Katrin Horn

About Katrin Horn:
No description specified

LHA ID: 83TNHDVX05-6

Location:  Germany

ORCID: https://orcid.org/0000-0002-5307-6936

Joined: 10th Sep 2020

Expertise: Not specified

Tools: Not specified

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Related items

LIFE - Leipzig Research Center for Civilization Diseases: inactive since

Goal of the Leipzig Research Center for Civilization Diseases (LIFE) is the investigation of civilization diseases like depression, diabetes, allergies or cardiovascular diseases. For this purpose we collect as much data as possible regarding health and living conditions of the population in Leipzig and provide these data for scientists of the University of Leipzig and other research institutions.

Programme: Epidemiology

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

Start date: 1st Jan 2009

LIFE Heart

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. ...

Programme: Epidemiology

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

Start date: 1st Jan 2009

Genetical Statistics and Systems Biology

The group is interested in omic-level studies including the genome, methylome, transcriptome, and metabolome of the general population as well as of various diseases including cardiovascular diseases, pneumonia, sepsis, obesity, and brain cancers. Additionally, we aim at transfering results of biomathematical model simulations into clinical practice e.g. by haematopoietic growth-factor opimization during cytotoxic chemotherapy and optimization of EPO applications in chronic kidney disease.

The ...

Programme: This Project is not associated with a Programme

Public web page: http://www.imise.uni-leipzig.de/en/Groups/GenStat/

Start date: 1st Jan 2013

LIFE Adult

This population-based study examined 10,000 participants randomly selected from the Leipzig population (2011 to 2014). A follow-up is to be carried out from 2017 - 2020. The study mainly included people aged between 40 and 79. All participants underwent a 6-hour study program and people over 60 years of age were invited two more times to in-depth study of cognition and depression and the brain (MRI, EEG). Extensive measurements of genome, metabolome and transcriptome are available. The LIFE-ADULT ...

Programme: Epidemiology

Public web page: http://life.uni-leipzig.de/en/adults/life_adult.html

Start date: 1st Jan 2009

DNA methylation patterns reflect individual lifestyle independent from obesity
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart
No description specified

Submitter: Katrin Horn

Investigation: OMICS Investigations

Resources: Gene Expression data, LIFE-Adult EPIC data

Study type: Not specified

LIFE-Adult EPIC data
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart
No description specified

Submitter: Katrin Horn

Resource type: Experimental Assay Type

Technology type: Technology Type

Investigation: OMICS Investigations

Study: DNA methylation patterns reflect individual lif...

Gene Expression data
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart
No description specified

Submitter: Katrin Horn

Resource type: Gene Expression Profiling

Technology type: Technology Type

Investigation: OMICS Investigations

Study: DNA methylation patterns reflect individual lif...

A biomathematical model of human erythropoiesis and iron metabolism
Genetical Statistics and Systems Biology

Abstract (Expand)

Anaemia therapy or perisurgical support of erythropoiesis often require both, EPO and iron medication. However, excessive iron medication can result in iron overload and it is challenging to control … haemoglobin levels in a desired range. To support this task, we develop a biomathematical model to simulate EPO- and iron medication in humans. We combine our previously established model of human erythropoiesis including comprehensive pharmacokinetic models of EPO applications with a newly developed model of iron metabolism including iron supplementation. Equations were derived by translating known biological mechanisms into ordinary differential equations. Qualitative model behaviour is studied in detail considering a variety of interventions such as bleeding, iron malnutrition and medication. The model can explain time courses of erythrocytes, reticulocytes, haemoglobin, haematocrit, red blood cells, EPO, serum iron, ferritin, transferrin saturation, and transferrin under a variety of scenarios including EPO and iron application into healthy volunteers or chemotherapy patients. Unknown model parameters were determined by fitting the predictions of the model to time series data from literature. We demonstrate how the model can be used to make predictions of untested therapy options such as cytotoxic chemotherapy supported by iron and EPO. Following our ultimate goal of establishing a model of anaemia treatment in chronic kidney disease, we aim at translating our model to this pathological condition in the near future.

