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A recombined allele of the lipase gene CEL and its pseudogene CELP confers susceptibility to chronic pancreatitis
Genetical Statistics and Systems Biology

Abstract (Expand)

Carboxyl ester lipase is a digestive pancreatic enzyme encoded by the CEL gene. Mutations in CEL cause maturity-onset diabetes of the young as well as pancreatic exocrine dysfunction. Here we describe … a hybrid allele (CEL-HYB) originating from a crossover between CEL and its neighboring pseudogene, CELP. In a discovery series of familial chronic pancreatitis cases, we observed CEL-HYB in 14.1% (10/71) of cases compared to 1.0% (5/478) of controls (odds ratio (OR) = 15.5; 95% confidence interval (CI) = 5.1-46.9; P = 1.3 \times 10(-6) by two-tailed Fisher’s exact test). In three replication studies of nonalcoholic chronic pancreatitis, we identified CEL-HYB in a total of 3.7% (42/1,122) cases and 0.7% (30/4,152) controls (OR = 5.2; 95% CI = 3.2-8.5; P = 1.2 \times 10(-11); formal meta-analysis). The allele was also enriched in alcoholic chronic pancreatitis. Expression of CEL-HYB in cellular models showed reduced lipolytic activity, impaired secretion, prominent intracellular accumulation and induced autophagy. These findings implicate a new pathway distinct from the protease-antiprotease system of pancreatic acinar cells in chronic pancreatitis.   Carboxyl ester lipase is a digestive pancreatic enzyme encoded by the CEL gene. Mutations in CEL cause maturity-onset diabetes of the young as well as pancreatic exocrine dysfunction. Here we describe a hybrid allele (CEL-HYB) originating from a crossover between CEL and its neighboring pseudogene, CELP. In a discovery series of familial chronic pancreatitis cases, we observed CEL-HYB in 14.1% (10/71) of cases compared to 1.0% (5/478) of controls (odds ratio (OR) = 15.5; 95% confidence interval (CI) = 5.1-46.9; P = 1.3 \times 10(-6) by two-tailed Fisher’s exact test). In three replication studies of nonalcoholic chronic pancreatitis, we identified CEL-HYB in a total of 3.7% (42/1,122) cases and 0.7% (30/4,152) controls (OR = 5.2; 95% CI = 3.2-8.5; P = 1.2 \times 10(-11); formal meta-analysis). The allele was also enriched in alcoholic chronic pancreatitis. Expression of CEL-HYB in cellular models showed reduced lipolytic activity, impaired secretion, prominent intracellular accumulation and induced autophagy. These findings implicate a new pathway distinct from the protease-antiprotease system of pancreatic acinar cells in chronic pancreatitis.   Carboxyl ester lipase is a digestive pancreatic enzyme encoded by the CEL gene. Mutations in CEL cause maturity-onset diabetes of the young as well as pancreatic exocrine dysfunction. Here we describe a hybrid allele (CEL-HYB) originating from a crossover between CEL and its neighboring pseudogene, CELP. In a discovery series of familial chronic pancreatitis cases, we observed CEL-HYB in 14.1% (10/71) of cases compared to 1.0% (5/478) of controls (odds ratio (OR) = 15.5; 95% confidence interval (CI) = 5.1-46.9; P = 1.3 \times 10(-6) by two-tailed Fisher’s exact test). In three replication studies of nonalcoholic chronic pancreatitis, we identified CEL-HYB in a total of 3.7% (42/1,122) cases and 0.7% (30/4,152) controls (OR = 5.2; 95% CI = 3.2-8.5; P = 1.2 \times 10(-11); formal meta-analysis). The allele was also enriched in alcoholic chronic pancreatitis. Expression of CEL-HYB in cellular models showed reduced lipolytic activity, impaired secretion, prominent intracellular accumulation and induced autophagy. These findings implicate a new pathway distinct from the protease-antiprotease system of pancreatic acinar cells in chronic pancreatitis.   Carboxyl ester lipase is a digestive pancreatic enzyme encoded by the CEL gene. Mutations in CEL cause maturity-onset diabetes of the young as well as pancreatic exocrine dysfunction. Here we describe a hybrid allele (CEL-HYB) originating from a crossover between CEL and its neighboring pseudogene, CELP. In a discovery series of familial chronic pancreatitis cases, we observed CEL-HYB in 14.1% (10/71) of cases compared to 1.0% (5/478) of controls (odds ratio (OR) = 15.5; 95% confidence interval (CI) = 5.1-46.9; P = 1.3 \times 10(-6) by two-tailed Fisher’s exact test). In three replication studies of nonalcoholic chronic pancreatitis, we identified CEL-HYB in a total of 3.7% (42/1,122) cases and 0.7% (30/4,152) controls (OR = 5.2; 95% CI = 3.2-8.5; P = 1.2 \times 10(-11); formal meta-analysis). The allele was also enriched in alcoholic chronic pancreatitis. Expression of CEL-HYB in cellular models showed reduced lipolytic activity, impaired secretion, prominent intracellular accumulation and induced autophagy. These findings implicate a new pathway distinct from the protease-antiprotease system of pancreatic acinar cells in chronic pancreatitis. //  Carboxyl ester lipase is a digestive pancreatic enzyme encoded by the CEL gene. Mutations in CEL cause maturity-onset diabetes of the young as well as pancreatic exocrine dysfunction. Here we describe a hybrid allele (CEL-HYB) originating from a crossover between CEL and its neighboring pseudogene, CELP. In a discovery series of familial chronic pancreatitis cases, we observed CEL-HYB in 14.1% (10/71) of cases compared to 1.0% (5/478) of controls (odds ratio (OR) = 15.5; 95% confidence interval (CI) = 5.1-46.9; P = 1.3 \times 10(-6) by two-tailed Fisher’s exact test). In three replication studies of nonalcoholic chronic pancreatitis, we identified CEL-HYB in a total of 3.7% (42/1,122) cases and 0.7% (30/4,152) controls (OR = 5.2; 95% CI = 3.2-8.5; P = 1.2 \times 10(-11); formal meta-analysis). The allele was also enriched in alcoholic chronic pancreatitis. Expression of CEL-HYB in cellular models showed reduced lipolytic activity, impaired secretion, prominent intracellular accumulation and induced autophagy. These findings implicate a new pathway distinct from the protease-antiprotease system of pancreatic acinar cells in chronic pancreatitis.

