Schütz, Ekkehard

[["dc.bibliographiccitation.artnumber","e0154602"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Wehrhahn, Christin"],["dc.contributor.author","Wanjek, Marius"],["dc.contributor.author","Bortfeld, Ralf"],["dc.contributor.author","Wemheuer, Wilhelm E."],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Brenig, Bertram"],["dc.date.accessioned","2018-11-07T10:15:21Z"],["dc.date.available","2018-11-07T10:15:21Z"],["dc.date.issued","2016"],["dc.description.abstract","Background With the availability of massive SNP data for several economically important cattle breeds, haplotype tests have been performed to identify unknown recessive disorders. A number of so-called lethal haplotypes, have been uncovered in Holstein Friesian cattle and, for at least seven of these, the causative mutations have been identified in candidate genes. However, several lethal haplotypes still remain elusive. Here we report the molecular genetic causes of lethal haplotype 5 (HH5) and cholesterol deficiency (CDH). A targeted enrichment for the known genomic regions, followed by massive parallel sequencing was used to interrogate for causative mutations in a case/control approach. Methods Targeted enrichment for the known genomic regions, followed by massive parallel sequencing was used in a case/control approach. PCRs for the causing mutations were developed and compared to routine imputing in 2,100 (HH5) and 3,100 (CDH) cattle. Results HH5 is caused by a deletion of 138kbp, spanning position 93,233kb to 93,371kb on chromosome 9 (BTA9), harboring only dimethyl-adenosine transferase 1 (TFB1M). The deletion breakpoints are flanked by bovine long interspersed nuclear elements Bov-B (upstream) and L1ME3 (downstream), suggesting a homologous recombination/deletion event. TFB1M di-methylates adenine residues in the hairpin loop at the 3'-end of mitochondrial 12S rRNA, being essential for synthesis and function of the small ribosomal subunit of mitochondria. Homozygous TFB1M(-/-) mice reportedly exhibit embryonal lethality with developmental defects. A 2.8% allelic frequency was determined for the German HF population. CDH results from a 1.3kbp insertion of an endogenous retrovirus (ERV2-1-LTR_BT) into exon 5 of the APOB gene at BTA11: 77,959kb. The insertion is flanked by 6bp target site duplications as described for insertions mediated by retroviral integrases. A premature stop codon in the open reading frame of APOB is generated, resulting in a truncation of the protein to a length of only < 140 amino acids. Such early truncations have been shown to cause an inability of chylomicron excretion from intestinal cells, resulting in malabsorption of cholesterol. The allelic frequency of this mutation in the German HF population was 6.7%, which is substantially higher than reported so far. Compared to PCR assays inferring the genetic variants directly, the routine imputing used so far showed a diagnostic sensitivity of as low as 91% (HH5) and 88% (CDH), with a high specificity for both (>= 99.7%). Conclusion With the availability of direct genetic tests it will now be possible to more effectively reduce the carrier frequency and ultimately eliminate the disorders from the HF populations. Beside this, the fact that repetitive genomic elements (RE) are involved in both diseases, underline the evolutionary importance of RE, which can be detrimental as here, but also advantageous over generations."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.identifier.doi","10.1371/journal.pone.0154602"],["dc.identifier.isi","000375212600046"],["dc.identifier.pmid","27128314"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13249"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40795"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights.access","openAccess"],["dc.title","The Holstein Friesian Lethal Haplotype 5 (HH5) Results from a Complete Deletion of TBF1M and Cholesterol Deficiency (CDH) from an ERV-(LTR) Insertion into the Coding Region of APOB"],["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.firstpage","549"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cancer Cell"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Berg, Tobias"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Alexe, Gabriela"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schnuetgen, Frank"],["dc.contributor.author","Cremer, Anjali"],["dc.contributor.author","Haetscher, Nadine"],["dc.contributor.author","Goellner, Stefanie"],["dc.contributor.author","Rouhi, Arefeh"],["dc.contributor.author","Palmqvist, Lars"],["dc.contributor.author","Rieger, Michael A."],["dc.contributor.author","Schroeder, Timm"],["dc.contributor.author","Boenig, Halvard"],["dc.contributor.author","Meuller-Tidow, Carsten"],["dc.contributor.author","Kuchenbauer, Florian"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Green, Anthony R."