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LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Overview

One of the tasks of the healthy liver is to store fat. Yet, at some stage, too much fat makes the liver sick. One critical time point occurs when a healthy fatty liver becomes inflamed and progresses to steatohepatitis, or NASH.
LiSyM-Pillar I will identify what events lead to this transition. Does it occur in all parts of the liver? Which molecules indicate that it is taking place? Can the degeneration be stopped or undone - and if so, how?

SEEK ID: https://seek.lisym.org/projects/3

Public web page: http://www.lisym.org/our-work/pillar-research/zones-of-the-liver

Organisms: Mus musculus, Rattus rattus, Rattus norvegicus, Homo sapiens

FAIRDOM PALs: Vincent Moser, Lutz Brusch, Annika Schneider, Mario Brosch

Project start date: 1st Jan 2016

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Johannes Bausch : inactive since 2018-04-30

Projects: LiSyM Core Infrastructure and Management (LiSyM-PD), LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP), LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM Pillar IV: Liver Function Diagnostics (LiSyM-LiFuDi), LiSyM Pillar III: Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF), LiSyM network, LiSyM Scientific Leadership Team (LiSyM-LT)

Institutions: University of Freiburg - Institute of Physics, LiSyM programme directorate

https://orcid.org/0000-0002-1003-1682
Ann-Kristin Becker

Projects: LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM network

Institutions: University Medicine Greifswald - Institute of Bioinformatics

Mario Brosch pal

Projects: LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM network, LiSyM-Krebs Partnering

Institutions: Universitätsklinikum Dresden - Medizinische Klinik I, Bereich Gastroenterologie & Hepatologie

Lutz Brusch pal

Projects: LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM PALs, LiSyM network, LiSyM-Krebs Partnering

Institutions: Zentrum für Informationsdienste und Hochleistungsrechnen (ZIH), Technische Universität Dresden

https://orcid.org/0000-0003-0137-5106
Stephan Buch

Projects: LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Institutions: Universitätsklinikum Dresden - Medizinische Klinik I, Bereich Gastroenterologie & Hepatologie

LiSyM Pillar I: Early Metabolic Injury
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)
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Mouse expression dataset (Comparison of Gene Expression Patterns Between Mouse Models of Nonalcoholic Fatty Liver Disease and Liver Tissues From Patients.)
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

BACKGROUND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder in industrialized countries. Mouse models of NAFLD have been used in studies of pathogenesis and treatment, and have certain features of the human disease. We performed a systematic transcriptome-wide analysis of liver tissues from patients at different stages of NAFLD progression (ranging from healthy obese individuals to those with steatosis), as well as rodent models of NAFLD, to identify
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Creators: Mario Brosch, Jochen Hampe, Clemens Schafmayer, Witigo von Schönfels

Submitter: Mario Brosch

Human expression dataset (Comparison of Gene Expression Patterns Between Mouse Models of Nonalcoholic Fatty Liver Disease and Liver Tissues From Patients.)
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

BACKGROUND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder in industrialized countries. Mouse models of NAFLD have been used in studies of pathogenesis and treatment, and have certain features of the human disease. We performed a systematic transcriptome-wide analysis of liver tissues from patients at different stages of NAFLD progression (ranging from healthy obese individuals to those with steatosis), as well as rodent models of NAFLD, to identify
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Creators: Mario Brosch, Jochen Hampe, Clemens Schafmayer, Witigo von Schönfels

Submitter: Mario Brosch

PALs Meeting Hünfeld 2017 Agenda
LiSyM Core Infrastructure and Management (LiSyM-PD), LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM Pillar II: Chronic Liver Disease Progression (LiSyM-DP), LiSyM Pillar III: Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF), LiSyM Pillar IV: Liver Function Diagnostics (LiSyM-LiFuDi), Model Guided Pharmacotherapy In Chronic Liver Disease (LiSyM-MGP), Molecular Steatosis - Imaging & Modeling (LiSyM-MSIM), The Hedgehog Signalling Pathway (LiSyM-JGMMS), Multi-Scale Models for Personalized Liver Function Tests (LiSyM-MM-PLF)
No description specified