Authors: Karianne Fjeld, Frank Ulrich Weiss, Denise Lasher, Jonas Rosendahl, Jian-Min Chen, Bente B. Johansson, Holger Kirsten, Claudia Ruffert, Emmanuelle Masson, Solrun J. Steine, Peter Bugert, Miriam Cnop, Robert Grützmann, Julia Mayerle, Joachim Mössner, Monika Ringdal, Hans-Ulrich Schulz, Matthias Sendler, Peter Simon, Paweł Sztromwasser, Janniche Torsvik, Markus Scholz, Erling Tjora, Claude Férec, Heiko Witt, Markus M. Lerch, Pål R. Njølstad, Stefan Johansson, Anders Molven

Date Published: 1st May 2015

Publication Type: Journal article

Common genomic variation in the FER gene: useful to stratify patients with sepsis due to pneumonia?
LIFE - Leipzig Research Center for Civilization Diseases

Abstract

Not specified

Authors: F. Schoneweck, E. Kuhnt, M. Scholz, F. M. Brunkhorst, A. Scherag

Date Published: 30th Apr 2015

Publication Type: Not specified

Human Diseases: bacterial infectious disease, pneumonia

Age- and gender-specific norms for the German version of the Three-Factor Eating-Questionnaire (TFEQ).
LIFE Adult

Abstract (Expand)

The 'Fragebogen zum Essverhalten' (FEV) is the German version of the Three-factor-Eating-Questionnaire (TFEQ). This questionnaire covers three domains of eating behaviour ('cognitive … restraint', 'disinhibition' and 'hunger') as well as common problems (e.g. craving for sweets). So far, there is a lack of normative data of the FEV especially for the middle-aged and older population. Aim of this study therefore was to provide age- and gender-specific norms of the FEV for the general population aged 40-79 years. We studied 3144 participants of the ongoing large community-based Leipzig Research Center for Civilization Diseases (LIFE) Health Care Study. We provided age- (four age groups: 40-49, 50-59, 60-69, and 70-79 years) and gender-specific percentile ranks and T-scores for the three domains of the FEV as well as age- and gender-specific frequencies of the common problems in eating behaviour. Females scored significantly higher than males in all three domains of the FEV (p < 0.001). Older individuals showed significantly higher mean scores than the younger ones in the domain of cognitive restraint, but lower mean scores in disinhibition and hunger (p < 0.001). 45.1% of the males and 69.9% of the females reported specific problems in eating. The main problem in both genders was craving for sweets (38.6%). Eating in response to stress was mostly reported in younger individuals. The present study offers current normative data for the FEV in the middle-aged and older general population that can be applied in clinical and non-clinical settings. Information on eating behaviour can be helpful in understanding body weight modulation, and thus, may help to improve interventive and preventive programmes for overweight, obesity, and eating disorders.