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Stegmaier, Kimberly"],["dc.contributor.author","Humphries, R. Keith"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:25:02Z"],["dc.date.available","2018-11-07T10:25:02Z"],["dc.date.issued","2017"],["dc.description.abstract","The transcription factor Meis1 drives myeloid leukemogenesis in the context of Hox gene overexpression but is currently considered undruggable. We therefore investigated whether myeloid progenitor cells transformed by Hoxa9 and Meis1 become addicted to targetable signaling pathways. A comprehensive (phospho) proteomic analysis revealed that Meis1 increased Syk protein expression and activity. Syk upregulation occurs through a Meis1-dependent feedback loop. By dissecting this loop, we show that Syk is a direct target of miR-146a, whose expression is indirectly regulated by Meis1 through the transcription factor PU. 1. In the context of Hoxa9 overexpression, Syk signaling induces Meis1, recapitulating several leukemogenic features of Hoxa9/Meis1-driven leukemia. Finally, Syk inhibition disrupts the identified regulatory loop, prolonging survival of mice with Hoxa9/Meis1-driven leukemia."],["dc.identifier.doi","10.1016/j.ccell.2017.03.001"],["dc.identifier.isi","000398670600010"],["dc.identifier.pmid","28399410"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42772"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","1878-3686"],["dc.relation.issn","1535-6108"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia"],["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.journal","Haematologica"],["dc.bibliographiccitation.volume","100"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Beck, J."],["dc.contributor.author","Pan, K.-T."],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schuetz, Eckehardt"],["dc.contributor.author","Tomska, Katarzyna"],["dc.contributor.author","Sellner, L."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.date.accessioned","2018-11-07T09:56:10Z"],["dc.date.available","2018-11-07T09:56:10Z"],["dc.date.issued","2015"],["dc.format.extent","178"],["dc.identifier.isi","000361204901386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36907"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ferrata Storti Foundation"],["dc.publisher.place","Pavia"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","0390-6078"],["dc.title","THE B CELL RECEPTOR SIGNALING OUTPUT IN BURKITT'S LYMPHOMA IS GENOTYPE-SPECIFIC AND IMPACTS SENSITIVITY TOWARDS BCR SIGNALING INHIBITORS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Therapeutic Drug Monitoring"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Shipkova, Maria"],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Wieland, Eberhard"],["dc.contributor.author","Weber, Lutz T."],["dc.contributor.author","Tonshoff, B."],["dc.contributor.author","Armstrong, Victor William"],["dc.date.accessioned","2018-11-07T10:55:24Z"],["dc.date.available","2018-11-07T10:55:24Z"],["dc.date.issued","2000"],["dc.description.abstract","The need for mycophenolic acid (MPA) monitoring is still under discussion. Key issues for the PK/PD relationships of this drug are: the role of metabolites, the usefulness of AUC versus predose levels, and the need to monitor the free concentration of MPA (f-MPA). Recent advances have revealed that, in addition to 7-O-MPAG, three additional MPA metabolites are present in the plasma of transplant recipients. One of these metabolites (M-2), identified as an acyl glucuronide of MPA, was found to inhibit IMPDH-II in vitro. This active metabolite was also found to cross-react in the Emit assay for MPA. In an ongoing multicenter study, the authors are evaluating the relevance of monitoring total (t-MPA) and free mycophenolic acid (f-MPA) in pediatric renal