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LIFE Heart

Overview
Description:

The LIFE-Heart study recruited 7,000 patients with suspected coronary heart disease, manifest heart disease or myocardial infarction. All patients received coronary angiography so that the vascular status in the heart is precisely known. In principle, this examination is not feasible in population-related studies. In addition, the patients were thoroughly examined with regard to the general vascular status and the health of the cardiovascular system. Extensive environmental factors were recorded. The cohort is also deeply molecularly and laboratory-medically characterized. These investigations are identical to those in LIFE-Adult, so that there are extensive possibilities for comparison between the cohorts. The LIFE-Heart study is the largest coronary angiographically characterized cohort in Germany and one of the largest worldwide.

Programme: Epidemiology

Health Atlas ID: 7Q0AQTKU2T-9

Funding codes:
  • EFRE

Public web page: http://life.uni-leipzig.de/

Organisms: Homo sapiens

Human Diseases: Cardiovascular system disease

Health Atlas PALs: No PALs for this Project

Project Coordinators: No Project coordinators for this Project

Project start date: 1st Jan 2009

Project Hierarchy

Related items

OMICS Investigations
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Resutls of different OMICS-level using LIFE Adult and LIFE Heart data are presented (Publications, Supplemental Data, & Summary Statistics).

Snapshots: No snapshots

GWAS Pulse Wave Velocity
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

We analysed if measuring PWV in different segments of the body leads to association with different genetic variants, as well as different heritability and different genetic correlation with other biological traits. Furthermore we searched for shared genetic architecture concerning PWV, blood pressure (BP) and coronary artery disease (CAD) and examined the causal relationship between PWV and BP.

Person responsible: Janne Pott

Snapshots: No snapshots

Study type: Genetic study

GWAS Carotid Plaque Burden
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

We defined six operationalizations of CPB considering plaques in common carotid arteries, carotid bulb, and internal carotid arteries (maximal plaque area, mean plaque area, sum of plaque areas at all six regions, maximal degree of stenosis, mean degree of stenosis, and sum of stenosis at all six regions).
Link to publication (PMID, DOI), Supplemental Figures and Tables, and Summary Statistics of GWAS will be made available upon acceptance of our manuscript.

Person responsible: Janne Pott

Snapshots: No snapshots

Study type: Genetic study

GWAS Steroid Hormones
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Supplement Data for Publication including Supplement Material & Results (eQTL annotation, Mendelian Randomization (MR), further significant loci), Figures (correlation plot of steroid hormones, scatter plot of genetic effect sizes, regional association plots, scatter plots of MR) and Tables (Correlations, GWAS summary statistics, interaction tests, MR results)

Person responsible: Janne Pott

Snapshots: No snapshots

Study type: Genetic study

1 hidden item
Summary Statistic for PWV GWAS
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAS of baPWV, bfPWV, cfPWV
All samples (adjusted for age, sex and log_sys)

These data is intended for research purposes only.

Citation: tbc

When using this data acknowledge the source as follows: 'Data on PWV has been contributed by LIFE-Adult investigators and has been downloaded from https://www.health-atlas.de/assays/34'

For any enquiries about the datasets, please contact Michael Rode (michael.rode@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de)
...

Submitter: Michael Rode

Resource type: Genome Wide Association

Technology type: SNP Array

Snapshots: No snapshots

Summary Statistics
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

We are releasing the summary data from our GWAS of carotid plaque burden traits, pending on acceptance of our publication, to empower other researchers to examine variants or loci in which they are interested for associations. These data are intended for research purposes only.

Citation:

When using this data acknowledge the source as follows: 'Data on carotid plaque burden has been contributed by LIFE-Adult investigators and has been downloaded from https://www.health-atlas.de/assays/31 '

For any
...

Submitter: Janne Pott

Resource type: Genome Wide Association

Technology type: SNP Array

Snapshots: No snapshots

Summary Statistics
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

We are releasing the summary data from our meta-analyses of steroid hormones, to empower other researchers to examine variants or loci in which they are interested for association with these hormonal traits. These data are intended for research purposes only.

Citation:
Pott et al. (2019) Genetic Association Study of Eight Steroid Hormones and Implications for Sexual Dimorphism of Coronary Artery Disease. J Clin Endocrinol Metab 104: 5008–5023. PubMed ID: 31169883

When using this data acknowledge
...