Authors: A. Loffler, T. Luck, F. S. Then, M. Luppa, C. Sikorski, P. Kovacs, A. Tonjes, Y. Bottcher, J. Breitfeld, A. Horstmann, M. Loffler, C. Engel, J. Thiery, M. Stumvoll, S. G. Riedel-Heller

Date Published: 19th Apr 2015

Publication Type: Not specified

Human Diseases: obesity, eating disorder

DNA methylation array analyses identified breast cancer-associated HYAL2 methylation in peripheral blood
GC-HBOC - German Consortium for Hereditary Breast and Ovarian Cancer

Abstract (Expand)

Breast cancer (BC) is the leading cause of cancer-related mortality in women worldwide. Changes in DNA methylation in peripheral blood could be associated with malignancy at early stage. However, the … BC-associated DNA methylation signatures in peripheral blood were largely unknown. Here, we performed a genome-wide methylation screening and identified a BC-associated differentially methylated CpG site cg27091787 in the hyaluronoglucosaminidase 2 gene (HYAL2) (discovery round with 72 BC case and 24 controls: p = 2.61 \times 10(-9) adjusted for cell-type proportions). The substantially decreased methylation of cg27091787 in BC cases was confirmed in two validation rounds (first validation round with 338 BC case and 507 controls: p \textless 0.0001; second validation round with 189 BC case and 189 controls: p \textless 0.0001). In addition to cg27091787, the decreased methylation of a 650-bp CpG island shore of HYAL2 was also associated with increased risk of BC. Moreover, the expression and methylation of HYAL2 were inversely correlated with a p-value of 0.006. To note, the BC-associated decreased HYAL2 methylation was replicated in the T-cell fraction (p = 0.034). The cg27091787 methylation level enabled a powerful discrimination of early-stage BC cases (stages 0 and I) from healthy controls [area under curve (AUC) = 0.89], and was robust for the detection of BC in younger women as well (age \textless 50, AUC = 0.87). Our study reveals a strong association between decreased HYAL2 methylation in peripheral blood and BC, and provides a promising blood-based marker for the detection of early BC.

Authors: Rongxi Yang, Katrin Pfütze, Manuela Zucknick, Christian Sutter, Barbara Wappenschmidt, Frederik Marme, Bin Qu, Katarina Cuk, Christoph Engel, Sarah Schott, Andreas Schneeweiss, Hermann Brenner, Rainer Claus, Christoph Plass, Peter Bugert, Markus Hoth, Christof Sohn, Rita Schmutzler, Claus R. Bartram, Barbara Burwinkel

Date Published: 15th Apr 2015

Publication Type: Journal article

Human Diseases: hereditary breast ovarian cancer syndrome

Association of type and location of BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer
GC-HBOC - German Consortium for Hereditary Breast and Ovarian Cancer

Abstract (Expand)

