000295875400006"],["dc.identifier.pmid","21952521"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21862"],["dc.language.iso","en"],["dc.notes","This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively."],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/8159"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1421-9824"],["dc.relation.issn","1420-8008"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Amyloid beta-Peptides"],["dc.subject.mesh","Cerebrospinal Fluid"],["dc.subject.mesh","Cerebrospinal Fluid Proteins"],["dc.subject.mesh","Dementia"],["dc.subject.mesh","Enzyme-Linked Immunosorbent Assay"],["dc.subject.mesh","Equipment Design"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Pseudomonas aeruginosa"],["dc.subject.mesh","Quality Control"],["dc.subject.mesh","Specimen Handling"],["dc.subject.mesh","Stenotrophomonas maltophilia"],["dc.subject.mesh","tau Proteins"],["dc.title","Bacterial Contamination and the Transport Vial Material Affect Cerebrospinal Fluid Concentrations of beta-Amyloid and Tau Protein as Determined by Enzyme Immunoassay"],["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.artnumber","15"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Fluids and Barriers of the CNS"],["dc.bibliographiccitation.lastpage","5"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Bunkowski, Stephanie"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2017-09-07T11:44:33Z"],["dc.date.available","2017-09-07T11:44:33Z"],["dc.date.issued","2016"],["dc.description.abstract","Background The composition of the cerebrospinal fluid (CSF) is not homogeneous, and concentrations of proteins from different origins diverge among ventricular, cisternal and lumbar CSF fractions. Concentrations of blood-derived proteins increase and of brain-derived proteins decrease from ventricular to lumbar fractions. We studied whether the origin of the CSF portion analysed may affect results in CSF analysis for dementia. Methods In 16 geriatric patients with suspected normal pressure hydrocephalus [age 82.5 (76/87) years; median (25th/75th percentile)] a lumbar spinal tap of 40 ml was performed. The CSF was sequentially collected in 8 fractions of 5 ml with the 1st fraction corresponding to lumbar CSF, the 8th to cisterna magna-near CSF. Fractions were analysed for total protein, albumin, Tau protein (Tau), phosphorylated Tau (pTau), Amyloid beta 1–42 (Aβ1–42), Amyloid beta 1–40 (Aβ1–40), and the Aβ1–42/Aβ1–40 ratio. Results The concentrations of total protein and albumin increased from cisternal to lumbar fractions due to diffusion-related accumulation from blood to CSF with significantly higher concentrations in fraction 1 compared to fraction 8. The concentrations of Tau showed a non-significant trend towards decreased values in lumbar samples, and pTau was slightly, but significantly decreased in the lumbar fraction 1 [26.5 (22.5/35.0) pg/ml] compared to the cistern-near fraction 8 [27.0 (24.2/36.3) pg/ml] (p = 0.02, Wilcoxon signed rank test). Aβ1-42, Aβ1-40, and the Aβ1-42/Aβ1-40 ratio remained almost constant. Conclusions According to the flow-related diverging dynamics of blood-derived and brain-derived proteins in CSF, the concentrations of Tau and pTau tended to be lower in lumbar compared to cisternal CSF fractions after a spinal tap of 40 ml. The differences reached statistical significance for pTau only. The small differences will not affect clinical interpretation of markers of dementia in the vast majority of cases."],["dc.identifier.doi","10.1186/s12987-016-0039-9"],["dc.identifier.gro","3151687"],["dc.identifier.pmid","27581842"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13876"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8505"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","2045-8118"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Small cisterno-lumbar gradient of phosphorylated Tau protein in geriatric patients with suspected normal pressure hydrocephalus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","410"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Sciences"],["dc.bibliographiccitation.volume","12"],["dc.contributor.affiliation","Konen, Franz Felix; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Lange, Peter; 2Department of Neurology, University Medical Center Göttingen (UMG), 37075 Göttingen, Germany; peter-la@med.uni-goettingen.de"],["dc.contributor.affiliation","Wurster, Ulrich; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Jendretzky, Konstantin Fritz; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Gingele, Stefan; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Möhn, Nora; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Sühs, Kurt-Wolfram; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Stangel, Martin; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Skripuletz, Thomas; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.affiliation","Schwenkenbecher, Philipp; 1Clinical Neuroimmunology and Neurochemistry, Department of Neurology, Hannover Medical School, 30625 Hannover, Germany; konen.felix@mh-hannover.de (F.F.K.); wurster.ulrich@mh-hannover.de (U.W.); jendretzky.konstantin@mh-hannover.de (K.F.J.); gingele.stefan@mh-hannover.de (S.G.); moehn.nora@mh-hannover.de (N.M.); suehs.kurt-wolfram@mh-hannover.de (K.