subject:(Reperfusion)

1. Olland, Anne. Intérêt des microparticules pour l'étude de l'ischémie reperfusion en tranplantation pulmonaire basé sur un modèle de perfusion ventilation pulmonaire ex vivo chez le rat : Relevance of microparticles for the study of ischemia reperfusion in lung transplantation using an experimental model of ex vivo rat lung reperfusion and ventilation.

Degree: Docteur es, Sciences de la vie et de la santé, 2016, Université de Strasbourg

URL: http://www.theses.fr/2016STRAJ035

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L’ischémie reperfusion pulmonaire et sa traduction clinique la dysfonction primaire du greffon sont responsables d’une morbi-mortalité importante en transplantation pulmonaire aussi bien à court terme… (more)

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L’ischémie reperfusion pulmonaire et sa traduction clinique la dysfonction primaire du greffon sont responsables d’une morbi-mortalité importante en transplantation pulmonaire aussi bien à court terme qu’à long terme. Nous avons voulu faire la démonstration de la pertinence des microparticules comme marqueur de l’ischémie reperfusion pulmonaire. Nous avons reproduit et validé la stabilité d’un modèle de perfusion ventilation ex vivo de poumon de rat aussi bien en conditions normales (pas d’ischémie pulmonaire avant reperfusion) qu’en conditions extrêmes (1 h d’ischémie chaude avant reperfusion pulmonaire). Nous avons étudié la génération de microparticules par des poumons soumis à des conditions variables d’ischémie froide et d’ischémie chaude. Les poumons soumis à de fortes conditions d’ischémie froide (20h) produisent un pic précoce de microparticules d’origine épithéliale alvéolaire, leucocytaire et endothéliale. Nous en concluons que le modèle de perfusion ventilation ex vivo de poumons de rats est un modèle pertinent pour l’étude des réactions d’ischémie reperfusion. Les microparticules apparaissent comme un marqueur précoce des lésions d’ischémie reperfusion pulmonaires dans ce modèle.

Lung ischemia reperfusion and its clinical expression as primary graft dysfunction are provider of immediate and long term morbidity and mortality for patients. We aimed at demonstrating the usefulness and relevance of microparticles as biomarkers for lung ischemia reperfusion injury. We first reproduced an ex vivo rat lung perfusion and ventilation experimental model. Stability of the model was validated for normal conditions (no ischemia before reperfusion) as well as for extreme conditions (1 hour warm ischemia before reperfusion). The generation of microparticles was studied in that model for variable conditions of cold ischemia and for warm ischemia. Lung submitted to strong ischemic injury (20hours cold ischemia) generate an early pike of microparticles originated from leukocyes, endothelial cells, and epithelial alveolar cells. We may conclude the ex vivo model of rat lung perfusion and ventilation is relevant for the study of lung ischemia reperfusion injury. Microparticles are relevant markers of rat lung ischemia reperfusion injury in our model.

Advisors/Committee Members: Massard, Gilbert (thesis director).

Subjects/Keywords: Ischémie reperfusion; Reperfusion ex vivo; Microparticules; Ischemia reperfusion; Ex vivo reperfusion; Microparticles; 571.96; 617.9

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APA (6^th Edition):

Olland, A. (2016). Intérêt des microparticules pour l'étude de l'ischémie reperfusion en tranplantation pulmonaire basé sur un modèle de perfusion ventilation pulmonaire ex vivo chez le rat : Relevance of microparticles for the study of ischemia reperfusion in lung transplantation using an experimental model of ex vivo rat lung reperfusion and ventilation. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2016STRAJ035

Chicago Manual of Style (16^th Edition):

Olland, Anne. “Intérêt des microparticules pour l'étude de l'ischémie reperfusion en tranplantation pulmonaire basé sur un modèle de perfusion ventilation pulmonaire ex vivo chez le rat : Relevance of microparticles for the study of ischemia reperfusion in lung transplantation using an experimental model of ex vivo rat lung reperfusion and ventilation.” 2016. Doctoral Dissertation, Université de Strasbourg. Accessed March 07, 2021. http://www.theses.fr/2016STRAJ035.

MLA Handbook (7^th Edition):

Olland, Anne. “Intérêt des microparticules pour l'étude de l'ischémie reperfusion en tranplantation pulmonaire basé sur un modèle de perfusion ventilation pulmonaire ex vivo chez le rat : Relevance of microparticles for the study of ischemia reperfusion in lung transplantation using an experimental model of ex vivo rat lung reperfusion and ventilation.” 2016. Web. 07 Mar 2021.

Vancouver:

Olland A. Intérêt des microparticules pour l'étude de l'ischémie reperfusion en tranplantation pulmonaire basé sur un modèle de perfusion ventilation pulmonaire ex vivo chez le rat : Relevance of microparticles for the study of ischemia reperfusion in lung transplantation using an experimental model of ex vivo rat lung reperfusion and ventilation. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2016. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2016STRAJ035.

Council of Science Editors:

Olland A. Intérêt des microparticules pour l'étude de l'ischémie reperfusion en tranplantation pulmonaire basé sur un modèle de perfusion ventilation pulmonaire ex vivo chez le rat : Relevance of microparticles for the study of ischemia reperfusion in lung transplantation using an experimental model of ex vivo rat lung reperfusion and ventilation. [Doctoral Dissertation]. Université de Strasbourg; 2016. Available from: http://www.theses.fr/2016STRAJ035

Universiteit Utrecht

2. Soyal, M. Forkhead Box O in ischemia/reperfusion injury: a potential therapeutic target.

Degree: 2012, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/254301

► Acute myocardial infarction (AMI) is a major cause of morbidity. AMI is caused by a blockage of one or multiple coronary arteries, leading to an… (more)

Subjects/Keywords: AMI; FOXO; ischemia/reperfusion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Soyal, M. (2012). Forkhead Box O in ischemia/reperfusion injury: a potential therapeutic target. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/254301

Chicago Manual of Style (16^th Edition):

Soyal, M. “Forkhead Box O in ischemia/reperfusion injury: a potential therapeutic target.” 2012. Masters Thesis, Universiteit Utrecht. Accessed March 07, 2021. http://dspace.library.uu.nl:8080/handle/1874/254301.

MLA Handbook (7^th Edition):

Soyal, M. “Forkhead Box O in ischemia/reperfusion injury: a potential therapeutic target.” 2012. Web. 07 Mar 2021.

Vancouver:

Soyal M. Forkhead Box O in ischemia/reperfusion injury: a potential therapeutic target. [Internet] [Masters thesis]. Universiteit Utrecht; 2012. [cited 2021 Mar 07]. Available from: http://dspace.library.uu.nl:8080/handle/1874/254301.

Council of Science Editors:

Soyal M. Forkhead Box O in ischemia/reperfusion injury: a potential therapeutic target. [Masters Thesis]. Universiteit Utrecht; 2012. Available from: http://dspace.library.uu.nl:8080/handle/1874/254301

University of Cambridge

3. Allen, Fay Marie. Mitochondrial metabolism elucidated by rapid fractionation from tissue.

Degree: PhD, 2020, University of Cambridge

URL: https://doi.org/10.17863/CAM.49510 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801797

► Mitochondria are metabolic hubs, with many diseases found to have altered metabolism and mitochondrial dysfunction, such as ischaemia-reperfusion injury. A detailed understanding of the metabolic… (more)

Subjects/Keywords: Mitochondria; Metabolism; Ischaemia-Reperfusion Injury

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Allen, F. M. (2020). Mitochondrial metabolism elucidated by rapid fractionation from tissue. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.49510 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801797

Chicago Manual of Style (16^th Edition):

Allen, Fay Marie. “Mitochondrial metabolism elucidated by rapid fractionation from tissue.” 2020. Doctoral Dissertation, University of Cambridge. Accessed March 07, 2021. https://doi.org/10.17863/CAM.49510 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801797.

MLA Handbook (7^th Edition):

Allen, Fay Marie. “Mitochondrial metabolism elucidated by rapid fractionation from tissue.” 2020. Web. 07 Mar 2021.

Vancouver:

Allen FM. Mitochondrial metabolism elucidated by rapid fractionation from tissue. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Mar 07]. Available from: https://doi.org/10.17863/CAM.49510 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801797.

Council of Science Editors:

Allen FM. Mitochondrial metabolism elucidated by rapid fractionation from tissue. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://doi.org/10.17863/CAM.49510 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.801797

University of Cambridge

4. Martin, Jack. The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/294351

► Summary The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation Ischaemia and subsequent reperfusion is inherent to solid organ transplantation and contributes to… (more)

▼ Summary The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation Ischaemia and subsequent reperfusion is inherent to solid organ transplantation and contributes to tissue damage, organ dysfunction, and worse recipient outcome. Demand for organs for transplantation in the UK has led to the increasing use of ‘less-than-ideal’ deceased organs that are less tolerant of ischaemia or have been exposed to greater ischaemic insults. Furthermore, outcomes from clinical transplantation suggest that increasing ischaemia-reperfusion (IR) injury influences not only short-term outcomes but also longer-term outcomes by increasing the rate of chronic organ rejection. Mitochondria are recognised as being integral to IR injury generating a burst of reactive oxygen species that initiates downstream tissue damage. There is emerging evidence that this process is driven by a specific metabolic pathway rather than by a series of random damaging events. A better understanding of this pathophysiology and the mechanisms underpinning IR injury will increase the opportunity for the development of rational therapeutic approaches. In this work, I have characterised ischaemic metabolism during warm and cold organ storage in murine, porcine and human myocardial tissue. I have demonstrated succinate accumulation to be a conserved signature of ischaemia across species and have demonstrated the ability to moderate metabolic pathways in the mouse heart during organ storage using metabolic inhibitors. In order to investigate the effects of the metabolic changes during ischaemia on reperfusion I developed a novel, small animal model of solid organ transplantation incorporating a warm ischaemic insult. I then used this model to examine the therapeutic efficacy of ameliorating succinate accumulation during ischaemia to reduce organ dysfunction upon reperfusion. Finally, I explored the impact of reperfusion injury on chronic rejection in a previously well characterised model of organ rejection. Jack Lewis Martin

Subjects/Keywords: Organ transplantation; Mitochondria; Ischaemia-Reperfusion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Martin, J. (2019). The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/294351

Chicago Manual of Style (16^th Edition):

Martin, Jack. “The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 07, 2021. https://www.repository.cam.ac.uk/handle/1810/294351.

MLA Handbook (7^th Edition):

Martin, Jack. “The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation.” 2019. Web. 07 Mar 2021.

Vancouver:

Martin J. The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 07]. Available from: https://www.repository.cam.ac.uk/handle/1810/294351.