IMPORTANCE Limited information about the relationship between specific mutations in BRCA1 or BRCA2 (BRCA1/2) and cancer risk exists. OBJECTIVE To identify mutation-specific cancer risks for carriers …ers of BRCA1/2. DESIGN, SETTING, AND PARTICIPANTS Observational study of women who were ascertained between 1937 and 2011 (median, 1999) and found to carry disease-associated BRCA1 or BRCA2 mutations. The international sample comprised 19,581 carriers of BRCA1 mutations and 11,900 carriers of BRCA2 mutations from 55 centers in 33 countries on 6 continents. We estimated hazard ratios for breast and ovarian cancer based on mutation type, function, and nucleotide position. We also estimated RHR, the ratio of breast vs ovarian cancer hazard ratios. A value of RHR greater than 1 indicated elevated breast cancer risk; a value of RHR less than 1 indicated elevated ovarian cancer risk. EXPOSURES Mutations of BRCA1 or BRCA2. MAIN OUTCOMES AND MEASURES Breast and ovarian cancer risks. RESULTS Among BRCA1 mutation carriers, 9052 women (46%) were diagnosed with breast cancer, 2317 (12%) with ovarian cancer, 1041 (5%) with breast and ovarian cancer, and 7171 (37%) without cancer. Among BRCA2 mutation carriers, 6180 women (52%) were diagnosed with breast cancer, 682 (6%) with ovarian cancer, 272 (2%) with breast and ovarian cancer, and 4766 (40%) without cancer. In BRCA1, we identified 3 breast cancer cluster regions (BCCRs) located at c.179 to c.505 (BCCR1; RHR = 1.46; 95% CI, 1.22-1.74; P = 2 \times 10(-6)), c.4328 to c.4945 (BCCR2; RHR = 1.34; 95% CI, 1.01-1.78; P = .04), and c. 5261 to c.5563 (BCCR2’, RHR = 1.38; 95% CI, 1.22-1.55; P = 6 \times 10(-9)). We also identified an ovarian cancer cluster region (OCCR) from c.1380 to c.4062 (approximately exon 11) with RHR = 0.62 (95% CI, 0.56-0.70; P = 9 \times 10(-17)). In BRCA2, we observed multiple BCCRs spanning c.1 to c.596 (BCCR1; RHR = 1.71; 95% CI, 1.06-2.78; P = .03), c.772 to c.1806 (BCCR1’; RHR = 1.63; 95% CI, 1.10-2.40; P = .01), and c.7394 to c.8904 (BCCR2; RHR = 2.31; 95% CI, 1.69-3.16; P = .00002). We also identified 3 OCCRs: the first (OCCR1) spanned c.3249 to c.5681 that was adjacent to c.5946delT (6174delT; RHR = 0.51; 95% CI, 0.44-0.60; P = 6 \times 10(-17)). The second OCCR spanned c.6645 to c.7471 (OCCR2; RHR = 0.57; 95% CI, 0.41-0.80; P = .001). Mutations conferring nonsense-mediated decay were associated with differential breast or ovarian cancer risks and an earlier age of breast cancer diagnosis for both BRCA1 and BRCA2 mutation carriers. CONCLUSIONS AND RELEVANCE Breast and ovarian cancer risks varied by type and location of BRCA1/2 mutations. With appropriate validation, these data may have implications for risk assessment and cancer prevention decision making for carriers of BRCA1 and BRCA2 mutations.

