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9 results on '"Jockel, K.H."'

1. Evidence for increased genetic risk load for major depression in patients assigned to electroconvulsive therapy

Author

Foo, J.C., Streit, F., Frank, J., Witt, S.H., Treutlein, J., Baune, B.T., Moebus, S., Jockel, K.H., Forstner, A.J., Nothen, M.M., Rietschel, M., Sartorius, A., Kranaster, L., Wray, N.R., Ripke, S., Mattheisen, M., Trzaskowski, M., Byrne, E.M., Abdellaoui, A., Adams, M.J., Agerbo, E., Air, T.M., Andlauer, T.F.M., Bacanu, S.A., Baekvad-Hansen, M., Beekman, A.T.F., Bigdeli, T.B., Binder, E.B., Blackwood, D.H.R., Bryois, J., Buttenschon, H.N., Bybjerg-Grauholm, J., Cai, N., Castelao, E., Christensen, J.H., Clarke, T.K., Coleman, J.R.I., Colodro-Conde, L., Couvy-Duchesne, B., Craddock, N., Crawford, G.E., Davies, G., Deary, I.J., Degenhardt, F., Derks, E.M., Direk, N., Dolan, C.V., Dunn, E.C., Eley, T.C., Escott-Price, V., Kiadeh, F.F.H., Finucane, H.K., Gaspar, H.A., Gill, M., Goes, F.S., Gordon, S.D., Grove, J., Hall, L.S., Hansen, C.S., Hansen, T.F., Herms, S., Hickie, I.B., Hoffmann, P., Homuth, G., Horn, C., Hottenga, J.J., Hougaard, D.M., Ising, M., Jansen, R., Jones, I., Jones, L.A., Jorgenson, E., Knowles, J.A., Kohane, I.S., Kraft, J., Kretzschmar, W.W., Krogh, J., Kutalik, Z., Li, Y.H., Lind, P.A., MacIntyre, D.J., MacKinnon, D.F., Maier, R.M., Maier, W., Marchini, J., Mbarek, H., McGrath, P., McGuffin, P., Medland, S.E., Mehta, D., Middeldorp, C.M., Mihailov, E., Milaneschi, Y., Milani, L., Mondimore, F.M., Montgomery, G.W., Mostafavi, S., Mullins, N., Nauck, M., Ng, B., Nivard, M.G., Nyholt, D.R., O'Reilly, P.F., Oskarsson, H., Owen, M.J., Painter, J.N., Pedersen, C.B., Pedersen, M.G., Peterson, R.E., Pettersson, E., Peyrot, W.J., Pistis, G., Posthuma, D., Quiroz, J.A., Qvist, P., Rice, J.P., Riley, B.P., Rivera, M., Mirza, S.S., Schoevers, R., Schulte, E.C., Shen, L., Shi, J.X., Shyn, S.I., Sigurdsson, E., Sinnamon, G.C.B., Smit, J.H., Smith, D.J., Stefansson, H., Steinberg, S., Strohmaier, J., Tansey, K.E., Teismann, H., Teumer, A., Thompson, W., Thomson, P.A., Thorgeirsson, T.E., Traylor, M., Trubetskoy, V., Uitterlinden, A.G., Umbricht, D., Auwera, S. van der, Hemert, A.M. van, Viktorin, A., Visscher, P.M., Wang, Y., Webb, B.T., Weinsheimer, S.M., Wellmann, J., Willemsen, G., Wu, Y., Xi, H.L.S., Yang, J., Zhang, F.T., Arolt, V., Berger, K., Boomsma, D.I., Cichon, S., Dannlowski, U., Geus, E.J.C. de, DePaulo, J.R., Domenici, E., Domschke, K., Esko, T., Grabe, H.J., Hamilton, S.P., Hayward, C., Heath, A.C., Kendler, K.S., Kloiber, S., Lewis, G., Li, Q.Q.S., Lucae, S., Madden, P.A.F., Magnusson, P.K., Martin, N.G., McIntosh, A.M., Metspalu, A., Mors, O., Mortensen, P.B., Muller-Myhsok, B., Nordentoft, M., O'Donovan, M.C., Paciga, S.A., Pedersen, N.L., Penninx, B.W.J.H., Perlis, R.H., Porteous, D.J., Potash, J.B., Preisig, M., Schaefer, C., Schulze, T.G., Smoller, J.W., Stefansson, K., Tiemeier, H., Uher, R., Voelzke, H., Weissman, M.M., Werge, T., Lewis, C.M., Levinson, D.F., Breen, G., Borglum, A.D., Sullivan, P.F., and Major Depressive Disorder Worki