Council of Science Editors:

Martin J. The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/294351

University of Cambridge

5. Allen, Fay Marie. Mitochondrial Metabolism Elucidated by Rapid Fractionation from Tissue.

Degree: PhD, 2020, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/302439

► Mitochondria are metabolic hubs, with many diseases found to have altered metabolism and mitochondrial dysfunction, such as ischaemia-reperfusion injury. A detailed understanding of the metabolic… (more)

Subjects/Keywords: Mitochondria; Metabolism; Ischaemia-Reperfusion Injury

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Allen, F. M. (2020). Mitochondrial Metabolism Elucidated by Rapid Fractionation from Tissue. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/302439

Chicago Manual of Style (16^th Edition):

Allen, Fay Marie. “Mitochondrial Metabolism Elucidated by Rapid Fractionation from Tissue.” 2020. Doctoral Dissertation, University of Cambridge. Accessed March 07, 2021. https://www.repository.cam.ac.uk/handle/1810/302439.

MLA Handbook (7^th Edition):

Allen, Fay Marie. “Mitochondrial Metabolism Elucidated by Rapid Fractionation from Tissue.” 2020. Web. 07 Mar 2021.

Vancouver:

Allen FM. Mitochondrial Metabolism Elucidated by Rapid Fractionation from Tissue. [Internet] [Doctoral dissertation]. University of Cambridge; 2020. [cited 2021 Mar 07]. Available from: https://www.repository.cam.ac.uk/handle/1810/302439.

Council of Science Editors:

Allen FM. Mitochondrial Metabolism Elucidated by Rapid Fractionation from Tissue. [Doctoral Dissertation]. University of Cambridge; 2020. Available from: https://www.repository.cam.ac.uk/handle/1810/302439

University of Melbourne

6. Thacker, Michelle Anne. Structural damage to the enteric nervous system following ischemia / reperfusion injury.

Degree: 2012, University of Melbourne

URL: http://hdl.handle.net/11343/37853

► Ischemia reperfusion (I/R) injury can occur in a number of organs, however the intestine is possibly the most susceptible to I/R damage. Intestinal I/R injury… (more)

▼ Ischemia reperfusion (I/R) injury can occur in a number of organs, however the intestine is possibly the most susceptible to I/R damage. Intestinal I/R injury is treated as a life threatening injury as tissue necrosis can rapidly progress and the non specific clinical presentation of the disease makes it difficult to diagnose. In addition, I/R injury is an inevitable consequence of intestinal transplantation and, with an increasing success rate, the demand for intestinal transplantation for end stage organ failure patients has increased. The damage caused to the intestine following a period of I/R has been well documented for a number of cell types, and results have demonstrated mucosal sloughing, muscle degeneration, and the damage caused to enteric neurons. However, the level of damage inflicted on enteric glia following I/R remains unexplored, despite the knowledge that glia contribute to neuronal maintenance and survival and are involved in maintaining mucosal integrity. Through the use of immunohistochemistry, this study shows for the first time that major damage to enteric glia occurs 3 hr following I/R injury, earlier than the peak of neuronal damage, and that structural damage to glia, revealed by cytoskeletal disruption (glial fibrillary acidic protein, GFAP, disaggregation) and loss of S100B, is associated with changes to the enteric neuronal protein, Hu in neighbouring neurons. I was able to quantify these changes, and to determine if the GFAP, S100B or Hu were differentially affected following arterial (A), venous (V), or arterial plus venous (AV) occlusion. In addition, through histochemistry, this study also documented the structural damage to the mucosa following A, V and AV occlusion. My study has added to our knowledge on the damaging effects of intestinal I/R injury on enteric glia, and has identified an association between the damage observed in enteric glia and neighbouring neurons. These results highlights the possible importance of enteric glia in I/R and may be beneficial for future studies investigating neuroprotective strategies against intestinal I/R injury.

Subjects/Keywords: enteric glia; ischemia reperfusion injury

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Thacker, M. A. (2012). Structural damage to the enteric nervous system following ischemia / reperfusion injury. (Masters Thesis). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37853

Chicago Manual of Style (16^th Edition):

Thacker, Michelle Anne. “Structural damage to the enteric nervous system following ischemia / reperfusion injury.” 2012. Masters Thesis, University of Melbourne. Accessed March 07, 2021. http://hdl.handle.net/11343/37853.

MLA Handbook (7^th Edition):

Thacker, Michelle Anne. “Structural damage to the enteric nervous system following ischemia / reperfusion injury.” 2012. Web. 07 Mar 2021.

Vancouver:

Thacker MA. Structural damage to the enteric nervous system following ischemia / reperfusion injury. [Internet] [Masters thesis]. University of Melbourne; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/11343/37853.

Council of Science Editors:

Thacker MA. Structural damage to the enteric nervous system following ischemia / reperfusion injury. [Masters Thesis]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/37853

University of Cambridge

7. Martin, Jack. The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation.

Degree: PhD, 2019, University of Cambridge

URL: https://doi.org/10.17863/CAM.41449 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782895

► The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation Ischaemia and subsequent reperfusion is inherent to solid organ transplantation and contributes to tissue… (more)

▼ The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation Ischaemia and subsequent reperfusion is inherent to solid organ transplantation and contributes to tissue damage, organ dysfunction, and worse recipient outcome. Demand for organs for transplantation in the UK has led to the increasing use of 'less-than-ideal' deceased organs that are less tolerant of ischaemia or have been exposed to greater ischaemic insults. Furthermore, outcomes from clinical transplantation suggest that increasing ischaemia-reperfusion (IR) injury influences not only short-term outcomes but also longer-term outcomes by increasing the rate of chronic organ rejection. Mitochondria are recognised as being integral to IR injury generating a burst of reactive oxygen species that initiates downstream tissue damage. There is emerging evidence that this process is driven by a specific metabolic pathway rather than by a series of random damaging events. A better understanding of this pathophysiology and the mechanisms underpinning IR injury will increase the opportunity for the development of rational therapeutic approaches. In this work, I have characterised ischaemic metabolism during warm and cold organ storage in murine, porcine and human myocardial tissue. I have demonstrated succinate accumulation to be a conserved signature of ischaemia across species and have demonstrated the ability to moderate metabolic pathways in the mouse heart during organ storage using metabolic inhibitors. In order to investigate the effects of the metabolic changes during ischaemia on reperfusion I developed a novel, small animal model of solid organ transplantation incorporating a warm ischaemic insult. I then used this model to examine the therapeutic efficacy of ameliorating succinate accumulation during ischaemia to reduce organ dysfunction upon reperfusion. Finally, I explored the impact of reperfusion injury on chronic rejection in a previously well characterised model of organ rejection.

Subjects/Keywords: Organ transplantation; Mitochondria; Ischaemia-Reperfusion

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Martin, J. (2019). The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.41449 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782895

Chicago Manual of Style (16^th Edition):

Martin, Jack. “The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 07, 2021. https://doi.org/10.17863/CAM.41449 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782895.

MLA Handbook (7^th Edition):

Martin, Jack. “The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation.” 2019. Web. 07 Mar 2021.

Vancouver:

Martin J. The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 07]. Available from: https://doi.org/10.17863/CAM.41449 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782895.

Council of Science Editors:

Martin J. The role of ischaemia-reperfusion injury and mitochondrial dysfunction in organ transplantation. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.41449 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.782895

8. Hoang, Quoc thang. Aspects diagnostiques et thérapeutiques du modèle d'ischémie - reperfusion mésentérique : Diagnostic and treatment aspects of mesenteric ischemia - reperfusion model.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie. Biothérapies, 2016, Sorbonne Paris Cité

URL: http://www.theses.fr/2016USPCC196

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Introduction: La lésion d'ischémie - reperfusion (I/R) intestinale est associée à une mortalité élevée.Le rôle de la transmigration des neutrophiles est probablement essentiel dans le… (more)

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Introduction: La lésion d'ischémie - reperfusion (I/R) intestinale est associée à une mortalité élevée.Le rôle de la transmigration des neutrophiles est probablement essentiel dans le dysfonctionnement de la barrière induit par la lésion I/R et la nécrose subséquente. Le but de notre étude était d'évaluer, au niveau pré-clinique, la valeur thérapeutique potentielle du peptide P8RI (un agoniste de CD31) dans la lésion I/R de l'intestine grêle.Méthodes: I/R intestinale a été induite chez des rats Wistar par clampage de l'artère mésentérique supérieure (AMS) pendant 30 min suivi par 4 h de reperfusion. Trois groupes de rats ont été comparés:P8RI (n = 20, I/R et P8RI 2,5 mg/kg/h de reperfusion), I/R témoins positifs (n = 21, I/R et infusion de sérum physiologique) et témoins (n = 14, dissection de l'AMS sans clampage et infusion de sérum physiologique). La matrix métallopeptidase 9 (MMP-9) dans la plasma, le liquide péritonéal et l'intestin; la MPO intestinale, l'ADN libre plasmatique, les taux d'hémoglobine intraluminale e tl'épaisseur épithéliale ont été évalués comme marqueurs intermédiaires de la lésion intestinale. La détection du matériel génétique d'E.coli par PCR quantitative dans le sang a été également réalisée chez les témoins positifs et chez les rats traités par P8RI pendant la période de reperfusion. Le CD31clivé dans le plasma a été mesuré par une méthode d'ELISA maison. Résultats: La grade histologique de l'intestin grêle chez les animaux traités par P8RI est supérieur àcelui des témoins positifs d'I/R (p < 0,05). P8RI protège l'intestin grêle contre la destruction épithéliale induite par lésion I/R (p < 0,01). Il y a une corrélation négative significative entre l'abrasion épithéliale et le score de Chiu de classement histologique de la lésion I/R mésentérique (r = -0,7245, p < 0.001).P8RI protège l'intestin grêle de la MPO in situ, de la libération de la MMP-9 (p < 0,05) et des complications hémorragiques digestives causées par lésion I/R (p < 0,01). Les taux plasmatiques et péritonéaux accrus de MMP-9, induits par I/R, sont significativement réduits par P8RI (p < 0,05 et p <0,01, respectivement). L'ADN d'E.coli circulant est significativement plus élevé chez les rats de témoins positifs que dans le groupe P8RI (p < 0,05). L'ADN libre plasmatique pendant la reperfusion chez les rats de témoins positifs augmente significativement plus que celle des rats du groupe P8RI (p< 0,05). P8RI n'a aucun effet sur le compte neutrophilaire sanguin, mais induit une diminution significative de CD31 clivé dans le plasma pendant l'I/R mésentérique (p < 0,01). Les corrélations entre l'abrasion épithéliale et l'ADN libre, MMP-9, CD31 clivé plasmatiques, les taux de MMP-9 et MPO intestinale suggèrent que le mécanisme protecteur de P8RI implique l'inhibition de l'activation neutrophilaire, y compris le clivage de CD31. Conclusions: Cette étude suggère que le traitement par le peptide P8RI, un agoniste de CD31, réduit de la façon préventive, la lésion I/R de l'intestin grêle chez les rats.