-W.S.); stangel.martin@mh-hannover.de (M.S.); skripuletz.thomas@mh-hannover.de (T.S.)"],["dc.contributor.author","Konen, Franz Felix"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Wurster, Ulrich"],["dc.contributor.author","Jendretzky, Konstantin Fritz"],["dc.contributor.author","Gingele, Stefan"],["dc.contributor.author","Möhn, Nora"],["dc.contributor.author","Sühs, Kurt-Wolfram"],["dc.contributor.author","Stangel, Martin"],["dc.contributor.author","Skripuletz, Thomas"],["dc.contributor.author","Schwenkenbecher, Philipp"],["dc.date.accessioned","2022-04-01T10:02:04Z"],["dc.date.available","2022-04-01T10:02:04Z"],["dc.date.issued","2022"],["dc.date.updated","2022-04-08T08:24:49Z"],["dc.description.abstract","Background: Cerebrospinal fluid (CSF) samples from patients with non-inflammatory neurological diseases are used for control groups in biomarker studies. Since large amounts of CSF are withdrawn, patients with idiopathic intracranial hypertension (IIH) or normal pressure hydrocephalus (NPH) are especially suitable. The serially taken CSF portions are usually collected in different tubes. We aimed to investigate whether the later random choice of one of these tubes for CSF investigations might harbor the risk of different CSF protein findings due to the so-called ventriculo-lumbar CSF gradient. Methods: Patients with IIH (9) and NPH (7) were included. CSF was serially taken and collected in six tubes of 5 mL each. Concentrations and CSF-serum quotients of immunoglobulins, albumin and the virus-specific antibody index (AI) were determined in the first, fourth and sixth CSF fraction. Results: CSF immunoglobulin and albumin concentrations and CSF-serum protein quotients were significantly lower in the fourth and sixth CSF fraction compared with the first CSF fraction. Virus-specific AI did not significantly differ in the different CSF fractions. Conclusions: CSF protein analytics should be performed in the first CSF fraction in order to avoid different measurement results and achieve comparability within a control group and between different control and patient groups."],["dc.identifier.doi","10.3390/brainsci12030410"],["dc.identifier.pii","brainsci12030410"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105817"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2076-3425"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.title","The Influence of the Ventricular-Lumbar Gradient on Cerebrospinal Fluid Analysis in Serial Samples"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical Case Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Giotaki, Ioanna"],["dc.contributor.author","Gross, Uwe"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Rustenbeck, Hans-Heino"],["dc.contributor.author","Bahn, Erik"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2022-05-02T08:09:51Z"],["dc.date.available","2022-05-02T08:09:51Z"],["dc.date.issued","2022"],["dc.description.abstract","The outcome of chronic meningitis depends to a large degree on the causative pathogen and the interval between onset of symptoms and diagnosis. We present a patient with a delayed diagnosis and several complications, for whom adequate therapy resulted in a favorable outcome. In a 76-year-old male patient, Candida albicans meningitis was diagnosed 4 months after the onset of symptoms. CSF findings (protein >1000 mg/L, predominance of intrathecal immunoglobulin A synthesis, lactate concentrations of approx. 10 mmol/L, leukocyte counts around 1000/μl, variable differential leukocyte counts) resembled tuberculous meningitis. In spite of the long interval without treatment, voriconazole 200 mg every 12 h for 7 weeks followed by fluconazole 300 mg/day maintenance therapy for 7 months led to a recovery with only mild deficits. The case illustrates that 1. C. albicans can cause chronic meningitis in patients without severe immune defects, 2. patients can survive C. albicans meningitis with mild long-term sequelae even when diagnosis and adequate treatment are delayed, and 3. voriconazole as a sole agent may be suitable for treatment of C. albicans meningitis."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.1002/ccr3.5664"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107483"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","2050-0904"],["dc.relation.issn","2050-0904"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc/4.0/"],["dc.title","Chronic Candida albicans meningitis misdiagnosed as polymyalgia rheumatica and successfully treated with voriconazole"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","174"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Djukic, Marija"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Erbguth, Frank"],["dc.contributor.author","Nau, Roland"],["dc.date.accessioned","2022-08-04T12:03:57Z"],["dc.date.available","2022-08-04T12:03:57Z"],["dc.date.issued","2022-07-06"],["dc.date.updated","2022-07-25T11:18:55Z"],["dc.description.abstract","The cerebrospinal fluid (CSF) space is convoluted. CSF flow oscillates with a net flow from