Subjects
treatment-resistance, polygenic risk scores, depression, major depression, electroconvulsive therapy
Abstract

Electroconvulsive therapy (ECT) is the treatment of choice for severe and treatment-resistantdepression; disorder severity and unfavorable treatment outcomes are shown to be influencedby an increased genetic burden for major depression (MD). Here, we tested whether ECT assign-ment and response/nonresponse are associated with an increased genetic burden for majordepression (MD) using polygenic risk score (PRS), which summarize the contribution of disease-related common risk variants. Fifty-one psychiatric inpatients suffering from a major depressiveepisode underwent ECT. MD-PRS were calculated for these inpatients and a separatepopulation-based sample (n = 3,547 healthy; n = 426 self-reported depression) based on sum-mary statistics from the Psychiatric Genomics Consortium MDD-working group (Cases:n = 59,851; Controls: n = 113,154). MD-PRS explained a significant proportion of disease statusbetween ECT patients and healthy controls (p = .022, R2 = 1.173%); patients showed higherMD-PRS. MD-PRS in population-based depression self-reporters were intermediate betweenECT patients and controls (n.s.). Significant associations between MD-PRS and ECT response(50% reduction in Hamilton depression rating scale scores) were not observed. Our findings indi-cate that ECT cohorts show an increased genetic burden for MD and are consistent with thehypothesis that treatment-resistant MD patients represent a subgroup with an increased geneticrisk for MD. Larger samples are needed to better substantiate these findings.

Published
2019

2. Systematic Evaluation of Pleiotropy Identifies 6 Further Loci Associated With Coronary Artery Disease

Author

Webb, T.R., Erdmann, J., Stirrups, K.E., Stitziel, N.O., Masca, N.G.D., Jansen, H., Kanoni, S., Nelson, C.P., Ferrario, P.G., Konig, I.R., Eicher, J.D., Johnson, A.D., Hamby, S.E., Betsholtz, C., Ruusalepp, A., Franzen, O., Schadt, E.E., Bjorkegren, J.L.M., Weeke, P.E., Auer, P.L., Schick, U.M., Lu, Y.C., Zhang, H., Dube, M.P., Goel, A., Farrall, M., Peloso, G.M., Won, H.H., R. do, Iperen, E. van, Kruppa, J., Mahajan, A., Scott, R.A., Willenborg, C., Braund, P.S., Capelleveen, J.C. van, Doney, A.S.F., Donnelly, L.A., Asselta, R., Merlini, P.A., Duga, S., Marziliano, N., Denny, J.C., Shaffer, C., El-Mokhtari, N.E., Franke, A., Heilmann, S., Hengstenberg, C., Hoffmann, P., Holmen, O.L., Hveem, K., Jansson, J.H., Jockel, K.H., Kessler, T., Kriebel, J., Laugwitz, K.L., Marouli, E., Martinelli, N., McCarthy, M.I., Zuydam, N.R. van, Meisinger, C., Esko, T., Mihailov, E., Escher, S.A., Alver, M., Moebus, S., Morris, A.D., Virtamo, J., Nikpay, M., Olivieri, O., Provost, S., AlQarawi, A., Robertson, N.R., Akinsansya, K.O., Reilly, D.F., Vogt, T.F., Yin, W., Asselbergs, F.W., Kooperberg, C., Jackson, R.D., Stahl, E., Muller-Nurasyid, M., Strauch, K., Varga, T.V., Waldenberger, M., Zeng, L.Y., Chowdhury, R., Salomaa, V., Ford, I., Jukema, J.W., Amouyel, P., Kontto, J., Nordestgaard, B.G., Ferrieres, J., Saleheen, D., Sattar, N., Surendran, P., Wagner, A., Young, R., Howson, J.M.M., Butterworth, A.S., Danesh, J., Ardissino, D., Bottinger, E.P., Erbel, R., Franks, P.W., Girelli, D., Hall, A.S., Hovingh, G.K., Kastrati, A., Lieb, W., Meitinger, T., Kraus, W.E., Shah, S.H., McPherson, R., Orho-Melander, M., Melander, O., Metspalu, A., Palmer, C.N.A., Peters, A., Rader, D.J., Reilly, M.P., Loos, R.J.F., Reiner, A.P., Roden, D.M., Tardif, J.C., Thompson, J.R., Wareham, N.J., Watkins, H., Willer, C.J., Samani, N.J., Schunkert, H., Deloukas, P., Kathiresan, S., Wellcome Trust Case Control, MORGAM Investigators, and Myocardial Infarction Genetics

