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Your search keyword '"Winkelmann, Juliane"' showing total 11 results
Start Over Author "Winkelmann, Juliane" Publisher biomed central
11 results on '"Winkelmann, Juliane"'

1. Epigenome-wide association study of dietary fatty acid intake

Author

Lange de Luna, Julia, Nounu, Aayah, Neumeyer, Sonja, Sinke, Lucy, Wilson, Rory, Hellbach, Fabian, Matías-García, Pamela R., Delerue, Thomas, Winkelmann, Juliane, Peters, Annette, Thorand, Barbara, Beekman, Marian, Heijmans, Bastiaan T., Slagboom, Eline, Gieger, Christian, Linseisen, Jakob, and Waldenberger, Melanie

Published
2024
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2. Exploring variation of coverage and access to dental care for adults in 11 European countries: a vignette approach

Author

Winkelmann, Juliane, Gómez Rossi, Jesús, Schwendicke, Falk, Dimova, Antoniya, Atanasova, Elka, Habicht, Triin, Kasekamp, Kaija, Gandré, Coralie, Or, Zeynep, McAuliffe, Úna, Murauskiene, Liubove, Kroneman, Madelon, de Jong, Judith, Kowalska-Bobko, Iwona, Badora-Musiał, Katarzyna, Motyl, Sylwia, Figueiredo Augusto, Gonçalo, Pažitný, Peter, Kandilaki, Daniela, Löffler, Lubica, Lundgren, Carl, Janlöv, Nils, van Ginneken, Ewout, and Panteli, Dimitra

Published
2022
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3. DNAm-based signatures of accelerated aging and mortality in blood are associated with low renal function

Author

Matías-García, Pamela R., Ward-Caviness, Cavin K., Raffield, Laura M., Gao, Xu, Zhang, Yan, Wilson, Rory, Gào, Xīn, Nano, Jana, Bostom, Andrew, Colicino, Elena, Correa, Adolfo, Coull, Brent, Eaton, Charles, Hou, Lifang, Just, Allan C., Kunze, Sonja, Lange, Leslie, Lange, Ethan, Lin, Xihong, Liu, Simin, Nwanaji-Enwerem, Jamaji C., Reiner, Alex, Shen, Jincheng, Schöttker, Ben, Vokonas, Pantel, Zheng, Yinan, Young, Bessie, Schwartz, Joel, Horvath, Steve, Lu, Ake, Whitsel, Eric A., Koenig, Wolfgang, Adamski, Jerzy, Winkelmann, Juliane, Brenner, Hermann, Baccarelli, Andrea A., Gieger, Christian, Peters, Annette, Franceschini, Nora, and Waldenberger, Melanie

Published
2021
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5. Methylation status of nc886 epiallele reflects periconceptional conditions and is associated with glucose metabolism through nc886 RNAs

Author

Marttila, Saara, Viiri, Leena E., Mishra, Pashupati P., Kühnel, Brigitte, Matias-Garcia, Pamela R., Lyytikäinen, Leo-Pekka, Ceder, Tiina, Mononen, Nina, Rathmann, Wolfgang, Winkelmann, Juliane, Peters, Annette, Kähönen, Mika, Hutri-Kähönen, Nina, Juonala, Markus, Aalto-Setälä, Katriina, Raitakari, Olli, Lehtimäki, Terho, Waldenberger, Melanie, and Raitoharju, Emma

Published
2021
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8. Systematic protein-protein interaction and pathway analyses in the idiopathic inflammatory myopathies