Background: Intestinal…

Advisors/Committee Members: Michel, Jean-Baptiste (thesis director), Tran Dinh, Alexy (thesis director).

Subjects/Keywords: Ischémie - reperfusion mésentérique; P8RI; Mesenteric ischemia - reperfusion; P8RI

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hoang, Q. t. (2016). Aspects diagnostiques et thérapeutiques du modèle d'ischémie - reperfusion mésentérique : Diagnostic and treatment aspects of mesenteric ischemia - reperfusion model. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2016USPCC196

Chicago Manual of Style (16^th Edition):

Hoang, Quoc thang. “Aspects diagnostiques et thérapeutiques du modèle d'ischémie - reperfusion mésentérique : Diagnostic and treatment aspects of mesenteric ischemia - reperfusion model.” 2016. Doctoral Dissertation, Sorbonne Paris Cité. Accessed March 07, 2021. http://www.theses.fr/2016USPCC196.

MLA Handbook (7^th Edition):

Hoang, Quoc thang. “Aspects diagnostiques et thérapeutiques du modèle d'ischémie - reperfusion mésentérique : Diagnostic and treatment aspects of mesenteric ischemia - reperfusion model.” 2016. Web. 07 Mar 2021.

Vancouver:

Hoang Qt. Aspects diagnostiques et thérapeutiques du modèle d'ischémie - reperfusion mésentérique : Diagnostic and treatment aspects of mesenteric ischemia - reperfusion model. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2016. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2016USPCC196.

Council of Science Editors:

Hoang Qt. Aspects diagnostiques et thérapeutiques du modèle d'ischémie - reperfusion mésentérique : Diagnostic and treatment aspects of mesenteric ischemia - reperfusion model. [Doctoral Dissertation]. Sorbonne Paris Cité; 2016. Available from: http://www.theses.fr/2016USPCC196

9. Sportouch-Dukhan, Catherine. Effets cardioprotecteurs du glutamate contre les lésions d'ischémie-reperfusion myocardique chez la souris. Evaluation échocardiographique. : Cardioprotective effects of glutamate against ischemia-reperfusion injury in the mouse heart. Echocardiographic evaluation.

Degree: Docteur es, Biochimie et biologie moléculaire, 2012, Université Montpellier I

URL: http://www.theses.fr/2012MON1T021

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L'infarctus du myocarde est la première cause de mortalité cardiovasculaire dans les pays occidentaux. La reperfusion la plus précoce possible est actuellement le seul traitement… (more)

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L'infarctus du myocarde est la première cause de mortalité cardiovasculaire dans les pays occidentaux. La reperfusion la plus précoce possible est actuellement le seul traitement validé pour réduire la taille d'infarctus, facteur pronostique fondamental de morbi-mortalité. Cependant, la reperfusion engendre des lésions d'ischémie-reperfusion (IR) irréversibles qui précipitent la mort par apoptose des cardiomyocytes. Une approche transcriptomique nous a permis d'identifier les gènes spécifiques du postconditionnement ischémique (PostC) dans le cœur de souris. Parmi ceux-ci, l'expression du gène codant pour le récepteur métabotrope de type 1 du glutamate (mGluR1) est augmentée par le PostC. L'objectif de mon travail de thèse a été d'étudier le rôle de mGluR1 au cours de l'IR myocardique. Notre stratégie, basée sur l'utilisation de souris knock-out, a permis de confirmer l'implication de mGluR1 dans la cardioprotection. L'injection de glutamate au moment de la reperfusion myocardique permet de diminuer significativement la taille de l'infarctus par inhibition de l'apoptose. Cet effet cardioprotecteur est diminué en présence de l'antagoniste spécifique YM 298198 ou en présence de wortmannin, inhibiteur de la PI3-kinase, activée dans la cascade de signalisation du récepteur. La réduction de la taille d'infarctus par le glutamate semble associée à une amélioration de la fonction contractile du ventricule gauche en échocardiographie (par speckle tracking, méthode de quantification de la déformation myocardique) dans un modèle murin d'IR myocardique. Ces résultats, bien que préliminaires, semblent prometteurs et nous permettent d'envisager une application clinique chez le patient coronarien.

Myocardial infarction is the major cause of cardiovascular mortality in western countries. Reperfusion as early as possible is the only treatment recognized to reduce infarct size, crucial prognostic factor of morbidity and mortality. However, reperfusion leads to ischemia-reperfusion (IR) injury leading to irreversible apoptotic death of cardiomyocytes. A transcriptomic approach has allowed us to identify genes specifically regulated upon ischemic postconditioning (PostC) in the mouse heart. Among them, the expression of the metabotropic glutamate receptor type 1 (mGluR1) gene is up-regulated by PostC. The aim of my thesis work was to study the role of mGluR1 during myocardial IR. Our strategy, based on the use of knockout mice, confirmed the involvement of mGluR1 in cardioprotection. Injection of glutamate at the time of reperfusion significantly reduced infarct size via apoptosis inhibition. This cardioprotective effect was reduced in presence of the specific antagonist YM 298198 or in presence of wortmannin, an inhibitor of PI3-kinase, which is activated downstream mGluR1. In our mouse model of myocardial IR injury, decrease in infarct size after glutamate treatment seems to be associated to an improved left ventricular contractile function assessed by echocardiography (speckle tracking method quantifying myocardial strain). These…

Advisors/Committee Members: Lemaire, Stéphanie (thesis director), Piot, Christophe (thesis director).

Subjects/Keywords: Cardioprotection; Infarctus; Ischémie-reperfusion; Échocardiographie; Cardioprotection; Infarction; Ischemia-reperfusion; Echocardiography

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sportouch-Dukhan, C. (2012). Effets cardioprotecteurs du glutamate contre les lésions d'ischémie-reperfusion myocardique chez la souris. Evaluation échocardiographique. : Cardioprotective effects of glutamate against ischemia-reperfusion injury in the mouse heart. Echocardiographic evaluation. (Doctoral Dissertation). Université Montpellier I. Retrieved from http://www.theses.fr/2012MON1T021

Chicago Manual of Style (16^th Edition):

Sportouch-Dukhan, Catherine. “Effets cardioprotecteurs du glutamate contre les lésions d'ischémie-reperfusion myocardique chez la souris. Evaluation échocardiographique. : Cardioprotective effects of glutamate against ischemia-reperfusion injury in the mouse heart. Echocardiographic evaluation.” 2012. Doctoral Dissertation, Université Montpellier I. Accessed March 07, 2021. http://www.theses.fr/2012MON1T021.

MLA Handbook (7^th Edition):

Sportouch-Dukhan, Catherine. “Effets cardioprotecteurs du glutamate contre les lésions d'ischémie-reperfusion myocardique chez la souris. Evaluation échocardiographique. : Cardioprotective effects of glutamate against ischemia-reperfusion injury in the mouse heart. Echocardiographic evaluation.” 2012. Web. 07 Mar 2021.

Vancouver:

Sportouch-Dukhan C. Effets cardioprotecteurs du glutamate contre les lésions d'ischémie-reperfusion myocardique chez la souris. Evaluation échocardiographique. : Cardioprotective effects of glutamate against ischemia-reperfusion injury in the mouse heart. Echocardiographic evaluation. [Internet] [Doctoral dissertation]. Université Montpellier I; 2012. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2012MON1T021.

Council of Science Editors:

Sportouch-Dukhan C. Effets cardioprotecteurs du glutamate contre les lésions d'ischémie-reperfusion myocardique chez la souris. Evaluation échocardiographique. : Cardioprotective effects of glutamate against ischemia-reperfusion injury in the mouse heart. Echocardiographic evaluation. [Doctoral Dissertation]. Université Montpellier I; 2012. Available from: http://www.theses.fr/2012MON1T021

10. Chevallier, Stéphane. Elastokines et Lactosylcéramide : cardioprotection et vieillissement : Elastokines et Lactosylceramide : cardioprotection et Ageing.

Degree: Docteur es, Pharmacologie, 2011, Reims

URL: http://www.theses.fr/2011REIMM203

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La maladie cardiovasculaire la plus courante dans les pays industrialisés est la maladie coronarienne responsable d’une ischémie du tissu cardiaque pouvant conduire à l’infarctus du… (more)

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La maladie cardiovasculaire la plus courante dans les pays industrialisés est la maladie coronarienne responsable d’une ischémie du tissu cardiaque pouvant conduire à l’infarctus du myocarde. Bien que les améliorations de la prise en charge aient considérablement réduit les délais de la reperfusion (seul remède à l’ischémie), l’ischémie/reperfusion (I/R) entraîne des dommages cellulaires et tissulaires ainsi qu’une diminution des capacités fonctionnelles du coeur. Il existe néanmoins des systèmes de cardioprotection endogènes (comme le préconditionnement (préC) ou le postconditionnement (postC)) que l’on peut activer via l’administration de substances pharmacologiques. L’élastine, une protéine fibreuse de la matrice extracellulaire, est responsable de l’élasticité de certains de nos tissus (poumons, peau, <). Des peptides issus de la dégradation de l’élastine (PE) exercent un effet cardioprotecteur envers l’I/R en activant la voie de survie cellulaire RISK. Dans des fibroblastes dermiques, la transduction du signal induit par les peptides d’élastine est médiée de façon précoce par un second messager : le lactosylcéramide (LacCer). Cette étude constitue une première approche des effets du LacCer dans la cardioprotection envers l’I/R. Nous avons montré que le LacCer est un médiateur précoce du signal cardioprotecteur induit par les PE et qu’il protège le coeur des dommages liés à l’I/R dans un modèle de coeur isolé et perfusé en postC. Lors du vieillissement, de nombreuses modifications physiologiques sont à l’origine d’une perte d’efficacité des mécanismes de cardioprotection. Dans ce travail, nous avons également étudié les effets cardioprotecteurs des PE, du LacCer et de l’inhibition de p38MAPK (une protéine probablement impliquée dans la perte des mécanismes cardioprotecteurs liée au vieillissement) envers les dommages liés à l’I/R chez les rats âgés. Nous avons montré que les PE exercent un effet cardioprotecteur en pré+postC contre l’I/R au niveau de la survie cellulaire et au niveau de la récupération des capacités contractiles cardiaques. Le LacCer n’exerce un effet protecteur qu’au niveau de la survie cellulaire et l’inhibition de p38MAPK entraine une meilleure récupération des capacités contractiles sans améliorer la survie cellulaire.

In developed countries the most common cardiovascular disease is coronary heart disease that is responsible for myocardial ischemia and can lead to myocardial infarction. Reperfusion is the only cure for ischemia. Care improvement has dramatically reduced reperfusion delay but ischemia/reperfusion (I/R) causes a lot of cellular and tissular damages and a reduction of cardiac contractile abilities. Nevertheless cardioprotective pathways (like preconditionning (preC) and postconditionning (postC) can be pharmacologically triggered to reduce I/R injury. Elastin is a fibrous protein from extracellular matrix and is responsible for tissues elasticity in lungs, skin, < Peptides derived from elastin fragmentation (EP) exhibit cardioprotective function against I/R by triggering the…

Advisors/Committee Members: Nguyen, Philippe (thesis director).