Submitter: Janne Pott

Resource type: Genome Wide Association

Technology type: SNP Array

Snapshots: No snapshots

Supplement Data
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

The primary goal of this study was to identify genetic loci associated with steroid hormone levels (cortisol, DHEA-S, testosterone, estradiol, progesterone, 17-hydroxyprogesterone, androstenedione, and aldosterone). In a secondary analysis, we searched for causal effects of steroid hormones on coronary artery disease.

Submitter: René Hänsel

Resource type: Experimental Assay Type

Technology type: Technology Type

Snapshots: No snapshots

1 hidden item
Meta-analysis uncovers genome-wide significant variants for rapid kidney function decline.
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Abstract (Expand)

Rapid decline of glomerular filtration rate estimated from creatinine (eGFRcrea) is associated with severe clinical endpoints. In contrast to cross-sectionally assessed eGFRcrea, the genetic basis for … rapid eGFRcrea decline is largely unknown. To help define this, we meta-analyzed 42 genome-wide association studies from the Chronic Kidney Diseases Genetics Consortium and United Kingdom Biobank to identify genetic loci for rapid eGFRcrea decline. Two definitions of eGFRcrea decline were used: 3 mL/min/1.73m(2)/year or more ("Rapid3"; encompassing 34,874 cases, 107,090 controls) and eGFRcrea decline 25% or more and eGFRcrea under 60 mL/min/1.73m(2) at follow-up among those with eGFRcrea 60 mL/min/1.73m(2) or more at baseline ("CKDi25"; encompassing 19,901 cases, 175,244 controls). Seven independent variants were identified across six loci for Rapid3 and/or CKDi25: consisting of five variants at four loci with genome-wide significance (near UMOD-PDILT (2), PRKAG2, WDR72, OR2S2) and two variants among 265 known eGFRcrea variants (near GATM, LARP4B). All these loci were novel for Rapid3 and/or CKDi25 and our bioinformatic follow-up prioritized variants and genes underneath these loci. The OR2S2 locus is novel for any eGFRcrea trait including interesting candidates. For the five genome-wide significant lead variants, we found supporting effects for annual change in blood urea nitrogen or cystatin-based eGFR, but not for GATM or LARP4B. Individuals at high compared to those at low genetic risk (8-14 vs 0-5 adverse alleles) had a 1.20-fold increased risk of acute kidney injury (95% confidence interval 1.08-1.33). Thus, our identified loci for rapid kidney function decline may help prioritize therapeutic targets and identify mechanisms and individuals at risk for sustained deterioration of kidney function.

Authors: M. Gorski, B. Jung, Y. Li, P. R. Matias-Garcia, M. Wuttke, S. Coassin, C. H. L. Thio, M. E. Kleber, T. W. Winkler, V. Wanner, J. F. Chai, A. Y. Chu, M. Cocca, M. F. Feitosa, S. Ghasemi, A. Hoppmann, K. Horn, M. Li, T. Nutile, M. Scholz, K. B. Sieber, A. Teumer, A. Tin, J. Wang, B. O. Tayo, T. S. Ahluwalia, P. Almgren, S. J. L. Bakker, B. Banas, N. Bansal, M. L. Biggs, E. Boerwinkle, E. P. Bottinger, H. Brenner, R. J. Carroll, J. Chalmers, M. L. Chee, M. L. Chee, C. Y. Cheng, J. Coresh, M. H. de Borst, F. Degenhardt, K. U. Eckardt, K. Endlich, A. Franke, S. Freitag-Wolf, P. Gampawar, R. T. Gansevoort, M. Ghanbari, C. Gieger, P. Hamet, K. Ho, E. Hofer, B. Holleczek, V. H. Xian Foo, N. Hutri-Kahonen, S. J. Hwang, M. A. Ikram, N. S. Josyula, M. Kahonen, C. C. Khor, W. Koenig, H. Kramer, B. K. Kramer, B. Kuhnel, L. A. Lange, T. Lehtimaki, W. Lieb, R. J. F. Loos, M. A. Lukas, L. P. Lyytikainen, C. Meisinger, T. Meitinger, O. Melander, Y. Milaneschi, P. P. Mishra, N. Mononen, J. C. Mychaleckyj, G. N. Nadkarni, M. Nauck, K. Nikus, B. Ning, I. M. Nolte, M. L. O'Donoghue, M. Orho-Melander, S. A. Pendergrass, B. W. J. H. Penninx, M. H. Preuss, B. M. Psaty, L. M. Raffield, O. T. Raitakari, R. Rettig, M. Rheinberger, K. M. Rice, A. R. Rosenkranz, P. Rossing, J. I. Rotter, C. Sabanayagam, H. Schmidt, R. Schmidt, B. Schottker, C. A. Schulz, S. Sedaghat, C. M. Shaffer, K. Strauch, S. Szymczak, K. D. Taylor, J. Tremblay, L. Chaker, P. van der Harst, P. J. van der Most, N. Verweij, U. Volker, M. Waldenberger, L. Wallentin, D. M. Waterworth, H. D. White, J. G. Wilson, T. Y. Wong, M. Woodward, Q. Yang, M. Yasuda, L. M. Yerges-Armstrong, Y. Zhang, H. Snieder, C. Wanner, C. A. Boger, A. Kottgen, F. Kronenberg, C. Pattaro, I. M. Heid