transplant recipients. As in adults, a time-dependant increase of t-MPA-AUC(0-12h) within the first 3 months posttransplant (35 versus 64 mg x L/h, 3 weeks versus 3 months respectively; daily dosage: 0.6 g/m(2) bid) was seen. Receiver operating characteristics curve analyses were used to test the ability of predose levels or AUC(0-12h) to discriminate between cases with no complications and those with acute rejection, adverse events (severe infections, leukopenia), or gastrointestinal disorders observed during the early posttransplant course, In agreement with observations in adults, a significant (p = 0.001) association was observed between AUC(0-12h) and acute rejection. A t-MPA-AUC(0-12h) of approximately 30-60 mg x L/h, as determined by HPLC, seems to be a reasonable target for the early posttransplant period. It remains to be elucidated whether regular predose level monitoring may be of more practical value. A higher incidence of rejection was observed at predose MPA concentrations less than or equal to 1 mg/L, as measured by HPLC. In contrast to t-MPA, f-MPA-AUC(0-12h) was significantly related to seven infections and leukopenia. The risk for severe adverse events was increased at f-MPA- AUC(0-12h) values greater than or equal to 600 mu g x Uh. On the basis of these data and the observed variability in the pharmacokinetics of MPA, the development of monitoring strategies for this drug appears to he promising."],["dc.identifier.doi","10.1097/00007691-200002000-00004"],["dc.identifier.isi","000085149700004"],["dc.identifier.pmid","10688252"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49780"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0163-4356"],["dc.title","Pharmacokinetic and metabolic investigations of mycophenolic acid in pediatric patients after renal transplantation: Implications for therapeutic drug monitoring"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","477"],["dc.bibliographiccitation.journal","Annals of the New York Academy of Sciences"],["dc.bibliographiccitation.lastpage","491"],["dc.bibliographiccitation.volume","1069"],["dc.contributor.author","Schedel, Jörg"],["dc.contributor.author","Gödde, Andrea"],["dc.contributor.author","Schütz, Ekkehard"],["dc.contributor.author","Bongartz, Tim A."],["dc.contributor.author","Lang, Bernhard"],["dc.contributor.author","Schölmerich, Jürgen"],["dc.contributor.author","Müller-Ladner, Ulf"],["dc.date.accessioned","2018-11-07T10:30:44Z"],["dc.date.available","2018-11-07T10:30:44Z"],["dc.date.issued","2006"],["dc.description.abstract","As azathioprine is one of the standard immunosuppressive drugs used for treatment of patients with different chronic inflammatory diseases, the effect of the azathioprine metabolizing enzyme thiopurine methyltransferase (TPMT) activity on incidence of adverse events (AE) was examined. In addition, potential correlations between the concentration of the azathioprine metabolite 6-thioguanine nucleotide (6-TGN) in erythrocytes (RBC) and inflammatory disease activity as well as hematological AE were investigated. TPMT activities were investigated prospectively in 139 patients (35 mate, 104 female) with chronic inflammatory diseases [systemic lupus erythematosus (SLE, 38), progressive systemic sclerosis (PSS, 13), Wegener's granulomatosis (4), rheumatoid arthritis (RA, 5), and other chronic inflammatory diseases (79)]. In addition, 6-TGN concentrations were investigated in a second cohort of 58 patients (17 patients with SLE, 5 with PSS, 5 with vasculitides, 4 with undifferentiated connective tissue diseases, 1 with dermatomyositis, 1 with Sjogren's syndrome, 1 with RA, 20 with Crohn's disease, and 4 with ulcerative colitis) prior to and during therapy with azathioprine. The distribution of activities of TPMT in 139 patients showed a normal Gaussian distribution in the Caucasian population. Within the group of 96 patients taking azathioprine, known azathioprine-related AE could be observed: minor AE (sickness, rash, and increase in cholestasis parameters) in 11 patients (11.4%), and severe AE (bone marrow toxicity) in 7 patients (7.3%). Below a \"cutoff\" value of 11.9 nmol/mL REC x h of TPMT activity, AE were significantly more frequent. In the second cohort of patients, no significant correlations could be observed between 6-TGN concentrations and parameters