Meyer, Thomas J.

[["dc.bibliographiccitation.firstpage","1818"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Medical Virology"],["dc.bibliographiccitation.lastpage","1825"],["dc.bibliographiccitation.volume","83"],["dc.contributor.author","Ruppert, Volker"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Balbach, Anna"],["dc.contributor.author","Richter, Anette"],["dc.contributor.author","Mueller, Hans-Helge"],["dc.contributor.author","Maisch, Bernhard"],["dc.contributor.author","Pankuweit, Sabine"],["dc.date.accessioned","2018-11-07T08:51:36Z"],["dc.date.available","2018-11-07T08:51:36Z"],["dc.date.issued","2011"],["dc.description.abstract","Genotype-specific effects of parvovirus B19 (B19V) infections on left ventricular function in patients with dilated cardiomyopathy (DCM) have not been investigated so far. In this prospective clinical study, the prevalences of B19V genotypes in endomyocardial biopsies from patients presenting with inflammatory heart disease and DCM were determined. A total of 139 consecutive patients were included in the study; among them 53 patients were diagnosed as DCM. Among the total study cohort, B19V DNA was detected in 65 study participants (46.8%). Genotyping of the B19V genomes in the total cohort identified genotype 1 in 38 samples (27.3%), genotype 2 in 25 samples (18.0%), and genotype 3 in only two patients (1.4%). During an average follow-up period of 8 months left ventricular ejection fraction (LVEF) improved significantly both in 819V-positive (7.1 +/- 13.8%, n = 17, P=0.038) as well as B19V-negative patients with DCM (9.5 +/- 13.9%, n = 20, P=0.017). However, mean LVEF improved only in patients with genotype 1 (11.0 +/- 14.4%, n = 7), whereas it even decreased in patients with genotype 2 (-6.2 +/- 6.3%, n = 5, P=0.033). These data from a small sample of patients diagnosed as DCM suggested that myocardial function during short-time follow-up differed between genetic variants of B19V. Patients with genotype 1 were on average younger than genotype 2 and appeared to be more prone to a beneficial course of left ventricular function than patients with genotype 2. Future studies with larger sample sizes and longer follow-up periods will be required to confirm this observation. J. Med. Virol. 83:1818-1825, 2011. (C) 2011 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/jmv.22187"],["dc.identifier.isi","000293985900020"],["dc.identifier.pmid","21837800"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21972"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0146-6615"],["dc.title","Genotype-Specific Effects on Left Ventricular Function in Parvovirus B19-Positive Patients With Dilated Cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","416"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Gene"],["dc.bibliographiccitation.lastpage","420"],["dc.bibliographiccitation.volume","527"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Pankuweit, Sabine"],["dc.contributor.author","Richter, Anette"],["dc.contributor.author","Maisch, Bernhard"],["dc.contributor.author","Ruppert, Volker"],["dc.date.accessioned","2018-11-07T09:19:54Z"],["dc.date.available","2018-11-07T09:19:54Z"],["dc.date.issued","2013"],["dc.description.abstract","Hypertrophic cardiomyopathy (HCM) is a cardiovascular disease with autosomal dominant inheritance caused by mutations in genes coding for sarcomeric and/or regulatory proteins expressed in cardiomyocytes. In a small cohort of HCM patients (n = 8), we searched for mutations in the two most common genes responsible for HCM and found four missense mutations in the MYH7 gene encoding cardiac beta-myosin heavy chain (R204H, M493V, R719W, and R870H) and three mutations in the myosin-binding protein C3 gene (MYBPC3) including one missense (A848V) and two frameshift mutations (c3713delTG and c.702ins26bp). The c.702ins26bp insertion resulted from the duplication of a 26-bp fragment in a 54-year-old female HCM patient presenting with clinical signs of heart failure due to diastolic dysfunction. Although such large duplications (>10 bp) in the MYBPC3 gene are very rare and have been identified only in 4 families reported so far, the identical duplication mutation was found earlier in a Dutch patient, demonstrating that it may constitute a hitherto unknown founder mutation in central European populations. This observation underscores the significance of insertions into the coding sequence of the MYBPC3 gene for the development and pathogenesis of HCM. (C) 2013 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.gene.2013.06.025"],["dc.identifier.isi","000323589100059"],["dc.identifier.pmid","23816408"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28751"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0378-1119"],["dc.title","Detection of a large duplication mutation in the myosin-binding protein C3 gene in a case of hypertrophic cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","206"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Gene"],["dc.bibliographiccitation.lastpage","210"],["dc.bibliographiccitation.volume","512"],["dc.contributor.author","Ruppert, Volker"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Richter, Anette"],["dc.contributor.author","Maisch, Bernhard"],["dc.contributor.author","Pankuweit, Sabine"],["dc.date.accessioned","2018-11-07T09:29:14Z"],["dc.date.available","2018-11-07T09:29:14Z"],["dc.date.issued","2013"],["dc.description.abstract","In a heterogeneous cohort of patients (n = 255) with sporadic and familial dilated cardiomyopathy (DCM), we searched for novel disease-associated mutations in the human melusin-encoding ITGB1BP2 gene and found only one missense mutation, which was a substitution of alanine for glycine at position 313 located in the carboxy-terminal spacer region of the molecule. This point mutation (c.938C>G) was identified in a 45-year-old male with familial DCM and severe impairment of left-ventricular function, but was absent in 300 healthy control subjects. However, its functional significance in the context of heart failure is unclear, as this amino acid substitution was predicted to be without disease-causing effects. In this report, we confirm the low prevalence of mutations and single nucleotide polymorphisms in the coding sequence of the human melusin gene in patients with DCM, ruling out the possibility that genetic variations in this myocardially transcribed gene may have a significant impact on the epidemiology of DCM-induced heart failure. (c) 2012 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.gene.2012.10.055"],["dc.identifier.isi","000313768900006"],["dc.identifier.pmid","23124043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30971"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0378-1119"],["dc.title","Identification of a missense mutation in the melusin-encoding ITGB1BP2 gene in a patient with dilated cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","653"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","APOPTOSIS"],["dc.bibliographiccitation.lastpage","663"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Stahl, Philipp"],["dc.contributor.author","Ruppert, Volker"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Schmidt, Joerg"],["dc.contributor.author","Campos, Marco A."],["dc.contributor.author","Gazzinelli, Ricardo T."],["dc.contributor.author","Maisch, Bernhard"],["dc.contributor.author","Schwarz, Ralph T."],["dc.contributor.author","Debierre-Grockiego, Francoise"],["dc.date.accessioned","2018-11-07T09:24:30Z"],["dc.date.available","2018-11-07T09:24:30Z"],["dc.date.issued","2013"],["dc.description.abstract","The haemoflagellate Trypanosoma cruzi is the causative agent of Chagas' disease that occurs in approximately 8 million people in Latin America. Patients infected with T. cruzi frequently suffer of cardiomegaly and may die of myocardial failure. Here we show that T. cruzi trypomastigotes (extracellular form) increased in vitro apoptosis of rat cardiomyocytes. Additionally, we demonstrated that amastigotes (intracellular form), for which a method for purification was established, were also able to induce cardiomyocyte apoptosis. Increase of apoptosis was associated with up-regulation of the apoptotic gene bax by trypomastigotes, while expression of the anti-apoptotic gene bcl-2 was down-regulated by amastigotes. The transcription factor STAT3 but not STAT1 was activated in cardiomyocytes by trypomastigotes. In addition, tlr7 gene expression was up-regulated in cardiomyocytes incubated with trypomastigotes, suggesting that this Toll-like receptor is involved in the intracellular recognition after host cell invasion by T. cruzi. Glycosylphosphatidylinositols purified from trypomastigotes did not induce cardiomyocyte apoptosis and STAT activation but down-regulated tlr7 gene expression. In conclusion, cardiomyopathy observed in Chagas' disease might be in part due to apoptosis of cardiomyocytes induced directly by the parasite."],["dc.identifier.doi","10.1007/s10495-013-0822-x"],["dc.identifier.isi","000318299300001"],["dc.identifier.pmid","23435997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29838"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1360-8185"],["dc.title","Trypomastigotes and amastigotes of Trypanosoma cruzi induce apoptosis and STAT3 activation in cardiomyocytes in vitro"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","180"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Gene"],["dc.bibliographiccitation.lastpage","183"],["dc.bibliographiccitation.volume","531"],["dc.contributor.author","Pankuweit, Sabine"],["dc.contributor.author","Ruppert, Volker"],["dc.contributor.author","Jonsdottir, Puriour"],["dc.contributor.author","Mueller, Hans-Helge"],["dc.contributor.author","Meyer, Thomas"],["dc.date.accessioned","2018-11-07T09:17:19Z"],["dc.date.available","2018-11-07T09:17:19Z"],["dc.date.issued","2013"],["dc.description.abstract","Previous