Kroemer, Heyo Klaus

[["dc.bibliographiccitation.artnumber","e96875"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Schwedhelm, Edzard"],["dc.contributor.author","Wallaschofski, Henri"],["dc.contributor.author","Atzler, Dorothee"],["dc.contributor.author","Dörr, Marcus"],["dc.contributor.author","Nauck, Matthias"],["dc.contributor.author","Volker, Uwe"],["dc.contributor.author","Kroemer, Heyo K."],["dc.contributor.author","Volzke, Henry"],["dc.contributor.author","Böger, Rainer H."],["dc.contributor.author","Friedrich, Nele"],["dc.date.accessioned","2018-08-15T06:50:42Z"],["dc.date.available","2018-08-15T06:50:42Z"],["dc.date.issued","2014"],["dc.description.abstract","BACKGROUND: L-Arginine and its dimethylated derivatives asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) have been associated with cardiovascular (CV) and all-cause mortality in populations at risk. The present study aimed to investigate the prognostic value of L-arginine and its derivatives in the general population. METHODS AND RESULTS: We evaluated 3,952 individuals (1,936 men and 2,016 women) aged 20-81 (median (IQR) 51 (37; 64) years) from the population-based Study of Health in Pomerania (SHIP). Associations of continuous [per standard deviation (SD) increase] and categorized (age- and sex-specific tertiles) serum L-arginine, ADMA, and SDMA concentrations with all-cause and cause-specific mortality were analysed. During a median (IQR) follow-up period of 10.1 (9.3; 10.8) years (38,476 person-years), 426 deaths (10.8%) were observed, including 139 CV deaths (3.5%), and 150 cancer deaths (3.8%). After multivariable adjustment, we revealed a positive association of SDMA with all-cause [hazard ratio (HR) per SD increase: 1.16, 95% confidence interval (CI): 1.07-1.25] and CV mortality [HR: 1.19, 95% CI: 1.05-1.35]. In contrast, we did not observe any association of SDMA with cancer mortality. Neither L-arginine nor ADMA were associated with all-cause or CV mortality. CONCLUSION: SDMA, but not ADMA, is an independent predictor of all-cause and CV mortality in a large population-based cohort of European ancestry."],["dc.identifier.doi","10.1371/journal.pone.0096875"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/15305"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Incidence of all-cause and cardiovascular mortality predicted by symmetric dimethylarginine in the population-based study of health in pomerania"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","144"],["dc.bibliographiccitation.journal","Journal of Translational Medicine"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Grabe, Hans Joergen"],["dc.contributor.author","Assel, Heinrich"],["dc.contributor.author","Bahls, Thomas"],["dc.contributor.author","Doerr, Marcus"],["dc.contributor.author","Endlich, Karlhans"],["dc.contributor.author","Endlich, Nicole"],["dc.contributor.author","Erdmann, Pia"],["dc.contributor.author","Ewert, Ralf"],["dc.contributor.author","Felix, Stephan B."],["dc.contributor.author","Fiene, Beate"],["dc.contributor.author","Fischer, Tobias"],["dc.contributor.author","Flessa, Steffen"],["dc.contributor.author","Friedrich, Nele"],["dc.contributor.author","Gadebusch-Bondio, Mariacarla"],["dc.contributor.author","Salazar, Manuela Gesell"],["dc.contributor.author","Hammer, Elke"],["dc.contributor.author","Haring, Robin"],["dc.contributor.author","Havemann, Christoph"],["dc.contributor.author","Hecker, Michael"],["dc.contributor.author","Hoffmann, Wolfgang"],["dc.contributor.author","Holtfreter, Birte"],["dc.contributor.author","Kacprowski, Tim"],["dc.contributor.author","Klein, Kathleen"],["dc.contributor.author","Kocher, Thomas"],["dc.contributor.author","Kock, Holger"],["dc.contributor.author","Krafczyk, Janina"],["dc.contributor.author","Kuhn, Jana"],["dc.contributor.author","Langanke, Martin"],["dc.contributor.author","Lendeckel, Uwe"],["dc.contributor.author","Lerch, Markus M."],["dc.contributor.author","Lieb, Wolfgang"],["dc.contributor.author","Lorbeer, Roberto"],["dc.contributor.author","Mayerle, Julia"],["dc.contributor.author","Meissner, Konrad"],["dc.contributor.author","Schwabedissen, Henriette