the ventricles towards the cerebral and spinal subarachnoid space. This flow is influenced by heartbeats, breath, head or body movements as well as the activity of the ciliated epithelium of the plexus and ventricular ependyma. The shape of the CSF space and the CSF flow preclude rapid equilibration of cells, proteins and smaller compounds between the different parts of the compartment. In this review including reinterpretation of previously published data we illustrate, how anatomical and (patho)physiological conditions can influence routine CSF analysis. Equilibration of the components of the CSF depends on the size of the molecule or particle, e.g., lactate is distributed in the CSF more homogeneously than proteins or cells. The concentrations of blood-derived compounds usually increase from the ventricles to the lumbar CSF space, whereas the concentrations of brain-derived compounds usually decrease. Under special conditions, in particular when distribution is impaired, the rostro-caudal gradient of blood-derived compounds can be reversed. In the last century, several researchers attempted to define typical CSF findings for the diagnosis of several inflammatory diseases based on routine parameters. Because of the high spatial and temporal variations, findings considered typical of certain CNS diseases often are absent in parts of or even in the entire CSF compartment. In CNS infections, identification of the pathogen by culture, antigen detection or molecular methods is essential for diagnosis."],["dc.identifier.citation","Journal of Neuroinflammation. 2022 Jul 06;19(1):174"],["dc.identifier.doi","10.1186/s12974-022-02538-3"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112646"],["dc.language.iso","en"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Cerebrospinal fluid"],["dc.subject","Blood–CSF barrier"],["dc.subject","Blood–brain barrier"],["dc.subject","Lactate"],["dc.subject","Intrathecal immunoglobulin synthesis"],["dc.subject","CSF flow"],["dc.title","Spatial and temporal variation of routine parameters: pitfalls in the cerebrospinal fluid analysis in central nervous system infections"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","A67"],["dc.bibliographiccitation.journal","Astronomy and Astrophysics"],["dc.bibliographiccitation.volume","557"],["dc.contributor.author","Vidotto, A. A."],["dc.contributor.author","Jardine, M."],["dc.contributor.author","Morin, Julien"],["dc.contributor.author","Donati, J.-F."],["dc.contributor.author","Lang, P."],["dc.contributor.author","Russell, A. J. B."],["dc.date.accessioned","2018-11-07T09:20:26Z"],["dc.date.available","2018-11-07T09:20:26Z"],["dc.date.issued","2013"],["dc.description.abstract","We investigate the effect of the magnetic fields of M dwarf (dM) stars on potentially habitable Earth-like planets. These fields can reduce the size of planetary magnetospheres to such an extent that a significant fraction of the planet's atmosphere may be exposed to erosion by the stellar wind. We used a sample of 15 active dM stars, for which surface magnetic-field maps were reconstructed, to determine the magnetic pressure at the planet orbit and hence the largest size of its magnetosphere, which would only be decreased by considering the stellar wind. Our method provides a fast means to assess which planets are most affected by the stellar magnetic field, which can be used as a first study to be followed by more sophisticated models. We show that hypothetical Earth-like planets with similar terrestrial magnetisation (similar to 1 G) orbiting at the inner (outer) edge of the habitable zone of these stars would present magnetospheres that extend at most up to 6 (11.7) planetary radii. To be able to sustain an Earth-sized magnetosphere, with the exception of only a few cases, the terrestrial planet would either (1) need to orbit significantly farther out than the traditional limits of the habitable zone; or else, (2) if it were orbiting within the habitable zone, it would require at least a magnetic field ranging from a few G to up to a few thousand G. By assuming a magnetospheric size that is more appropriate for the young-Earth (3.4 Gyr ago), the required planetary magnetic fields are one order of magnitude weaker. However, in this case, the polar-cap area of the planet, which is unprotected from transport of particles to/from interplanetary space, is twice as large. At present, we do not know how small the smallest area of the planetary surface is that could be exposed and would still not affect the potential for formation and development of life in a planet. As the star becomes older and, therefore, its rotation rate and magnetic field reduce, the interplanetary magnetic pressure decreases and the magnetosphere of planets probably expands. Using an empirically derived rotation-activity/magnetism relation, we provide an analytical expression for estimating the shortest stellar rotation period for which an Earth-analogue in the habitable zone could sustain an Earth-sized magnetosphere. We find that the required rotation rate of the early- and mid-dM stars (with periods greater than or similar to 37-202 days) is slower than the