Subjects/Keywords: Ischémie; Reperfusion; Elastine; Lactosylcéramides; Ischemia; Reperfusion; Elastin; Lactosylceramides

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chevallier, S. (2011). Elastokines et Lactosylcéramide : cardioprotection et vieillissement : Elastokines et Lactosylceramide : cardioprotection et Ageing. (Doctoral Dissertation). Reims. Retrieved from http://www.theses.fr/2011REIMM203

Chicago Manual of Style (16^th Edition):

Chevallier, Stéphane. “Elastokines et Lactosylcéramide : cardioprotection et vieillissement : Elastokines et Lactosylceramide : cardioprotection et Ageing.” 2011. Doctoral Dissertation, Reims. Accessed March 07, 2021. http://www.theses.fr/2011REIMM203.

MLA Handbook (7^th Edition):

Chevallier, Stéphane. “Elastokines et Lactosylcéramide : cardioprotection et vieillissement : Elastokines et Lactosylceramide : cardioprotection et Ageing.” 2011. Web. 07 Mar 2021.

Vancouver:

Chevallier S. Elastokines et Lactosylcéramide : cardioprotection et vieillissement : Elastokines et Lactosylceramide : cardioprotection et Ageing. [Internet] [Doctoral dissertation]. Reims; 2011. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2011REIMM203.

Council of Science Editors:

Chevallier S. Elastokines et Lactosylcéramide : cardioprotection et vieillissement : Elastokines et Lactosylceramide : cardioprotection et Ageing. [Doctoral Dissertation]. Reims; 2011. Available from: http://www.theses.fr/2011REIMM203

11. Paradis, Stephanie. Effet cardioprotecteur des ligands de la protéine translocatrice mitochondriale (TSPO) au cours de l'ischémie-reperfusion myocardique expérimentale : rôle du cholestérol. : Cardioprotective effect of mitochondrial translocator protein (TSPO) ligands during experimental myocardial ischemia-reperfusion : role of cholesterol.

Degree: Docteur es, Pharmacologie et Biothérapies, 2012, Université Paris-Est

URL: http://www.theses.fr/2012PEST0071

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Dans ce travail, nous avons montré qu'un nouveau ligand du TSPO, le TRO40303, possède des propriétés cardioprotectrices, confirmant que le TSPO joue un rôle important… (more)

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Dans ce travail, nous avons montré qu'un nouveau ligand du TSPO, le TRO40303, possède des propriétés cardioprotectrices, confirmant que le TSPO joue un rôle important dans les effets délétères engendrés par l'ischémie-reperfusion myocardique. Des effets similaires ont déjà été observés avec d'autres ligands du TSPO, notamment le 4'-chlorodiazépam, mais le mécanisme d'action par lequel ces molécules exercent leur effet cardioprotecteur reste pour une large part encore mal connu. Nous avons montré chez le rat que la reperfusion d'un myocarde ischémié s'accompagne d'une augmentation du cholestérol mitochondrial, de la formation d'oxystérols et d'un stress oxydant majeur. Le 4'-chlorodiazépam inhibe ces effets et améliore les fonctions mitochondriales post-ischémiques, révélant que le TSPO est responsable du transport du cholestérol dans la mitochondrie cardiaque et que ce dernier, sous des formes oxydées ou non, pourrait participer aux effets délétères de la reperfusion. La limitation de l'entrée du cholestérol dans la mitochondrie lors de la reperfusion d'un myocarde ischémié est un mécanisme original qui pourrait donc contribuer à l'effet cardioprotecteur des ligands du TSPO. Enfin, nous avons montré que chez des rats génétiquement modifiés et associant hypercholestérolémie, obésité et diabète de type II, le cholestérol mitochondrial est d'une part très élevé, avec ou sans ischémie-reperfusion myocardique et d'autre part que le 4'-chlorodiazépam n'a pas d'effet sur le cholestérol mitochondrial après ischémie-reperfusion. Ces résultats suggèrent que les mécanismes d'action des ligands du TSPO sont probablement différents et que les traitements doivent être adaptés en présence de facteurs de co-morbidité.

In the present work we showed that a new TSPO ligand, TRO40303, has cardioprotective properties confirming that TSPO plays a key role in the deleterious effects of myocardial ischemia-reperfusion. Similar effects have been observed with other TSPO ligands, such as 4'-chlorodiazepam, but the mechanism of action of these molecules is not known. We showed that ischemia-reperfusion in rats increased mitochondrial concentration of cholesterol, oxysterol formation and oxidative stress. 4'-Chlorodiazepam inhibited these effects and improved post-ischemic mitochondrial functions, revealing that TSPO is responsible for cholesterol transport in cardiac mitochondria and that cholesterol, in oxidized or non-oxidized forms, could participate in the deleterious effects of reperfusion. The limitation of the increase in cholesterol in mitochondria during ischemia-reperfusion is an original mechanism which could contribute to the cardioprotective effect of TSPO ligands. We then showed, in genetically modified rats with hypercholesterolemia, obesity and type II diabetes, that the concentration of mitochondrial cholesterol is very high with or without ischemia-reperfusion. We further demonstrated that 4'-chlorodiazepam has no effect on mitochondrial cholesterol after ischemia-reperfusion. These results suggest that the mechanisms of…

Advisors/Committee Members: Morin, Didier (thesis director).

Subjects/Keywords: Cholestérol; Ischémie reperfusion; Mitochondrie; Cardioprotection; Cholesterol; Ischemia reperfusion; Mitochondria; Cardioprotection

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Paradis, S. (2012). Effet cardioprotecteur des ligands de la protéine translocatrice mitochondriale (TSPO) au cours de l'ischémie-reperfusion myocardique expérimentale : rôle du cholestérol. : Cardioprotective effect of mitochondrial translocator protein (TSPO) ligands during experimental myocardial ischemia-reperfusion : role of cholesterol. (Doctoral Dissertation). Université Paris-Est. Retrieved from http://www.theses.fr/2012PEST0071

Chicago Manual of Style (16^th Edition):

Paradis, Stephanie. “Effet cardioprotecteur des ligands de la protéine translocatrice mitochondriale (TSPO) au cours de l'ischémie-reperfusion myocardique expérimentale : rôle du cholestérol. : Cardioprotective effect of mitochondrial translocator protein (TSPO) ligands during experimental myocardial ischemia-reperfusion : role of cholesterol.” 2012. Doctoral Dissertation, Université Paris-Est. Accessed March 07, 2021. http://www.theses.fr/2012PEST0071.

MLA Handbook (7^th Edition):

Paradis, Stephanie. “Effet cardioprotecteur des ligands de la protéine translocatrice mitochondriale (TSPO) au cours de l'ischémie-reperfusion myocardique expérimentale : rôle du cholestérol. : Cardioprotective effect of mitochondrial translocator protein (TSPO) ligands during experimental myocardial ischemia-reperfusion : role of cholesterol.” 2012. Web. 07 Mar 2021.

Vancouver:

Paradis S. Effet cardioprotecteur des ligands de la protéine translocatrice mitochondriale (TSPO) au cours de l'ischémie-reperfusion myocardique expérimentale : rôle du cholestérol. : Cardioprotective effect of mitochondrial translocator protein (TSPO) ligands during experimental myocardial ischemia-reperfusion : role of cholesterol. [Internet] [Doctoral dissertation]. Université Paris-Est; 2012. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2012PEST0071.

Council of Science Editors:

Paradis S. Effet cardioprotecteur des ligands de la protéine translocatrice mitochondriale (TSPO) au cours de l'ischémie-reperfusion myocardique expérimentale : rôle du cholestérol. : Cardioprotective effect of mitochondrial translocator protein (TSPO) ligands during experimental myocardial ischemia-reperfusion : role of cholesterol. [Doctoral Dissertation]. Université Paris-Est; 2012. Available from: http://www.theses.fr/2012PEST0071

12. Noll, Éric. Ischémie-reperfusion musculaire squelettique expérimentale : place de la lactatémie capillaire dans le monitorage de la reperfusion et transposition au modèle intestinal : Experimental skeletal muscle ischemia-reperfusion : capillary lactate for reperfusion monitoring.

Degree: Docteur es, Recherche clinique et innovation technologique, 2016, Université de Strasbourg

URL: http://www.theses.fr/2016STRAJ006

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Les objectifs de ce travail expérimental étaient : 1. Évaluer la place de la lactatémie capillaire comme dispositif de monitorage de l’ischémie et de la… (more)

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Les objectifs de ce travail expérimental étaient : 1. Évaluer la place de la lactatémie capillaire comme dispositif de monitorage de l’ischémie et de la reperfusion tissulaire. 2. Comparer le suivi local du taux de lactate, au niveau du compartiment ischémié, par rapport au taux systémique du lactate lors des l’ischémie de membre, l’ischémie intestinale ainsi que durant le choc hémorragique. La mesure capillaire du taux de lactate pourrait permettre: 1. d’affirmer l’existence d’une ischémie tissulaire régionale. Le taux systémique du lactate ne permet ce diagnostic, 2. de confirmer l’efficacité d’une reperfusion au niveau d’un membre préalablement ischémique tandis que la mesure systémique des lactates ne le permet pas. L’affirmation de l’efficacité de la reperfusion et de sa constance, par une mesure aussi simple que la lactatémie capillaire compartimentale représente une avancée majeure en comparaison avec les autres méthodes existantes. La mesure capillaire du taux de lactate systémique dans une situation d’hypoperfusion par choc hémorragique n’est pas associée à augmentation du taux de lactate intra-musculaire.

Our objectives for this experimental work were: 1. Assessment of capillary lactate for tissue ischemia and reperfusion monitoring. 2. Compare the local and systemic capillary lactate time course during compartmental ischemia insults like limb ischemia, intestinal ischemia or during hemorrhagic shock. The capillary measurement of the lactate in IR could be interesting for: 1. Assessing a limb or intestinal tissue ischemia. On the opposite, the systemic measurement could not assess this diagnosis. 2. Assessing the efficiency of a limb reperfusion. On the opposite, the systemic measurement could not assess this diagnosis. The systemic capillary lactate measurement during haemorrhagic shock related hypo perfusion could not be associated with an increase in intra muscular lactate.

Advisors/Committee Members: Geny, Bernard (thesis director), Diemunsch, Pierre (thesis director).