E. Meyer zu"],["dc.contributor.author","Nauck, Matthias"],["dc.contributor.author","Ott, Konrad"],["dc.contributor.author","Rathmann, Wolfgang"],["dc.contributor.author","Rettig, Rainer"],["dc.contributor.author","Richardt, Claudia"],["dc.contributor.author","Salje, Karen"],["dc.contributor.author","Schminke, Ulf"],["dc.contributor.author","Schulz, Andrea"],["dc.contributor.author","Schwab, Matthias"],["dc.contributor.author","Siegmund, Werner"],["dc.contributor.author","Stracke, Sylvia"],["dc.contributor.author","Suhre, Karsten"],["dc.contributor.author","Ueffing, Marius"],["dc.contributor.author","Ungerer, Saskia"],["dc.contributor.author","Voelker, Uwe"],["dc.contributor.author","Voelzke, Henry"],["dc.contributor.author","Wallaschofski, Henri"],["dc.contributor.author","Werner, Vivian"],["dc.contributor.author","Zygmunt, Marek T."],["dc.contributor.author","Kroemer, Heyo K."],["dc.date.accessioned","2018-11-07T09:39:59Z"],["dc.date.available","2018-11-07T09:39:59Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Individualized Medicine aims at providing optimal treatment for an individual patient at a given time based on his specific genetic and molecular characteristics. This requires excellent clinical stratification of patients as well as the availability of genomic data and biomarkers as prerequisites for the development of novel diagnostic tools and therapeutic strategies. The University Medicine Greifswald, Germany, has launched the \"Greifswald Approach to Individualized Medicine\" (GANI_MED) project to address major challenges of Individualized Medicine. Herein, we describe the implementation of the scientific and clinical infrastructure that allows future translation of findings relevant to Individualized Medicine into clinical practice. Methods/design: Clinical patient cohorts (N > 5,000) with an emphasis on metabolic and cardiovascular diseases are being established following a standardized protocol for the assessment of medical history, laboratory biomarkers, and the collection of various biosamples for bio-banking purposes. A multi-omics based biomarker assessment including genome-wide genotyping, transcriptome, metabolome, and proteome analyses complements the multi-level approach of GANI_MED. Comparisons with the general background population as characterized by our Study of Health in Pomerania (SHIP) are performed. A central data management structure has been implemented to capture and integrate all relevant clinical data for research purposes. Ethical research projects on informed consent procedures, reporting of incidental findings, and economic evaluations were launched in parallel."],["dc.identifier.doi","10.1186/1479-5876-12-144"],["dc.identifier.isi","000338469800002"],["dc.identifier.pmid","24886498"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10153"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33415"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1479-5876"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Cohort profile: Greifswald approach to individualized medicine (GANI_MED)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","688"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","688"],["dc.bibliographiccitation.journal","BMC Research Notes"],["dc.bibliographiccitation.lastpage","6"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Meyer zu Schwabedissen, Henriette Elisabeth"],["dc.contributor.author","Siegmund, Werner"],["dc.contributor.author","Kroemer, Heyo Klaus"],["dc.contributor.author","Rollnik, Jens D."],["dc.date.accessioned","2019-04-30T12:38:18Z"],["dc.date.available","2019-04-30T12:38:18Z"],["dc.date.issued","2014"],["dc.description.abstract","BACKGROUND: Genetic factors as predictor of the individual outcome of drug therapy is one aim of personalized medicine approaches. CASE PRESENTATION: We report a drug metabolism based analysis of genetic polymorphisms in a Caucasian patient receiving fluvastatin and