Creator: Martin Golebiewski

Submitter: Martin Golebiewski

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Wnt-Hh Interaction Model
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Model for the interaction of Wnt and Hh as published in Kolbe et al.: Mutual Zonated Interactions of Wnt and Hh Signaling Are Orchestrating the Metabolism of the Adult Liver in Mice and Human, Cell Reports, 29,4553,

https://doi.org/10.1016/j.celrep.2019.11.104

Creators: Michael Kücken, Lutz Brusch

Submitters: Lutz Brusch, Michael Kücken

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Spatio-temporal model of YAP activation during liver regeneration
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM network

For the spatio-temporal dynamics of bile transport, bile canalicular dilation, mechanical stimulation and transduction of YAP signaling during liver regeneration see the open access publication and its appendix:
Meyer et al. (2020) Bile canaliculi remodeling activates YAP via the actin cytoskeleton during liver regeneration. Molecular Systems Biology 16:e8985. https://doi.org/10.15252/msb.20198985

The model format is MorpheusML that can readily be loaded and run in the free and open source software
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Creator: Lutz Brusch

Submitter: Lutz Brusch

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Morpheus: open source modelling and simulation framework for multicellular systems
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM PALs

Morpheus is the modelling and simulation framework for multicellular systems biology developed at Technische Universität Dresden.
Manual, examples and binaries for Windows, Linux, MacOS at: https://morpheus.gitlab.io
Open source code at: https://gitlab.com/morpheus.lab/morpheus

Creators: Lutz Brusch, Jörn Starruß, Walter de Back, Andreas Deutsch

Submitter: Lutz Brusch

Bile flow model
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Code for the bile flow model in Segovia-Miranda et al.: Three-dimensional spatially resolved geometrical and functional models of human liver tissue reveal new aspects of NAFLD progression (https://www.nature.com/articles/s41591-019-0660-7)

See the README file in the link for details installing and running the code.

Creators: Michael Kücken, Lutz Brusch

Submitter: Michael Kücken

External Link
Morpheus model of spatio-temporal Smo regulation in response to Hh signaling
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

The model is adapted from A.P. Kupinski, I. Raabe, M. Michel, D. Ail, L. Brusch, T. Weidemann, C. Bökel (2013) Phosphorylation of the Smo tail is controlled by membrane localization and is dispensable for clustering, J. Cell Sci., 126, 20, 4684-4697 doi: 10.1242/​jcs.128926

The model format is MorpheusML that can readily be loaded and run in Morpheus: https://imc.zih.tu-dresden.de//wiki/morpheus

Creator: Lutz Brusch

Submitter: Lutz Brusch

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rs641738C>T near MBOAT7 is associated with liver fat, ALT, and fibrosis in NAFLD: a meta-analysis.
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Abstract (Expand)

BACKGROUND & AIMS: A common genetic variant near MBOAT7 (rs641738C>T) has been previously associated with hepatic fat and advanced histology in non-alcoholic fatty liver disease (NAFLD), however, … these findings have not been consistently replicated in the literature. We aimed to establish whether rs641738C>T is a risk factor across the spectrum of NAFLD and characterize its role in the regulation of related metabolic phenotypes through meta-analysis. METHODS: We performed meta-analysis of studies with data on the association between rs641738C>T genotype and: liver fat, NAFLD histology, and serum ALT, lipids, or insulin. These included directly genotyped studies and population-level data from genome-wide association studies (GWAS). We performed random effects meta-analysis using recessive, additive, and dominant genetic models. RESULTS: Data from 1,066,175 participants (9,688 with liver biopsies) across 42 studies were included in the meta-analysis. rs641738C>T was associated with higher liver fat on CT/MRI (+0.03 standard deviations [95% CI: 0.02 - 0.05], pz=4.8x10(-5)) and diagnosis of NAFLD (OR 1.17 [95% CI 1.05 - 1.3], pz=0.003) in Caucasian adults. The variant was also positively associated with presence of advanced fibrosis (OR 1.22 [95% CI: 1.03 - 1.45], pz=0.021) in Caucasian adults using a recessive model of inheritance (CC+CT vs. TT). Meta-analysis of data from previous GWAS found the variant to be associated with higher ALT (pz=0.002) and lower serum triglycerides (pz=1.5x10(-4)). rs641738C>T was not associated with fasting insulin and no effect was observed in children with NAFLD. CONCLUSION: Our study validates rs641738C>T near MBOAT7 as a risk factor for the presence and severity of NAFLD in individuals of European descent.