Subjects/Keywords: Ischémie-Reperfusion; Lactate; Ischemia-Reperfusion; Lactate; 571.5; 616.13

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Noll, �. (2016). Ischémie-reperfusion musculaire squelettique expérimentale : place de la lactatémie capillaire dans le monitorage de la reperfusion et transposition au modèle intestinal : Experimental skeletal muscle ischemia-reperfusion : capillary lactate for reperfusion monitoring. (Doctoral Dissertation). Université de Strasbourg. Retrieved from http://www.theses.fr/2016STRAJ006

Chicago Manual of Style (16^th Edition):

Noll, Éric. “Ischémie-reperfusion musculaire squelettique expérimentale : place de la lactatémie capillaire dans le monitorage de la reperfusion et transposition au modèle intestinal : Experimental skeletal muscle ischemia-reperfusion : capillary lactate for reperfusion monitoring.” 2016. Doctoral Dissertation, Université de Strasbourg. Accessed March 07, 2021. http://www.theses.fr/2016STRAJ006.

MLA Handbook (7^th Edition):

Noll, Éric. “Ischémie-reperfusion musculaire squelettique expérimentale : place de la lactatémie capillaire dans le monitorage de la reperfusion et transposition au modèle intestinal : Experimental skeletal muscle ischemia-reperfusion : capillary lactate for reperfusion monitoring.” 2016. Web. 07 Mar 2021.

Vancouver:

Noll �. Ischémie-reperfusion musculaire squelettique expérimentale : place de la lactatémie capillaire dans le monitorage de la reperfusion et transposition au modèle intestinal : Experimental skeletal muscle ischemia-reperfusion : capillary lactate for reperfusion monitoring. [Internet] [Doctoral dissertation]. Université de Strasbourg; 2016. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2016STRAJ006.

Council of Science Editors:

Noll �. Ischémie-reperfusion musculaire squelettique expérimentale : place de la lactatémie capillaire dans le monitorage de la reperfusion et transposition au modèle intestinal : Experimental skeletal muscle ischemia-reperfusion : capillary lactate for reperfusion monitoring. [Doctoral Dissertation]. Université de Strasbourg; 2016. Available from: http://www.theses.fr/2016STRAJ006

University of Hong Kong

13. 毛晓雯. Peroxynitrite/Ho-1 interaction in propofol post-conditioning protection against myocardial ischemia reperfusion injury.

Degree: 2013, University of Hong Kong

URL: http://hdl.handle.net/10722/193463

► Coronary artery disease limits myocardial blood flow and results in myocardial infarction. Reperfusion therapies restore coronary flow, but may also cause myocardial ischemia reperfusion injury… (more)

▼ Coronary artery disease limits myocardial blood flow and results in myocardial infarction. Reperfusion therapies restore coronary flow, but may also cause myocardial ischemia reperfusion injury (MIRI). Multiple critical factors contribute to MIRI and among them, oxidative stress plays an important role. This burst of oxidative stress during reperfusion is caused by a variety of sources which collectively are called reactive oxygen species (ROS). Peroxynitrite is more cytotoxic than other ROSs, which at high concentration serves as a detrimental molecule with a variety of target. Peroxynitrite is largely produced during the early reperfusion due to the dramatically increased concentrations of superoxide (O2●-) and nitric oxide (NO). Current cardioprotective therapies against MIRI include exogenous antioxidant treatment and conditioning treatment that induced endogenous antioxidant signaling which upregulates heme oxygenase1 (HO-1), which confers its antioxidant effect in cells and tissues by degrading the latent oxidant heme and generating downstream antioxidant molecules. More importantly, peroxynitrite is closely related to HO-1 in pathogenesis of MIRI and pharmacological or genetic methods that induce over-expression of HO-1 in turn decrease the peroxynitrite generation. In this thesis we report the results of three studies designed to explore the interaction of peroxynitrite and HO-1 in cardioprotection against MIRI. In the first study we demonstrated that HO-1 plays an essential role in chronic antioxidant treatment against MIRI in 4-week diabetic rats. Chronic antioxidant treatment with two kinds of antioxidants that target different sources of ROSs was administrated in an in vivo study with streptozotocin (STZ)-induced type 1 diabetic rats. Antioxidant treatments synergistically attenuate MIRI and cardiac dysfunction in type 1 diabetic rats by enhancing HO-1 expression, and inhibition of HO-1 expression cancelled antioxidant cardioprotection. This finding was supported by in vitro experiments in a cardiomyocyte hypoxia-reoxygenation model. The second study explored the peroxynitrite/HO-1 interaction in propofol post-conditioning (PPC) in acute MIRI with both ex vivo and in vivo animal models. We showed that PPC conferred similar cardioprotection as an established intervention˗ischemic post-conditioning (I-PostC). PPC cardioprotection was achieved through down-regulating peroxynitrite formation and activation of HO-1 and its related signaling molecules. This finding indicates that anaesthetic post-conditioning treatment (such as PPC) can achieve similar cardioprotection as ischemic post-conditioning and can avoid potential mechanical injury that may be caused by I-PostC. Inhibition of peroxynitrite reduction and subsequent enhanced HO-1 expression may be the fundamental mechanism of PPC cardioprotection. Lastly, we further explored PPC cardioprotection against MIRI in diabetic rats. We found that the diabetic heart lost its sensitivity to PPC and the diminished effect of PPC in inducing HO-1… Advisors/Committee Members: Xia, Z (advisor), Vanhoutte, PMGR (advisor).

Subjects/Keywords: Myocardial reperfusion; Reperfusion injury

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

毛晓雯. (2013). Peroxynitrite/Ho-1 interaction in propofol post-conditioning protection against myocardial ischemia reperfusion injury. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/193463

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

毛晓雯. “Peroxynitrite/Ho-1 interaction in propofol post-conditioning protection against myocardial ischemia reperfusion injury.” 2013. Thesis, University of Hong Kong. Accessed March 07, 2021. http://hdl.handle.net/10722/193463.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

毛晓雯. “Peroxynitrite/Ho-1 interaction in propofol post-conditioning protection against myocardial ischemia reperfusion injury.” 2013. Web. 07 Mar 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

毛晓雯. Peroxynitrite/Ho-1 interaction in propofol post-conditioning protection against myocardial ischemia reperfusion injury. [Internet] [Thesis]. University of Hong Kong; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10722/193463.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

毛晓雯. Peroxynitrite/Ho-1 interaction in propofol post-conditioning protection against myocardial ischemia reperfusion injury. [Thesis]. University of Hong Kong; 2013. Available from: http://hdl.handle.net/10722/193463

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

14. Feliu, Catherine. Implication des récepteurs P1 et P2 dans la protection des cellules endothéliales au cours de l’hypoxie-reoxygenation : Involvement of P1 and P2 receptors in the protection of endothelial cells during hypoxia-reoxygenation.

Degree: Docteur es, Médecine, 2019, Reims

URL: http://www.theses.fr/2019REIMM202

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Au cours de l’ischémie cardiaque, la lésion est initiée au niveau de l’endothélium, et progresse aux cardiomyocytes environnants. La signalisation purinergique joue un rôle important… (more)

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Au cours de l’ischémie cardiaque, la lésion est initiée au niveau de l’endothélium, et progresse aux cardiomyocytes environnants. La signalisation purinergique joue un rôle important au cours d’épisodes l’ischémie/reperfusion (I/R). De multiples travaux ont portés sur l’étude des mécanismes de protection des nucléotides et nucléosides, sans pour autant étudier leurs rôles spécifiques sur l’endothélium. Dans ce travail, nous mettons en évidence une augmentation des concentrations extracellulaires en ATP et adénosine provenant de l’endothélium soumis à une hypoxie. Au niveau endothélial, nous mettons en évidence un effet protecteur de l’ATP extracellulaire ainsi qu’un rôle complémentaire des récepteurs P2 et P1. Les récepteurs P2 impliquent les voies de signalisation PI3K, ERK1/2, le canal mKATP et mettent également en jeu la NOS. La protection médiée par les récepteurs P1 implique les voies MEK/ERK1/2, PKA et NOS. Dans un second temps, nous rapportons un nouveau mécanisme cytoprotecteur du ticagrelor, indépendant des éléments figurés du sang et de son effet antiagrégant plaquettaire. Ce mécanisme est initié par l’augmentation de la biodisponibilité de l’adénosine extracellulaire qui déclenche les effets protecteurs via ses récepteurs A3 et A2A. Ceci peut expliquer, en partie, les effets cardioprotecteurs du ticagrelor décrit chez l’homme. L’ensemble de nos données conforte le rôle protecteur de l’ATP et de l’adénosine vis-à-vis de l’hypoxie au niveau endothélial et suggèrent un rôle bénéfique de ces médiateurs dans diverses ischémies notamment cardiaque, rénale ou cérébrale.

During cardiac ischemia, the lesion is triggered in the endothelium and progresses to the surrounding cardiomyocytes. Purinergic signalling plays an important role during ischemia/reperfusion (I/R) events. Many studies have been carried out to study the mechanisms of protection of nucleotides and nucleosides, without studying their specific roles on the endothelium. In this work, we report an increase in extracellular concentrations of ATP and adenosine from the endothelium exposed to hypoxia. We report a protective effect of extracellular ATP and a complementary role of the P2 and P1 receptors. P2 receptors protective effects involve the PI3K, ERK1/2, mKATP channel signalling and also involve NOS. The protection mediated by the P1 receptors involves the MEK/ERK1/2, PKA and NOS. In a second step, we describe a new cytoprotective mechanism of ticagrelor, independent of the blood element and its antiplatelet anti-aggregating effect. This mechanism is initiated by the increased of extracellular adenosine bioavailability, which triggers protective effects via its A3 and A2A receptors. This may explain, in part, the reported cardioprotective effects of the ticagrelor in clinical studies. Together, our data support the protective role of ATP and adenosine against deleterious effects ofendothelium hypoxia and suggest a beneficial role for these mediators in different ischemia, including cardiac, renal or cerebral ischemia.

Advisors/Committee Members: Millart, Hervé (thesis director).

Subjects/Keywords: Cardioprotection; Cellules endothéliales; Ischémie/reperfusion; Ischemia/reperfusion; Endothelial cells; Cardioprotection

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Feliu, C. (2019). Implication des récepteurs P1 et P2 dans la protection des cellules endothéliales au cours de l’hypoxie-reoxygenation : Involvement of P1 and P2 receptors in the protection of endothelial cells during hypoxia-reoxygenation. (Doctoral Dissertation). Reims. Retrieved from http://www.theses.fr/2019REIMM202

Chicago Manual of Style (16^th Edition):

Feliu, Catherine. “Implication des récepteurs P1 et P2 dans la protection des cellules endothéliales au cours de l’hypoxie-reoxygenation : Involvement of P1 and P2 receptors in the protection of endothelial cells during hypoxia-reoxygenation.” 2019. Doctoral Dissertation, Reims. Accessed March 07, 2021. http://www.theses.fr/2019REIMM202.

MLA Handbook (7^th Edition):

Feliu, Catherine. “Implication des récepteurs P1 et P2 dans la protection des cellules endothéliales au cours de l’hypoxie-reoxygenation : Involvement of P1 and P2 receptors in the protection of endothelial cells during hypoxia-reoxygenation.” 2019. Web. 07 Mar 2021.

