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Showing 1 to 12 of 18 entries
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Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies.

Current opinion in biomedical engineering

Aboelkassem Y, Powers JD, McCabe KJ, McCulloch AD.
PMID: 31886450
Curr Opin Biomed Eng. 2019 Sep;11:35-44. doi: 10.1016/j.cobme.2019.09.005. Epub 2019 Sep 18.

Myocardial hypertrophy is the result of sustained perturbations to the mechanical and/or neurohormonal homeostasis of cardiac cells and is driven by integrated, multiscale biophysical and biochemical processes that are currently not well defined. In this brief review, we highlight...

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Aboelkassem Y, Powers JD, McCabe KJ, et al. Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies. Curr Opin Biomed Eng. 2019;11:35-44doi: 10.1016/j.cobme.2019.09.005.
Aboelkassem, Y., Powers, J. D., McCabe, K. J., & McCulloch, A. D. (2019). Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies. Current opinion in biomedical engineering, 1135-44. https://doi.org/10.1016/j.cobme.2019.09.005
Aboelkassem, Yasser, et al. "Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies." Current opinion in biomedical engineering vol. 11 (2019): 35-44. doi: https://doi.org/10.1016/j.cobme.2019.09.005
Aboelkassem Y, Powers JD, McCabe KJ, McCulloch AD. Multiscale Models of Cardiac Muscle Biophysics and Tissue Remodeling in Hypertrophic Cardiomyopathies. Curr Opin Biomed Eng. 2019 Sep;11:35-44. doi: 10.1016/j.cobme.2019.09.005. Epub 2019 Sep 18. PMID: 31886450; PMCID: PMC6934086.
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Qualitative causal analyses of biosimulation models.

CEUR workshop proceedings

Neal ML, Gennari JH, Cook DL.
PMID: 28804276
CEUR Workshop Proc. 2016 Aug;1747. Epub 2016 Nov 29.

We describe an approach for performing qualitative, systems-level causal analyses on biosimulation models that leverages semantics-based modeling formats, formal ontology, and automated inference. The approach allows users to quickly investigate how a qualitative perturbation to an element within a...

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Neal ML, Gennari JH, Cook DL. Qualitative causal analyses of biosimulation models. CEUR Workshop Proc. 2016;1747
Neal, M. L., Gennari, J. H., & Cook, D. L. (2016). Qualitative causal analyses of biosimulation models. CEUR workshop proceedings, 1747.
Neal, Maxwell L, et al. "Qualitative causal analyses of biosimulation models." CEUR workshop proceedings vol. 1747 (2016).
Neal ML, Gennari JH, Cook DL. Qualitative causal analyses of biosimulation models. CEUR Workshop Proc. 2016 Aug;1747. Epub 2016 Nov 29. PMID: 28804276; PMCID: PMC5551042.
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Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape.

Frontiers in pediatrics

Dewan S, Krishnamurthy A, Kole D, Conca G, Kerckhoffs R, Puchalski MD, Omens JH, Sun H, Nigam V, McCulloch AD.
PMID: 28275592
Front Pediatr. 2017 Feb 22;5:25. doi: 10.3389/fped.2017.00025. eCollection 2017.

INTRODUCTION: Hypoplastic left heart syndrome (HLHS) is a congenital condition with an underdeveloped left ventricle (LV) that provides inadequate systemic blood flow postnatally. The development of HLHS is postulated to be due to altered biomechanical stimuli during gestation. Predicting...

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Dewan S, Krishnamurthy A, Kole D, et al. Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape. Front Pediatr. 2017;5:25doi: 10.3389/fped.2017.00025.
Dewan, S., Krishnamurthy, A., Kole, D., Conca, G., Kerckhoffs, R., Puchalski, M. D., Omens, J. H., Sun, H., Nigam, V., & McCulloch, A. D. (2017). Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape. Frontiers in pediatrics, 525. https://doi.org/10.3389/fped.2017.00025
Dewan, Sukriti, et al. "Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape." Frontiers in pediatrics vol. 5 (2017): 25. doi: https://doi.org/10.3389/fped.2017.00025
Dewan S, Krishnamurthy A, Kole D, Conca G, Kerckhoffs R, Puchalski MD, Omens JH, Sun H, Nigam V, McCulloch AD. Model of Human Fetal Growth in Hypoplastic Left Heart Syndrome: Reduced Ventricular Growth Due to Decreased Ventricular Filling and Altered Shape. Front Pediatr. 2017 Feb 22;5:25. doi: 10.3389/fped.2017.00025. eCollection 2017. PMID: 28275592; PMCID: PMC5319967.
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Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype.