Authors: Sibylle Schirm, Markus Scholz

Date Published: 1st Dec 2020

Publication Type: Journal article

Dynamics of cytokines, immune cell counts and disease severity in patients with community-acquired pneumonia - Unravelling potential causal relationships
Genetical Statistics and Systems Biology

Abstract (Expand)

BACKGROUND Community acquired pneumonia (CAP) is a severe and often rapidly deteriorating disease. To better understand its dynamics and potential causal relationships, we analyzed time series data of …f cytokines, blood and clinical parameters in hospitalized CAP patients. METHODS Time series data of 10 circulating cytokines, blood counts and clinical parameters were related to baseline characteristics of 403 CAP patients using univariate mixed models. Bivariate mixed models were applied to analyze correlations between the time series. To identify potential causal relationships, we inferred cross-lagged relationships between pairs of parameters using latent curve models with structured residuals. RESULTS IL-6 levels decreased faster over time in younger patients (Padj = 0.06). IL-8, VCAM-1, and IL-6 correlated strongly with disease severity as assessed by the sequential organ failure assessment (SOFA) score (r = 0.49, 0.48, 0.46, respectively; all Padj \textless 0.001). IL-6 and bilirubin correlated with respect to their mean levels and slopes over time (r = 0.36 and r = 0.46, respectively; Padj \textless 0.001). A number of potential causal relationships were identified, e.g., a negative effect of ICAM-1 on MCP-1, or a positive effect of the level of creatinine on the subsequent VCAM-1 concentration (P \textless 0.001). CONCLUSIONS These results suggest that IL-6 trajectories of CAP patients are associated with age and run parallel to bilirubin levels. The time series analysis also unraveled directed, potentially causal relationships between cytokines, blood parameters and clinical outcomes. This will facilitate the development of mechanistic models of CAP, and with it, improvements in treatment or surveillance strategies for this disease. TRIAL REGISTRATION clinicaltrials.gov NCT02782013, May 25, 2016, retrospectively registered.

Authors: Maciej Rosolowski, Volker Oberle, Peter Ahnert, Petra Creutz, Martin Witzenrath, Michael Kiehntopf, Markus Loeffler, Norbert Suttorp, Markus Scholz

Date Published: 1st Dec 2020

Publication Type: Journal article

Integration of mathematical model predictions into routine workflows to support clinical decision making in haematology
Genetical Statistics and Systems Biology

Abstract (Expand)

BACKGROUND Individualization and patient-specific optimization of treatment is a major goal of modern health care. One way to achieve this goal is the application of high-resolution diagnostics together …r with the application of targeted therapies. However, the rising number of different treatment modalities also induces new challenges: Whereas randomized clinical trials focus on proving average treatment effects in specific groups of patients, direct conclusions at the individual patient level are problematic. Thus, the identification of the best patient-specific treatment options remains an open question. Systems medicine, specifically mechanistic mathematical models, can substantially support individual treatment optimization. In addition to providing a better general understanding of disease mechanisms and treatment effects, these models allow for an identification of patient-specific parameterizations and, therefore, provide individualized predictions for the effect of different treatment modalities. RESULTS In the following we describe a software framework that facilitates the integration of mathematical models and computer simulations into routine clinical processes to support decision-making. This is achieved by combining standard data management and data exploration tools, with the generation and visualization of mathematical model predictions for treatment options at an individual patient level. CONCLUSIONS By integrating model results in an audit trail compatible manner into established clinical workflows, our framework has the potential to foster the use of systems-medical approaches in clinical practice. We illustrate the framework application by two use cases from the field of haematological oncology.

Authors: Katja Hoffmann, Katja Cazemier, Christoph Baldow, Silvio Schuster, Yuri Kheifetz, Sibylle Schirm, Matthias Horn, Thomas Ernst, Constanze Volgmann, Christian Thiede, Andreas Hochhaus, Martin Bornhäuser, Meinolf Suttorp, Markus Scholz, Ingmar Glauche, Markus Loeffler, Ingo Roeder

Date Published: 1st Dec 2020

Publication Type: Journal article

Genome-wide association meta-analysis for early age-related macular degeneration highlights novel loci and insights for advanced disease
Genetical Statistics and Systems Biology

Abstract (Expand)