Date Published: 30th Oct 2020

Publication Type: Journal article

Genetic association study of eight steroid hormones and implications for sexual dimorphism of coronary artery disease
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Abstract (Expand)

CONTEXT: Steroid hormones are important regulators of physiological processes in humans and are under genetic control. A link to coronary artery disease (CAD) is supposed. OBJECTIVE: Our main objective …e was to identify genetic loci influencing steroid hormone levels. As secondary aim, we searched for causal effects of steroid hormones on CAD. DESIGN: We conducted genome-wide meta-association studies for eight steroid hormones: cortisol, DHEA-S, estradiol and testosterone in two independent cohorts (LIFE-Adult, LIFE-Heart, max. n=7667), and progesterone, 17-hydroxyprogesterone, androstenedione and aldosterone in LIFE-Heart only (max. n=2070). All genome-wide significant loci were tested for sex interactions. Further, we tested if previously reported CAD SNPs were associated with our steroid hormone panel and investigated causal links between hormone levels and CAD status using Mendelian Randomization (MR) approaches. RESULTS: We discovered 15 novel associated loci for 17-hydroxyprogesterone, progesterone, DHEA-S, cortisol, androstenedione, and estradiol. Five of these loci relate to genes directly involved in steroid metabolism: CYP21A1, CYP11B1, CYP17A1, STS, and HSD17B12, almost completing the set of steroidogenic enzymes with genetic associations. Sexual dimorphisms were found for seven of the novel loci. Other loci correspond, e.g., to the WNT4/β-catenin pathway. MR revealed that cortisol, androstenedione, 17-hydroxyprogesterone and DHEA-S had causal effects on CAD. We also observed enrichment of cortisol and testosterone associations among known CAD hits. CONCLUSION: Our study greatly improves insight into genetic regulation of steroid hormones and their dependency on sex. These results could serve as a basis for analyzing sex-dimorphisms in other complex diseases.

Authors: J. Pott, YJ. Bae, K. Horn, A. Teren, Andreas Kühnapfel, H. Kirsten, U. Ceglarek, Markus Löffler, J. Thiery, J. Kratzsch, Markus Scholz

Date Published: 6th Jun 2019

Publication Type: Not specified

Human Diseases: coronary artery disease

Relations between lipoprotein(a) concentrations, LPA genetic variants, and the risk of mortality in patients with established coronary heart disease: a molecular and genetic association study.
Genetical Statistics and Systems Biology, LIFE Heart

Abstract (Expand)