Vancouver:

Feliu C. Implication des récepteurs P1 et P2 dans la protection des cellules endothéliales au cours de l’hypoxie-reoxygenation : Involvement of P1 and P2 receptors in the protection of endothelial cells during hypoxia-reoxygenation. [Internet] [Doctoral dissertation]. Reims; 2019. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2019REIMM202.

Council of Science Editors:

Feliu C. Implication des récepteurs P1 et P2 dans la protection des cellules endothéliales au cours de l’hypoxie-reoxygenation : Involvement of P1 and P2 receptors in the protection of endothelial cells during hypoxia-reoxygenation. [Doctoral Dissertation]. Reims; 2019. Available from: http://www.theses.fr/2019REIMM202

University of Florida

15. Kirkby, Kristin. The Effects of Low Level Laser Therapy on Intestinal Ischemia Reperfusion Injury.

Degree: PhD, Veterinary Medical Sciences - Veterinary Medicine, 2012, University of Florida

URL: https://ufdc.ufl.edu/UFE0044834

► Intestinal ischemia reperfusion injury (IRI) in animals andhumans is associated with mortality rates between 50-80%. Various pharmacologicagents have been studied as potential treatments for IRI;… (more)

Subjects/Keywords: Dosage; Ischemia; Laser therapy; Lasers; Lungs; Oxygen; Physical trauma; Rats; Reperfusion; Reperfusion injury; injury – intestine – ischemia – laser – lung – rat – reperfusion – therapy

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kirkby, K. (2012). The Effects of Low Level Laser Therapy on Intestinal Ischemia Reperfusion Injury. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0044834

Chicago Manual of Style (16^th Edition):

Kirkby, Kristin. “The Effects of Low Level Laser Therapy on Intestinal Ischemia Reperfusion Injury.” 2012. Doctoral Dissertation, University of Florida. Accessed March 07, 2021. https://ufdc.ufl.edu/UFE0044834.

MLA Handbook (7^th Edition):

Kirkby, Kristin. “The Effects of Low Level Laser Therapy on Intestinal Ischemia Reperfusion Injury.” 2012. Web. 07 Mar 2021.

Vancouver:

Kirkby K. The Effects of Low Level Laser Therapy on Intestinal Ischemia Reperfusion Injury. [Internet] [Doctoral dissertation]. University of Florida; 2012. [cited 2021 Mar 07]. Available from: https://ufdc.ufl.edu/UFE0044834.

Council of Science Editors:

Kirkby K. The Effects of Low Level Laser Therapy on Intestinal Ischemia Reperfusion Injury. [Doctoral Dissertation]. University of Florida; 2012. Available from: https://ufdc.ufl.edu/UFE0044834

Ruhr Universität Bochum

16. Appukuttan, Avinash. Role of type 10 "soluble" adenylyl cyclase in regulation of apoptosis : relevance to cardiovascular diseases.

Degree: 2012, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-38004

► In der Arbeit wurde die Rolle der intrazellulär lokalisierten löslichen Adenylylcyclase (LAC) bei der Apoptose- Regulation untersucht. Dazu wurden (1) Behandlung mit einem spezifischen Hemmstoff,… (more)

Subjects/Keywords: Ischämie; Reperfusion; Apoptosis; In vitro; Translokation

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APA (6^th Edition):

Appukuttan, A. (2012). Role of type 10 "soluble" adenylyl cyclase in regulation of apoptosis : relevance to cardiovascular diseases. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-38004

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Appukuttan, Avinash. “Role of type 10 "soluble" adenylyl cyclase in regulation of apoptosis : relevance to cardiovascular diseases.” 2012. Thesis, Ruhr Universität Bochum. Accessed March 07, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-38004.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Appukuttan, Avinash. “Role of type 10 "soluble" adenylyl cyclase in regulation of apoptosis : relevance to cardiovascular diseases.” 2012. Web. 07 Mar 2021.

Vancouver:

Appukuttan A. Role of type 10 "soluble" adenylyl cyclase in regulation of apoptosis : relevance to cardiovascular diseases. [Internet] [Thesis]. Ruhr Universität Bochum; 2012. [cited 2021 Mar 07]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-38004.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Appukuttan A. Role of type 10 "soluble" adenylyl cyclase in regulation of apoptosis : relevance to cardiovascular diseases. [Thesis]. Ruhr Universität Bochum; 2012. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-38004

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. 下内, 昭人. 網膜虚血再灌流障害における分散ヘスペレチンの神経保護効果 : Neuroprotective effect of water-dispersible hesperetin in retinal ischemia reperfusion injury.

Degree: 博士（医学）, 2016, Asahikawa Medical University / 旭川医科大学

URL: http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20160325_K492

►

First online: 25 September 2015The final publication is available at Springer via http://dx.doi.org/10.1007/s10384-015-0415-z

PurposeTo determine whether water-dispersible hesperetin (WD-Hpt) can prevent degeneration of ganglion cell… (more)

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First online: 25 September 2015The final publication is available at Springer via http://dx.doi.org/10.1007/s10384-015-0415-z

PurposeTo determine whether water-dispersible hesperetin (WD-Hpt) can prevent degeneration of ganglion cell neurons in the ischemic retina.MethodsIschemia reperfusion (I/R) injury was induced by increasing the intraocular pressure of mice to 110 mmHg for 40 min. Mice received daily intraperitoneal injections with either normal saline (NS, 0.3 ml/day) or WD-Hpt (0.3 ml, 200 mg/kg/day). Reactive oxygen species (ROS) was assessed by dihydroethidium and nitrotyrosine formation. Inflammation was estimated by microglial morphology in the retina. Lipopolysaccharide (LPS)-stimulated BV-2 cells were used to explore the anti-inflammatory effect of WD-Hpt on activated microglia by quantifying the expression of IL-1β using real-time quantitative reverse transcription-polymerase chain reaction. Ganglion cell loss was assessed by immunohistochemistry of NeuN. Glial activation was quantified with glial fibrillary acidic protein (GFAP) immunoreactivity. Apoptosis was evaluated with a terminal deoxynucleotidyl transferase (TUNEL) assay and immunohistochemistry of cleaved caspase-3. Phosphorylation of extracellular signal-regulated kinase (p-ERK) was surveyed by western blotting.ResultsWD-Hpt decreased I/R-induced ROS formation. WD-Hpt alleviated microglial activation induced by I/R and reduced mRNA levels of IL-1β in LPS-stimulated BV-2. I/R resulted in a 37 % reduction in the number of ganglion cells in the NS-treated mice, whereas the reduction was only 5 % in the WD-Hpt-treated mice. In addition, WD-Hpt mitigated the immunoreactivity of GFAP, increased expression of cleaved caspase-3, increased number of TUNEL positive cells and p-ERK after I/R.ConclusionsWD-Hpt protected ganglion cells from I/R injury by inhibiting oxidative stress and modulating cell death signaling. Moreover, WD-Hpt had an anti-inflammatory effect through the suppression of activated microglia.

Subjects/Keywords: Hesperetin; Ischemia–reperfusion; Neuroprotection; Retina; Inflammation

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APA (6^th Edition):

下内, �. (2016). 網膜虚血再灌流障害における分散ヘスペレチンの神経保護効果 : Neuroprotective effect of water-dispersible hesperetin in retinal ischemia reperfusion injury. (Thesis). Asahikawa Medical University / 旭川医科大学. Retrieved from http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20160325_K492

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

下内, 昭人. “網膜虚血再灌流障害における分散ヘスペレチンの神経保護効果 : Neuroprotective effect of water-dispersible hesperetin in retinal ischemia reperfusion injury.” 2016. Thesis, Asahikawa Medical University / 旭川医科大学. Accessed March 07, 2021. http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20160325_K492.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

下内, 昭人. “網膜虚血再灌流障害における分散ヘスペレチンの神経保護効果 : Neuroprotective effect of water-dispersible hesperetin in retinal ischemia reperfusion injury.” 2016. Web. 07 Mar 2021.

Vancouver:

下内 �. 網膜虚血再灌流障害における分散ヘスペレチンの神経保護効果 : Neuroprotective effect of water-dispersible hesperetin in retinal ischemia reperfusion injury. [Internet] [Thesis]. Asahikawa Medical University / 旭川医科大学; 2016. [cited 2021 Mar 07]. Available from: http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20160325_K492.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

下内 �. 網膜虚血再灌流障害における分散ヘスペレチンの神経保護効果 : Neuroprotective effect of water-dispersible hesperetin in retinal ischemia reperfusion injury. [Thesis]. Asahikawa Medical University / 旭川医科大学; 2016. Available from: http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20160325_K492

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. 畑地, 豪. The Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor PJ34 Reduces Pulmonary Ischemia-Reperfusion Injury in Rats : ポリADPリボースポリメレース阻害薬(PJ34)はラットにおける肺虚血再灌流障害を軽減する.

Degree: 博士(医学), 2014, Nagasaki University / 長崎大学

URL: http://hdl.handle.net/10069/35827

► Background: Ischemia-reperfusion (I/R) injury after lung transplantation causes alveolar damage, lung edema, and acute rejection. Poly(adenosine diphosphate-ribose) polymerase (PARP) is a single-stranded DNA repair enzyme… (more)

Subjects/Keywords: Ischemia-reperfusion injury; PARP inhibitor; PJ34; Antioxidants

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APA (6^th Edition):

畑地, �. (2014). The Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor PJ34 Reduces Pulmonary Ischemia-Reperfusion Injury in Rats : ポリADPリボースポリメレース阻害薬(PJ34)はラットにおける肺虚血再灌流障害を軽減する. (Thesis). Nagasaki University / 長崎大学. Retrieved from http://hdl.handle.net/10069/35827

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

畑地, 豪. “The Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor PJ34 Reduces Pulmonary Ischemia-Reperfusion Injury in Rats : ポリADPリボースポリメレース阻害薬(PJ34)はラットにおける肺虚血再灌流障害を軽減する.” 2014. Thesis, Nagasaki University / 長崎大学. Accessed March 07, 2021. http://hdl.handle.net/10069/35827.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

畑地, 豪. “The Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor PJ34 Reduces Pulmonary Ischemia-Reperfusion Injury in Rats : ポリADPリボースポリメレース阻害薬(PJ34)はラットにおける肺虚血再灌流障害を軽減する.” 2014. Web. 07 Mar 2021.

