Ciesielczyk, Barbara

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Kiesel, Petra"],["dc.contributor.author","Gibson, Toby J."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Bodemer, Walter"],["dc.contributor.author","Zischler, Hans"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:44:50Z"],["dc.date.available","2018-11-07T08:44:50Z"],["dc.date.issued","2010"],["dc.description.abstract","Alu DNA elements were long considered to be of no biological significance and thus have been only poorly defined. However, in the past Alu DNA elements with well-defined nucleotide sequences have been suspected to contribute to disease, but the role of Alu DNA element transcripts has rarely been investigated. For the first time, we determined in a real-time approach Alu DNA element transcription in buffy coat cells isolated from the blood of humans suffering from sporadic Creutzfeldt-Jakob disease (sCJD) and other neurodegenerative disorders. The reverse transcribed Alu transcripts were amplified and their cDNA sequences were aligned to genomic regions best fitted to database genomic Alu DNA element sequences deposited in the UCSC and NCBI data bases. Our cloned Alu RNA/cDNA sequences were widely distributed in the human genome and preferably belonged to the \"young\" Alu Y family. We also observed that some RNA/cDNA clones could be aligned to several chromosomes because of the same degree of identity and score to resident genomic Alu DNA elements. These elements, called paralogues, have purportedly been recently generated by retrotransposition. Along with cases of sCJD we also included cases of dementia and Alzheimer disease (AD). Each group revealed a divergent pattern of transcribed Alu elements. Chromosome 2 was the most preferred site in sCJD cases, besides chromosome 17; in AD cases chromosome 11 was overrepresented whereas chromosomes 2, 3 and 17 were preferred active Alu loci in controls. Chromosomes 2, 12 and 17 gave rise to Alu transcripts in dementia cases. The detection of putative Alu paralogues widely differed depending on the disease. A detailed data search revealed that some cloned Alu transcripts originated from RNA polymerase III transcription since the genomic sites of their Alu elements were found between genes. Other Alu DNA elements could be located close to or within coding regions of genes. In general, our observations suggest that identification and genomic localization of active Alu DNA elements could be further developed as a surrogate marker for differential gene expression in disease. A sufficient number of cases are necessary for statistical significance before Alu DNA elements can be considered useful to differentiate neurodegenerative diseases from controls."],["dc.identifier.isi","000280388200006"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20288"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1933-6896"],["dc.title","Transcription of Alu DNA elements in blood cells of sporadic Creutzfeldt-Jakob disease (sCJD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1591"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","ARCHIVES OF NEUROLOGY"],["dc.bibliographiccitation.lastpage","1594"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:55:05Z"],["dc.date.available","2018-11-07T10:55:05Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: In neurodegenerative diseases, increasing attention has been focused on inflammatory mediators such as pro-inflammatory and anti-inflammatory cytokines and their potential influence in the process of neurodegeneration. In prion diseases, much data has been gained on the cell culture and animal disease models level, but only limited information is available on humans affected by Creutzfeldt-Jakob disease (CJD). Objective: To obtain data on anti-inflammatory cytokines interleukin 4 and interleukin 10 in the cerebrospinal fluid of patients with CJD, patients with other dementia, and nondemented neurological patients and controls. Design: Cerebrospinal fluid samples were collected from CJD patients and control subjects, and concentrations of the anti-inflammatory cytokines interleukin 4 and interleukin 10 were determined using an enzyme-linked immunosorbent assay. Patients: Cerebrospinal fluid samples from 61 patients were analyzed. The group was composed of patients with CJD (n = 20), patients with other forms of dementia (n = 10), patients with motoneuron disease (n = 6), patients with normal pressure hydrocephalus (n = 5), and control subjects (n = 20). Conclusions: Elevated levels of the anti-inflammatory cytokines interleukin 4 and interleukin 10 in cerebrospinal fluid of patients with CJD are new findings. The data of the present study provide a clue toward the possible role of cytokines as immunological modifiers in the neurodegenerative process of CJD."],["dc.identifier.doi","10.1001/archneur.62.10.1591"],["dc.identifier.isi","000232502900014"],["dc.identifier.pmid","16216944"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49709"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","Interleukin 4 and interleukin 10 levels are elevated in the cerebrospinal fluid of patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","87"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Kiesel, Petra"],["dc.contributor.author","Gibson, Toby J."