solar one, and even slower for the late-dM stars (greater than or similar to 63-263 days). Planets orbiting in the habitable zone of dM stars that rotate faster than this have smaller magnetospheric sizes than that of the Earth magnetosphere. Because many late-dM stars are fast rotators, conditions for terrestrial planets to harbour Earth-sized magnetospheres are more easily achieved for planets orbiting slowly rotating early- and mid-dM stars."],["dc.identifier.doi","10.1051/0004-6361/201321504"],["dc.identifier.isi","000325211900068"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10871"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28875"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Edp Sciences S A"],["dc.relation.issn","1432-0746"],["dc.relation.orgunit","Fakultät für Physik"],["dc.title","Effects of M dwarf magnetic fields on potentially habitable planets"],["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.artnumber","289"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in aging neuroscience"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Knipper, Tobias"],["dc.contributor.author","Schmidt, Christian"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Hermann, Peter"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-01-09T14:55:23Z"],["dc.date.available","2018-01-09T14:55:23Z"],["dc.date.issued","2017"],["dc.description.abstract","Vascular factors increase the risks of developing Alzheimer's disease (AD) and they contribute to AD pathology. Since amyloid beta (Aβ) deposits can be observed in both diseases, there is an overlap which impedes a clear discrimination and difficult clinical diagnosis. In the present study, we compared cerebrospinal fluid (CSF) profiles of neurodegenerative and inflammatory biomarkers in a patient cohort of controls (n = 50), AD (n = 65) and vascular dementia (VaD) (n = 31) cases. Main results were validated in a second cohort composed of AD (n = 26), rapidly progressive AD (rpAD) (n = 15), VaD (n = 21), and cognitively unimpaired patients with vascular encephalopathy (VE) (n = 25) cases. In the study, cohort significant differences were detected in tau, p-tau, and Aβ1-42 (Aβ42) levels between AD and VaD patients, but not for the neuron-specific enolase (NSE), S100B protein, 14-3-3 and YKL-40. Differential tau, p-tau, and Aβ42 levels between AD and VaD were confirmed in the validation cohort, which additionally showed no differences between AD and rpAD, nor between VaD and VE. The evaluation of the biomarker performance in discrimination between AD and VaD patients revealed that the best diagnostic accuracy could be obtained when tau, p-tau, and Aβ42 were combined in form of Aβ42/p-tau (AUC 0.84-0.90, sensitivity 77-81%, specificity 80-93%) and (tau × p-tau)/Aβ42 ratio (AUC 0.83-0.87, sensitivity 73-81%, specificity 78-87%). Altogether, our studies provided neurodegenerative biomarker profiles in two cohorts of AD and VaD patients favoring the combination of CSF biomarker to differentiate between diseases."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.3389/fnagi.2017.00289"],["dc.identifier.pmid","28955218"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14625"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11611"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cerebrospinal Fluid Biomarkers of Alzheimer's Disease Show Different but Partially Overlapping Profile Compared to Vascular Dementia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3363"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Journal of Clinical Oncology"],["dc.bibliographiccitation.lastpage","3369"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Burkhardt, Birgit"],["dc.contributor.author","Reiter, Alfred"],["dc.contributor.author","Landmann, Eva"],["dc.contributor.author","Lang, Peter"],["dc.contributor.author","Lassay, Lisa"],["dc.contributor.author","Dickerhoff, Roswitha"],["dc.contributor.author","Lakomek, Max"],["dc.contributor.author","Henze, Guenter"],["dc.contributor.author","von Stackelberg, Arend"],["dc.date.accessioned","2018-11-07T08:27:47Z"],["dc.date.available","2018-11-07T08:27:47Z"],["dc.date.issued","2009"],["dc.description.abstract","Purpose Little is known about the outcome of pediatric patients with lymphoblastic lymphoma (LBL) who suffer from progressive disease or relapse. Patients and Methods We analyzed the pattern of LBL relapses after current non-Hodgkin's lymphoma Berlin-Frankfurt-Muenster (BFM) frontline therapy between April 1990 and March 2003. Relapse therapy was according to acute lymphoblastic leukemia (ALL)-Relapse-BFM protocols or ALL-BFM protocols for high-risk patients. Results Twenty-eight (11%) of 251 registered patients with precursor T-cell LBL (T-LBL) and six (8%) of 73 patients with precursor B-cell LBL (pB-LBL) suffered from relapse. Of the 28 patients with T-LBL, one died from infection during relapse chemotherapy, 18 failed to achieve stable remission and died from disease progression, and nine reached allogeneic stem-cell transplantation (SCT). Two of these nine patients who underwent SCT died from transplantation-associated toxicity, three died from disease progression, and four