studies have shown weak associations between human dilated cardiomyopathy (DCM) and certain human leucocyte antigen (HLA) class II polymorphisms. Using a sequence-specific primer-PCR (SSP-PCR) technology, we compared the allelic distribution in the HLA-DQ and -DR locus in a cohort of German DCM patients (n = 165) and DCM-free controls (n = 79). With the exception of HLA-DQB1 0309, we found no significant differences between the two groups, even without adjustment for multiple testing. The HIA-DQB1 0309 allele, however, was detected more frequently in DCM patients as compared to controls (28.5% versus 10.1%, p = 0.0010), leading to an odds ratio of 3.5 (95% confidence interval = 1.5-9.1). The frequency of this allele was significantly higher in DCM patients without lymphocytic infiltrates in endomyocardial biopsies as compared to patients classified histologically as inflammatory DCM (33.1% versus 14.6%, p = 0.028). There was no significant difference in the allelic HLA-DQB1 0309 distribution between DCM patients with and without viral genomes detected in the heart (24.2% versus 29.5%, p = 0.668). In summary, the frequency of the HLA-DQB1 0309 allele is overrepresented in DCM patients, suggesting that carriers of this HIA class II variant are associated with an increased risk for developing DCM. Although Bonferroni adjustment was applied, controlled studies in larger samples of DCM patients and in different ethnic populations are warranted to confirm this observation and reveal the pathophysiological mechanisms behind this association. (C) 2013 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.gene.2013.09.022"],["dc.identifier.isi","000326846800008"],["dc.identifier.pmid","24050898"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28134"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1879-0038"],["dc.relation.issn","0378-1119"],["dc.title","The HLA class II allele DQB1 0309 is associated with dilated cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","294"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Human Genetics"],["dc.bibliographiccitation.lastpage","300"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Ruppert, Volker"],["dc.contributor.author","Ackermann, Sarah"],["dc.contributor.author","Richter, Anette"],["dc.contributor.author","Perrot, Andreas"],["dc.contributor.author","Sperling, Silke R."],["dc.contributor.author","Posch, Maximilian G."],["dc.contributor.author","Maisch, Bernhard"],["dc.contributor.author","Pankuweit, Sabine"],["dc.date.accessioned","2018-11-07T09:27:36Z"],["dc.date.available","2018-11-07T09:27:36Z"],["dc.date.issued","2013"],["dc.description.abstract","Recently, missense mutations in titin-associated proteins have been linked to the pathogenesis of dilated cardiomyopathy (DCM). The objective of this study was to search for novel disease-associated mutations in the two human titin-binding proteins myopalladin and its amino-terminal-interacting partner cardiac ankyrin-repeat protein (CARP). In a cohort of 255 cases with familial and sporadic DCM, we analyzed the coding regions and all corresponding intron flanks located in the MYPN and CARP-encoding ANKRD1 gene. Two heterozygous missense mutations were detected in the MYPN gene (p.R955W and p.P961L), but neither of these mutations was found in 300 healthy controls. Both mutations were located in the a-actinin-binding region of myopalladin. Endomyocardial biopsies from the p.R955W carrier showed normal subcellular localization of myopalladin and a-actinin in cardiac myocytes, while their regular sarcomeric staining pattern was significantly disrupted in the p.P961L carrier, indicating that disturbed myofibrillogenesis and altered sarcomere assembly are the cause of the disease. In the ANKRD1 gene, we identified synonymous base exchanges (c.108T>C and c.-79C>T, respectively), but no non-synonymous mutations. In summary, we have identified novel missense mutations in the third immunoglobulin-like domain of myopalladin, which have either no or profound effects on the molecular composition of the sarcomere. According to our epidemiological data, the prevalence of ANKRD1 mutations seems to be lower than that of its binding partner myopalladin, indicating the clinical significance of myopalladin for the functional integrity of the sarcomeric apparatus and the protection against DCM. European Journal of Human Genetics (2013) 21, 294-300; doi:10.1038/ejhg.2012.173; published online 15 August 2012"],["dc.identifier.doi","10.1038/ejhg.2012.173"],["dc.identifier.isi","000315754800010"],["dc.identifier.pmid","22892539"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30577"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1018-4813"],["dc.title","Novel mutations in the sarcomeric protein myopalladin in patients with dilated cardiomyopathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]