BACKGROUND Advanced age-related macular degeneration (AMD) is a leading cause of blindness. While around half of the genetic contribution to advanced AMD has been uncovered, little is known about the … genetic architecture of early AMD. METHODS To identify genetic factors for early AMD, we conducted a genome-wide association study (GWAS) meta-analysis (14,034 cases, 91,214 controls, 11 sources of data including the International AMD Genomics Consortium, IAMDGC, and UK Biobank, UKBB). We ascertained early AMD via color fundus photographs by manual grading for 10 sources and via an automated machine learning approach for > 170,000 photographs from UKBB. We searched for early AMD loci via GWAS and via a candidate approach based on 14 previously suggested early AMD variants. RESULTS Altogether, we identified 10 independent loci with statistical significance for early AMD: (i) 8 from our GWAS with genome-wide significance (P < 5 × 10- 8), (ii) one previously suggested locus with experiment-wise significance (P < 0.05/14) in our non-overlapping data and with genome-wide significance when combining the reported and our non-overlapping data (together 17,539 cases, 105,395 controls), and (iii) one further previously suggested locus with experiment-wise significance in our non-overlapping data. Of these 10 identified loci, 8 were novel and 2 known for early AMD. Most of the 10 loci overlapped with known advanced AMD loci (near ARMS2/HTRA1, CFH, C2, C3, CETP, TNFRSF10A, VEGFA, APOE), except two that have not yet been identified with statistical significance for any AMD. Among the 17 genes within these two loci, in-silico functional annotation suggested CD46 and TYR as the most likely responsible genes. Presence or absence of an early AMD effect distinguished the known pathways of advanced AMD genetics (complement/lipid pathways versus extracellular matrix metabolism). CONCLUSIONS Our GWAS on early AMD identified novel loci, highlighted shared and distinct genetics between early and advanced AMD and provides insights into AMD etiology. Our data provide a resource comparable in size to the existing IAMDGC data on advanced AMD genetics enabling a joint view. The biological relevance of this joint view is underscored by the ability of early AMD effects to differentiate the major pathways for advanced AMD.

Authors: Thomas W. Winkler, Felix Grassmann, Caroline Brandl, Christina Kiel, Felix Günther, Tobias Strunz, Lorraine Weidner, Martina E. Zimmermann, Christina A. Korb, Alicia Poplawski, Alexander K. Schuster, Martina Müller-Nurasyid, Annette Peters, Franziska G. Rauscher, Tobias Elze, Katrin Horn, Markus Scholz, Marisa Cañadas-Garre, Amy Jayne McKnight, Nicola Quinn, Ruth E. Hogg, Helmut Küchenhoff, Iris M. Heid, Klaus J. Stark, Bernhard H. F. Weber

Date Published: 1st Dec 2020

Publication Type: Journal article

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

Prevalence of atrial fibrillation dependent on coronary artery status: Insights from the LIFE-Heart Study.
Genetical Statistics and Systems Biology

Abstract (Expand)

BACKGROUND: Coronary artery disease (CAD) is a significant risk factor for atrial fibrillation (AF). Experimental studies demonstrated that atrial ischemia induced by right coronary artery (RCA) stenosis … promote AF triggers and development of electro-anatomical substrate for AF. AIM: To analyze the association between AF prevalence and coronary arteries status in the LIFE-Heart Study. METHODS: This analysis included patients with available coronary catheterization data recruited between 2006 and 2014. Patients with acute myocardial infarction were excluded. CAD was defined as stenosis >/=75%, while coronary artery sclerosis (CAS) was defined as non-critical plaque(s) <75%. RESULTS: In total, 3.458 patients (median age 63 years, 34% women) were included into analysis. AF was diagnosed in 238 (6.7%) patients. There were 681 (19.7%) patients with CAS and 1.411 (40.8%) with CAD (27.5% with single, 32.4% with double, and 40.1% with triple vessel CAD). In multivariable analysis, there was a significant association between prevalent AF and coronary artery status (OR 0.64, 95% CI 0.53-0.78, Ptrend < .001). Similarly, AF risk was lower in patients with higher CAD extent (OR 0.54, 95%CI 0.35-0.83, Ptrend = .005). Compared to single vessel CAD, the risk of AF was lower in double (OR 0.42, 95%CI 0.19-0.95, P = .037) and triple CAD (OR 0.31, 95%CI 0.13-0.71, P = .006). Finally, no association was found between AF prevalence and CAD origin among patients with single vessel CAD. CONCLUSION: In the LIFE-Heart Study, CAS but not CAD was associated with increased risk of AF.

