Parkinson's disease mouse brain proteome profiling
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion
ORGANISM(S): Mus Musculus (ncbitaxon:10090)
SUBMITTER: 
Sung Jung
PROVIDER: MSV000080437 | MassIVE | Sun Dec 25 20:45:00 GMT 2016
SECONDARY ACCESSION(S): PXD005626
REPOSITORIES: MassIVE
Publications
An Anatomically Resolved Mouse Brain Proteome Reveals Parkinson Disease-relevant Pathways.
Jung Sung Yun SY Choi Jong Min JM Rousseaux Maxime W C MW Malovannaya Anna A Kim Jean J JJ Kutzera Joachim J Wang Yi Y Huang Yin Y Zhu Weimin W Maity Suman S Zoghbi Huda Yahya HY Qin Jun J
Molecular & cellular proteomics : MCP 20170202 4
Here, we present a mouse brain protein atlas that covers 17 surgically distinct neuroanatomical regions of the adult mouse brain, each less than 1 mm<sup>3</sup> in size. The protein expression levels are determined for 6,500 to 7,500 gene protein products from each region and over 12,000 gene protein products for the entire brain, documenting the physiological repertoire of mouse brain proteins in an anatomically resolved and comprehensive manner. We explored the utility of our spatially define ...[more]
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Project description:This a model from the article:
The canine virtual ventricular wall: a platform for dissecting pharmacological
effects on propagation and arrhythmogenesis.
Benson AP, Aslanidi OV, Zhang H, Holden AV. Prog Biophys Mol Biol
2008 Jan-Apr;96(1-3):187-208 17915298
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Abstract:
We have constructed computational models of canine ventricular cells and
tissues, ultimately combining detailed tissue architecture and heterogeneous
transmural electrophysiology. The heterogeneity is introduced by modifying the
Hund-Rudy canine cell model in order to reproduce experimentally reported
electrophysiological properties of endocardial, midmyocardial (M) and epicardial
cells. These models are validated against experimental data for individual ionic
current and action potential characteristics, and their rate dependencies. 1D
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This suggests an electrophysiological mechanism for the anti- and proarrhythmic
effects of the class III drugs: the relative safety of amiodarone in comparison
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This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Benson AP, Aslanidi OV, Zhang H, Holden AV. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230101 | BioModels
Project description:This a model from the article:
The canine virtual ventricular wall: a platform for dissecting pharmacological
effects on propagation and arrhythmogenesis.
Benson AP, Aslanidi OV, Zhang H, Holden AV. Prog Biophys Mol Biol
2008 Jan-Apr;96(1-3):187-208 17915298
,
Abstract:
We have constructed computational models of canine ventricular cells and
tissues, ultimately combining detailed tissue architecture and heterogeneous
transmural electrophysiology. The heterogeneity is introduced by modifying the
Hund-Rudy canine cell model in order to reproduce experimentally reported
electrophysiological properties of endocardial, midmyocardial (M) and epicardial
cells. These models are validated against experimental data for individual ionic
current and action potential characteristics, and their rate dependencies. 1D
and 3D heterogeneous virtual tissues are constructed, with detailed tissue
architecture (anisotropy and orthotropy, due to fibre orientation and sheet
structure) of the left ventricular wall wedge extracted from a diffusion tensor
imaging data set. The models are used to study the effects of tissue
heterogeneity and class III drugs on transmural propagation and tissue
vulnerability to re-entry. We have determined relationships between the
transmural dispersion of action potential duration (APD) and the vulnerable
window in the 1D virtual ventricular wall, and demonstrated how changes in the
transmural heterogeneity, and hence tissue vulnerability, can lead to generation
of re-entry in the 3D ventricular wedge. Two class III drugs with opposite
qualitative effects on transmural APD heterogeneity are considered: d-sotalol
that increases transmural APD dispersion, and amiodarone that decreases it.
Simulations with the 1D virtual ventricular wall show that under d-sotalol
conditions the vulnerable window is substantially wider compared to amiodarone
conditions, primarily in the epicardial region where unidirectional conduction
block persists until the adjacent M cells are fully repolarised. Further
simulations with the 3D ventricular wedge have shown that ectopic stimulation of
the epicardial region results in generation of sustained re-entry under
d-sotalol conditions, but not under amiodarone conditions or in control. Again,
APD increase in M cells was identified as the major contributor to tissue
vulnerability--re-entry was initiated primarily due to ectopic excitation
propagating around the unidirectional conduction block in the M cell region.
This suggests an electrophysiological mechanism for the anti- and proarrhythmic
effects of the class III drugs: the relative safety of amiodarone in comparison
to d-sotalol can be explained by relatively low transmural APD dispersion, and
hence, a narrow vulnerable window and low probability of re-entry in the tissue.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Benson AP, Aslanidi OV, Zhang H, Holden AV. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230078 | BioModels
Project description:This a model from the article:
The canine virtual ventricular wall: a platform for dissecting pharmacological
effects on propagation and arrhythmogenesis.
Benson AP, Aslanidi OV, Zhang H, Holden AV. Prog Biophys Mol Biol
2008 Jan-Apr;96(1-3):187-208 17915298
,
Abstract:
We have constructed computational models of canine ventricular cells and
tissues, ultimately combining detailed tissue architecture and heterogeneous
transmural electrophysiology. The heterogeneity is introduced by modifying the
Hund-Rudy canine cell model in order to reproduce experimentally reported
electrophysiological properties of endocardial, midmyocardial (M) and epicardial
cells. These models are validated against experimental data for individual ionic
current and action potential characteristics, and their rate dependencies. 1D
and 3D heterogeneous virtual tissues are constructed, with detailed tissue
architecture (anisotropy and orthotropy, due to fibre orientation and sheet
structure) of the left ventricular wall wedge extracted from a diffusion tensor
imaging data set. The models are used to study the effects of tissue
heterogeneity and class III drugs on transmural propagation and tissue
vulnerability to re-entry. We have determined relationships between the
transmural dispersion of action potential duration (APD) and the vulnerable
window in the 1D virtual ventricular wall, and demonstrated how changes in the
transmural heterogeneity, and hence tissue vulnerability, can lead to generation
of re-entry in the 3D ventricular wedge. Two class III drugs with opposite
qualitative effects on transmural APD heterogeneity are considered: d-sotalol
that increases transmural APD dispersion, and amiodarone that decreases it.
Simulations with the 1D virtual ventricular wall show that under d-sotalol
conditions the vulnerable window is substantially wider compared to amiodarone
conditions, primarily in the epicardial region where unidirectional conduction
block persists until the adjacent M cells are fully repolarised. Further
simulations with the 3D ventricular wedge have shown that ectopic stimulation of
the epicardial region results in generation of sustained re-entry under
d-sotalol conditions, but not under amiodarone conditions or in control. Again,
APD increase in M cells was identified as the major contributor to tissue
vulnerability--re-entry was initiated primarily due to ectopic excitation
propagating around the unidirectional conduction block in the M cell region.
This suggests an electrophysiological mechanism for the anti- and proarrhythmic
effects of the class III drugs: the relative safety of amiodarone in comparison
to d-sotalol can be explained by relatively low transmural APD dispersion, and
hence, a narrow vulnerable window and low probability of re-entry in the tissue.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Benson AP, Aslanidi OV, Zhang H, Holden AV. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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