are still alive. These four patients are in second remission of their lymphoma for 48, 68, 125, and 131 months, respectively, after allogeneic SCT. One of the four patients developed colon adenocarcinoma 47 months after SCT. Of the six patients with pB-LBL who experienced relapse, one patient died as a result of toxicity of relapse chemotherapy, two died from disease progression after chemotherapy, and three received allogeneic SCT. Of these, two died from subsequent disease progression, and one is still alive 57 months after allogeneic SCT. Conclusion Using modern conventional therapy in the frontline treatment of LBL, 10% of patients suffer from progressive disease or relapse. Because of the extremely poor reinduction success, the salvage rate for these patients is poor, with only a 14% (SE = 6%) overall survival. Long-term survival was only achieved in those few patients who were able to undergo an allogeneic SCT."],["dc.identifier.doi","10.1200/JCO.2008.19.3367"],["dc.identifier.isi","000267821400017"],["dc.identifier.pmid","19433688"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6241"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16276"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Clinical Oncology"],["dc.publisher.place","Alexandria"],["dc.relation.conference","50th Annual Meeting of the American-Society-of-Hematology/ASH/ASCO Joint Symposium"],["dc.relation.eventlocation","San Francisco, CA"],["dc.relation.issn","1527-7755"],["dc.relation.issn","0732-183X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Poor Outcome for Children and Adolescents With Progressive Disease or Relapse of Lymphoblastic Lymphoma: A Report From the Berlin-Frankfurt-Muenster Group"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Fluids and Barriers of the CNS"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Möhn, Nora"],["dc.contributor.author","Luo, Yi"],["dc.contributor.author","Skripuletz, Thomas"],["dc.contributor.author","Schwenkenbecher, Philipp"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Stangel, Martin"],["dc.date.accessioned","2020-12-10T18:39:01Z"],["dc.date.available","2020-12-10T18:39:01Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s12987-019-0148-3"],["dc.identifier.eissn","2045-8118"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77514"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Tau-protein concentrations are not elevated in cerebrospinal fluid of patients with progressive multifocal leukoencephalopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","212"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","216"],["dc.bibliographiccitation.volume","257"],["dc.contributor.author","Pohl, Daniela"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Jacobi, Christian"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Krone, Bernd"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T08:46:22Z"],["dc.date.available","2018-11-07T08:46:22Z"],["dc.date.issued","2010"],["dc.description.abstract","Epstein-Barr virus (EBV) has been implicated in the pathogenesis of multiple sclerosis (MS). Recent reports proposed an increased EBV-targeted humoral immune response in MS, which appears to be more pronounced in pediatric patients. However, little is known about the CNS-derived antibody production against EBV in patients with MS. The objective of this study was to assess the frequency and intensity of intrathecal antibody production against EBV as compared to other neurotropic viruses in pediatric and adult onset MS. In cohorts of 43 childhood, 50 adult onset MS patients, 20 children and 12 adults with other CNS disorders, paired CSF and serum samples were studied. Frequency and intensity of intrathecal antibody production against EBV as compared to measles, rubella, varicella zoster (VZV) and herpes simplex virus (HSV) were analyzed by determination of virus-specific CSF-to-serum Antibody Indices (AI). Intrathecally synthesized EBV antibodies were detectable in 26% pediatric and 10% adult onset MS patients, compared to frequencies ranging in both groups from 10 to 60% for the other viruses. Median AIs for EBV were lower than those for all other viruses, with more than twofold higher median AI for measles, rubella and VZV. The EBV-targeted humoral immune response in the CNS is only part of the intrathecal polyspecific antibody production in MS, directed against various neurotropic viruses. Our results do not rule out the possibility that EBV is involved in the pathogenesis of MS by triggering diverse cellular immune mechanisms, but they argue against a direct pathogenic role of EBV-targeted humoral immune response within the CNS."],["dc.description.sponsorship","Hertie-Stiftung [GHS 191/00]"],["dc.identifier.doi","10.1007/s00415-009-5296-y"],["dc.identifier.isi","000274251700008"],["dc.identifier.pmid","19714396"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6746"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20676"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Intrathecal antibody production against Epstein-Barr and other neurotropic viruses in pediatric and adult onset 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"]]