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.

Published
2017

3. Genetic variation in FTO and mortality

Author

Zimmermann, E., Angquist, L.H., Mirza, S.S., Zhao, J.H., Chasman, D.I., Fischer, K., Qi, Q., Smith, A.V., Thinggaard, M., Jarczok, M.N., Nalls, M.A., Trompet, S., Timpson, N.J., Schmidt, B., Jackson, A.U., Lyytikainen, L.P., Verweij, N., Mueller-Nurasyid, M., Vikstrom, M., Marques-Vidal, P., Wong, A., Meidtner, K., Middelberg, R.P., Strawbridge, R.J., Christiansen, L., Kyvik, K.O., Hamsten, A., Jaaskelainen, T., Tjonneland, A., Eriksson, J.G., Whitfield, J.B., Boeing, H., Hardy, R., Vollenweider, P., Leander, K., Peters, A., Harst, P. van der, Kumari, M., Lehtimaki, T., Meirhaeghe, A., Tuomilehto, J., Jockel, K.H., Ben-Shlomo, Y., Sattar, N., Baumeister, S.E., Smith, G.D., Casas, J.P., Houston, D.K., Marz, W., Christensen, K., Gudnason, V., Hu, F.B., Metspalu, A., Ridker, P.M., Wareham, N.J., Loos, R.J.F., Tiemeier, H., Sonestedt, E., Sorensen, T.I.A., The FTO-Mortality Collaborating, Epidemiology, Surgery, Erasmus MC other, Child and Adolescent Psychiatry / Psychology, FTO-Mortality Collaborating Group, Orho-Melander, M., Zillikens, C., Ikram, A., Hofman, A., Luan, J., Khaw, KT., Rose, LM., Läll, K., Mägi, R., Qi, L., Sun, Q., Harris, TB., Launer, LJ., Eiriksdottir, G., Kleber, ME., Delgado, G., Liu, Y., Garcia, M., Teumer, A., Grabe, H., Homuth, G., Jukema, JW., Ford, I., de Craen AJ., Gallacher, J., Yarnell, J., Mahabadi, AA., Nöthen, MM., Erbel, R., Stringham, HM., Boehnke, M., Amouyel, P., Ferrières, J., Arveiler, D., Kähönen, M., Nikus, K., Nieminen, T., Sanchez, A., Kivimaki, M., van Vliet-Ostaptchouk JV., Hampel, R., Thorand, B., De Faire, U., Nyberg, F., Kuh, D., Martin, NG., Montgomery, GW., Heath, AC., Madden, PA., Osmond, C., Pulizzi, N., Roswall, N., Halkjaer, J., Overvad, K., Uusitupa, M., Kinnunen, L., Lindström, J., Saramies, J., Keinänen-Kiukaanniemi, S., Uusitalo, H., Hussi, E., Baldassarre, D., Veglia, F., Humphries, S., Tremoli, E., and Heitmann, B.

