Emmert, Steffen

[["dc.bibliographiccitation.firstpage","278"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Plasma Processes and Polymers"],["dc.bibliographiccitation.lastpage","286"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Helmke, Andreas"],["dc.contributor.author","Hoffmeister, Dennis"],["dc.contributor.author","Berge, Frank"],["dc.contributor.author","Emmert, Steffen"],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Mertens, Nina"],["dc.contributor.author","Vioel, Wolfgang"],["dc.contributor.author","Weltmann, Klaus-Dieter"],["dc.date.accessioned","2018-11-07T08:56:58Z"],["dc.date.available","2018-11-07T08:56:58Z"],["dc.date.issued","2011"],["dc.description.abstract","The inactivation of the Gram-positive bacteria Staphylococcus epidermidis (ATCC 12228) in its vegetative state was studied in vitro after exposure to cold atmospheric pressure plasma generated by direct dielectric barrier discharge (DBD). Compared to UV radiation at 254 nm, plasma UV emission yielded no significant contribution to bacterial inactivation. Analysis of bacterial growth inhibition revealed a pH dependency on growth media. Yet, measurements combined with numerical simulations excluded the pH shift induced by plasma generated reactive species as the main cause of bacterial inactivation. Scanning electron microscopy (SEM) images showed no alteration of cell walls, while fluorescence microscopy revealed lethal damage to cell membranes even after 1 s treatment. When the cell membrane was already severely damaged, also degradation of the bacterial DNA by plasma treatment was found. We conclude that membrane damage due to reactive oxygen species (ROS) and DNA degradation are the main mechanisms of plasma-induced bacterial death that is aggregated by milieu acidification."],["dc.identifier.doi","10.1002/ppap.201000168"],["dc.identifier.isi","000289999200001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23275"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-v C H Verlag Gmbh"],["dc.relation.issn","1612-8869"],["dc.relation.issn","1612-8850"],["dc.title","Physical and Microbiological Characterisation of Staphylococcus epidermidis Inactivation by Dielectric Barrier Discharge Plasma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1085"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Carcinogenesis"],["dc.bibliographiccitation.lastpage","1090"],["dc.bibliographiccitation.volume","26"],["dc.contributor.author","Blankenburg, S."],["dc.contributor.author","Konig, I. R."],["dc.contributor.author","Moessner, R."],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Thoms, Kai Martin"],["dc.contributor.author","Krueger, Ulrich"],["dc.contributor.author","Khan, Sajjad"],["dc.contributor.author","Westphal, G."],["dc.contributor.author","Berking, Carola"],["dc.contributor.author","Volkenandt, Matthias"],["dc.contributor.author","Reich, Kristian"],["dc.contributor.author","Neumann, C."],["dc.contributor.author","Ziegler, Andreas"],["dc.contributor.author","Kraemer, Kenneth H."],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T10:29:15Z"],["dc.date.available","2018-11-07T10:29:15Z"],["dc.date.issued","2005"],["dc.description.abstract","Individuals with the rare DNA repair deficiency syndrome xeroderma pigmentosum (XP) are sensitive to the sun and exhibit a 1000-fold increased risk for developing skin cancers, including cutaneous melanoma. Inherited polymorphisms of XP genes may contribute to subtle variations in DNA repair capacity and genetic susceptibility to melanoma. We investigated the role of three polymorphic alleles of the DNA repair gene XPC in a hospital-based case-control study of 294 Caucasian patients from Germany who had cutaneous melanoma and 375 healthy cancer-free sex-matched Caucasian control subjects from the same area. We confirmed that the XPC intron 9 PAT+, intron 11 -6A, and the exon 15 2920C polymorphisms are in a linkage disequilibrium. Only 1.6% of the 669 donors genotyped were discordant for these three polymorphisms. The allele frequencies (cases: controls) were for intron 9 PAT+ 41.7%:36.9%, for intron 11 -6A 41.8%:37.0% and for exon 15 2920C 41.3%:37.3%. Using multivariate logistic regression analyses to control for age, skin type and number of nevi, the three polymorphisms were significantly associated with increased risks of melanoma: OR 1.87 (95% CI: 1.10-3.19; P = 0.022), OR 1.83 (95% CI: 1.07-3.11; P = 0.026), and OR 1.82 (95% CI: 1.07-3.08; P = 