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244 results on '"Heilmann, S."'

63. Highly Cross-Linked Azlactone Functional Supports of Tailorable Polarity

Author

Drtina, G. J., Heilmann, S. M., Moren, D. M., Rasmussen, J. K., Krepski, L. R., Smith, H. K., II, Pranis, R. A., and Turek, T. C.

Abstract

Highly cross-linked azlactone functional supports were prepared by dispersion polymerization of 2-vinyl-4,4-dimethylazlactone (VDM), 2-hydroxyethyl methacrylate (HEMA), and trimethylolpropane trimethacrylate (TMPTMA). The supports were recovered in high yield and possessed high surface areas. Individual particles, which ranged from 10 to 300 μm in diameter, were irregularly shaped and comprised of filamentous strands. Support polarity was tailored through increases in the HEMA level in the polymer formulations and was quantified by a lipophilicity index derived from solvent partition data collected on the constituent monomers. Support reactivity, as determined by azlactone aminolysis and measured by IR, was found to increase linearly with increasing support polarity. This effect was shown to be independent of the support cross-link density.

Published
1996

65. Systematic evaluation of pleiotropy identifies 6 further loci associated with coronary artery disease

Author

Webb, T, Erdmann, J, Stirrups, K, Stitziel, N, Masca, N, Jansen, H, Kanoni, S, Nelson, C, Ferrario, P, König, I, Eicher, J, Johnson, A, Hamby, S, Betsholtz, C, Ruusalepp, A, Franzén, O, Schadt, E, Björkegren, J, Weeke, P, Auer, P, Schick, U, Lu, Y, Zhang, H, Dube, M, Goel, A, Farrall, M, Peloso, G, Won, H, Do, R, van Iperen, E, Kruppa, J, Mahajan, A, Scott, R, Willenborg, C, Braund, P, van Capelleveen, J, Doney, A, Donnelly, L, Asselta, R, Merlini, P, Duga, S, Marziliano, N, Denny, J, Shaffer, C, El-Mokhtari, N, Franke, A, Heilmann, S, Hengstenberg, C, Hoffmann, P, Holmen, O, Hveem, K, Jansson, J, Jöckel, K, Kessler, T, Kriebel, J, Laugwitz, K, Marouli, E, Martinelli, N, McCarthy, M, Van Zuydam, N, Meisinger, C, Esko, T, Mihailov, E, Escher, S, Alver, M, Moebus, S, Morris, A, Virtamo, J, Nikpay, M, Olivieri, O, Provost, S, AlQarawi, A, Robertson, N, Akinsansya, K, Reilly, D, Vogt, T, Yin, W, Asselbergs, F, Kooperberg, C, Jackson, R, Stahl, E, Müller-Nurasyid, M, Strauch, K, Varga, T, Waldenberger, M, Consortium, Wellcome Trust Case Control, Zeng, L, Chowdhury, R, Salomaa, V, Ford, I, Jukema, J, Amouyel, P, Kontto, J, Investigators, MORGAM, Nordestgaard, B, Ferrières, J, Saleheen, D, Sattar, N, Surendran, P, Wagner, A, Young, R, Howson, J, Butterworth, A, Danesh, J, Ardissino, D, Bottinger, E, Erbel, R, Franks, P, Girelli, D, Hall, A, Hovingh, G, Kastrati, A, Lieb, W, Meitinger, T, Kraus, W, Shah, S, McPherson, R, Orho-Melander, M, Melander, O, Metspalu, A, Palmer, C, Peters, A, Rader, D, Reilly, M, Loos, R, Reiner, A, Roden, D, Tardif, J, Thompson, J, Wareham, N, Watkins, H, Willer, C, Samani, N, Schunkert, H, Deloukas, P, Kathiresan, S, Investigators, Myocardial Infarction Genetics and CARDIoGRAM Exome Consortia, Johnson, Kathleen [0000-0002-6823-3252], Chowdhury, Rajiv [0000-0003-4881-5690], Surendran, Praveen [0000-0002-4911-6077], Howson, Joanna [0000-0001-7618-0050], Butterworth, Adam [0000-0002-6915-9015], Danesh, John [0000-0003-1158-6791], Wareham, Nicholas [0000-0003-1422-2993], and Apollo - University of Cambridge Repository

Subjects
expression quantitative trait loci, single nucleotide polymorphism, cholesteryl ester transfer protein, genome-wide association, genetics
Abstract

