Model model = doc.createModel("test_model");
Creator c = new Creator("Hans", "Wurst",
"Institute for Interesting Biology", "ovidiu.radulescu@univ-rennes1.fr");
History h = new History();
h.addCreator(c);
model.setHistory(h);
// model.appendNotes("This is a very interesting model.");
model.appendNotes("<body xmlns=\"http://www.w3.org/1999/xhtml\"><h1>Model of “Apoptosis” in “Homo sapiens (human)”</h1>Apoptosis is a genetically controlled mechanisms of cell death involved in the regulation of tissue homeostasis. The 2 major pathways of apoptosis are the extrinsic (Fas and other TNFR superfamily members and ligands) and the intrinsic (mitochondria-associated) pathways, both of which are found in the cytoplasm. The extrinsic pathway is triggered by death receptor engagement, which initiates a signaling cascade mediated by caspase-8 activation. Caspase-8 both feeds directly into caspase-3 activation and stimulates the release of cytochrome c by the mitochondria. Caspase-3 activation leads to the degradation of cellular proteins necessary to maintain cell survival and integrity. The intrinsic pathway occurs when various apoptotic stimuli trigger the release of cytochrome c from the mitochondria (independently of caspase-8 activation). Cytochrome c interacts with Apaf-1 and caspase-9 to promote the activation of caspase-3. Recent studies point to the ER as a third subcellular compartment implicated in apoptotic execution. Alterations in Ca2+ homeostasis and accumulation of misfolded proteins in the ER cause ER stress. Prolonged ER stress can result in the activation of BAD and/or caspase-12, and execute apoptosis.<br/><a href=\"http://www.genome.jp/kegg/pathway/hsa/hsa04210.png\"><img src=\"http://www.genome.jp/kegg/pathway/hsa/hsa04210.png\" alt=\"http://www.genome.jp/kegg-bin/show_pathway?hsa04210\"/></a><br/><a href=\"http://www.genome.jp/kegg-bin/show_pathway?hsa04210\">Original Entry</a><br/><div align=\"right\"></div><br/></body>");
Parameter k1 = model.createParameter("k1");