telmisartan experiencing myotoxicity (myalgia and moderate creatine kinase elevation). CONCLUSIONS: The obtained findings suggest that heterocygocity of cytochrome P450 CYP2C9 3 variant in combination with multidrug resistance-associated protein MRP2-24C > T functions as risk factor predisposing to experience drug-drug interaction combing those drugs."],["dc.identifier.doi","10.1186/1756-0500-7-688"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10966"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57892"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1756-0500"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Creatine kinase elevation caused by a combination of fluvastatin and telmisartan in a patient heterozygous for the CYP2C9 3 and ABCC2 -24C T variants: a case report"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","617"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Cancer"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Oberstadt, Moritz C."],["dc.contributor.author","Bien-Möller, Sandra"],["dc.contributor.author","Weitmann, Kerstin"],["dc.contributor.author","Herzog, Susann"],["dc.contributor.author","Hentschel, Katharina"],["dc.contributor.author","Rimmbach, Christian"],["dc.contributor.author","Vogelgesang, Silke"],["dc.contributor.author","Balz, Ellen"],["dc.contributor.author","Fink, Matthias"],["dc.contributor.author","Michael, Heike"],["dc.contributor.author","Zeden, Jan-Philip"],["dc.contributor.author","Bruckmüller, Henrike"],["dc.contributor.author","Werk, Anneke N."],["dc.contributor.author","Cascorbi, Ingolf"],["dc.contributor.author","Hoffmann, Wolfgang"],["dc.contributor.author","Rosskopf, Dieter"],["dc.contributor.author","Schroeder, Henry W.S."],["dc.contributor.author","Kroemer, Heyo K."],["dc.date.accessioned","2019-07-09T11:39:41Z"],["dc.date.available","2019-07-09T11:39:41Z"],["dc.date.issued","2013"],["dc.description.abstract","Background Resistance of the highly aggressive glioblastoma multiforme (GBM) to drug therapy is a major clinical problem resulting in a poor patient’s prognosis. Beside promoter methylation of the O 6 -methylguanine-DNA-methyltransferase (MGMT) gene the efflux transporters ABCB1 and ABCG2 have been suggested as pivotal factors contributing to drug resistance, but the methylation of ABCB1 and ABCG2 has not been assessed before in GBM. Methods Therefore, we evaluated the proportion and prognostic significance of promoter methylation of MGMT, ABCB1 and ABCG2 in 64 GBM patient samples using pyrosequencing technology. Further, the single nucleotide polymorphisms MGMT C-56 T (rs16906252), ABCB1 C3435T (rs1045642) and ABCG2 C421A (rs2231142) were determined using the restriction fragment length polymorphism method (RFLP). To study a correlation between promoter methylation and gene expression, we analyzed MGMT, ABCB1 and ABCG2 expression in 20 glioblastoma and 7 non-neoplastic brain samples. Results Despite a significantly increased MGMT and ABCB1 promoter methylation in GBM tissue, multivariate regression analysis revealed no significant association between overall survival of glioblastoma patients and MGMT or ABCB1 promoter methylation. However, a significant negative correlation between promoter methylation and expression could be identified for MGMT but not for ABCB1 and ABCG2. Furthermore, MGMT promoter methylation was significantly associated with the genotypes of the MGMT C-56 T polymorphism showing a higher methylation level in the T allele bearing GBM. Conclusions In summary, the data of this study confirm the previous published relation of MGMT promoter methylation and gene expression, but argue for no pivotal role of MGMT, ABCB1 and ABCG2 promoter methylation in GBM patients’ survival."],["dc.identifier.doi","10.1186/1471-2407-13-617"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58024"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Epigenetic modulation of the drug resistance genes MGMT, ABCB1 and ABCG2 in glioblastoma multiforme"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]