BioModelsapplication/xmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001.pdfhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001-biopax2.owlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001-biopax3.owlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001_url.xmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001_urn.xmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001.vcmlhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001.mhttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001.scihttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001.pnghttps://www.ebi.ac.uk/biomodels/model/download/MODEL0912160001?filename=MODEL0912160001.xppprimaryOK200Vijayalakshmi ChelliahNon-curatedordinary differential equation modelL2V4https://www.ebi.ac.uk/biomodels/MODEL09121600014334846falseBioModelsSBMLModelsGuyton1972 Electrolytes1972MODEL0912160001A C Guyton, T G Coleman, H J GrangerA C Guyton4334846, null. null, 34. nullviji@ebi.ac.ukEMBL-EBICirculation: overall regulation.Guyton A C AC, Coleman T G TG, Granger H J HJElectrolyte.extent, Public Sectors, Activity, determination, 2410041A17Rik, Laboratory, ACTG, ACTE, NetrinA, AUTSX5, D430049E23Rik, fs(1)M34, NOVH, congenital defects, CCN3, csp2, Act5, QM, aplasia, Social Controls, l(1)G0420, DmelCG12051, Calculators, Dynamics Analyses, Techniques, Tier, Method, HEL-176, CG4601, Analysis, Research Activity, Public Enterprise, Laboratory Research, Formal Social Controls, fs(1)M104, Priorities, Animalia, Multicase, A, C, Elkh, cyt5C, Man (Taxonomy), Analyses, DHO, Systems Approachs, Personnel, long, developmental field, Public Domains, EK6, hypoplasia, CG18572, SAP-2, Sap-2, DmelCG4063, Social, IBP-9, neuroendocrine tumour, Methodological Studies, Solute carrier family 6 member 2, act 42A, Ac5C, CT27014, Medicine, CG4027, NET1, SLC6A5, ACT, Act, Tbl1, TBL1, Medicines, Research Priority, netA, NOVh, Thinkings, Elk, ELK, l(1)G0330, Actin/BAP47, completeness, CTE-II, Neuronally-expressed EPH-related tyrosine kinase, animalia, Complexity, AACT, Modern, CTE-IIa, act, Digital Computers, Research Priorities, Ach1, hBACH, Systems Oriented, ACH1, SAP2, future organ, 9330129L11, Procedure, LACH1, results, deformities, act42A, neuroendocrine neoplasm, Literatures, GIG25, Su(b), Alpha-1-antichymotrypsin His-Pro-less, Norepinephrine transporter, Public Domain, AFFX-Dros-ACTIN_M_r_at, GIG24, Domains, DFNA26, actin, EPH-like kinase 6, NOV, LACH, PlexA1, GAT, DFNA20, Domain, Systems Medicines, Research and Development, Computers, atresia, Approachs, Epistemology, figures, Plxn1, Clinical Investigator, DmelCG4027, whole organism, CG4063, Review, Modeling, System, l(1)G0117, Systems Analyses, malformations, Control, nov, Researcher, Actin, Methodological, hEK6, Controls, Hardware, Methodological Study, beta-actin/Bap47, E-2f, mKIAA4053, human, E-2g, fs(1)Y[b], experimental procedures, Agent-Based, Activities, l(1)G0486, l(1)G0245, DmelCG18657, actin5C, Sector, l(1)G0009, Digital Computer, ACTL3, Lach1, C130088N23Rik, anomalies, Koerper, PLXN1, Review of Reported Cases, Systems Oriented Approachs, DXS648E, Modelings, Regulation, BACH, Programmable Calculator, Systems Thinkings, l(1)Ab, Regulations, AW488255, Act5c, Agent Based Modeling, Sectors, l(1)G0010, Thinking, human being, Procedures, Agent-Based Modelings, Tb11, YB, experimental, Programmable, System Dynamics Analysis, number, ACT5C, CG12051, Copyrights, study person role, Serpin A3, Computer, Bach, Human, FBXW4, netrin, l(1)G0025, method, organ field, Homo sapiens, Yb, Hek6, method used in an experiment, Studies, Survey, Cek6, Cell growth-inhibiting gene 24|25 protein, field, Animal, defects, Enterprises, Technique, Man, CG2706, ENSMUSG00000074119, study, ERP, APUDoma, Erp, Complexity Analyses, act5C, anatomical systems, methods, Clinical, Academic, Research, experimental section, Ebi, EBI, BRWS2, Investigators, Tyrosine-protein kinase receptor EPH-2, Clinical Investigators, metazoa, IGFBP9, Public Enterprises, fs(1)829, Study, Act42a, anon-EST:fe2D2, Kiaa4053, Abstract, 2.7.10.1, 1700027G07Rik, L10, DmelCG18572, Etrp, NAT1, Development and Research, T11, Systems