Authors: J. Kornej, S. Henger, T. Seewoster, A. Teren, R. Burkhardt, H. Thiele, J. Thiery, M. Scholz

Date Published: 27th Oct 2020

Publication Type: Journal article

Higher BMI, but not obesity-related genetic polymorphisms, correlates with lower structural connectivity of the reward network in a population-based study.
Genetical Statistics and Systems Biology

Abstract (Expand)

BACKGROUND: Obesity is of complex origin, involving genetic and neurobehavioral factors. Genetic polymorphisms may increase the risk for developing obesity by modulating dopamine-dependent behaviors, … such as reward processing. Yet, few studies have investigated the association of obesity, related genetic variants, and structural connectivity of the dopaminergic reward network. METHODS: We analyzed 347 participants (age range: 20-59 years, BMI range: 17-38 kg/m(2)) of the LIFE-Adult Study. Genotyping for the single nucleotid polymorphisms rs1558902 (FTO) and rs1800497 (near dopamine D2 receptor) was performed on a microarray. Structural connectivity of the reward network was derived from diffusion-weighted magnetic resonance imaging at 3 T using deterministic tractography of Freesurfer-derived regions of interest. Using graph metrics, we extracted summary measures of clustering coefficient and connectivity strength between frontal and striatal brain regions. We used linear models to test the association of BMI, risk alleles of both variants, and reward network connectivity. RESULTS: Higher BMI was significantly associated with lower connectivity strength for number of streamlines (beta = -0.0025, 95%-C.I.: [-0.004, -0.0008], p = 0.0042), and, to lesser degree, fractional anisotropy (beta = -0.0009, 95%-C.I. [-0.0016, -0.00008], p = 0.031), but not clustering coefficient. Strongest associations were found for left putamen, right accumbens, and right lateral orbitofrontal cortex. As expected, the polymorphism rs1558902 in FTO was associated with higher BMI (F = 6.9, p < 0.001). None of the genetic variants was associated with reward network structural connectivity. CONCLUSIONS: Here, we provide evidence that higher BMI correlates with lower reward network structural connectivity. This result is in line with previous findings of obesity-related decline in white matter microstructure. We did not observe an association of variants in FTO or near DRD2 receptor with reward network structural connectivity in this population-based cohort with a wide range of BMI and age. Future research should further investigate the link between genetics, obesity and fronto-striatal structural connectivity.

Authors: F. Beyer, R. Zhang, M. Scholz, K. Wirkner, M. Loeffler, M. Stumvoll, A. Villringer, A. V. Witte

Date Published: 25th Oct 2020

Publication Type: Journal article

Neurobiological origins of individual differences in mathematical ability.
Genetical Statistics and Systems Biology

Abstract (Expand)

Mathematical ability is heritable and related to several genes expressing proteins in the brain. It is unknown, however, which intermediate neural phenotypes could explain how these genes relate to … mathematical ability. Here, we examined genetic effects on cerebral cortical volume of 3-6-year-old children without mathematical training to predict mathematical ability in school at 7-9 years of age. To this end, we followed an exploration sample (n = 101) and an independent replication sample (n = 77). We found that ROBO1, a gene known to regulate prenatal growth of cerebral cortical layers, is associated with the volume of the right parietal cortex, a key region for quantity representation. Individual volume differences in this region predicted up to a fifth of the behavioral variance in mathematical ability. Our findings indicate that a fundamental genetic component of the quantity processing system is rooted in the early development of the parietal cortex.