Frontiers in physiology

Dewan S, McCabe KJ, Regnier M, McCulloch AD.
PMID: 28352236
Front Physiol. 2017 Mar 14;8:151. doi: 10.3389/fphys.2017.00151. eCollection 2017.

Dilated Cardiomyopathy (DCM) is a leading cause of sudden cardiac death characterized by impaired pump function and dilatation of cardiac ventricles. In this review we discuss various

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Dewan S, McCabe KJ, Regnier M, et al. Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype. Front Physiol. 2017;8:151doi: 10.3389/fphys.2017.00151.
Dewan, S., McCabe, K. J., Regnier, M., & McCulloch, A. D. (2017). Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype. Frontiers in physiology, 8151. https://doi.org/10.3389/fphys.2017.00151
Dewan, Sukriti, et al. "Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype." Frontiers in physiology vol. 8 (2017): 151. doi: https://doi.org/10.3389/fphys.2017.00151
Dewan S, McCabe KJ, Regnier M, McCulloch AD. Insights and Challenges of Multi-Scale Modeling of Sarcomere Mechanics in cTn and Tm DCM Mutants-Genotype to Cellular Phenotype. Front Physiol. 2017 Mar 14;8:151. doi: 10.3389/fphys.2017.00151. eCollection 2017. PMID: 28352236; PMCID: PMC5348544.
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Tellurium notebooks-An environment for reproducible dynamical modeling in systems biology.

PLoS computational biology

Medley JK, Choi K, König M, Smith L, Gu S, Hellerstein J, Sealfon SC, Sauro HM.
PMID: 29906293
PLoS Comput Biol. 2018 Jun 15;14(6):e1006220. doi: 10.1371/journal.pcbi.1006220. eCollection 2018 Jun.

The considerable difficulty encountered in reproducing the results of published dynamical models limits validation, exploration and reuse of this increasingly large biomedical research resource. To address this problem, we have developed Tellurium Notebook, a software system for model authoring,...

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Medley JK, Choi K, König M, et al. Tellurium notebooks-An environment for reproducible dynamical modeling in systems biology. PLoS Comput Biol. 2018;14(6):e1006220doi: 10.1371/journal.pcbi.1006220.
Medley, J. K., Choi, K., König, M., Smith, L., Gu, S., Hellerstein, J., Sealfon, S. C., & Sauro, H. M. (2018). Tellurium notebooks-An environment for reproducible dynamical modeling in systems biology. PLoS computational biology, 14(6), e1006220. https://doi.org/10.1371/journal.pcbi.1006220
Medley, J Kyle, et al. "Tellurium notebooks-An environment for reproducible dynamical modeling in systems biology." PLoS computational biology vol. 14,6 (2018): e1006220. doi: https://doi.org/10.1371/journal.pcbi.1006220
Medley JK, Choi K, König M, Smith L, Gu S, Hellerstein J, Sealfon SC, Sauro HM. Tellurium notebooks-An environment for reproducible dynamical modeling in systems biology. PLoS Comput Biol. 2018 Jun 15;14(6):e1006220. doi: 10.1371/journal.pcbi.1006220. eCollection 2018 Jun. PMID: 29906293; PMCID: PMC6021116.
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Optical Cryoimaging Reveals a Heterogeneous Distribution of Mitochondrial Redox State in ex vivo Guinea Pig Hearts and Its Alteration During Ischemia and Reperfusion.

IEEE journal of translational engineering in health and medicine

Ranji M, Motlagh MM, Salehpour F, Sepehr R, Heisner JS, Dash RK, Camara AK.
PMID: 27574574
IEEE J Transl Eng Health Med. 2016 Jun 15;4:1800210. doi: 10.1109/JTEHM.2016.2570219. eCollection 2016.

Oxidation of substrates to generate ATP in mitochondria is mediated by redox reactions of NADH and FADH2. Cardiac ischemia and reperfusion (IR) injury compromises mitochondrial oxidative phosphorylation. We hypothesize that IR alters the metabolic heterogeneity of mitochondrial redox state...