BACKGROUND: Lipoprotein(a) concentrations in plasma are associated with cardiovascular risk in the general population. Whether lipoprotein(a) concentrations or LPA genetic variants predict long-term … mortality in patients with established coronary heart disease remains less clear. METHODS: We obtained data from 3313 patients with established coronary heart disease in the Ludwigshafen Risk and Cardiovascular Health (LURIC) study. We tested associations of tertiles of lipoprotein(a) concentration in plasma and two LPA single-nucleotide polymorphisms ([SNPs] rs10455872 and rs3798220) with all-cause mortality and cardiovascular mortality by Cox regression analysis and with severity of disease by generalised linear modelling, with and without adjustment for age, sex, diabetes diagnosis, systolic blood pressure, BMI, smoking status, estimated glomerular filtration rate, LDL-cholesterol concentration, and use of lipid-lowering therapy. Results for plasma lipoprotein(a) concentrations were validated in five independent studies involving 10 195 patients with established coronary heart disease. Results for genetic associations were replicated through large-scale collaborative analysis in the GENIUS-CHD consortium, comprising 106 353 patients with established coronary heart disease and 19 332 deaths in 22 studies or cohorts. FINDINGS: The median follow-up was 9.9 years. Increased severity of coronary heart disease was associated with lipoprotein(a) concentrations in plasma in the highest tertile (adjusted hazard radio [HR] 1.44, 95% CI 1.14-1.83) and the presence of either LPA SNP (1.88, 1.40-2.53). No associations were found in LURIC with all-cause mortality (highest tertile of lipoprotein(a) concentration in plasma 0.95, 0.81-1.11 and either LPA SNP 1.10, 0.92-1.31) or cardiovascular mortality (0.99, 0.81-1.2 and 1.13, 0.90-1.40, respectively) or in the validation studies. INTERPRETATION: In patients with prevalent coronary heart disease, lipoprotein(a) concentrations and genetic variants showed no associations with mortality. We conclude that these variables are not useful risk factors to measure to predict progression to death after coronary heart disease is established. FUNDING: Seventh Framework Programme for Research and Technical Development (AtheroRemo and RiskyCAD), INTERREG IV Oberrhein Programme, Deutsche Nierenstiftung, Else-Kroener Fresenius Foundation, Deutsche Stiftung fur Herzforschung, Deutsche Forschungsgemeinschaft, Saarland University, German Federal Ministry of Education and Research, Willy Robert Pitzer Foundation, and Waldburg-Zeil Clinics Isny.

Authors: S. Zewinger, M. E. Kleber, V. Tragante, R. O. McCubrey, A. F. Schmidt, K. Direk, U. Laufs, C. Werner, W. Koenig, D. Rothenbacher, U. Mons, L. P. Breitling, H. Brenner, R. T. Jennings, I. Petrakis, S. Triem, M. Klug, A. Filips, S. Blankenberg, C. Waldeyer, C. Sinning, R. B. Schnabel, K. J. Lackner, E. Vlachopoulou, O. Nygard, G. F. T. Svingen, E. R. Pedersen, G. S. Tell, J. Sinisalo, M. S. Nieminen, R. Laaksonen, S. Trompet, R. A. J. Smit, N. Sattar, J. W. Jukema, H. V. Groesdonk, G. Delgado, T. Stojakovic, A. P. Pilbrow, V. A. Cameron, A. M. Richards, R. N. Doughty, Y. Gong, R. Cooper-DeHoff, J. Johnson, M. Scholz, F. Beutner, J. Thiery, J. G. Smith, R. O. Vilmundarson, R. McPherson, A. F. R. Stewart, S. Cresci, P. A. Lenzini, J. A. Spertus, O. Olivieri, D. Girelli, N. I. Martinelli, A. Leiherer, C. H. Saely, H. Drexel, A. Mundlein, P. S. Braund, C. P. Nelson, N. J. Samani, D. Kofink, I. E. Hoefer, G. Pasterkamp, A. A. Quyyumi, Y. A. Ko, J. A. Hartiala, H. Allayee, W. H. W. Tang, S. L. Hazen, N. Eriksson, C. Held, E. Hagstrom, L. Wallentin, A. Akerblom, A. Siegbahn, I. Karp, C. Labos, L. Pilote, J. C. Engert, J. M. Brophy, G. Thanassoulis, P. Bogaty, W. Szczeklik, M. Kaczor, M. Sanak, S. S. Virani, C. M. Ballantyne, V. V. Lee, E. Boerwinkle, M. V. Holmes, B. D. Horne, A. Hingorani, F. W. Asselbergs, R. S. Patel, B. K. Kramer, H. Scharnagl, D. Fliser, W. Marz, T. Speer

Date Published: 2nd Jun 2017

Publication Type: Journal article

Alteration of Multiple Leukocyte Gene Expression Networks is Linked with Magnetic Resonance Markers of Prognosis After Acute ST-Elevation Myocardial Infarction.
LIFE Heart

Abstract (Expand)