Authors: M. A. Skeide, K. Wehrmann, Z. Emami, H. Kirsten, A. M. Hartmann, D. Rujescu

Date Published: 22nd Oct 2020

Publication Type: Journal article

The Obesity-Susceptibility Gene TMEM18 Promotes Adipogenesis through Activation of PPARG.
Genetical Statistics and Systems Biology

Abstract (Expand)

TMEM18 is the strongest candidate for childhood obesity identified from GWASs, yet as for most GWAS-derived obesity-susceptibility genes, the functional mechanism remains elusive. We here investigate … the relevance of TMEM18 for adipose tissue development and obesity. We demonstrate that adipocyte TMEM18 expression is downregulated in children with obesity. Functionally, downregulation of TMEM18 impairs adipocyte formation in zebrafish and in human preadipocytes, indicating that TMEM18 is important for adipocyte differentiation in vivo and in vitro. On the molecular level, TMEM18 activates PPARG, particularly upregulating PPARG1 promoter activity, and this activation is repressed by inflammatory stimuli. The relationship between TMEM18 and PPARG1 is also evident in adipocytes of children and is clinically associated with obesity and adipocyte hypertrophy, inflammation, and insulin resistance. Our findings indicate a role of TMEM18 as an upstream regulator of PPARG signaling driving healthy adipogenesis, which is dysregulated with adipose tissue dysfunction and obesity.

Authors: K. Landgraf, N. Kloting, M. Gericke, N. Maixner, E. Guiu-Jurado, M. Scholz, A. V. Witte, F. Beyer, J. T. Schwartze, M. Lacher, A. Villringer, P. Kovacs, A. Rudich, M. Bluher, W. Kiess, A. Korner

Date Published: 20th Oct 2020

Publication Type: Journal article

Genome-wide association study reveals new insights into the heritability and genetic correlates of developmental dyslexia.
Genetical Statistics and Systems Biology

Abstract (Expand)

Developmental dyslexia (DD) is a learning disorder affecting the ability to read, with a heritability of 40-60%. A notable part of this heritability remains unexplained, and large genetic studies are … warranted to identify new susceptibility genes and clarify the genetic bases of dyslexia. We carried out a genome-wide association study (GWAS) on 2274 dyslexia cases and 6272 controls, testing associations at the single variant, gene, and pathway level, and estimating heritability using single-nucleotide polymorphism (SNP) data. We also calculated polygenic scores (PGSs) based on large-scale GWAS data for different neuropsychiatric disorders and cortical brain measures, educational attainment, and fluid intelligence, testing them for association with dyslexia status in our sample. We observed statistically significant (p < 2.8 x 10(-6)) enrichment of associations at the gene level, for LOC388780 (20p13; uncharacterized gene), and for VEPH1 (3q25), a gene implicated in brain development. We estimated an SNP-based heritability of 20-25% for DD, and observed significant associations of dyslexia risk with PGSs for attention deficit hyperactivity disorder (at pT = 0.05 in the training GWAS: OR = 1.23[1.16; 1.30] per standard deviation increase; p = 8 x 10(-13)), bipolar disorder (1.53[1.44; 1.63]; p = 1 x 10(-43)), schizophrenia (1.36[1.28; 1.45]; p = 4 x 10(-22)), psychiatric cross-disorder susceptibility (1.23[1.16; 1.30]; p = 3 x 10(-12)), cortical thickness of the transverse temporal gyrus (0.90[0.86; 0.96]; p = 5 x 10(-4)), educational attainment (0.86[0.82; 0.91]; p = 2 x 10(-7)), and intelligence (0.72[0.68; 0.76]; p = 9 x 10(-29)). This study suggests an important contribution of common genetic variants to dyslexia risk, and novel genomic overlaps with psychiatric conditions like bipolar disorder, schizophrenia, and cross-disorder susceptibility. Moreover, it revealed the presence of shared genetic foundations with a neural correlate previously implicated in dyslexia by neuroimaging evidence.

Authors: A. Gialluisi, T. F. M. Andlauer, N. Mirza-Schreiber, K. Moll, J. Becker, P. Hoffmann, K. U. Ludwig, D. Czamara, B. S. Pourcain, F. Honbolygo, D. Toth, V. Csepe, G. Huguet, Y. Chaix, S. Iannuzzi, J. F. Demonet, A. P. Morris, J. Hulslander, E. G. Willcutt, J. C. DeFries, R. K. Olson, S. D. Smith, B. F. Pennington, A. Vaessen, U. Maurer, H. Lyytinen, M. Peyrard-Janvid, P. H. T. Leppanen, D. Brandeis, M. Bonte, J. F. Stein, J. B. Talcott, F. Fauchereau, A. Wilcke, H. Kirsten, B. Muller, C. Francks, T. Bourgeron, A. P. Monaco, F. Ramus, K. Landerl, J. Kere, T. S. Scerri, S. Paracchini, S. E. Fisher, J. Schumacher, M. M. Nothen, B. Muller-Myhsok, G. Schulte-Korne