Authors: K. Teo, K. W. M. Abeysekera, L. Adams, E. Aigner, Q. M. Anstee, J. M. Banales, R. Banerjee, P. Basu, T. Berg, P. Bhatnagar, S. Buch, A. Canbay, S. Caprio, A. Chatterjee, Y. D. Ida Chen, A. Chowdhury, A. K. Daly, C. Datz, D. de Gracia Hahn, J. K. DiStefano, J. Dong, A. Duret, C. Emdin, M. Fairey, G. S. Gerhard, X. Guo, J. Hampe, M. Hickman, L. Heintz, C. Hudert, H. Hunter, M. Kelly, J. Kozlitina, M. Krawczyk, F. Lammert, C. Langenberg, J. Lavine, L. Li, H. K. Lim, R. Loomba, P. K. Luukkonen, P. E. Melton, T. A. Mori, N. D. Palmer, C. A. Parisinos, S. G. Pillai, F. Qayyum, M. C. Reichert, S. Romeo, J. I. Rotter, Y. R. Im, N. Santoro, C. Schafmayer, E. K. Speliotes, S. Stender, F. Stickel, C. D. Still, P. Strnad, K. D. Taylor, A. Tybjaerg-Hansen, G. R. Umano, M. Utukuri, L. Valenti, L. E. Wagenknecht, N. J. Wareham, R. M. Watanabe, J. Wattacheril, H. Yaghootkar, H. Yki-Jarvinen, K. A. Young, J. P. Mann

Date Published: 31st Aug 2020

Publication Type: Journal

Diploid hepatocytes drive physiological liver renewal in adult humans
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Abstract (Expand)

Physiological liver cell replacement is central to maintaining the organ’s high metabolic activity, although its characteristics are difficult to study in humans. Using retrospective 14C birth dating … of cells, we report that human hepatocytes show continuous and lifelong turnover, maintaining the liver a young organ (average age < 3 years). Hepatocyte renewal is highly dependent on the ploidy level. Diploid hepatocytes show an seven-fold higher annual exchange rate than polyploid hepatocytes. These observations support the view that physiological liver cell renewal in humans is mainly dependent on diploid hepatocytes, whereas polyploid cells are compromised in their ability to divide. Moreover, cellular transitions between these two subpopulations are limited, with minimal contribution to the respective other ploidy class under homeostatic conditions. With these findings, we present a new integrated model of homeostatic liver cell generation in humans that provides fundamental insights into liver cell turnover dynamics.

Authors: Paula Heinke, Fabian Rost, Julian Rode, Thilo Welsch, Kanar Alkass, Joshua Feddema, Mehran Salehpour, Göran Possnert, Henrik Druid, Lutz Brusch, Olaf Bergmann

Date Published: 7th Aug 2020

Publication Type: Unpublished

Resilience of three-dimensional sinusoidal networks in liver tissue.
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Abstract (Expand)