Authors: Timothy R. Rebbeck, Nandita Mitra, Fei Wan, Olga M. Sinilnikova, Sue Healey, Lesley McGuffog, Sylvie Mazoyer, Georgia Chenevix-Trench, Douglas F. Easton, Antonis C. Antoniou, Katherine L. Nathanson, Yael Laitman, Anya Kushnir, Shani Paluch-Shimon, Raanan Berger, Jamal Zidan, Eitan Friedman, Hans Ehrencrona, Marie Stenmark-Askmalm, Zakaria Einbeigi, Niklas Loman, Katja Harbst, Johanna Rantala, Beatrice Melin, Dezheng Huo, Olufunmilayo I. Olopade, Joyce Seldon, Patricia A. Ganz, Robert L. Nussbaum, Salina B. Chan, Kunle Odunsi, Simon A. Gayther, Susan M. Domchek, Banu K. Arun, Karen H. Lu, Gillian Mitchell, Beth Y. Karlan, Christine Walsh, Jenny Lester, Andrew K. Godwin, Harsh Pathak, Eric Ross, Mary B. Daly, Alice S. Whittemore, Esther M. John, Alexander Miron, Mary Beth Terry, Wendy K. Chung, David E. Goldgar, Saundra S. Buys, Ramunas Janavicius, Laima Tihomirova, Nadine Tung, Cecilia M. Dorfling, Elizabeth J. van Rensburg, Linda Steele, Susan L. Neuhausen, Yuan Chun Ding, Bent Ejlertsen, Anne-Marie Gerdes, Thomas v. O. Hansen, Teresa Ramón y Cajal, Ana Osorio, Javier Benitez, Javier Godino, Maria-Isabel Tejada, Mercedes Duran, Jeffrey N. Weitzel, Kristie A. Bobolis, Sharon R. Sand, Annette Fontaine, Antonella Savarese, Barbara Pasini, Bernard Peissel, Bernardo Bonanni, Daniela Zaffaroni, Francesca Vignolo-Lutati, Giulietta Scuvera, Giuseppe Giannini, Loris Bernard, Maurizio Genuardi, Paolo Radice, Riccardo Dolcetti, Siranoush Manoukian, Valeria Pensotti, Viviana Gismondi, Drakoulis Yannoukakos, Florentia Fostira, Judy Garber, Diana Torres, Muhammad Usman Rashid, Ute Hamann, Susan Peock, Debra Frost, Radka Platte, D. Gareth Evans, Rosalind Eeles, Rosemarie Davidson, Diana Eccles, Trevor Cole, Jackie Cook, Carole Brewer, Shirley Hodgson, Patrick J. Morrison, Lisa Walker, Mary E. Porteous, M. John Kennedy, Louise Izatt, Julian Adlard, Alan Donaldson, Steve Ellis, Priyanka Sharma, Rita Katharina Schmutzler, Barbara Wappenschmidt, Alexandra Becker, Kerstin Rhiem, Eric Hahnen, Christoph Engel, Alfons Meindl, Stefanie Engert, Nina Ditsch, Norbert Arnold, Hans Jörg Plendl, Christoph Mundhenke, Dieter Niederacher, Markus Fleisch, Christian Sutter, C. R. Bartram, Nicola Dikow, Shan Wang-Gohrke, Dorothea Gadzicki, Doris Steinemann, Karin Kast, Marit Beer, Raymonda Varon-Mateeva, Andrea Gehrig, Bernhard H. Weber, Dominique Stoppa-Lyonnet, Claude Houdayer, Muriel Belotti, Marion Gauthier-Villars, Francesca Damiola, Nadia Boutry-Kryza, Christine Lasset, Hagay Sobol, Jean-Philippe Peyrat, Danièle Muller, Jean-Pierre Fricker, Marie-Agnès Collonge-Rame, Isabelle Mortemousque, Catherine Nogues, Etienne Rouleau, Claudine Isaacs, Anne de Paepe, Bruce Poppe, Kathleen Claes, Kim de Leeneer, Marion Piedmonte, Gustavo Rodriguez, Katie Wakely, John Boggess, Stephanie V. Blank, Jack Basil, Masoud Azodi, Kelly-Anne Phillips, Trinidad Caldes, Miguel de La Hoya, Atocha Romero, Heli Nevanlinna, Kristiina Aittomäki, Annemarie H. van der Hout, Frans B. L. Hogervorst, Senno Verhoef, J. Margriet Collée, Caroline Seynaeve, Jan C. Oosterwijk, Johannes J. P. Gille, Juul T. Wijnen, Encarna B. Gómez Garcia, Carolien M. Kets, Margreet G. E. M. Ausems, Cora M. Aalfs, Peter Devilee, Arjen R. Mensenkamp, Ava Kwong, Edith Olah, Janos Papp, Orland Diez, Conxi Lazaro, Esther Darder, Ignacio Blanco, Mónica Salinas, Anna Jakubowska, Jan Lubinski, Jacek Gronwald, Katarzyna Jaworska-Bieniek, Katarzyna Durda, Grzegorz Sukiennicki, Tomasz Huzarski, Tomasz Byrski, Cezary Cybulski, Aleksandra Toloczko-Grabarek, Elżbieta Złowocka-Perłowska, Janusz Menkiszak, Adalgeir Arason, Rosa B. Barkardottir, Jacques Simard, Rachel Laframboise, Marco Montagna, Simona Agata, Elisa Alducci, Ana Peixoto, Manuel R. Teixeira, Amanda B. Spurdle, Min Hyuk Lee, Sue K. Park, Sung-Won Kim, Tara M. Friebel, Fergus J. Couch, Noralane M. Lindor, Vernon S. Pankratz, Lucia Guidugli, Xianshu Wang, Marc Tischkowitz, Lenka Foretova, Joseph Vijai, Kenneth Offit, Mark Robson, Rohini Rau-Murthy, Noah Kauff, Anneliese Fink-Retter, Christian F. Singer, Christine Rappaport, Daphne Gschwantler-Kaulich, Georg Pfeiler, Muy-Kheng Tea, Andreas Berger, Mark H. Greene, Phuong L. Mai, Evgeny N. Imyanitov, Amanda Ewart Toland, Leigha Senter, Anders Bojesen, Inge Sokilde Pedersen, Anne-Bine Skytte, Lone Sunde, Mads Thomassen, Sanne Traasdahl Moeller, Torben A. Kruse, Uffe Birk Jensen, Maria Adelaide Caligo, Paolo Aretini, Soo-Hwang Teo, Christina G. Selkirk, Peter J. Hulick, Irene Andrulis