Subjects
obesity, nutritional and metabolic diseases, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Genetic Variation, Proteins, mortality, Polymorphism, Single Nucleotide, Article, Body Mass Index, meta-analysis, Observational Studies as Topic, Humans, Genetic Predisposition to Disease, Waist Circumference, FTO, Adiposity, Genome-Wide Association Study
Abstract

Previously, a single nucleotide polymorphism (SNP), rs9939609, in the FTO gene showed a much stronger association with all-cause mortality than expected from its association with body mass index (BMI), body fat mass index (FMI) and waist circumference (WC). This finding implies that the SNP has strong pleiotropic effects on adiposity and adiposity-independent pathological pathways that leads to increased mortality. To investigate this further, we conducted a meta-analysis of similar data from 34 longitudinal studies including 169,551 adult Caucasians among whom 27,100 died during follow-up. Linear regression showed that the minor allele of the FTO SNP was associated with greater BMI (n = 169,551; 0.32 kg m(-2) ; 95% CI 0.28-0.32, P

Published
2015

4. Making use of longitudinal information in pattern recognition

Author

Aksman, L.M., Lythgoe, D.J., Williams, S.C.R., Jokisch, M., Monninghoff, C., Streffer, J., Jockel, K.H., Weimar, C., Marquand, A.F., Aksman, L.M., Lythgoe, D.J., Williams, S.C.R., Jokisch, M., Monninghoff, C., Streffer, J., Jockel, K.H., Weimar, C., and Marquand, A.F.

Abstract

Contains fulltext : 167931.pdf (publisher's version ) (Open Access), Longitudinal designs are widely used in medical studies as a means of observing within-subject changes over time in groups of subjects, thereby aiming to improve sensitivity for detecting disease effects. Paralleling an increased use of such studies in neuroimaging has been the adoption of pattern recognition algorithms for making individualized predictions of disease. However, at present few pattern recognition methods exist to make full use of neuroimaging data that have been collected longitudinally, with most methods relying instead on cross-sectional style analysis. This article presents a principal component analysis-based feature construction method that uses longitudinal high-dimensional data to improve predictive performance of pattern recognition algorithms. The method can be applied to data from a wide range of longitudinal study designs and permits an arbitrary number of time-points per subject. We apply the method to two longitudinal datasets, one containing subjects with mild cognitive impairment along with healthy controls, the other with early dementia subjects and healthy controls. Across both datasets, we show improvements in predictive accuracy relative to cross-sectional classifiers for discriminating disease subjects from healthy controls on the basis of whole-brain structural magnetic resonance image-based voxels. In addition, we can transfer longitudinal information from one set of subjects to make disease predictions in another set of subjects. The proposed method is simple and, as a feature construction method, flexible with respect to the choice of classifier and image registration algorithm. Hum Brain Mapp 37:4385-4404, 2016. (c) 2016 Wiley Periodicals, Inc.