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Ranji M, Motlagh MM, Salehpour F, et al. Optical Cryoimaging Reveals a Heterogeneous Distribution of Mitochondrial Redox State in ex vivo Guinea Pig Hearts and Its Alteration During Ischemia and Reperfusion. IEEE J Transl Eng Health Med. 2016;4:1800210doi: 10.1109/JTEHM.2016.2570219.
Ranji, M., Motlagh, M. M., Salehpour, F., Sepehr, R., Heisner, J. S., Dash, R. K., & Camara, A. K. (2016). Optical Cryoimaging Reveals a Heterogeneous Distribution of Mitochondrial Redox State in ex vivo Guinea Pig Hearts and Its Alteration During Ischemia and Reperfusion. IEEE journal of translational engineering in health and medicine, 41800210. https://doi.org/10.1109/JTEHM.2016.2570219
Ranji, Mahsa, et al. "Optical Cryoimaging Reveals a Heterogeneous Distribution of Mitochondrial Redox State in ex vivo Guinea Pig Hearts and Its Alteration During Ischemia and Reperfusion." IEEE journal of translational engineering in health and medicine vol. 4 (2016): 1800210. doi: https://doi.org/10.1109/JTEHM.2016.2570219
Ranji M, Motlagh MM, Salehpour F, Sepehr R, Heisner JS, Dash RK, Camara AK. Optical Cryoimaging Reveals a Heterogeneous Distribution of Mitochondrial Redox State in ex vivo Guinea Pig Hearts and Its Alteration During Ischemia and Reperfusion. IEEE J Transl Eng Health Med. 2016 Jun 15;4:1800210. doi: 10.1109/JTEHM.2016.2570219. eCollection 2016. PMID: 27574574; PMCID: PMC4993131.
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Biomechanics Simulations Using Cubic Hermite Meshes with Extraordinary Nodes for Isogeometric Cardiac Modeling.

Computer aided geometric design

Krishnamurthy A, Gonzales MJ, Sturgeon G, Segars WP, McCulloch AD.
PMID: 27182096
Comput Aided Geom Des. 2016 Mar;43:27-38. doi: 10.1016/j.cagd.2016.02.016.

Cubic Hermite hexahedral finite element meshes have some well-known advantages over linear tetrahedral finite element meshes in biomechanical and anatomic modeling using isogeometric analysis. These include faster convergence rates as well as the ability to easily model rule-based anatomic...

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Krishnamurthy A, Gonzales MJ, Sturgeon G, et al. Biomechanics Simulations Using Cubic Hermite Meshes with Extraordinary Nodes for Isogeometric Cardiac Modeling. Comput Aided Geom Des. 2016;43:27-38doi: 10.1016/j.cagd.2016.02.016.
Krishnamurthy, A., Gonzales, M. J., Sturgeon, G., Segars, W. P., & McCulloch, A. D. (2016). Biomechanics Simulations Using Cubic Hermite Meshes with Extraordinary Nodes for Isogeometric Cardiac Modeling. Computer aided geometric design, 4327-38. https://doi.org/10.1016/j.cagd.2016.02.016
Krishnamurthy, Adarsh, et al. "Biomechanics Simulations Using Cubic Hermite Meshes with Extraordinary Nodes for Isogeometric Cardiac Modeling." Computer aided geometric design vol. 43 (2016): 27-38. doi: https://doi.org/10.1016/j.cagd.2016.02.016
Krishnamurthy A, Gonzales MJ, Sturgeon G, Segars WP, McCulloch AD. Biomechanics Simulations Using Cubic Hermite Meshes with Extraordinary Nodes for Isogeometric Cardiac Modeling. Comput Aided Geom Des. 2016 Mar;43:27-38. doi: 10.1016/j.cagd.2016.02.016. PMID: 27182096; PMCID: PMC4862616.
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Translation of Cardiac Myosin Activation with 2-deoxy-ATP to Treat Heart Failure via an Experimental Ribonucleotide Reductase-Based Gene Therapy.

JACC. Basic to translational science

Thomson KS, Odom GL, Murry CE, Mahairas GG, Moussavi-Harami F, Teichman SL, Chen X, Hauschka SD, Chamberlain JS, Regnier M.
PMID: 28553667
JACC Basic Transl Sci. 2016 Dec;1(7):666-679. doi: 10.1016/j.jacbts.2016.07.006.

Despite recent advances, chronic heart failure remains a significant and growing unmet medical need, reaching epidemic proportions carrying substantial morbidity, mortality, and costs. A safe and convenient therapeutic agent that produces sustained inotropic effects could ameliorate symptoms, and improve...