Can three-dimensional, microvasculature networks still ensure blood supply if individual links fail? We address this question in the sinusoidal network, a plexus-like microvasculature network, which … transports nutrient-rich blood to every hepatocyte in liver tissue, by building on recent advances in high-resolution imaging and digital reconstruction of adult mice liver tissue. We find that the topology of the three-dimensional sinusoidal network reflects its two design requirements of a space-filling network that connects all hepatocytes, while using shortest transport routes: sinusoidal networks are sub-graphs of the Delaunay graph of their set of branching points, and also contain the corresponding minimum spanning tree, both to good approximation. To overcome the spatial limitations of experimental samples and generate arbitrarily-sized networks, we developed a network generation algorithm that reproduces the statistical features of 0.3-mm-sized samples of sinusoidal networks, using multi-objective optimization for node degree and edge length distribution. Nematic order in these simulated networks implies anisotropic transport properties, characterized by an empirical linear relation between a nematic order parameter and the anisotropy of the permeability tensor. Under the assumption that all sinusoid tubes have a constant and equal flow resistance, we predict that the distribution of currents in the network is very inhomogeneous, with a small number of edges carrying a substantial part of the flow-a feature known for hierarchical networks, but unexpected for plexus-like networks. We quantify network resilience in terms of a permeability-at-risk, i.e., permeability as function of the fraction of removed edges. We find that sinusoidal networks are resilient to random removal of edges, but vulnerable to the removal of high-current edges. Our findings suggest the existence of a mechanism counteracting flow inhomogeneity to balance metabolic load on the liver.

Authors: J. Karschau, A. Scholich, J. Wise, H. Morales-Navarrete, Y. Kalaidzidis, M. Zerial, B. M. Friedrich

Date Published: 1st Jul 2020

Publication Type: Journal

Loss of hepatic Mboat7 leads to liver fibrosis.
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM network

Abstract (Expand)

OBJECTIVE: The rs641738C>T variant located near the membrane-bound O-acyltransferase domain containing 7 (MBOAT7) locus is associated with fibrosis in liver diseases, including non-alcoholic fatty … liver disease (NAFLD), alcohol-related liver disease, hepatitis B and C. We aim to understand the mechanism by which the rs641738C>T variant contributes to pathogenesis of NAFLD. DESIGN: Mice with hepatocyte-specific deletion of MBOAT7 (Mboat7(Deltahep)) were generated and livers were characterised by histology, flow cytometry, qPCR, RNA sequencing and lipidomics. We analysed the association of rs641738C>T genotype with liver inflammation and fibrosis in 846 NAFLD patients and obtained genotype-specific liver lipidomes from 280 human biopsies. RESULTS: Allelic imbalance analysis of heterozygous human liver samples pointed to lower expression of the MBOAT7 transcript on the rs641738C>T haplotype. Mboat7(Deltahep) mice showed spontaneous steatosis characterised by increased hepatic cholesterol ester content after 10 weeks. After 6 weeks on a high fat, methionine-low, choline-deficient diet, mice developed increased hepatic fibrosis as measured by picrosirius staining (p<0.05), hydroxyproline content (p<0.05) and transcriptomics, while the inflammatory cell populations and inflammatory mediators were minimally affected. In a human biopsied NAFLD cohort, MBOAT7 rs641738C>T was associated with fibrosis (p=0.004) independent of the presence of histological inflammation. Liver lipidomes of Mboat7(Deltahep) mice and human rs641738TT carriers with fibrosis showed increased total lysophosphatidylinositol levels. The altered lysophosphatidylinositol and phosphatidylinositol subspecies in MBOAT7(Deltahep) livers and human rs641738TT carriers were similar. CONCLUSION: Mboat7 deficiency in mice and human points to an inflammation-independent pathway of liver fibrosis that may be mediated by lipid signalling and a potentially targetable treatment option in NAFLD.

