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value: 2.0E7
name: Amax
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value: 1.0E-8
name: e2
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metaid_0000045
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value: 0.4
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BIOMD0000000381
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species: metaid_0000036
parameter: metaid_0000048
parameter: metaid_0000052
is version of: GO:0006909
species: metaid_0000037
parameter: metaid_0000053
parameter: metaid_0000055
modified:
  W3 CDTF: Thu Mar 08 12:33:17 GMT 2012
parameter: metaid_0000044
occurs in: http://identifiers.org/taxonomy/10090
parameter: metaid_0000056
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parameter: metaid_0000057
parameter: metaid_0000041
rule: metaid_0000032
parameter: metaid_0000049
parameter: metaid_0000042
parameter: metaid_0000054
species: metaid_0000039
volume units: 498095
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species: metaid_0000040
substance units: 949014
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curated: true
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rule: metaid_0000029
is version of: GO:0042116
name: Maree2006_DuCa_Type1DiabetesModel
area units: 498119
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is described by: http://identifiers.org/pubmed/16608707
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parameter: metaid_0000050
created:
  W3 CDTF: Fri Oct 07 16:36:41 BST 2011
notes: This a model from the article: Modelling the onset of Type 1 diabetes: can impaired macrophage phagocytosis make the difference between health and disease? Maree AF, Kublik R, Finegood DT, Edelstein-Keshet L. Philos Transact A Math Phys Eng Sci. 2006 May 15;364(1842):1267-82. 16608707 , Abstract: A wave of apoptosis (programmed cell death) occurs normally in pancreatic beta-cells of newborn mice. We previously showed that macrophages from non-obese diabetic (NOD) mice become activated more slowly and engulf apoptotic cells at a lower rate than macrophages from control (Balb/c) mice. It has been hypothesized that this low clearance could result in secondary necrosis, escalating inflammation and self-antigen presentation that later triggers autoimmune, Type 1 diabetes (T1D). We here investigate whether this hypothesis could offer a reasonable and parsimonious explanation for onset of T1D in NOD mice. We quantify variants of the Copenhagen model (Freiesleben De Blasio et al. 1999 Diabetes 48, 1677), based on parameters from NOD and Balb/c experimental data. We show that the original Copenhagen model fails to explain observed phenomena within a reasonable range of parameter values, predicting an unrealistic all-or-none disease occurrence for both strains. However, if we take into account that, in general, activated macrophages produce harmful cytokines only when engulfing necrotic (but not apoptotic) cells, then the revised model becomes qualitatively and quantitatively reasonable. Further, we show that known differences between NOD and Balb/c mouse macrophage kinetics are large enough to account for the fact that an apoptotic wave can trigger escalating inflammatory response in NOD, but not Balb/c mice. In Balb/c mice, macrophages clear the apoptotic wave so efficiently, that chronic inflammation is prevented. 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 BioM…
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type: SBMLModel
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    orgname: EMBL-EBI
  n:
    given: Ishan
    family: Ajmera
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metaid_0000046
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metaid_0000044
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