Vancouver:

畑地 �. The Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor PJ34 Reduces Pulmonary Ischemia-Reperfusion Injury in Rats : ポリADPリボースポリメレース阻害薬(PJ34)はラットにおける肺虚血再灌流障害を軽減する. [Internet] [Thesis]. Nagasaki University / 長崎大学; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10069/35827.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

畑地 �. The Poly(Adenosine Diphosphate-Ribose) Polymerase Inhibitor PJ34 Reduces Pulmonary Ischemia-Reperfusion Injury in Rats : ポリADPリボースポリメレース阻害薬(PJ34)はラットにおける肺虚血再灌流障害を軽減する. [Thesis]. Nagasaki University / 長崎大学; 2014. Available from: http://hdl.handle.net/10069/35827

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. Gory, Benjamin. Caractérisation IRM d’un modèle murin d’ischémie-reperfusion cérébrale induit par cathétérisme de l’artère cérébrale moyenne et évaluation du post-conditionnement à la Cyclosporine A : MRI characterization of brain ischemia-reperfusion model induced by middle cerebral artery catheterization in rat and evaluation of Cyclosporine A postconditioning.

Degree: Docteur es, Neurosciences, 2016, Lyon

URL: http://www.theses.fr/2016LYSE1208

► La reperfusion complète et précoce est le moyen le plus efficace pour limiter l'extension de l'infarctus cérébral et les séquelles neurologiques. Le traitement de l'infarctus… (more)

▼ La reperfusion complète et précoce est le moyen le plus efficace pour limiter l'extension de l'infarctus cérébral et les séquelles neurologiques. Le traitement de l'infarctus cérébral a été révolutionné par la thrombectomie mécanique intra-artérielle en permettant une recanalisation dans plus de 70% des cas et une réduction significative de la morbidité comparativement à la thrombolyse seule pour le territoire carotidien. Le pronostic des occlusions basilaires reste dramatique et aucun essai n'a démontré le bénéfice de l'approche intra-artérielle à l'heure actuelle. Dans la première partie du travail, nous avons réalisé une méta-analyse sur la thrombectomie par «stent-retriever» des occlusions basilaires, à partir des résultats publiés dans MEDLINE entre novembre 2010 et avril 2014: recanalisation angiographique (TICI≥2b)=81% (IC 95%: 73-87); hémorragie cérébrale symptomatique à 24 heures=4% (IC 95%: 2-8); évolution neurologique favorable (mRS≤2 à 3 mois)=42% (IC 95%: 36-48); mortalité=30% (IC 95%: 25-36). L'approche intra-artérielle ouvre une nouvelle ère thérapeutique, cependant un modèle animal adapté et pertinent est nécessaire pour l'évaluation pré-clinique. Dans la deuxième partie du travail, nous avons caractérisé l'évolution spatio-temporelle précoce de l'infarctus par IRM multimodale dans un modèle d'ischémie cérébrale focale transitoire réalisé par occlusion sélective intra-artérielle de l'artère cérébrale moyenne chez le rat adulte. Une occlusion complète de l'artère cérébrale moyenne proximale était observée dans 75% des 16 rats opérés, et un mismatch diffusion/perfusion dans 77% des cas. Le volume ischémique durant l'occlusion artérielle, définie sur la séquence de diffusion, était de 90±64 mm3 et de 57±67 mm3 à 24 heures sur la séquence T2. La recanalisation artérielle s'associe à une reperfusion tissulaire dans 36% des cas. L'hypoperfusion persistait chez la majorité des animaux 3 heures après recanalisation. L'infarctus était de localisation cortical dans 31%, striatale dans 25%, et cortico-striatale dans 44%. Tous les animaux étaient en vie à 24 heures confirmant le caractère mini-invasif de ce modèle. Bien que la reperfusion sauve incontestablement une partie du parenchyme ischémique, elle s'accompagne également de lésions irréversibles spécifiques, dites de reperfusion, s'ajoutant aux lésions initiales. Limiter l'importance des lésions de reperfusion représente un objectif thérapeutique majeur. Dans la troisième partie, nous avons testé l'effet neuroprotecteur de la Cyclosporine A sur la réduction du volume de l'infarctus cérébral et sur le pronostic clinique. Une procédure d'ischémie reperfusion cérébrale de 60 minutes a été réalisée chez 48 animaux, puis ont été randomisés en quatre groupes (groupe témoin, pré-conditionnement, postconditionnement intraveineux et intra-artériel avec la Cyclosporine A à la dose de 10 mg/kg dans les 30 secondes suivant la reperfusion). Sur les 43 animaux inclus dans l'analyse, il n'a pas été observé de réduction du volume ischémique ni une amélioration du pronostic… Advisors/Committee Members: Turjman, Francis (thesis director).

Subjects/Keywords: Infarctus cérébral; Thrombectomie; Reperfusion; Recanalisation artérielle; Lésions de reperfusion; Cyclosporine A; Neuroprotection; Post-conditionnement; Ischemic stroke; Thrombectomy; Reperfusion; Arterial recanalization; Reperfusion injuries; Cyclosporine A; Neuroprotection; Postconditioning; 612.8

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gory, B. (2016). Caractérisation IRM d’un modèle murin d’ischémie-reperfusion cérébrale induit par cathétérisme de l’artère cérébrale moyenne et évaluation du post-conditionnement à la Cyclosporine A : MRI characterization of brain ischemia-reperfusion model induced by middle cerebral artery catheterization in rat and evaluation of Cyclosporine A postconditioning. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2016LYSE1208

Chicago Manual of Style (16^th Edition):

Gory, Benjamin. “Caractérisation IRM d’un modèle murin d’ischémie-reperfusion cérébrale induit par cathétérisme de l’artère cérébrale moyenne et évaluation du post-conditionnement à la Cyclosporine A : MRI characterization of brain ischemia-reperfusion model induced by middle cerebral artery catheterization in rat and evaluation of Cyclosporine A postconditioning.” 2016. Doctoral Dissertation, Lyon. Accessed March 07, 2021. http://www.theses.fr/2016LYSE1208.

MLA Handbook (7^th Edition):

Gory, Benjamin. “Caractérisation IRM d’un modèle murin d’ischémie-reperfusion cérébrale induit par cathétérisme de l’artère cérébrale moyenne et évaluation du post-conditionnement à la Cyclosporine A : MRI characterization of brain ischemia-reperfusion model induced by middle cerebral artery catheterization in rat and evaluation of Cyclosporine A postconditioning.” 2016. Web. 07 Mar 2021.

Vancouver:

Gory B. Caractérisation IRM d’un modèle murin d’ischémie-reperfusion cérébrale induit par cathétérisme de l’artère cérébrale moyenne et évaluation du post-conditionnement à la Cyclosporine A : MRI characterization of brain ischemia-reperfusion model induced by middle cerebral artery catheterization in rat and evaluation of Cyclosporine A postconditioning. [Internet] [Doctoral dissertation]. Lyon; 2016. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2016LYSE1208.

Council of Science Editors:

Gory B. Caractérisation IRM d’un modèle murin d’ischémie-reperfusion cérébrale induit par cathétérisme de l’artère cérébrale moyenne et évaluation du post-conditionnement à la Cyclosporine A : MRI characterization of brain ischemia-reperfusion model induced by middle cerebral artery catheterization in rat and evaluation of Cyclosporine A postconditioning. [Doctoral Dissertation]. Lyon; 2016. Available from: http://www.theses.fr/2016LYSE1208

University of Alberta

20. Qadhi, Rawabi. Docosahexaenoic Acid Induced Apoptosis In H9c2 Cells And Changed Cardiac Function After Ischemia-Reperfusion Injury.

Degree: MS, Faculty of Pharmacy and Pharmaceutical Sciences, 2013, University of Alberta

URL: https://era.library.ualberta.ca/files/fx719m76s

► Cardiovascular disease (CVD) remains one of the leading causes of death worldwide. As such, a vast amount of research has investigated novel therapies for preventing… (more)

▼ Cardiovascular disease (CVD) remains one of the leading causes of death worldwide. As such, a vast amount of research has investigated novel therapies for preventing and/or reducing CVD. Much evidence has demonstrated the importance of dietary composition in increasing or lowering risks of CVD. While the role played by dietary n-3 polyunsaturated fatty acids (PUFAs) in reducing CVD has been recognized for many years, the protective mechanisms of these molecules, notably toward ischemia-reperfusion (IR) injury, remain unknown. Ecosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3, DHA) are two of the most important n-3 PUFAs. Both are present in fish oil. The objective of this study is to investigate the effect of acute administration of DHA on IR injury. Methods: Hearts from male C57BL6 mice were isolated and perfused in Langendorff mode and then subjected to IR injury. Hearts were perfused with different concentrations of DHA (0, 10, 50 and 100 µM) to determine its effect on cardiac function and recovery. Mechanistic studies were performed using rat myoblast cells (H9c2 cells) in an anoxia-reoxygenation protocol. Cell viability (MTT assay), cytochrome c release, and caspase-3 and caspase-8 activities were measured to compare cellular injury in DHA treated cells versus controls. The impact of DHA on mitochondrial morphology and function was assessed using epifluorescent microscopy. Results: Data demonstrated that DHA has adverse effects on both pre- and post-ischemic left ventricular developed pressures and on the heart rate, systolic and diastolic heart rates. Cell experiments revealed that significant cell death occurs in a concentration-dependent manner when H9c2 cells are treated with DHA and subjected to anoxia-reoxygenation injury. Moreover, apoptotic cell death is caused by DHA treatment, during which cytochrome c is released and caspases-8 and -3 are activated. Significant mitochondrial fragmentation and loss of membrane potential were observed with high concentrations of DHA. Conclusion: Our data suggest that acute treatment with DHA impedes the function of isolated hearts and triggers apoptotic cell death.

Subjects/Keywords: H9c2 cells; Apoptosis; DHA; Ischemia/reperfusion injury

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Qadhi, R. (2013). Docosahexaenoic Acid Induced Apoptosis In H9c2 Cells And Changed Cardiac Function After Ischemia-Reperfusion Injury. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/fx719m76s

Chicago Manual of Style (16^th Edition):

Qadhi, Rawabi. “Docosahexaenoic Acid Induced Apoptosis In H9c2 Cells And Changed Cardiac Function After Ischemia-Reperfusion Injury.” 2013. Masters Thesis, University of Alberta. Accessed March 07, 2021. https://era.library.ualberta.ca/files/fx719m76s.

MLA Handbook (7^th Edition):

Qadhi, Rawabi. “Docosahexaenoic Acid Induced Apoptosis In H9c2 Cells And Changed Cardiac Function After Ischemia-Reperfusion Injury.” 2013. Web. 07 Mar 2021.

Vancouver:

Qadhi R. Docosahexaenoic Acid Induced Apoptosis In H9c2 Cells And Changed Cardiac Function After Ischemia-Reperfusion Injury. [Internet] [Masters thesis]. University of Alberta; 2013. [cited 2021 Mar 07]. Available from: https://era.library.ualberta.ca/files/fx719m76s.