Authors: V. R. Thangapandi, O. Knittelfelder, M. Brosch, E. Patsenker, O. Vvedenskaya, S. Buch, S. Hinz, A. Hendricks, M. Nati, A. Herrmann, D. R. Rekhade, T. Berg, M. Matz-Soja, K. Huse, E. Klipp, J. K. Pauling, J. A. Wodke, J. Miranda Ackerman, M. V. Bonin, E. Aigner, C. Datz, W. von Schonfels, S. Nehring, S. Zeissig, C. Rocken, A. Dahl, T. Chavakis, F. Stickel, A. Shevchenko, C. Schafmayer, J. Hampe, P. Subramanian

Date Published: 26th Jun 2020

Publication Type: Journal

Genome-Wide Association Study for Alcohol-Related Cirrhosis Identifies Risk Loci in MARC1 and HNRNPUL1.
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Abstract (Expand)

BACKGROUND AND AIMS: Little is known about genetic factors that affect development of alcohol-related cirrhosis. We performed a genome-wide association study (GWAS) of samples from the United Kingdom … Biobank (UKB) to identify polymorphisms associated with risk of alcohol-related liver disease. METHODS: We performed a GWAS of 35,839 participants in the UKB with high intake of alcohol against markers of hepatic fibrosis (FIB-4, APRI, and Forns index scores) and hepatocellular injury (levels of aminotransferases). Loci identified in the discovery analysis were tested for their association with alcohol-related cirrhosis in 3 separate European cohorts (phase 1 validation cohort; n=2545). Variants associated with alcohol-related cirrhosis in the validation at a false discovery rate of less than 20% were then directly genotyped in 2 additional European validation cohorts (phase 2 validation, n=2068). RESULTS: In the GWAS of the discovery cohort, we identified 50 independent risk loci with genome-wide significance (P < 5 x 10(-8)). Nine of these loci were significantly associated with alcohol-related cirrhosis in the phase 1 validation cohort; 6 of these 9 loci were significantly associated with alcohol-related cirrhosis in phase 2 validation cohort, at a false discovery rate below 5%. The loci included variants in the mitochondrial amidoxime reducing component 1 gene (MARC1) and the heterogeneous nuclear ribonucleoprotein U like 1 gene (HNRNPUL1). After we adjusted for age, sex, body mass index, and type-2 diabetes in the phase 2 validation cohort, the minor A allele of MARC1:rs2642438 was associated with reduced risk of alcohol-related cirrhosis (adjusted odds ratio, 0.76; P=.0027); conversely, the minor C allele of HNRNPUL1:rs15052 was associated with an increased risk of alcohol-related cirrhosis (adjusted odds ratio, 1.30; P=.020). CONCLUSIONS: In a GWAS of samples from the UKB, we identified and validated (in 5 European cohorts) single-nucleotide polymorphisms that affect risk of alcohol-related cirrhosis in opposite directions: the minor A allele in MARC1:rs2642438 decreases risk, whereas the minor C allele in HNRNPUL1:rs15052 increases risk.

Authors: H. Innes, S. Buch, S. Hutchinson, I. N. Guha, J. R. Morling, E. Barnes, W. Irving, E. Forrest, V. Pedergnan, D. Goldberg, E. Aspinall, S. Barclay, P. Hayes, J. Dillon, H. D. Nischalke, P. Lutz, U. Spengler, J. Fischer, T. Berg, M. Brosch, F. Eyer, C. Datz, S. Mueller, T. Peccerella, P. Deltenre, A. Marot, M. Soyka, A. McQuillin, M. Y. Morgan, J. Hampe, F. Stickel

Date Published: 16th Jun 2020

Publication Type: Journal

Morpheus: A user-friendly and extensible simulation framework supporting declarative modeling
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)

Computational modeling and simulation become increasingly important for Systems Medicine. A number of corresponding software tools have been developed but require scientists to encode their models in an imperative programming language. Morpheus [1,2], on the other hand, is an extensible open-source software framework that is entirely based on declarative modeling. It uses the domain-specific language MorpheusML to define multicellular models through a user-friendly GUI and has since proven
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Creators: Lutz Brusch, Michael Kücken

Submitter: Lutz Brusch

Poster 8 LiSyM-Midterm_Evaluation_Hampe
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM network
No description specified