Date Published: 14th Oct 2020

Publication Type: Journal article

LIFE-Adult EPIC data idat files
LIFE Adult, Genetical Statistics and Systems Biology
No description specified

Creators: None

Submitter: Katrin Horn

Data file type: Not specified

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Gene Expression probe info
LIFE Adult, Genetical Statistics and Systems Biology
No description specified

Creators: None

Submitter: Katrin Horn

Data file type: Not specified

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Summary statistics for stigmasterol (part 2)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of stigmasterol (stf_chf, free stigmasterol to free cholesterol; stt_cht, total stigmasterol to total cholesterol; stf_laf, free stigmasterol to free lanosterol; stt_laf, total stigmasterol to free lanosterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: tba

When ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

Summary statistics for stigmasterol (part 1)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of stigmasterol (ste, esterified stigmasterol; stf, free stigmasterol; stt, total stigmasterol; stf_ste, free to esterified stigmasterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: tba

When using this data acknowledge the source as follows: 'Data on stigmasterol ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

Summary statistics for sitosterol (part 2)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of sitosterol (sif_chf, free sitosterol to free cholesterol; sit_cht, total sitosterol to total cholesterol; sif_laf, free sitosterol to free lanosterol; sit_laf, total sitosterol to free lanosterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: tba

When using this ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

Summary statistics for sitosterol (part 1)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of sitosterol (sie, esterified sitosterol; sif, free sitosterol; sit, total sitosterol; sif_sie, free to esterified sitosterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: tba

When using this data acknowledge the source as follows: 'Data on sitosterol has been ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

Summary statistics for campesterol (part 2)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of campesterol (caf_chf, free campesterol to free cholesterol; cat_cht, total campesterol to total cholesterol; caf_laf, free campesterol to free lanosterol; cat_laf, total campesterol to free lanosterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: tba

When using ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

Summary statistics for campesterol (part 1)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of campesterol (cae, esterified campesterol; caf, free campesterol; cat, total campesterol; caf_cae, free to esterified campesterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: tba

When using this data acknowledge the source as follows: 'Data on campesterol has been ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

Summary statistics for brassicasterol (part 2)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of brassicasterol (brf_chf, free brassicasterol to free cholesterol; brt_cht, total brassicasterol to total cholesterol; brf_laf, free brassicasterol to free lanosterol; brt_laf, total brassicasterol to free lanosterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

Summary statistics for brassicasterol (part 1)
LIFE Adult, Genetical Statistics and Systems Biology, LIFE Heart

Summary statistics from GWAMA of brassicasterol (bre, esterified brassicasterol; brf, free brassicasterol; brt, total brassicasterol; brf_bre, free to esterified brassicasterol). These data are intended for research purposes only, and available upon publication. For any enquiries about the datasets, please contact Janne Pott (janne.pott@imise.uni-leipzig.de) or Markus Scholz (markus.scholz@imise.uni-leipzig.de).

Citation: tba

When using this data acknowledge the source as follows: 'Data on ...

Creators: Katrin Horn, Markus Scholz, Janne Pott

Submitter: Janne Pott

Data file type: Other OMICs Data

LIFE-Adult EPIC Samples Sheet
LIFE Adult, Genetical Statistics and Systems Biology
No description specified

Creator: Katrin Horn

Submitter: Katrin Horn

Download
LIFE-Adult EPIC mSetSqFlt.rds
LIFE Adult, Genetical Statistics and Systems Biology
No description specified

Creator: Katrin Horn

Submitter: Katrin Horn

Download
Gene Expression sample information
LIFE Adult, Genetical Statistics and Systems Biology
No description specified

Creator: Katrin Horn

Submitter: Katrin Horn

Download
Gene Expression Data Dictionary
LIFE Adult, Genetical Statistics and Systems Biology
No description specified

Creator: Katrin Horn

Submitter: Katrin Horn

Download

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