Inductive and Deductive Approaches to Acute Cell Injury
Many clinically relevant forms of acute injury, such as stroke, traumatic brain injury, and myocardial infarction, have resisted treatments to prevent cell death following injury. The clinical failures can be linked to the currently used inductive models based on biological specifics of the injury s...
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Published in | International scholarly research notices Vol. 2014; pp. 859341 - 15 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Hindawi Publishing Corporation
2014
John Wiley & Sons, Inc Hindawi Limited |
Subjects | |
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Abstract | Many clinically relevant forms of acute injury, such as stroke, traumatic brain injury, and myocardial infarction, have resisted treatments to prevent cell death following injury. The clinical failures can be linked to the currently used inductive models based on biological specifics of the injury system. Here we contrast the application of inductive and deductive models of acute cell injury. Using brain ischemia as a case study, we discuss limitations in inductive inferences, including the inability to unambiguously assign cell death causality and the lack of a systematic quantitative framework. These limitations follow from an overemphasis on qualitative molecular pathways specific to the injured system. Our recently developed nonlinear dynamical theory of cell injury provides a generic, systematic approach to cell injury in which attractor states and system parameters are used to quantitatively characterize acute injury systems. The theoretical, empirical, and therapeutic implications of shifting to a deductive framework are discussed. We illustrate how a deductive mathematical framework offers tangible advantages over qualitative inductive models for the development of therapeutics of acutely injured biological systems. |
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AbstractList | Many clinically relevant forms of acute injury, such as stroke, traumatic brain injury, and myocardial infarction, have resisted treatments to prevent cell death following injury. The clinical failures can be linked to the currently used inductive models based on biological specifics of the injury system. Here we contrast the application of inductive and deductive models of acute cell injury. Using brain ischemia as a case study, we discuss limitations in inductive inferences, including the inability to unambiguously assign cell death causality and the lack of a systematic quantitative framework. These limitations follow from an overemphasis on qualitative molecular pathways specific to the injured system. Our recently developed nonlinear dynamical theory of cell injury provides a generic, systematic approach to cell injury in which attractor states and system parameters are used to quantitatively characterize acute injury systems. The theoretical, empirical, and therapeutic implications of shifting to a deductive framework are discussed. We illustrate how a deductive mathematical framework offers tangible advantages over qualitative inductive models for the development of therapeutics of acutely injured biological systems. |
Audience | Academic |
Author | Tri Anggraini, Fika DeGracia, Donald J. Taha, Doaa Taha Metwally Huang, Zhi-Feng |
AuthorAffiliation | 1 Department of Physiology, Wayne State University, 4116 Scott Hall, 540 East Canfield Avenue, Detroit, MI 48201, USA 2 Department of Physics and Astronomy, Wayne State University, Detroit, MI 48201, USA |
AuthorAffiliation_xml | – name: 1 Department of Physiology, Wayne State University, 4116 Scott Hall, 540 East Canfield Avenue, Detroit, MI 48201, USA – name: 2 Department of Physics and Astronomy, Wayne State University, Detroit, MI 48201, USA |
Author_xml | – sequence: 1 givenname: Donald J. surname: DeGracia fullname: DeGracia, Donald J. organization: Department of Physiology Wayne State University 4116 Scott Hall 540 East Canfield Avenue Detroit MI 48201 USA wayne.edu – sequence: 2 givenname: Fika surname: Tri Anggraini fullname: Tri Anggraini, Fika organization: Department of Physiology Wayne State University 4116 Scott Hall 540 East Canfield Avenue Detroit MI 48201 USA wayne.edu – sequence: 3 givenname: Doaa Taha Metwally surname: Taha fullname: Taha, Doaa Taha Metwally organization: Department of Physics and Astronomy Wayne State University Detroit MI 48201 USA wayne.edu – sequence: 4 givenname: Zhi-Feng surname: Huang fullname: Huang, Zhi-Feng organization: Department of Physics and Astronomy Wayne State University Detroit MI 48201 USA wayne.edu |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27437490$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | Copyright © 2014 Donald J. DeGracia et al. COPYRIGHT 2014 John Wiley & Sons, Inc. Copyright © 2014 Donald J. DeGracia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2014 Donald J. DeGracia et al. 2014 |
Copyright_xml | – notice: Copyright © 2014 Donald J. DeGracia et al. – notice: COPYRIGHT 2014 John Wiley & Sons, Inc. – notice: Copyright © 2014 Donald J. DeGracia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright © 2014 Donald J. DeGracia et al. 2014 |
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Snippet | Many clinically relevant forms of acute injury, such as stroke, traumatic brain injury, and myocardial infarction, have resisted treatments to prevent cell... |
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SubjectTerms | Anatomy & physiology Apoptosis Biology Cell death Cerebral ischemia Clinical trials Heart attacks Injuries Ischemia Physics Review Science Studies Theory |
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Title | Inductive and Deductive Approaches to Acute Cell Injury |
URI | https://dx.doi.org/10.1155/2014/859341 https://www.ncbi.nlm.nih.gov/pubmed/27437490 https://www.proquest.com/docview/1760294029 https://search.proquest.com/docview/1806080070 https://pubmed.ncbi.nlm.nih.gov/PMC4897055 |
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