Date Published: 7th Apr 2015

Publication Type: Journal article

Human Diseases: hereditary breast ovarian cancer syndrome

PET/MR in dementia and other neurodegenerative diseases.
LIFE Adult

Abstract (Expand)

The spectrum of neurodegenerative diseases covers the dementias, parkinsonian syndromes, Huntington disease, amyotrophic lateral sclerosis, and prion diseases. In these entities, brain MRI is often … used in clinical routine to exclude other pathologies and to demonstrate specific atrophy patterns. [18F]FDG PET delivers early and sensitive readouts of neural tissue loss, and more specific PET tracers currently in use clinically target beta-amyloid plaques or dopaminergic deficiency. The recent integration of PET into MR technology offers a new chance to improve early and differential diagnosis of many neurodegenerative diseases. Initial evidence in the literature is available to support this notion. New emerging PET tracers, such as tracers that bind to tau or alpha-synuclein aggregates, as well as MR techniques, like diffusion-tensor imaging, resting-state functional MRI, and arterial spin labeling, have the potential to broaden the diagnostic capabilities of combined PET/MRI to image dementias, Parkinson disease, and other neurodegenerative diseases. The ultimate goal is to establish combined PET/MRI as a first-line imaging technique to provide, in a one-stop-shop fashion with improved patient comfort, all biomarker information required to increase diagnostic confidence toward specific diagnoses. The technical challenge of accurate PET data attenuation correction within PET/MRI systems needs yet to be solved. Apart from the projected clinical routine applications, future research would need to answer the questions of whether combined brain PET/MRI is able to improve basic research of neurodegenerative diseases and antineurodegeneration drug testing.

Authors: H. Barthel, M. L. Schroeter, K. T. Hoffmann, O. Sabri

Date Published: 6th Apr 2015

Publication Type: Not specified

Human Diseases: dementia, neurodegenerative disease

Cost-utility analysis of a preventive home visit program for older adults in Germany.
LIFE Adult

Abstract (Expand)

BACKGROUND: Most older adults want to live independently in a familiar environment instead of moving to a nursing home. Preventive home visits based on multidimensional geriatric assessment can be one … strategy to support this preference and might additionally reduce health care costs, due to the avoidance of costly nursing home admissions. The purpose of this study was to analyse the cost-effectiveness of preventive home visits from a societal perspective in Germany. METHODS: This study is part of a multi-centre, non-blinded, randomised controlled trial aiming at the reduction of nursing home admissions. Participants were older than 80 years and living at home. Up to three home visits were conducted to identify self-care deficits and risk factors, to present recommendations and to implement solutions. The control group received usual care. A cost-utility analysis using quality-adjusted life years (QALY) based on the EQ-5D was performed. Resource utilization was assessed by means of the interview version of a patient questionnaire. A cost-effectiveness acceptability curve controlled for prognostic variables was constructed and a sensitivity analysis to control for the influence of the mode of QALY calculation was performed. RESULTS: 278 individuals (intervention group: 133; control group: 145) were included in the analysis. During 18 months follow-up mean adjusted total cost (mean: +4,401 EUR; bootstrapped standard error: 3,019.61 EUR) and number of QALY (mean: 0.0061 QALY; bootstrapped standard error: 0.0388 QALY) were higher in the intervention group, but differences were not significant. For preventive home visits the probability of an incremental cost-effectiveness ratio <50,000 EUR per QALY was only 15%. The results were robust with respect to the mode of QALY calculation. CONCLUSIONS: The evaluated preventive home visits programme is unlikely to be cost-effective. TRIAL REGISTRATION: Clinical Trials.gov Identifier: NCT00644826.

Authors: C. Brettschneider, T. Luck, S. Fleischer, G. Roling, K. Beutner, M. Luppa, J. Behrens, S. G. Riedel-Heller, H. H. Konig

Date Published: 3rd Apr 2015

Publication Type: Not specified

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