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Thomson KS, Odom GL, Murry CE, et al. Translation of Cardiac Myosin Activation with 2-deoxy-ATP to Treat Heart Failure via an Experimental Ribonucleotide Reductase-Based Gene Therapy. JACC Basic Transl Sci. 2016;1(7):666-679doi: 10.1016/j.jacbts.2016.07.006.
Thomson, K. S., Odom, G. L., Murry, C. E., Mahairas, G. G., Moussavi-Harami, F., Teichman, S. L., Chen, X., Hauschka, S. D., Chamberlain, J. S., & Regnier, M. (2016). Translation of Cardiac Myosin Activation with 2-deoxy-ATP to Treat Heart Failure via an Experimental Ribonucleotide Reductase-Based Gene Therapy. JACC. Basic to translational science, 1(7), 666-679. https://doi.org/10.1016/j.jacbts.2016.07.006
Thomson, Kassandra S, et al. "Translation of Cardiac Myosin Activation with 2-deoxy-ATP to Treat Heart Failure via an Experimental Ribonucleotide Reductase-Based Gene Therapy." JACC. Basic to translational science vol. 1,7 (2016): 666-679. doi: https://doi.org/10.1016/j.jacbts.2016.07.006
Thomson KS, Odom GL, Murry CE, Mahairas GG, Moussavi-Harami F, Teichman SL, Chen X, Hauschka SD, Chamberlain JS, Regnier M. Translation of Cardiac Myosin Activation with 2-deoxy-ATP to Treat Heart Failure via an Experimental Ribonucleotide Reductase-Based Gene Therapy. JACC Basic Transl Sci. 2016 Dec;1(7):666-679. doi: 10.1016/j.jacbts.2016.07.006. PMID: 28553667; PMCID: PMC5444879.
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Integrated Computational Model of Lung Tissue Bioenergetics.

Frontiers in physiology

Zhang X, Dash RK, Clough AV, Xie D, Jacobs ER, Audi SH.
PMID: 30906264
Front Physiol. 2019 Mar 08;10:191. doi: 10.3389/fphys.2019.00191. eCollection 2019.

Altered lung tissue bioenergetics plays a key role in the pathogenesis of lung diseases. A wealth of information exists regarding the bioenergetic processes in mitochondria isolated from rat lungs, cultured pulmonary endothelial cells, and intact rat lungs under physiological...

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Zhang X, Dash RK, Clough AV, et al. Integrated Computational Model of Lung Tissue Bioenergetics. Front Physiol. 2019;10:191doi: 10.3389/fphys.2019.00191.
Zhang, X., Dash, R. K., Clough, A. V., Xie, D., Jacobs, E. R., & Audi, S. H. (2019). Integrated Computational Model of Lung Tissue Bioenergetics. Frontiers in physiology, 10191. https://doi.org/10.3389/fphys.2019.00191
Zhang, Xiao, et al. "Integrated Computational Model of Lung Tissue Bioenergetics." Frontiers in physiology vol. 10 (2019): 191. doi: https://doi.org/10.3389/fphys.2019.00191
Zhang X, Dash RK, Clough AV, Xie D, Jacobs ER, Audi SH. Integrated Computational Model of Lung Tissue Bioenergetics. Front Physiol. 2019 Mar 08;10:191. doi: 10.3389/fphys.2019.00191. eCollection 2019. PMID: 30906264; PMCID: PMC6418344.
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Increased cell membrane capacitance is the dominant mechanism of stretch-dependent conduction slowing in the rabbit heart: a computational study.

Cellular and molecular bioengineering

de Oliveira BL, Pfeiffer ER, Sundnes J, Wall ST, McCulloch AD.
PMID: 27087858
Cell Mol Bioeng. 2015 Jun 01;8(2):237-246. doi: 10.1007/s12195-015-0384-9. Epub 2015 Mar 24.

Volume loading of the cardiac ventricles is known to slow electrical conduction in the rabbit heart, but the mechanisms remain unclear. Previous experimental and modeling studies have investigated some of these mechanisms, including stretch-activated membrane currents, reduced gap junctional...