Creators: Mario Brosch, Jochen Hampe

Submitter: Mario Brosch

LiSyM Midterm Evaluation Poster 7 - Schwab/Hofmann
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)
No description specified

Creators: Ute Hofmann, Matthias Schwab

Submitter: Ute Hofmann

LiSyM Midterm Evaluation 2018 poster 9 Shevchenko group
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI), LiSyM network

Shotgun lipidomics of microdissected periportal and pericentral zones; Characterization of NAFLD in Human Liver Biopsies by Shotgun Lipidomics

Creators: Oskar Knittelfelder, Olga Vvedenskaya

Submitter: Oskar Knittelfelder

Poster midterm evaluation Pillar I, WP6
LiSyM Pillar I: Early Metabolic Injury (LiSyM-EMI)
No description specified

Creator: Witigo von Schönfels

Submitter: Witigo von Schönfels

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First LiSyM PostDoc and PhD student retreat

The meeting will provide a great opportunity for discussion between modellers, experimentalists and clinicians and to organize and harmonize our future work within the LiSyM network on the grassroot level.

Start Date: 20th Nov 2017

End Date: 22nd Nov 2017

Event Website: Not specified

Country:  Germany

City: Hünfeld

First EASL Nonalcoholic Fatty Liver Disease (NAFLD) Summit: Target-oriented approach to Diagnosis and Pharmacotherapy of Nonalcoholic Steatohepatitis (NASH), a dialogue between Academia and Industry

This summit will cover both the basic and translational / clinical aspects of NAFLD, with a specific focus on novel drug target and prognostic signature development.

Key sessions include all crucial pathophysiological aspects currently known to affect development and progression of NAFLD, such as "lipid metabolism and lipotoxicity" and "insulin resistance, insulin and hormonal signaling". Furthermore, oxidative stress, ER stress, and mitochondrial dysfunction will be addressed. On the second day,
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Start Date: 9th Nov 2017

End Date: 11th Nov 2017

Event Website: https://events.easl.eu/EventPortal/Information/EventInformation.aspx?EventInformationPageCode=HOME&EventCode=nafld2017

Country:  Italy

City: Rome

18th International Conference on Systems Biology (ICSB 2017)

ICSB continues to be the flagship conference of the International Society for Systems Biology (ISSB). The conference will cover a variety of themes from Fundamental Biological Sciences, Network Analysis, to Metabolic Engineering and Cancer Biology. The conference will also include a variety of engaging plenary lectures, parallel sessions, poster sessions, and interactive networking opportunities.

Abstract submission deadline: May 13th, 2017

Start Date: 6th Aug 2017

End Date: 12th Aug 2017

Event Website: http://www.cpe.vt.edu/icsb2017/

Country:  United States

City: Blacksburg, Virginia

International Conference on Systems Biology of Human Disease (SBHD)

The International Conference on Systems Biology of Human Disease (SBHD) is a transatlantic event and communication platform for scientific exchange that takes place alternately between the United States and Germany.

SBHD 2017 is continuing a conference series launched by Peter Sorger and colleagues from Harvard Medical School in 2008. The conference focus is on mammalian systems biology, particularly on its application to human disease and therapy.

Start Date: 5th Jul 2017

End Date: 7th Jul 2017

Event Website: http://www.sbhd-conference.org/2017/index.php

Country:  Germany

City: Heidelberg

Joint LiSyM & ERASysAPP Data Management PALs Meeting

This event is a jointly organized Data Management PALs Meeting that involves PALs from the German LiSyM (Liver Systems Medicine) network and from the ERASysAPP (ERA-Net for Systems Biology Applications) initiative. PALs (Project Area Liaisons) are the front line experts of the data management teams of these projects. They act as data management advocates and help gathering user requirements and testing potential data management solutions. An important part of the meeting will be to gather the
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Start Date: 2nd May 2017

End Date: 3rd May 2017

Event Website: https://fairdomhub.org/events/64

Country:  Germany

City: 36088 Hünfeld bei Fulda

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