0.026), respectively. Exploratory multivariate analyses of distinct subgroups revealed that these polymorphisms were associated with increased risks for the development of multiple primary melanomas (n = 28). The results of our case-control study support the hypothesis that the intron 9 PAT+, intron 11 -6A and exon 15 2920C haplotype may contribute to the risk of developing cutaneous melanoma by increasing the rate of an alternatively spliced XPC mRNA isoform that skips exon 12 and leads to reduced DNA repair. Our results should be validated in independent samples in order to guard against false positive findings."],["dc.description.sponsorship","Intramural NIH HHS [Z01 BC004517-31]"],["dc.identifier.doi","10.1093/carcin/bgi055"],["dc.identifier.isi","000229700100008"],["dc.identifier.pmid","15731165"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43601"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0143-3334"],["dc.title","Assessment of 3 xeroderma pigmentosum group C gene polymorphisms and risk of cutaneous melanoma: a case-control study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","154"],["dc.bibliographiccitation.journal","JDDG Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.lastpage","155"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Thoms, K-M"],["dc.contributor.author","Kuschal, Christiane"],["dc.contributor.author","Mori, T."],["dc.contributor.author","Kobayashi, Nobuhiko"],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Boeckmann, L."],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T08:29:22Z"],["dc.date.available","2018-11-07T08:29:22Z"],["dc.date.issued","2009"],["dc.identifier.isi","000268960300506"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16637"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.issn","1610-0379"],["dc.title","Cyclosporin A but not everolimus inhibits the DNA-repair"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","486"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.lastpage","489"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Schaefer, Annika"],["dc.contributor.author","Gratchev, Alexei"],["dc.contributor.author","Seebode, Christina"],["dc.contributor.author","Hofmann, Lars"],["dc.contributor.author","Schubert, Steffen"],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Apel, Antje"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Tzvetkov, Mladen"],["dc.contributor.author","Weishaupt, Carsten"],["dc.contributor.author","Oji, Vinzenz"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T09:23:16Z"],["dc.date.available","2018-11-07T09:23:16Z"],["dc.date.issued","2013"],["dc.description.abstract","The xeroderma pigmentosum (XP) group D protein is involved in nucleotide excision repair (NER) as well as in basal transcription. Determined by the type of XPD mutation, six different clinical entities have been distinguished: XP, XP with neurological symptoms, trichothiodystrophy (TTD), XP/TTD complex, XP/Cockayne syndrome (CS) complex or the cerebro-oculo-facio-skeletal syndrome (COFS). We identified nine new XPD-deficient patients. Their fibroblasts showed reduced post-UV cell survival, reduced NER capacity, normal XPD mRNA expression and partly reduced XPD protein expression. Six patients exhibited a XP phenotype in accordance with established XP-causing mutations (c.2079G>A, p.R683Q; c.2078G>T, p.R683W; c.1833G>T, p.R601L; c.1878G>C, p.R616P; c.1878G>A, p.R616Q). One TTD patient was homozygous for the known TTD-causing mutation p.R722W (c.2195C>T). Two patients were compound heterozygous for a TTD-causing mutation (c.366G>A, p.R112H) and a novel p.D681H (c.2072G>C) amino acid exchange, but exhibited different TTD and XP/CS complex phenotypes, respectively. Interestingly, the XP/CS patient's cells exhibited a reduced but well detectable XPD protein expression compared with hardly detectable XPD expression of the TTD patient's cells. Same mutations with different clinical outcomes in NER-defective patients demonstrate the complexity of phenotype-genotype correlations, for example relating to additional genetic variations (parental consanguinity), different allelic expression due to SNPs or differences in the methylation status."],["dc.identifier.doi","10.1111/exd.12166"],["dc.identifier.isi","000320935600012"],["dc.identifier.pmid","23800062"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29540"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1600-0625"],["dc.relation.issn","0906-6705"],["dc.title","Functional