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3 results on '"Mathieu C, Rousseau"'

1. Technical and analytical approach to biventricular pressure-volume loops in swine including a completely endovascular, percutaneous closed-chest large animal model

Author

David P. Stonko, MD, MS, Mathieu C. Rousseau, MD, Colin Price, BS, Amy Benike, MS, Rebecca N. Treffalls, BS, Nichole E. Brunton, DO, Dorian Rosen, PhD, and Jonathan J. Morrison, MBChB, PhD

Subjects
Biventricular pressure-volume loops, LV PV loops, RV PV loops, Endovascular, Closed-chest, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Pressure-volume (PV) loop analysis is a sophisticated invasive approach to quantifying load-dependent and independent measures of cardiac function. Biventricular (BV) PV loops allow left and right ventricular function to be quantified simultaneously and independently, which is important for conditions and certain physiologic states, such as ventricular decoupling or acute physiologic changes. BV PV loops can be performed in an entirely endovascular, percutaneous, and closed-chest setting. This technique is helpful in a survival animal model, as a percutaneous monitoring system during endovascular device experiments, or in cases where chest wall compliance is being tested or may be a confounder. In this article, we describe the end-to-end implementation of a completely endovascular, totally percutaneous, and closed-chest large animal model to obtain contemporaneous BV PV loops in 40 to 70 kg swine. We describe the associated surgical and technical challenges and our solutions to obtaining endovascular BV PV loops, closed-chest cardiac output, and stroke volume (including validation of the correction factor necessary for thermodilution), as well as how to perform endovascular inferior vena cava occlusion in this swine model. We also include techniques for data acquisition and analysis that are required for this method. : Clinical Relevance: This article describes the end-to-end implementation of a completely endovascular, percutaneous, and closed-chest large animal model for obtaining biventricular pressure-volume loops in swine. This will allow researchers to obtain contemporaneous, continuous left and right ventricular physiology through a minimally invasive procedure that animals can survive and does not alter chest wall compliance. This model may be used to better quantify the physiology during clinical scenarios of ventricular decoupling, during procedures such as transcatheter aortic valve repair or those that alter left ventricular (LV) function, or during the initiation of resuscitative endovascular balloon occlusion of the aorta or extracorporeal cardiopulmonary resuscitation when LV and right ventricular filling become misaligned.

Published
2024
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2. Gram negative bacteria increase non-small cell lung cancer metastasisviatoll-like receptor 4 activation and mitogen-activated protein kinase phosphorylation

Author

Simon C. Chow, Stephen D. Gowing, Jonathan J. Cools-Lartigue, Crystal B. Chen, Julie Berube, Hee-Won Yoon, Carlos H.F. Chan, Mathieu C. Rousseau, France Bourdeau, Betty Giannias, Lucie Roussel, Salman T. Qureshi, Simon Rousseau, and Lorenzo E. Ferri

Subjects
Cancer Research, Toll-like receptor, biology, medicine.disease, 3. Good health, Metastasis, Fibronectin, chemistry.chemical_compound, Oncology, chemistry, Cancer cell, Immunology, medicine, Cancer research, biology.protein, Cell adhesion, Lung cancer, Receptor, Eritoran
Abstract

Surgery is required for the curative treatment of lung cancer but is associated with high rates of postoperative pneumonias predominantly caused by gram negative bacteria. Recent evidence suggests that these severe infectious complications may decrease long term survival after hospital discharge via cancer recurrence, but the mechanism is unclear. Lung cancer cells have recently been demonstrated to express Toll-like receptors (TLR) that mediate pathogen recognition. We hypothesized that incubation of non-small cell lung cancer (NSCLC) cells with heat-inactivated Escherichia coli can augment cancer cell adhesion, migration and metastasis via TLR4 signaling. Incubation of murine and human NSCLC cells with E. coli increased in vitro cell adhesion to collagen I, collagen IV and fibronectin, and enhanced in vitro migration. Using hepatic intravital microscopy, we demonstrated that NSCLC cells have increased in vivo adhesion to hepatic sinusoids after coincubation with gram negative bacteria. These enhanced cell adhesion and migration phenotypes following incubation with E. coli were attenuated at three levels: inhibition of TLR4 (Eritoran), p38 MAPK (BIRB0796) and ERK1/2 phosphorylation (PD184352). Incubation of murine NSCLC cells in vitro with E. coli prior to intrasplenic injection significantly augmented formation of in vivo hepatic metastases 2 weeks later. This increase was abrogated by NSCLC TLR4 blockade using Eritoran. TLR4 represents a potential therapeutic target to help prevent severe postoperative infection driven cancer metastasis.

Published
2014
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3. Gram negative bacteria increase non-small cell lung cancer metastasis via Toll-like receptor 4 activation and mitogen-activated protein kinase phosphorylation

Author

Simon C, Chow, Stephen D, Gowing, Jonathan J, Cools-Lartigue, Crystal B, Chen, Julie, Berube, Hee-Won, Yoon, Carlos H F, Chan, Mathieu C, Rousseau, France, Bourdeau, Betty, Giannias, Lucie, Roussel, Salman T, Qureshi, Simon, Rousseau, and Lorenzo E, Ferri

Subjects
Male, Mice, Inbred C57BL, Toll-Like Receptor 4, Mice, Lung Neoplasms, Carcinoma, Non-Small-Cell Lung, Cell Line, Tumor, Cell Adhesion, Escherichia coli, Animals, Humans, Mitogen-Activated Protein Kinases, Phosphorylation
Abstract

Surgery is required for the curative treatment of lung cancer but is associated with high rates of postoperative pneumonias predominantly caused by gram negative bacteria. Recent evidence suggests that these severe infectious complications may decrease long term survival after hospital discharge via cancer recurrence, but the mechanism is unclear. Lung cancer cells have recently been demonstrated to express Toll-like receptors (TLR) that mediate pathogen recognition. We hypothesized that incubation of non-small cell lung cancer (NSCLC) cells with heat-inactivated Escherichia coli can augment cancer cell adhesion, migration and metastasis via TLR4 signaling. Incubation of murine and human NSCLC cells with E. coli increased in vitro cell adhesion to collagen I, collagen IV and fibronectin, and enhanced in vitro migration. Using hepatic intravital microscopy, we demonstrated that NSCLC cells have increased in vivo adhesion to hepatic sinusoids after coincubation with gram negative bacteria. These enhanced cell adhesion and migration phenotypes following incubation with E. coli were attenuated at three levels: inhibition of TLR4 (Eritoran), p38 MAPK (BIRB0796) and ERK1/2 phosphorylation (PD184352). Incubation of murine NSCLC cells in vitro with E. coli prior to intrasplenic injection significantly augmented formation of in vivo hepatic metastases 2 weeks later. This increase was abrogated by NSCLC TLR4 blockade using Eritoran. TLR4 represents a potential therapeutic target to help prevent severe postoperative infection driven cancer metastasis.

Published
2014

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