Author

Parkes, Joanna E., Rothwell, Simon, Day, Philip J., McHugh, Neil J., Betteridge, Zoë E., Cooper, Robert G., Ollier, William E., Chinoy, Hector, Lamb, Janine A., Lundberg, Ingrid E., Miller, Frederick W., Gregersen, Peter K., Vencovsky, Jiri, Danko, Katalin, Limaye, Vidya, Selva-O'Callaghan, Albert, Machado, Pedro M., Hanna, Michael G., Pachman, Lauren M., Reed, Ann M., Rider, Lisa G., Platt, Hazel, Molberg, Øyvind, Benveniste, Olivier, Mathiesen, Pernille, Radstake, Timothy, Doria, Andrea, Bleecker, Jan De, Paepe, Boel De, Maurer, Britta, Padyukov, Leonid, O'Hanlon, Terrance P., Lee, Annette, Amos, Christopher I., Gieger, Christian, Meitinger, Thomas, Winkelmann, Juliane, Wedderburn, Lucy R., Denton, Christopher, Mann, Herman, Hilton-Jones, David, Kiely, Patrick, Plotz, Paul H., Gourley, Mark, Rouster-Stevens, Kelly, Huber, Adam M., Marder, Galina, Dimachkie, Mazen, Parkes, Joanna E., Rothwell, Simon, Day, Philip J., McHugh, Neil J., Betteridge, Zoë E., Cooper, Robert G., Ollier, William E., Chinoy, Hector, Lamb, Janine A., Lundberg, Ingrid E., Miller, Frederick W., Gregersen, Peter K., Vencovsky, Jiri, Danko, Katalin, Limaye, Vidya, Selva-O'Callaghan, Albert, Machado, Pedro M., Hanna, Michael G., Pachman, Lauren M., Reed, Ann M., Rider, Lisa G., Platt, Hazel, Molberg, Øyvind, Benveniste, Olivier, Mathiesen, Pernille, Radstake, Timothy, Doria, Andrea, Bleecker, Jan De, Paepe, Boel De, Maurer, Britta, Padyukov, Leonid, O'Hanlon, Terrance P., Lee, Annette, Amos, Christopher I., Gieger, Christian, Meitinger, Thomas, Winkelmann, Juliane, Wedderburn, Lucy R., Denton, Christopher, Mann, Herman, Hilton-Jones, David, Kiely, Patrick, Plotz, Paul H., Gourley, Mark, Rouster-Stevens, Kelly, Huber, Adam M., Marder, Galina, and Dimachkie, Mazen

Published
2016

9. Systematic protein-protein interaction and pathway analyses in the idiopathic inflammatory myopathies

Author

Translationele immunologie, Infection & Immunity, Parkes, Joanna E., Rothwell, Simon, Day, Philip J., McHugh, Neil J., Betteridge, Zoë E., Cooper, Robert G., Ollier, William E., Chinoy, Hector, Lamb, Janine A., Lundberg, Ingrid E., Miller, Frederick W., Gregersen, Peter K., Vencovsky, Jiri, Danko, Katalin, Limaye, Vidya, Selva-O'Callaghan, Albert, Machado, Pedro M., Hanna, Michael G., Pachman, Lauren M., Reed, Ann M., Rider, Lisa G., Platt, Hazel, Molberg, Øyvind, Benveniste, Olivier, Mathiesen, Pernille, Radstake, Timothy, Doria, Andrea, Bleecker, Jan De, Paepe, Boel De, Maurer, Britta, Padyukov, Leonid, O'Hanlon, Terrance P., Lee, Annette, Amos, Christopher I., Gieger, Christian, Meitinger, Thomas, Winkelmann, Juliane, Wedderburn, Lucy R., Denton, Christopher, Mann, Herman, Hilton-Jones, David, Kiely, Patrick, Plotz, Paul H., Gourley, Mark, Rouster-Stevens, Kelly, Huber, Adam M., Marder, Galina, Dimachkie, Mazen, Translationele immunologie, Infection & Immunity, Parkes, Joanna E., Rothwell, Simon, Day, Philip J., McHugh, Neil J., Betteridge, Zoë E., Cooper, Robert G., Ollier, William E., Chinoy, Hector, Lamb, Janine A., Lundberg, Ingrid E., Miller, Frederick W., Gregersen, Peter K., Vencovsky, Jiri, Danko, Katalin, Limaye, Vidya, Selva-O'Callaghan, Albert, Machado, Pedro M., Hanna, Michael G., Pachman, Lauren M., Reed, Ann M., Rider, Lisa G., Platt, Hazel, Molberg, Øyvind, Benveniste, Olivier, Mathiesen, Pernille, Radstake, Timothy, Doria, Andrea, Bleecker, Jan De, Paepe, Boel De, Maurer, Britta, Padyukov, Leonid, O'Hanlon, Terrance P., Lee, Annette, Amos, Christopher I., Gieger, Christian, Meitinger, Thomas, Winkelmann, Juliane, Wedderburn, Lucy R., Denton, Christopher, Mann, Herman, Hilton-Jones, David, Kiely, Patrick, Plotz, Paul H., Gourley, Mark, Rouster-Stevens, Kelly, Huber, Adam M., Marder, Galina, and Dimachkie, Mazen

Published
2016

10. Network-based SNP meta-analysis identifies joint and disjoint genetic features across common human diseases.

Author

Arnold, Matthias, Hartsperger, Mara L., Baurecht, Hansjörg, Rodríguez, Elke, Wachinger, Benedikt, Franke, Andre, Kabesch, Michael, Winkelmann, Juliane, Pfeufer, Arne, Romanos, Marcel, Illig, Thomas, Mewes, Hans-Werner, Stümpflen, Volker, and Weidinger, Stephan