Published
2016

5. Occupational exposure to organic dust increases lung cancer risk in the general population

Author

Peters, S., Kromhout, H., Olsson, A.C., Wichmann, H.E., Bruske, I., Consonni, D., Landi, M.T., Caporaso, N., Siemiatycki, J., Richiardi, L., Mirabelli, D., Simonato, L., Gustavsson, P., Plato, N., Jockel, K.H., Ahrens, W., Pohlabeln, H., Boffetta, P., Brennan, P., Zaridze, D., Cassidy, A., Lissowska, J, Szeszenia-Dabrowska, N., Rudnai, P., Fabianova, E., Forastiere, F., Bencko, V., Foretova, L., Janout, V., Stucker, I., Dumitru, R.S., Benhamou, S., Bueno-de-Mesquita, B., Kendzia, B., Pesch, B., Straif, K., Bruning, T., Vermeulen, R., Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Peters, S., Kromhout, H., Olsson, A.C., Wichmann, H.-E., Brüske, I., Consonni, D., Landi, M.T., Caporaso, N., Siemiatycki, J., Richiardi, L., Mirabelli, D., Simonato, L., Gustavsson, P., Plato, N., Jöckel, K.-H., Ahrens, W., Pohlabeln, H., Boffetta, P., Brennan, P., Zaridze, D., Cassidy, A., Lissowska, J., Szeszenia-Dabrowska, N., Rudnai, P., Fabianova, E., Forastiere, F., Bencko, V., Foretova, L., Janout, V., Stücker, I., Dumitru, R.S., Benhamou, S., Bueno-de-Mesquita, B., Kendzia, B., Pesch, B., Straif, K., Brüning, T., Vermeulen, R., Risk Assessment of Toxic and Immunomodulatory Agents, and Dep IRAS

Subjects
Adult, Male, Pulmonary and Respiratory Medicine, Canada, Lung Neoplasms, case-control study, Population, Medizin, Cumulative Exposure, Logistic regression, Article, Toxicology, Occupational Exposure, Environmental health, Humans, Medicine, Lung cancer, education, Aged, Asthma, education.field_of_study, business.industry, Smoking, Case-control study, Public Health, Environmental and Occupational Health, Dust, Middle Aged, medicine.disease, Occupational exposure to organic du, respiratory tract diseases, Europe, Occupational Diseases, lung cancer, Quartile, Case-Control Studies, Meta-analysis, Female, business
Abstract

Background: Organic dust is a complex mixture of particulate matter from microbial, plant or animal origin. Occupations with exposure to animal products have been associated with an increased lung cancer risk, while exposure to microbial components (eg, endotoxin) has been associated with a decreased risk. To date there has not been a comprehensive evaluation of the possible association between occupational organic dust exposure (and its specific constituents) and lung cancer risk in the general population. Methods: The SYNERGY project has pooled information on lifetime working and smoking from 13 300 lung cancer cases and 16 273 controls from 11 case - control studies conducted in Europe and Canada. A newly developed general population job-exposure matrix (assigning no, low or high exposure to organic dust, endotoxin, and contact with animals or fresh animal products) was applied to determine level of exposure. ORs for lung cancer were estimated by logistic regression, adjusted for age, sex, study, cigarette pack-years, time since quitting smoking, and ever employment in occupations with established lung cancer risk. Results: Occupational organic dust exposure was associated with increased lung cancer risk. The second to the fourth quartile of cumulative exposure showed significant risk estimates ranging from 1.12 to 1.24 in a dose-dependent manner (p

Published
2012

6. Occupational exposure to organic dust increases lung cancer risk in the general population.

Author

Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Peters, S., Kromhout, H., Olsson, A.C., Wichmann, H.E., Bruske, I., Consonni, D., Landi, M.T., Caporaso, N., Siemiatycki, J., Richiardi, L., Mirabelli, D., Simonato, L., Gustavsson, P., Plato, N., Jockel, K.H., Ahrens, W., Pohlabeln, H., Boffetta, P., Brennan, P., Zaridze, D., Cassidy, A., Lissowska, J, Szeszenia-Dabrowska, N., Rudnai, P., Fabianova, E., Forastiere, F., Bencko, V., Foretova, L., Janout, V., Stucker, I., Dumitru, R.S., Benhamou, S., Bueno-de-Mesquita, B., Kendzia, B., Pesch, B., Straif, K., Bruning, T., Vermeulen, R., Risk Assessment of Toxic and Immunomodulatory Agents, Dep IRAS, Peters, S., Kromhout, H., Olsson, A.C., Wichmann, H.E., Bruske, I., Consonni, D., Landi, M.T., Caporaso, N., Siemiatycki, J., Richiardi, L., Mirabelli, D., Simonato, L., Gustavsson, P., Plato, N., Jockel, K.H., Ahrens, W., Pohlabeln, H., Boffetta, P., Brennan, P., Zaridze, D., Cassidy, A., Lissowska, J, Szeszenia-Dabrowska, N., Rudnai, P., Fabianova, E., Forastiere, F., Bencko, V., Foretova, L., Janout, V., Stucker, I., Dumitru, R.S., Benhamou, S., Bueno-de-Mesquita, B., Kendzia, B., Pesch, B., Straif, K., Bruning, T., and Vermeulen, R.