Prognostic relevant pathways of leukocyte involvement in human myocardial ischemic-reperfusion injury are largely unknown. We enrolled 136 patients with ST-elevation myocardial infarction (STEMI) after … primary angioplasty within 12 h after onset of symptoms. Following reperfusion, whole blood was collected within a median time interval of 20 h (interquartile range: 15-25 h) for genome-wide gene expression analysis. Subsequent CMR scans were performed using a standard protocol to determine infarct size (IS), area at risk (AAR), myocardial salvage index (MSI) and the extent of late microvascular obstruction (lateMO). We found 398 genes associated with lateMO and two genes with IS. Neither AAR, nor MSI showed significant correlations with gene expression. Genes correlating with lateMO were strongly related to several canonical pathways, including positive regulation of T-cell activation (p = 3.44 x 10(-5)), and regulation of inflammatory response (p = 1.86 x 10(-3)). Network analysis of multiple gene expression alterations associated with larger lateMO identified the following functional consequences: facilitated utilisation and decreased concentration of free fatty acid, repressed cell differentiation, enhanced phagocyte movement, increased cell death, vascular disease and compensatory vasculogenesis. In conclusion, the extent of lateMO after acute, reperfused STEMI correlated with altered activation of multiple genes related to fatty acid utilisation, lymphocyte differentiation, phagocyte mobilisation, cell survival, and vascular dysfunction.

Authors: A. Teren, H. Kirsten, F. Beutner, M. Scholz, L. M. Holdt, D. Teupser, M. Gutberlet, J. Thiery, G. Schuler, I. Eitel

Date Published: 3rd Feb 2017

Publication Type: Journal article

Human Diseases: myocardial infarction

No Association of Coronary Artery Disease with X-Chromosomal Variants in Comprehensive International Meta-Analysis.
Genetical Statistics and Systems Biology, LIFE Heart

Abstract (Expand)

In recent years, genome-wide association studies have identified 58 independent risk loci for coronary artery disease (CAD) on the autosome. However, due to the sex-specific data structure of the X … chromosome, it has been excluded from most of these analyses. While females have 2 copies of chromosome X, males have only one. Also, one of the female X chromosomes may be inactivated. Therefore, special test statistics and quality control procedures are required. Thus, little is known about the role of X-chromosomal variants in CAD. To fill this gap, we conducted a comprehensive X-chromosome-wide meta-analysis including more than 43,000 CAD cases and 58,000 controls from 35 international study cohorts. For quality control, sex-specific filters were used to adequately take the special structure of X-chromosomal data into account. For single study analyses, several logistic regression models were calculated allowing for inactivation of one female X-chromosome, adjusting for sex and investigating interactions between sex and genetic variants. Then, meta-analyses including all 35 studies were conducted using random effects models. None of the investigated models revealed genome-wide significant associations for any variant. Although we analyzed the largest-to-date sample, currently available methods were not able to detect any associations of X-chromosomal variants with CAD.

Authors: C. Loley, M. Alver, T. L. Assimes, A. Bjonnes, A. Goel, S. Gustafsson, J. Hernesniemi, J. C. Hopewell, S. Kanoni, M. E. Kleber, K. W. Lau, Y. Lu, L. P. Lyytikainen, C. P. Nelson, M. Nikpay, L. Qu, E. Salfati, M. Scholz, T. Tukiainen, C. Willenborg, H. H. Won, L. Zeng, W. Zhang, S. S. Anand, F. Beutner, E. P. Bottinger, R. Clarke, G. Dedoussis, R. Do, T. Esko, M. Eskola, M. Farrall, D. Gauguier, V. Giedraitis, C. B. Granger, A. S. Hall, A. Hamsten, S. L. Hazen, J. Huang, M. Kahonen, T. Kyriakou, R. Laaksonen, L. Lind, C. Lindgren, P. K. Magnusson, E. Marouli, E. Mihailov, A. P. Morris, K. Nikus, N. Pedersen, L. Rallidis, V. Salomaa, S. H. Shah, A. F. Stewart, J. R. Thompson, P. A. Zalloua, J. C. Chambers, R. Collins, E. Ingelsson, C. Iribarren, P. J. Karhunen, J. S. Kooner, T. Lehtimaki, R. J. Loos, W. Marz, R. McPherson, A. Metspalu, M. P. Reilly, S. Ripatti, D. K. Sanghera, J. Thiery, H. Watkins, P. Deloukas, S. Kathiresan, N. J. Samani, H. Schunkert, J. Erdmann, I. R. Konig

Date Published: 12th Oct 2016

Publication Type: Journal article

Human Diseases: coronary artery disease

Supplementary Data for Dissecting the genetics of the human transcriptome identifies novel trait-related trans-eQTLs and corroborates the regulatory relevance of non-protein coding locidagger.
Genetical Statistics and Systems Biology, LIFE Heart
No description specified