Subjects
META-analysis, PHENOTYPES, ETIOLOGY of diseases, SINGLE nucleotide polymorphisms, NETWORK analysis (Planning)
Abstract

Background: Genome-wide association studies (GWAS) have provided a large set of genetic loci influencing the risk for many common diseases. Association studies typically analyze one specific trait in single populations in an isolated fashion without taking into account the potential phenotypic and genetic correlation between traits. However, GWA data can be efficiently used to identify overlapping loci with analogous or contrasting effects on different diseases. Results: Here, we describe a new approach to systematically prioritize and interpret available GWA data. We focus on the analysis of joint and disjoint genetic determinants across diseases. Using network analysis, we show that variant-based approaches are superior to locus-based analyses. In addition, we provide a prioritization of disease loci based on network properties and discuss the roles of hub loci across several diseases. We demonstrate that, in general, agonistic associations appear to reflect current disease classifications, and present the potential use of effect sizes in refining and revising these agonistic signals. We further identify potential branching points in disease etiologies based on antagonistic variants and describe plausible small-scale models of the underlying molecular switches. Conclusions: The observation that a surprisingly high fraction (>15%) of the SNPs considered in our study are associated both agonistically and antagonistically with related as well as unrelated disorders indicates that the molecular mechanisms influencing causes and progress of human diseases are in part interrelated. Genetic overlaps between two diseases also suggest the importance of the affected entities in the specific pathogenic pathways and should be investigated further. [ABSTRACT FROM AUTHOR]

Published
2012
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11. Novel SCARB2 mutation in action myoclonus-renal failure syndrome and evaluation of SCARB2 mutations in isolated AMRF features.

Author

Hopfner F, Schormair B, Knauf F, Berthele A, Tölle TR, Baron R, Maier C, Treede RD, Binder A, Sommer C, Maihöfner C, Kunz W, Zimprich F, Heemann U, Pfeufer A, Näbauer M, Kääb S, Nowak B, Gieger C, Lichtner P, Trenkwalder C, Oexle K, and Winkelmann J

Subjects
Adult, Base Sequence, DNA Mutational Analysis, Female, Humans, Male, Molecular Sequence Data, Myoclonic Epilepsies, Progressive complications, Myoclonic Epilepsies, Progressive physiopathology, Pedigree, Phenotype, Reverse Transcriptase Polymerase Chain Reaction, Young Adult, Cardiomyopathies genetics, Demyelinating Diseases genetics, Lysosomal Membrane Proteins genetics, Mutation, Myoclonic Epilepsies, Progressive genetics, Receptors, Scavenger genetics
Abstract

Background: Action myoclonus-renal failure syndrome is a hereditary form of progressive myoclonus epilepsy associated with renal failure. It is considered to be an autosomal-recessive disease related to loss-of-function mutations in SCARB2. We studied a German AMRF family, additionally showing signs of demyelinating polyneuropathy and dilated cardiomyopathy. To test the hypothesis whether isolated appearance of individual AMRF syndrome features could be related to heterozygote SCARB2 mutations, we screened for SCARB2 mutations in unrelated patients showing isolated AMRF features., Methods: In the AMRF family all exons of SCARB2 were analyzed by Sanger sequencing. The mutation screening of unrelated patients with isolated AMRF features affected by either epilepsy (n = 103, progressive myoclonus epilepsy or generalized epilepsy), demyelinating polyneuropathy (n = 103), renal failure (n = 192) or dilated cardiomyopathy (n = 85) was performed as high resolution melting curve analysis of the SCARB2 exons., Results: A novel homozygous 1 bp deletion (c.111delC) in SCARB2 was found by sequencing three affected homozygous siblings of the affected family. A heterozygous sister showed generalized seizures and reduction of nerve conduction velocity in her legs. No mutations were found in the epilepsy, renal failure or dilated cardiomyopathy samples. In the polyneuropathy sample two individuals with demyelinating disease were found to be carriers of a SCARB2 frameshift mutation (c.666delCCTTA)., Conclusions: Our findings indicate that demyelinating polyneuropathy and dilated cardiomyopathy are part of the action myoclonus-renal failure syndrome. Moreover, they raise the possibility that in rare cases heterozygous SCARB2 mutations may be associated with PNP features.

Published
2011
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