of disease activity. Reduced activity of TPMT in patients with chronic inflammatory diseases requiring immunosuppressive therapy with azathioprine, especially below a distinct cutoff, appears to inherit a substantial risk for development of AE."],["dc.identifier.doi","10.1196/annals.1351.048"],["dc.identifier.isi","000239951000047"],["dc.identifier.pmid","16855176"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43936"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","3rd International Conference on Neuroendocrine Immune Basis of the Rheumatic Diseases"],["dc.relation.eventend","2005-09-12"],["dc.relation.eventlocation","Genova, ITALY"],["dc.relation.eventstart","2005-09-10"],["dc.relation.isbn","1-57331-593-1"],["dc.relation.issn","0077-8923"],["dc.title","Impact of thiopurine methyltransferase activity and 6-thioguanine nucleotide concentrations in patients with chronic inflammatory diseases"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","156"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Chemistry"],["dc.bibliographiccitation.lastpage","161"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Oellerich, M."],["dc.contributor.author","Schutz, Ekkehard"],["dc.date.accessioned","2018-11-07T10:16:50Z"],["dc.date.available","2018-11-07T10:16:50Z"],["dc.date.issued","2000"],["dc.description.abstract","Background: alpha(1)-Antitrypsin is the major plasma serine protease inhibitor. Its deficiency is mainly associated with the alleles PI S and PI Z and can lead to obstructive lung disease in adults and to liver cirrhosis during childhood. Methods: A multiplex PCR method has been established that uses two sets of primers to amplify the gene regions covering the PI S or PI Z mutations sites. Mutation detection was performed on the LightCycler by melting curve analysis of detection probes labeled with two different fluorescent dyes, LC-Red640 and LC-Red705. Results: Unequivocal genotyping results were obtained for all investigated samples in an assay time of similar to 30 min. The color compensation procedure greatly improved the readability of the resulting diagnostic melting curves. Conclusions: To our knowledge, this is the first report of simultaneous detection of two mutations in a single tube by PCR of genomic DNA and the use of two different reporter dyes with the LightCycler color compensation feature. This approach is a rapid, convenient, and economic alternative to other methods described to date for the detection of alpha(1)-antitrypsin deficiency alleles. (C) 2000 American Association for Clinical Chemistry."],["dc.identifier.isi","000085288500004"],["dc.identifier.pmid","10657370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41113"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Clinical Chemistry"],["dc.publisher.place","Washington"],["dc.relation.conference","Meeting of the Deutsche-Gesellschaft-fur-Klinische-Chemie / Deutsche-Gesellschaft-fur-Laboratoriumsmedizin"],["dc.relation.eventlocation","REGENSBURG, GERMANY"],["dc.relation.issn","0009-9147"],["dc.title","Use of two reporter dyes without interference in a single-tube rapid-cycle PCR: alpha(1)-antitrypsin genotyping by multiplex real-time fluorescence PCR with the LightCycler"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","550"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","556"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Gordon, Paul M. K."],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Urnovitz, Howard B."],["dc.contributor.author","Graham, Catherine"],["dc.contributor.author","Clark, Renee"],["dc.contributor.author","Dudas, Sandor"],["dc.contributor.author","Czub, Stefanie"],["dc.contributor.author","Sensen, Maria"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Groschup, Martin H."],["dc.contributor.author","Church, Robert B."],["dc.contributor.author","Sensen, Christoph W."],["dc.date.accessioned","2018-11-07T08:33:15Z"],["dc.date.available","2018-11-07T08:33:15Z"],["dc.date.issued","2009"],["dc.description.abstract","To gain insight into the disease progression of transmissible spongiform encephalopathies (TSE), we searched for disease-specific patterns in circulating nucleic acids (CNA) in elk and cattle. In a 25-month time-course experiment, CNAs were isolated from blood samples of 24 elk (Cervus elaphus) orally challenged