Creator: Markus Scholz

Submitter: Christoph Beger

Data file type: Clinical Data

Download
Incremental value of Veterans Specific Activity Questionnaire and the YMCA-step test for the assessment of cardiorespiratory fitness in population-based studies.
LIFE Heart
No description specified

Creator: Silke Zachariae

Submitter: Silke Zachariae

Data file type: Not specified

GWAS_SteroidHormones_SupTables
LIFE Adult, LIFE Heart, Genetical Statistics and Systems Biology
No description specified

Creator: Janne Pott

Submitter: René Hänsel

Data file type: Clinical Data

Download
GWAS_SteroidHormones_SupData
LIFE Adult, LIFE Heart, Genetical Statistics and Systems Biology

Supplement Data for Publication including Supplement Material & Results (eQTL annotation, Mendelian Randomization (MR), further significant loci), Figures (correlation plot of steroid hormones, scatter plot of genetic effect sizes, regional association plots, scatter plots of MR) and Tables (Correlations, GWAS summary statistics, interaction tests, MR results)

Creator: Janne Pott

Submitter: René Hänsel

Download
Katrin Horn

Projects: LIFE Adult, LIFE - Leipzig Research Center for Civilization Diseases, LIFE Heart, Genetical Statistics and Systems Biology

Institutions: Institute for Medical Informatics, Statistics and Epidemiology

https://orcid.org/0000-0002-5307-6936
René Hänsel adminproject_administratorasset_housekeeperasset_gatekeeperprogramme_administrator

Projects: LHA - Leipzig Health Atlas, LIFE Adult, LIFE - Leipzig Research Center for Civilization Diseases, LIFE HNC - Head and Neck Cancer Group, LIFE Heart, MMML - Molecular mechanisms in malignant lymphoma, GLA - German Lymphoma Alliance, MMML Demonstrators - Molecular Mechanisms in Malignant Lymphomas - Demonstrators of Personalized Medicine, HaematoOpt - Individualized model-based managing of the next-cycle thrombopenia of CHOEP/CHOP treated patients based on platelets dynamics during the previous cycles, GC-HBOC - German Consortium for Hereditary Breast and Ovarian Cancer, GC-HNPCC - German Consortium for Hereditary Non-Polyposis Colorectal Cancer, MMML-MYC-SYS, NLP4CR - Natural Language Processing for Clinical Research, Genetical Statistics and Systems Biology, SepNet - German Competence Network Sepsis, LIFE Child, HNPCC-Sys - Genomic and transcriptomic heterogeneity of colorectal tumours arising in Lynch syndrome, GGN - German Glioma Network, CAPSys - Footprints of Sepsis Framed Within Community Acquired Pneumonia in the Blood Transcriptome, ProstataCA, SMITH - Smart Medical Information Technology for Healthcare, COVID-19 Leipzig, Management of health information systems

Institutions: Institute for Medical Informatics, Statistics and Epidemiology

https://orcid.org/0000-0001-8344-0658
Markus Kreuz project_administrator

Projects: LIFE HNC - Head and Neck Cancer Group, LIFE - Leipzig Research Center for Civilization Diseases, LIFE Heart, MMML - Molecular mechanisms in malignant lymphoma, GLA - German Lymphoma Alliance, MMML-MYC-SYS, GGN - German Glioma Network

Institutions: Institute for Medical Informatics, Statistics and Epidemiology

Andreas Kühnapfel

Projects: LIFE Adult, LIFE - Leipzig Research Center for Civilization Diseases, LIFE Heart, Genetical Statistics and Systems Biology

Institutions: Institute for Medical Informatics, Statistics and Epidemiology

https://orcid.org/0000-0003-3668-0784
Janne Pott project_administratorasset_housekeeper

Projects: LIFE Adult, LIFE - Leipzig Research Center for Civilization Diseases, LIFE Heart, Genetical Statistics and Systems Biology

Institutions: Institute for Medical Informatics, Statistics and Epidemiology

https://orcid.org/0000-0002-5983-5331
cardiovascular system disease
LIFE Heart

Taxonomy URI: http://purl.obolibrary.org/obo/DOID_1287

Synonyms: disease of subdivision of hemolymphoid system

Definitions: A disease of anatomical entity which occurs in the blood, heart, blood vessels or the lymphatic system that passes nutrients (such as amino acids and electrolytes), gases, hormones, blood cells or lymph to and from cells in the body to help fight diseases and help stabilize body temperature and pH to maintain homeostasis.

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