Published
2012

7. Genome-wide association study in German patients with attention deficit/hyperactivity disorder

Author

Hinney, A., Scherag, A., Jarick, I., Albayrak, O., Putter, C. de, Pechlivanis, S., Dauvermann, M.R., Beck, S., Weber, H., Scherag, S., Nguyen, T.T., Volckmar, A.L., Knoll, N., Faraone, S.V., Neale, B.M., Franke, B., Cichon, S., Hoffmann, P., Nothen, Markus, Schreiber, S., Jockel, K.H., Wichmann, H.E., Freitag, C., Lempp, T., Meyer, J., Gilsbach, S., Herpertz-Dahlmann, B., Sinzig, J., Lehmkuhl, G., Renner, T.J., Warnke, A., Romanos, M., Lesch, K.P., Reif, A., Schimmelmann, B.G., Hebebrand, J., Hinney, A., Scherag, A., Jarick, I., Albayrak, O., Putter, C. de, Pechlivanis, S., Dauvermann, M.R., Beck, S., Weber, H., Scherag, S., Nguyen, T.T., Volckmar, A.L., Knoll, N., Faraone, S.V., Neale, B.M., Franke, B., Cichon, S., Hoffmann, P., Nothen, Markus, Schreiber, S., Jockel, K.H., Wichmann, H.E., Freitag, C., Lempp, T., Meyer, J., Gilsbach, S., Herpertz-Dahlmann, B., Sinzig, J., Lehmkuhl, G., Renner, T.J., Warnke, A., Romanos, M., Lesch, K.P., Reif, A., Schimmelmann, B.G., and Hebebrand, J.

Abstract

Item does not contain fulltext, The heritability of attention deficit hyperactivity disorder (ADHD) is approximately 0.8. Despite several larger scale attempts, genome-wide association studies (GWAS) have not led to the identification of significant results. We performed a GWAS based on 495 German young patients with ADHD (according to DSM-IV criteria; Human660W-Quadv1; Illumina, San Diego, CA) and on 1,300 population-based adult controls (HumanHap550v3; Illumina). Some genes neighboring the single nucleotide polymorphisms (SNPs) with the lowest P-values (best P-value: 8.38 x 10(-7) ) have potential relevance for ADHD (e.g., glutamate receptor, metabotropic 5 gene, GRM5). After quality control, the 30 independent SNPs with the lowest P-values (P-values

Published
2011

8. A pooled analysis of bladder cancer case-control studies evaluating smoking in men and women

Author

Puente, D., Hartge, P., Greiser, E., Cantor, K.P., King, W.D., Gonzalez, C.A., Cordier, S., Vineis, P., Lynge, E., Chang-Claude, J., Porru, S., Tzonou, A., Jockel, K.H., Serra, C., Hours, M., Lynch, C.F., Ranft, U., Wahrendorf, J., Silverman, D., Fernandez, F., Boffetta, P., Kogevinas, M., Puente, D., Hartge, P., Greiser, E., Cantor, K.P., King, W.D., Gonzalez, C.A., Cordier, S., Vineis, P., Lynge, E., Chang-Claude, J., Porru, S., Tzonou, A., Jockel, K.H., Serra, C., Hours, M., Lynch, C.F., Ranft, U., Wahrendorf, J., Silverman, D., Fernandez, F., Boffetta, P., and Kogevinas, M.

Abstract

Udgivelsesdato: 2006/2

Published
2006

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