with chronic wasting disease (CWD) infectious material. In a separate experiment, blood-sample CNAs from 29 experimental cattle (Bos taurus) 40 months post-inoculation with clinical bovine spongiform encephalopathy (BSE) were analyzed according to the same protocol. Next-generation sequencing provided broad elucidation of sample CNAs: we detected infection-specific sequences as early as 11 months in elk (i.e. at least 3 months before the appearance of the first clinical signs) and we established CNA patterns related to BSE in cattle at least 4 months prior to clinical signs. In elk, a progression of CNA sequence patterns was found to precede and correlate with macro-observable disease progression, including delayed CWD progression in elk with PrP genotype LM. Some of the patterns identified contain transcription-factor-binding sites linked to endogenous retroviral integration. These patterns suggest that retroviruses may be connected to the manifestation of TSEs. Our results may become useful for the early diagnosis of TSE in live elk and cattle."],["dc.identifier.doi","10.1093/nar/gkn963"],["dc.identifier.isi","000262963400031"],["dc.identifier.pmid","19059996"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4005"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17531"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0305-1048"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Disease-specific motifs can be identified in circulating nucleic acids from live elk and cattle infected with transmissible spongiform encephalopathies"],["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","e75485"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Hennecke, Silvia"],["dc.contributor.author","Bornemann-Kolatzki, Kirsten"],["dc.contributor.author","Urnovitz, Howard B."],["dc.contributor.author","Neumann, Stephan"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.date.accessioned","2018-11-07T09:19:45Z"],["dc.date.available","2018-11-07T09:19:45Z"],["dc.date.issued","2013"],["dc.description.abstract","Mammary tumors are the most frequent cancers in female dogs exhibiting a variety of histopathological differences. There is lack of knowledge about the genomes of these common dog tumors. Five tumors of three different histological subtypes were evaluated. Massive parallel sequencing (MPS) was performed in comparison to the respective somatic genome of each animal. Copy number and structural aberrations were validated using droplet digital PCR (ddPCR). Using mate-pair sequencing chromosomal aneuploidies were found in two tumors, frequent smaller deletions were found in one, inter-chromosomal fusions in one other, whereas one tumor was almost normal. These aberrations affect several known cancer associated genes such as cMYC, and KIT. One common deletion of the proximal end of CFA27, harboring the tumor suppressor gene PFDN5 was detected in four tumors. Using ddPCR, this deletion was validated and detected in 50% of tumors (N = 20). Breakpoint specific dPCRs were established for four tumors and tumor specific cell-free DNA (cfDNA) was detected in the plasma. In one animal tumor-specific cfDNA was found >1 year after surgery, attributable to a lung metastasis. Paired-end sequencing proved that copy-number imbalances of the tumor are reflected by the cfDNA. This report on chromosomal instability of canine mammary cancers reveals similarities to human breast cancers as well as special canine alterations. This animal model provides a framework for using MPS for screening for individual cancer biomarkers with cost effective confirmation and monitoring using ddPCR. The possibility exists that ddPCR can be expanded to screening for common cancer related variants."],["dc.identifier.doi","10.1371/journal.pone.0075485"],["dc.identifier.isi","000325423500069"],["dc.identifier.pmid","24098698"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28716"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Genome Aberrations in Canine Mammary Carcinomas and Their Detection in Cell-Free Plasma DNA"],["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.firstpage","30"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","113"],["dc.contributor.author","Schmidt, H"],["dc.contributor.author","Tlustochowska, A."],["dc.contributor.author","Stuertz, K."],["dc.contributor.author","Djukic, M."