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de Oliveira BL, Pfeiffer ER, Sundnes J, et al. Increased cell membrane capacitance is the dominant mechanism of stretch-dependent conduction slowing in the rabbit heart: a computational study. Cell Mol Bioeng. 2015;8(2):237-246doi: 10.1007/s12195-015-0384-9.
de Oliveira, B. L., Pfeiffer, E. R., Sundnes, J., Wall, S. T., & McCulloch, A. D. (2015). Increased cell membrane capacitance is the dominant mechanism of stretch-dependent conduction slowing in the rabbit heart: a computational study. Cellular and molecular bioengineering, 8(2), 237-246. https://doi.org/10.1007/s12195-015-0384-9
de Oliveira, Bernardo L, et al. "Increased cell membrane capacitance is the dominant mechanism of stretch-dependent conduction slowing in the rabbit heart: a computational study." Cellular and molecular bioengineering vol. 8,2 (2015): 237-246. doi: https://doi.org/10.1007/s12195-015-0384-9
de Oliveira BL, Pfeiffer ER, Sundnes J, Wall ST, McCulloch AD. Increased cell membrane capacitance is the dominant mechanism of stretch-dependent conduction slowing in the rabbit heart: a computational study. Cell Mol Bioeng. 2015 Jun 01;8(2):237-246. doi: 10.1007/s12195-015-0384-9. Epub 2015 Mar 24. PMID: 27087858; PMCID: PMC4830494.
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Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts.

Frontiers in physiology

Lewalle A, Land S, Carruth E, Frank LR, Lamata P, Omens JH, McCulloch AD, Niederer SA, Smith NP.
PMID: 29527171
Front Physiol. 2018 Feb 23;9:37. doi: 10.3389/fphys.2018.00037. eCollection 2018.

The cardiac system compensates for variations in physiological and pathophysiological conditions through a dynamic remodeling at the organ, tissue, and intracellular levels in order to maintain function. However, on longer time scales following the onset of ventricular pressure overload,...

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Lewalle A, Land S, Carruth E, et al. Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts. Front Physiol. 2018;9:37doi: 10.3389/fphys.2018.00037.
Lewalle, A., Land, S., Carruth, E., Frank, L. R., Lamata, P., Omens, J. H., McCulloch, A. D., Niederer, S. A., & Smith, N. P. (2018). Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts. Frontiers in physiology, 937. https://doi.org/10.3389/fphys.2018.00037
Lewalle, Alexandre, et al. "Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts." Frontiers in physiology vol. 9 (2018): 37. doi: https://doi.org/10.3389/fphys.2018.00037
Lewalle A, Land S, Carruth E, Frank LR, Lamata P, Omens JH, McCulloch AD, Niederer SA, Smith NP. Decreasing Compensatory Ability of Concentric Ventricular Hypertrophy in Aortic-Banded Rat Hearts. Front Physiol. 2018 Feb 23;9:37. doi: 10.3389/fphys.2018.00037. eCollection 2018. PMID: 29527171; PMCID: PMC5829063.
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Semi-automated Modular Program Constructor for physiological modeling: Building cell and organ models.

F1000Research

Jardine B, Raymond GM, Bassingthwaighte JB.
PMID: 28698795
F1000Res. 2015 Dec 16;4:1461. doi: 10.12688/f1000research.7476.3. eCollection 2015.

The Modular Program Constructor (MPC) is an open-source Java based modeling utility, built upon JSim's Mathematical Modeling Language (MML) ( http://www.physiome.org/jsim/) that uses directives embedded in model code to construct larger, more complicated models quickly and with less error...

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Jardine B, Raymond GM, Bassingthwaighte JB. Semi-automated Modular Program Constructor for physiological modeling: Building cell and organ models. F1000Res. 2015;4:1461doi: 10.12688/f1000research.7476.3.
Jardine, B., Raymond, G. M., & Bassingthwaighte, J. B. (2015). Semi-automated Modular Program Constructor for physiological modeling: Building cell and organ models. F1000Research, 41461. https://doi.org/10.12688/f1000research.7476.3
Jardine, Bartholomew, et al. "Semi-automated Modular Program Constructor for physiological modeling: Building cell and organ models." F1000Research vol. 4 (2015): 1461. doi: https://doi.org/10.12688/f1000research.7476.3
Jardine B, Raymond GM, Bassingthwaighte JB. Semi-automated Modular Program Constructor for physiological modeling: Building cell and organ models. F1000Res. 2015 Dec 16;4:1461. doi: 10.12688/f1000research.7476.3. eCollection 2015. PMID: 28698795; PMCID: PMC5488124.
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Showing 1 to 12 of 18 entries