Oriented Approach, Enterprise, Act-5C, Cte-II, NET, Net, l(1)G0177, 42A, C130099E04Rik, CPS, Formal Social Control, body, Investigator, DmelCG2706, dJ393D12.2, EPH tyrosine kinase 2, DXS648, Computer Hardware, whole body, function, SMAP55, neuroendocrine tumor, net, System Dynamics Analyses, presence., System Dynamics, count in organism, Experiment, Priority, Review Literature, Dynamics Analysis, CAD, Social Control, IGFBP-9, beta-actin, Public, agenesis, Systems, chemical analysis, Metazoa, Research Activities, M32055, Act42, Systems Thinking, Approach, ACTA3, Complexity Analysis, Data Base, Survey Personnel, l(1)G0079, Digital, PYR1, Programmable Calculators, VSCM, investigator, act 5C, Calculator, Systems Medicine, CG18657, l(2)k16213, plan specification, Systems Approach, Agent-Based Modeling, EPHT2, Modern Man, birth defects, EG:95B7.8, DRORUD, Researchers, 2600013D04Rik, regulation, BAP47, assay, ACTSG, Bap47, netrin A, Actin5CSocial, Regulations, Control, regulation, Controls, Social Control, Regulation, Social Controls., Formal Social Controls, Formal Social ControlfalseGuyton1972_Electrolytes This a model from the article: Circulation: overall regulation. Guyton AC, Coleman TG, Granger HJ. Annu Rev Physiol 1972;34:13-46 4334846 , Abstract: This article is an experiment, one undertaken primarily because of the long-term belief of Dr. Victor Hall, Editor of the Annual Review of Physiology fo r many years, that physiology is, or at least should be, an analytical subject, and that a method not utilized to its fullest advantage for organizing review material is the systems analysis. Furthermore, one of the most likely areas in physiology for which a systems analysis could be of value would be in a discussion of circulatory regulation. Therefore, this article was undertaken directly at the request of the editors of the A ogy to attempt the welding togeth er of a systemsn annuaally Rsiesv ioewf coifr cPuhlaytsoiorlyregulation with a review of the current literature in this field. The systems analysis of circulatory regulation developed for this article is based on earlier, much less extensive analyses (Guyton and Coleman 1, 2); it i s illustrated in Figure 1. This analysis is comprised of 354 blocks, each of which represents one or more mathematical equations describing some physiological facet of circulatory function. In general, each of the functional blocks has been the subject of research investigation by one or many investigator s, but the analysis is based on cumulative knowledge of the circulation rather than simply on current literature. Therefore, the analysis presented here is not a review of the current literature but is a framework to show how the different regulations operate together in the overall system. Later in this review we will attempt to show some of the voids still present in our knowledge of circulatory regulation (which is perhaps the most important value of performing systems analyses), and we will discuss the current research that is attempting to fill these voids. A criticism that has often been made against systems analyses, and very justly so, is that they are usually designed to explain specific phenomena. Therefore, they too often are based on such bizarre concepts of function that they not only fail to give correct predictions (other than the specific ones for which they are designed) but, indeed, often give exactly reverse predictions. Therefore, the analysis of Figure 1 was based almost entirely on act ual experimental data, and it has been tested in computer simulations to see whether or not it can predict the animal or human results of many different types of circulatory stresses induced either experimentally or as the result of clinical abnormalities. Figures 2 through 5 present simulations of some of these experiments or clinical conditions. They will be described later in the article. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Guyton AC, Coleman TG, Granger HJ. (2008) - version02 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. 2010-02-032005-01-012009-12-16MODEL09121600014334846MODEL0912160001GO:00030739606