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Schutz, Ekkehard"],["dc.contributor.author","Kuhnt, U."],["dc.contributor.author","Nau, R."],["dc.date.accessioned","2021-06-01T10:50:09Z"],["dc.date.available","2021-06-01T10:50:09Z"],["dc.date.issued","2001"],["dc.description.abstract","Hippocampal slices of newborn rats were exposed to either heat-inactivated Streptococcus pneumoniae R6 (hiR6) equivalent to 10(6) and 10(8) CFU/ml, lipoteichoic acid (LTA) (0.3 mug/ml and 30 mug/ml), peptidoglycans (PG) (0.3, 30, 50 and 100 mug/ml), pneumococcal DNA (pDNA) (0.3 and 30 mug/ml) or medium only (control). Cell injury was examined by Nissl staining, Annexin V and NeuN immunohistochemistry, and quantified by propidium iodide (PI) uptake and by determining neuron-specific enolase (NSE) concentration in the culture medium. Necrotic and apoptotic cell damage occurred in all treatment groups. Overall damage (Nissl and PI staining) was most prominent after hiR6 (10(8) CFU/ml), followed by LTA (30 mug/ml), pDNA (30 mug/ml), and not detectable after PG (30 mug/ml) exposure. PG (100 mug/ml) induced severe damage. Apoptotic cells were most frequent after exposure to LTA and hiR6. Damage in the neuronal cell layers (NeuN, NSE) was most severe after treatment with hiR6 (10(8) CFU/ml), followed by PG (100 mug/ml), pDNA (30 mug/ml), and LTA (30 mug/ml). (C) 2001 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0165-5728(00)00402-1"],["dc.identifier.isi","000166575000004"],["dc.identifier.pmid","11137574"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86547"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0165-5728"],["dc.title","Organotypic hippocampal cultures A model of brain tissue damage in Streptococcus pneumoniae meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","228"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Forensic Science International Genetics"],["dc.bibliographiccitation.lastpage","231"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Brenig, Bertram"],["dc.contributor.author","Beck, J."],["dc.contributor.author","Schuetz, Eckehardt"],["dc.date.accessioned","2018-11-07T08:41:39Z"],["dc.date.available","2018-11-07T08:41:39Z"],["dc.date.issued","2010"],["dc.description.abstract","A detailed molecular analysis of blood or other biological stains at a crime scene is often hampered by the low quantity and quality of the extractable DNA. However, the determination of the origin and composition of a stain is in most cases a prerequisite for the final elucidation of a criminal case. Standard methodologies, e.g. amplification of DNA followed by microsatellite typing or mitochondrial DNA sequencing, are often not sensitive enough to result in sufficient and conclusive data. We have applied ultra-deep DNA sequencing using the 454 pyrosequencing technology on a whole genome amplified (WGA) environmental biological stain, which was analysed unsuccessfully with standard methodologies following WGA. With the combination of WGA and 454 pyrosequencing, however, we were able to generate 7242 single sequences with an average length of 195 bp. A total of 1,441,971 bp DNA sequences were generated and compared with public DNA sequence databases. Using RepeatMasker and basic logical alignment search tool (BLAST) searches against known microbial and mammalian genomes it was possible to determine the metagenomic composition of the stain, i.e. 4.2% bacterial DNA, 0.3% viral DNA, 2.7% fungal DNA, 10.3% mammalian repetitive DNA, 0.9% porcine DNA, 0.13% human DNA and 81.5% DNA of unknown origin. Our data demonstrate that 454 pyrosequencing has the potential to become a powerful tool not only in basic research but also in the metagenomic analysis of biological trace materials for forensic genetics. (C) 2009 Elsevier Ireland Ltd. All rights reserved."],["dc.description.sponsorship","Erxleben Research and Innovation Council ERIC [ERIC-BR1959-2008-01]"],["dc.identifier.doi","10.1016/j.fsigen.2009.10.001"],["dc.identifier.isi","000278592500002"],["dc.identifier.pmid","20457050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19523"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","1872-4973"],["dc.title","Shotgun metagenomics of biological stains using ultra-deep DNA sequencing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]