and molecular genetic analyses of nine newly identified XPD-deficient patients reveal a novel mutation resulting in TTD as well as in XP/CS complex phenotypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","580"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Scandinavian Journal of Clinical and Laboratory Investigation"],["dc.bibliographiccitation.lastpage","588"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Thoms, Kai Martin"],["dc.contributor.author","Baesecke, Joerg"],["dc.contributor.author","Emmert, Birgit"],["dc.contributor.author","Hermann, J."],["dc.contributor.author","Roedling, T."],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Leibeling, Diana"],["dc.contributor.author","Truemper, Lorenz H."],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T11:07:34Z"],["dc.date.available","2018-11-07T11:07:34Z"],["dc.date.issued","2007"],["dc.description.abstract","Deficiencies in individual DNA repair systems are involved in both de novo and therapy-related acute myeloid leukaemia (t-AML), as indicated by genetic markers involving nucleotide excision repair (NER gene polymorphisms), double-strand-break (DSB) or mismatch repair (microsatellite instability (MSI)). We modified a host cell reactivation (HCR) assay for functional DNA repair system analysis of living primary haematopoietic cells; 2 x 10(5) normal peripheral blood lymphocytes (PBLs) and cord blood CD34+ progenitor cells were cryopreserved, thawed and transfected with 75 250 ng luciferase reporter plasmid (pCMVLuc) using DEAE-dextran (0.1 mg/mL) in a transfection volume of 250 mu L. We obtained luciferase activities of similar to 300-fold above background in CD34+ progenitor cells and similar to 2000-fold in PBLs, thus rendering these cells applicable for DNA repair analysis. We then evaluated the NER (UV-irradiated pCMVLuc) and DSB repair capacity (linearized pCMVLuc) of normal lymphocytes and several leukaemic cell lineages. Kasumi-1 and HL-60 AML cells exhibited a reduced NER capacity compared to normal GM03715 lymphocytes, PBLs and CD34+ progenitor cells (6.2 +/- 0.9 %, 6.5 +/- 0.9% vs. 12.3 +/- 1.8 %, 13.5 +/- 0.7% and 13.5 +/- 2.0 %, respectively). Kasumi-1 AML cells exhibited a reduced DSB repair capacity compared to AG10107 and GM03715 normal lymphocytes as well as CEM acute T-cell lymphoblastic leukaemia cells (6.4 +/- 0.8% vs. 10.8 +/- 0.7 %, 27.3 +/- 1.1% and 20.5 +/- 1.6 %, respectively). The modified HCR assay can be used for functional DNA repair analysis in living cells of patients with pre- and post-leukaemic conditions as well as in leukaemic blasts to elucidate the role of DNA repair in de novo and t-AML leukaemogenesis and to determine the individual susceptibility to t-AML prior to chemotherapy."],["dc.identifier.doi","10.1080/00365510701230481"],["dc.identifier.isi","000249644300003"],["dc.identifier.pmid","17852814"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/52592"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis As"],["dc.relation.issn","0036-5513"],["dc.title","Functional DNA repair system analysis in haematopoietic progenitor cells using host cell reactivation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Jantke, M."],["dc.contributor.author","Tsvetkov, M."],["dc.contributor.author","Kamalapaskaran, S."],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Koenig, Inke R."],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T09:12:41Z"],["dc.date.available","2018-11-07T09:12:41Z"],["dc.date.issued","2012"],["dc.format.extent","e22"],["dc.identifier.isi","000300931700131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26998"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.conference","39th Annual Meeting of the Arbeitsgemeinschaft-Dermatologische-Forschung (ADF)"],["dc.relation.eventlocation","Marburg, GERMANY"],["dc.relation.issn","0906-6705"],["dc.title","Association of gene polymorphisms with cutaneous melanoma"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","JDDG Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Schaefer, Annika"],["dc.contributor.author","Schubert, Steffen"],["dc.contributor.author","Gratchev, Alexei"],["dc.contributor.author","Apel, Antje"],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Hofmann, Lars"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Mori, Toshio"],["dc.contributor.author","Kobayashi, Nobuhiko"],["dc.contributor.author","Schuerer, Anke"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T09:06:46Z"],["dc.date.available","2018-11-07T09:06:46Z"],["dc.date.issued","2012"],["dc.format.extent","678"],["dc.identifier.isi","000307881400026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25630"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1610-0379"],["dc.title","Characterization