BACKGROUND: Genome-wide association studies have so far identified 56 loci associated with risk of coronary artery disease (CAD). Many CAD loci show pleiotropy; that is, they are also associated with other diseases or traits. OBJECTIVES: This study sought to systematically test if genetic variants identified for non-CAD diseases/traits also associate with CAD and to undertake a comprehensive analysis of the extent of pleiotropy of all CAD loci. METHODS: In discovery analyses involving 42,335 CAD cases and 78,240 control subjects we tested the association of 29,383 common (minor allele frequency >5%) single nucleotide polymorphisms available on the exome array, which included a substantial proportion of known or suspected single nucleotide polymorphisms associated with common diseases or traits as of 2011. Suggestive association signals were replicated in an additional 30,533 cases and 42,530 control subjects. To evaluate pleiotropy, we tested CAD loci for association with cardiovascular risk factors (lipid traits, blood pressure phenotypes, body mass index, diabetes, and smoking behavior), as well as with other diseases/traits through interrogation of currently available genome-wide association study catalogs. RESULTS: We identified 6 new loci associated with CAD at genome-wide significance: on 2q37 (KCNJ13-GIGYF2), 6p21 (C2), 11p15 (MRVI1-CTR9), 12q13 (LRP1), 12q24 (SCARB1), and 16q13 (CETP). Risk allele frequencies ranged from 0.15 to 0.86, and odds ratio per copy of the risk allele ranged from 1.04 to 1.09. Of 62 new and known CAD loci, 24 (38.7%) showed statistical association with a traditional cardiovascular risk factor, with some showing multiple associations, and 29 (47%) showed associations at p < 1 × 10(-4) with a range of other diseases/traits. CONCLUSIONS: We identified 6 loci associated with CAD at genome-wide significance. Several CAD loci show substantial pleiotropy, which may help us understand the mechanisms by which these loci affect CAD risk.

66. Meta-analysis of genome-wide association studies in alopecia areata resolves HLA associations and reveals two new susceptibility loci

Author

Redler, S., Petukhova, L., Ripke, S., Huang, H., Menelaou, A., Becker, T., Heilmann, S., Yamany, T., Duvic, M., Hordinsky, M., Norris, D., Price, V., Mackay-Wiggan, J., Jong, A., Destefano, G., Moebus, S., Boehm, M., Blume-Peytavi, U., Wolff, H., Lutz, G., Kruse, R., Bian, L., Amos, C., Lee, A., Gregersen, P., Bettina Blaumeiser, Altshuler, D., Clynes, R., Bakker, P. I., Noethen, M. M., Daly, M. J., Christiano, A. M., and Betz, R. C.

Subjects
Medizin

96. Gegenstand und Methode

Author

Ziltener, Patrick, Blechinger-Talcott, V., editor, Heberer, T., editor, Heilmann, S., editor, Holbig, H., editor, Köllner, P., editor, Maull, H. W., editor, Schubert, G., editor, and Ziltener, Patrick

Published
2013
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98. Ergebnis: Ostasien als Weltregion

Author

Ziltener, Patrick, Blechinger-Talcott, V., editor, Heberer, T., editor, Heilmann, S., editor, Holbig, H., editor, Köllner, P., editor, Maull, H. W., editor, Schubert, G., editor, and Ziltener, Patrick

Published
2013
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99. Die Herausbildung der Weltregion Ostasien

Author

Ziltener, Patrick, Blechinger-Talcott, V., editor, Heberer, T., editor, Heilmann, S., editor, Holbig, H., editor, Köllner, P., editor, Maull, H. W., editor, Schubert, G., editor, and Ziltener, Patrick

Published
2013
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100. A genome-wide association study with tissue transcriptomics identifies genetic drivers for classic bladder exstrophy.

Author

Mingardo E, Beaman G, Grote P, Nordenskjöld A, Newman W, Woolf AS, Eckstein M, Hilger AC, Dworschak GC, Rösch W, Ebert AK, Stein R, Brusco A, Di Grazia M, Tamer A, Torres FM, Hernandez JL, Erben P, Maj C, Olmos JM, Riancho JA, Valero C, Hostettler IC, Houlden H, Werring DJ, Schumacher J, Gehlen J, Giel AS, Buerfent BC, Arkani S, Åkesson E, Rotstein E, Ludwig M, Holmdahl G, Giorgio E, Berettini A, Keene D, Cervellione RM, Younsi N, Ortlieb M, Oswald J, Haid B, Promm M, Neissner C, Hirsch K, Stehr M, Schäfer FM, Schmiedeke E, Boemers TM, van Rooij IALM, Feitz WFJ, Marcelis CLM, Lacher M, Nelson J, Ure B, Fortmann C, Gale DP, Chan MMY, Ludwig KU, Nöthen MM, Heilmann S, Zwink N, Jenetzky E, Odermatt B, Knapp M, and Reutter H

Subjects
Humans, Animals, Mice, Genome-Wide Association Study, Transcriptome, Ephrin-A1 genetics, Bladder Exstrophy genetics, Bladder Exstrophy complications, Urinary Bladder Neoplasms genetics
Abstract

Classic bladder exstrophy represents the most severe end of all human congenital anomalies of the kidney and urinary tract and is associated with bladder cancer susceptibility. Previous genetic studies identified one locus to be involved in classic bladder exstrophy, but were limited to a restrict number of cohort. Here we show the largest classic bladder exstrophy genome-wide association analysis to date where we identify eight genome-wide significant loci, seven of which are novel. In these regions reside ten coding and four non-coding genes. Among the coding genes is EFNA1, strongly expressed in mouse embryonic genital tubercle, urethra, and primitive bladder. Re-sequence of EFNA1 in the investigated classic bladder exstrophy cohort of our study displays an enrichment of rare protein altering variants. We show that all coding genes are expressed and/or significantly regulated in both mouse and human embryonic developmental bladder stages. Furthermore, nine of the coding genes residing in the regions of genome-wide significance are differentially expressed in bladder cancers. Our data suggest genetic drivers for classic bladder exstrophy, as well as a possible role for these drivers to relevant bladder cancer susceptibility., (© 2022. The Author(s).)

Published
2022
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