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Bodemer, Walter"],["dc.contributor.author","Zischler, Hans"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2022-10-06T13:26:54Z"],["dc.date.available","2022-10-06T13:26:54Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.4161/pri.4.2.11965"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115196"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1933-690X"],["dc.relation.issn","1933-6896"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Transcription of Alu DNA elements in blood cells of sporadic Creutzfeldt-Jakob disease (sCJD)"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","PII 931918862"],["dc.bibliographiccitation.firstpage","88"],["dc.bibliographiccitation.issue","2-4"],["dc.bibliographiccitation.journal","Journal of Toxicology and Environmental Health Part A"],["dc.bibliographiccitation.lastpage","95"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Kiesel, Petra"],["dc.contributor.author","Gibson, Toby J."],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Bodemer, Walter"],["dc.contributor.author","Zischler, Hans"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:01:37Z"],["dc.date.available","2018-11-07T09:01:37Z"],["dc.date.issued","2011"],["dc.description.abstract","Editing of RNA molecules gained major interest when coding mRNA was analyzed. A small, noncoding, Alu DNA element transcript that may act as regulatory RNA in cells was examined in this study. Alu DNA element transcription was determined in buffy coat from healthy humans and human sporadic Creutzfeldt-Jakob disease (sCJD) cases. In addition, non-sCJD controls, mostly dementia cases and Alzheimer's disease (AD) cases, were included. The Alu cDNA sequences were aligned to genomic Alu DNA elements by database search. A comparison of best aligned Alu DNA sequences with our RNA/cDNA clones revealed editing by deamination by ADAR (adenosine deaminase acting on RNA) and APOBEC (apolipoprotein B editing complex). Nucleotide exchanges like a G instead of an A or a T instead of a C in our cDNA sequences versus genomic Alu DNA pointed to recent mutations. To confirm this, our Alu cDNA sequences were aligned not only to genomic human Alu DNA but also to the respective genomic DNA of the chimpanzee and rhesus. Enhanced ADAR correlated with A-G exchanges in dementia, AD, and sCJD was noted when compared to healthy controls as well as APOBEC-related C-T exchanges. The APOBEC-related mutations were higher in healthy controls than in cases suffering from neurodegeneration, with the exception of the dementia group with the prion protein gene (PRNP) MV genotype. Hence, this study may be considered the first real-time analysis of Alu DNA element transcripts with regard to editing of the respective Alu transcripts in human blood cells."],["dc.identifier.doi","10.1080/15287394.2011.529057"],["dc.identifier.isi","000286822400003"],["dc.identifier.pmid","21218337"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24472"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Inc"],["dc.relation.issn","1528-7394"],["dc.title","Possible Editing of Alu Transcripts in Blood Cells of Sporadic Creutzfeldt-Jakob Disease (sCJD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","35"],["dc.bibliographiccitation.journal","BMC Neurology"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Boesenberg-Grosse, Constanze"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Ciesielczyk, Barbara"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Eigenbrod, Sabina"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:14:53Z"],["dc.date.available","2018-11-07T09:14:53Z"],["dc.date.issued","2006"],["dc.description.abstract","Background: Brain derived proteins such as 14-3-3, neuron-specific enolase (NSE), S 100b, tau, phosphorylated tau and A beta(1-42) were found to be altered in the cerebrospinal fluid (CSF) in Creutzfeldt-Jakob disease (CJD) patients. The pathogenic mechanisms leading to these abnormalities are not known, but a relation to rapid neuronal damage is assumed. No systematic analysis on brain-derived proteins in the CSF and neuropathological lesion profiles has been performed. Methods: CSF protein levels of brain-derived proteins and the degree of spongiform changes, neuronal loss and gliosis in various brain areas were analyzed in 57 CJD patients. Results: We observed three different patterns of CSF alteration associated with the degree of cortical and subcortical changes. NSE levels increased with lesion severity of subcortical areas. Tau and 14-3-3 levels increased with minor pathological changes, a negative correlation was observed with severity of cortical lesions. Levels of the physiological form of the prion protein (PrPc) and A beta(1-42) levels correlated negatively with cortical pathology, most clearly with temporal and occipital lesions. Conclusion: Our results indicate that the alteration of levels of brain-derived proteins in the CSF does not only reflect the degree of neuronal damage, but it is also modified by the localization on the brain pathology. Brain specific lesion patterns have to be considered when analyzing CSF neuronal proteins."],["dc.identifier.doi","10.1186/1471-2377-6-35"],["dc.identifier.isi","000240991000001"],["dc.identifier.pmid","16989662"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1372"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27536"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2377"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Brain-derived proteins in the CSF, do they correlate with brain pathology in CJD?"],["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"]]