of five novel XPG mutations in three XP-G patients: Missense mutations impair repair and transcription"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","JDDG Journal der Deutschen Dermatologischen Gesellschaft"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Lehmann, J."],["dc.contributor.author","Schubert, S."],["dc.contributor.author","Schaefer, A."],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Haenssle, Holger Andreas"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Gratchev, Alexei"],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T09:36:16Z"],["dc.date.available","2018-11-07T09:36:16Z"],["dc.date.issued","2014"],["dc.format.extent","40"],["dc.identifier.isi","000340532500112"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32577"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1610-0387"],["dc.relation.issn","1610-0379"],["dc.title","A novel mutation in the XPA gene results in two truncated protein variants and leads to a severe XP/neurological symptoms phenotype"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Kuschal, Christiane"],["dc.contributor.author","Thoms, Kai Martin"],["dc.contributor.author","Bueckmann, L."],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Apel, Antje"],["dc.contributor.author","Schoen, Michael Peter"],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T08:44:37Z"],["dc.date.available","2018-11-07T08:44:37Z"],["dc.date.issued","2010"],["dc.format.extent","S23"],["dc.identifier.isi","000276455100134"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20242"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.conference","Annual Meeting of the Society-for-Investigative-Dermatology"],["dc.relation.eventlocation","Atlanta, GA"],["dc.relation.issn","0022-202X"],["dc.title","Nucleotide excision repair is inhibited by Cyclosporin A via calcineurin-mediated down-regulation of the xeroderma pigmentosum group A and C proteins"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","225"],["dc.bibliographiccitation.issue","5-7"],["dc.bibliographiccitation.journal","Journal of Molecular Histology"],["dc.bibliographiccitation.lastpage","238"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Leibeling, Diana"],["dc.contributor.author","Laspe, Petra"],["dc.contributor.author","Emmert, Steffen"],["dc.date.accessioned","2018-11-07T09:20:32Z"],["dc.date.available","2018-11-07T09:20:32Z"],["dc.date.issued","2006"],["dc.description.abstract","Nucleotide excision repair (NER) is the most versatile and best studied DNA repair system in humans. NER can repair a variety of bulky DNA damages including UV-Iight induced DNA photoproducts. NER consists of a multistep process in which the DNA lesion is recognized and demarcated by DNA unwinding. Then, a similar to 28 bp DNA damage containing oligonucleotide is excised followed by gap filling using the undamaged DNA strand as a template. The consequences of defective NER are demonstrated by three rare autosomal-rezessive NER-defective syndromes: xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD). XP patients show severe sun sensitivity, freckling in sun exposed skin, and develop skin cancers already during childhood. CS patients exhibit sun sensitivity, severe neurologic abnormalities, and cachectic dwarfism. Clinical symptoms of TTD patients include sun sensitivity, freckling in sun exposed skin areas, and brittle sulfur-deficient hair. In contrast to XP patients, CS and TTD patients are not skin cancer prone. Studying these syndromes can increase the knowledge of skin cancer development including cutaneous melanoma as well as basal and squamous cell carcinoma in general that may lead to new preventional and therapeutic anticancer strategies in the normal population."],["dc.identifier.doi","10.1007/s10735-006-9041-x"],["dc.identifier.isi","000243864800006"],["dc.identifier.pmid","16855787"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28902"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1567-2387"],["dc.relation.issn","1567-2379"],["dc.title","Nucleotide excision repair and cancer"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]