Council of Science Editors:

Qadhi R. Docosahexaenoic Acid Induced Apoptosis In H9c2 Cells And Changed Cardiac Function After Ischemia-Reperfusion Injury. [Masters Thesis]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/fx719m76s

21. Güney, Türkan. Fukoidin’in rat aortik iskemi reperfüzyon modelinde böbrek ve akciğerler üzerine etkisi .

Degree: ESOGÜ, Tıp Fakültesi, Tıbbi Biyokimya, 2015, Eskisehir Osmangazi University

URL: http://hdl.handle.net/11684/631

► Aort cerrahisinde abdominal aortun klemplenmesi ile oluşan iskemide birçok dokuda uzak organ hasarı meydana gelmektedir. Bu çalışmada fukoidinin rat aortik iskemi reperfüzyon modelinde böbrek ve… (more)

▼ Aort cerrahisinde abdominal aortun klemplenmesi ile oluşan iskemide birçok dokuda uzak organ hasarı meydana gelmektedir. Bu çalışmada fukoidinin rat aortik iskemi reperfüzyon modelinde böbrek ve akciğerler üzerine etkisini araştırdık. Çalışmamızda 40 tane Wistar türü erkek sıçan, her grupta 8 tane olacak şekilde Grup 1 (Sham), Grup 2 (Kontrol), Grup 3 (İskemi öncesi) (İÖ), Grup 4 (Reperfüzyon öncesi) (RÖ), Grup 5 (Hem iskemi hem reperfüzyon öncesi) (İRÖ) olmak üzere 5 gruba ayrıldı. Sham grubuna, sadece laparotomi uygulandı. Diğer gruplara laparotomi ve infrarenal aortik iskemi reperfüzyon (AİR) uygulandı ( 120 dakika iskemi ardından 120 dakika reperfüzyon). İÖ iskemiden 10 dak. önce juguler venden 25mg/kg fukoidin verildi. RÖ grubuna, reperfüzyondan 10 dak. önce juguler venden 25mg/kg fukoidin verildi. İRÖ grubuna, iskemiden 10 dak. önce 12,5mg/kg ve reperfüzyondan 10 dak. önce 12,5mg/kg olmak üzere juguler venden toplam 25mg/kg fukoidin verildi. İşlemlerden sonra tüm hayvanlardan kan, böbrek ve akciğer dokuları alınarak sakrifiye edildi. Plazmada protein karbonil (PCO), protein sülfidril (P-SH) ve kitotriozidaz (CHIT), serumda iskemi modifiye albümin (İMA), kan üre azotu (BUN), kreatinin, malondialdehit (MDA), nitrik oksit (NO), myeloperoksidaz (MPO), böbrek ve akciğer doku örneklerinde, MDA, NO, MPO, katalaz (CAT) düzeyleri biyokimyasal olarak ölçüldü ve histolojik olarak doku örnekleri hemotoksilen-eosin boya ile boyanarak ışık mikroskobu ile değerlendirildi. Kontrol grubu ile RÖ ve İRÖ karşılaştırıldığında; PCO, CHIT, İMA, BUN, kreatinin, MDA, NO, MPO, CAT da istatistiksel olarak anlamlı azalma gözlenirken, P-SH grubunda istatistiksel olarak anlamlı artma olduğunu belirledik. Kontrol grubu ile İÖ grubu arasında ise istatistiksel olarak anlamlılık bulunmadı. Böbrek dokusu, kontrol grubu ile Grup 4 ve Grup 5 histoloji yönünden (fokal glomeruler nekroz, bowman kapsül dilatasyonu, tubuler epitel dejenerasyonu, tubuler epitel nekrozu, tubuler dilatasyon, interstisiyel inflamatuar infiltrasyon) değerlendirildiğinde toplam skorlara göre anlamlı azalma bulundu. Kontrol grubu ile İÖ grubu arasında ise istatistiksel olarak anlamlılık bulunmadı. Akciğer dokusu, kontrol grubu ile RÖ ve İRÖ grubu histoloji yönünden (fibrin platelet trombüs varlığı, kronik inflamasyon, intra alveolar kanama, ödem, konjesyon, PMNL) değerlendirildiğinde toplam skorlara göre anlamlı azalma bulundu. Kontrol grubu ile İÖ grubu arasında ise istatistiksel olarak anlamlılık bulunmadı. Aortaya infrarenal kros-klempin konması iskemi-reperfüzyonuna bağlı olarak böbreklerde ve akciğerde uzak organ hasarı meydana getirmiş ve fukoidinin reperfüzyondan önce uygulanması bu hasarı azalttı. Fukoidinin iskemi öncesi uygulamasında ise, iskemi de kan akışının tamamen durması nedeni ile, nötrofil infiltrasyonu ve serbest oksijen radikal hasarı meydana gelmediğinden, iskemi reperfüzyon hasarı üzerine koruyucu etki göstermedi. Fukoidinin reperfüzyon hasarından önce verilmesinin iskemi reperfüzyon hasarına karşı koruyucu… Advisors/Committee Members: Akyüz, Fahrettin (advisor).

Subjects/Keywords: İskemi/Reperfüzyon; Fukoidin; Ischemia; Reperfusion; Fucoidin

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Güney, T. (2015). Fukoidin’in rat aortik iskemi reperfüzyon modelinde böbrek ve akciğerler üzerine etkisi . (Thesis). Eskisehir Osmangazi University. Retrieved from http://hdl.handle.net/11684/631

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Güney, Türkan. “Fukoidin’in rat aortik iskemi reperfüzyon modelinde böbrek ve akciğerler üzerine etkisi .” 2015. Thesis, Eskisehir Osmangazi University. Accessed March 07, 2021. http://hdl.handle.net/11684/631.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Güney, Türkan. “Fukoidin’in rat aortik iskemi reperfüzyon modelinde böbrek ve akciğerler üzerine etkisi .” 2015. Web. 07 Mar 2021.

Vancouver:

Güney T. Fukoidin’in rat aortik iskemi reperfüzyon modelinde böbrek ve akciğerler üzerine etkisi . [Internet] [Thesis]. Eskisehir Osmangazi University; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/11684/631.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Güney T. Fukoidin’in rat aortik iskemi reperfüzyon modelinde böbrek ve akciğerler üzerine etkisi . [Thesis]. Eskisehir Osmangazi University; 2015. Available from: http://hdl.handle.net/11684/631

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queens University

22. Lafreniere, Gina. mRNA Variants of a Neuronal Sodium Channel in Rat Cardiac Myocytes .

Degree: Physiology, 2015, Queens University

URL: http://hdl.handle.net/1974/12682

► Death due to ischemic heart disease (IHD) is the result of cardiac arrhythmias and loss of cardiac pump function. One of the putative underlying mechanisms… (more)

▼ Death due to ischemic heart disease (IHD) is the result of cardiac arrhythmias and loss of cardiac pump function. One of the putative underlying mechanisms is impaired inactivation of voltage-gated sodium channels (VGSC), resulting in small persistent sodium currents. Nine VGSC (NaV1.1-NaV1.9) have been cloned and functionally expressed. Electrophysiological/pharmacological evidence suggests that “neuronal” isoform(s) exist in cardiomyocytes along with the cardiac-dominant NaV1.5. Given that persistent currents have been shown to be fundamental to the function of neuronal isoforms and that pharmacological evidence suggests that neuronal VGSC underlie increases in persistent currents during ischemic events, we hypothesized that neuronal VGSC are present in cardiomyocytes. Specifically, the purpose of this study was to demonstrate that the neuronal VGSC NaV1.1 exists in rat right ventricular myocytes. The full-length NaV1.1 coding sequence was cloned in overlapping segments. Through sequencing, we identified one amino acid difference from a published brain sequence (c.2935A>G) and four deletion variants (c.[del266_473], c.[del2012_2044], c.[del4004_4258], and c.[del4003_4284]). The deletion variants were not present in all sequenced amplicons. Deletions at the first and the third deletion sites were of particular interest as these involved regions of conserved sequence, likely essential to channel function. To explore this further, PCR primers were designed to amplify a partial transcript spanning both of these regions. Three RT-PCR bands were produced: 1) an ~4500 bp band that is likely a composite of two amplicons, one with a deletion at the first deletion site (c.[del266_473]) and one with a deletion at the third deletion site (either c.[del4004_4258] or c.[del4003_4284]); 2) an ~4200 bp band confirmed to contain an amplicon with a deletion at both the first and the third deletion sites (either c.[del266_473] and c.[del4004_4258], or c.[del266_473] and c.[del4003_4284]); and 3) an ~4075 bp band suggesting further unidentified deletion variants. We were unable to identify any amplicons that did not contain at least one deletion involving conserved sequence. Overall, these results demonstrate that multiple sequence variances of NaV1.1 exist in adult rat cardiomyocytes. Moreover it appears that under normal cellular conditions, at least one deletion that is likely to be devastating to channel function is always present.

Subjects/Keywords: Ischemia/Reperfusion ; Heart ; Voltage Gated Sodium Channels

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lafreniere, G. (2015). mRNA Variants of a Neuronal Sodium Channel in Rat Cardiac Myocytes . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/12682

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lafreniere, Gina. “mRNA Variants of a Neuronal Sodium Channel in Rat Cardiac Myocytes .” 2015. Thesis, Queens University. Accessed March 07, 2021. http://hdl.handle.net/1974/12682.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lafreniere, Gina. “mRNA Variants of a Neuronal Sodium Channel in Rat Cardiac Myocytes .” 2015. Web. 07 Mar 2021.

Vancouver:

Lafreniere G. mRNA Variants of a Neuronal Sodium Channel in Rat Cardiac Myocytes . [Internet] [Thesis]. Queens University; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1974/12682.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lafreniere G. mRNA Variants of a Neuronal Sodium Channel in Rat Cardiac Myocytes . [Thesis]. Queens University; 2015. Available from: http://hdl.handle.net/1974/12682

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Newcastle

23. Lin, Longting. Whole-brain CTP in acute ischemic stroke.

Degree: PhD, 2015, University of Newcastle

URL: http://hdl.handle.net/1959.13/1310399

►

Research Doctorate - Doctor of Philosophy (PhD)

Perfusion imaging technology not only enables stroke diagnosis by identifying the ischemic lesion earlier, but also helps the… (more)

▼

Research Doctorate - Doctor of Philosophy (PhD)

Perfusion imaging technology not only enables stroke diagnosis by identifying the ischemic lesion earlier, but also helps the clinician to make treatment decisions by further classifying the ischemic lesion into salvageable tissue and non-salvageable tissue. The imaging of salvageable tissue, penumbra, provides a direct target for reperfusion treatment. However, the accuracy of penumbra measurement with perfusion imaging has been questioned, especially with CT perfusion (CTP). Perfusion images, acquired on earlier generation instruments such as the16 or 64-detector scanners, have limited coverage of potentially ischemic brain, a factor recognised to reduce the accuracy of penumbra measurement. This limitation can be overcome by the advance in technology. The new generation “mega-detector” scanners, such as 320-detector Toshiba Aquilion One, provide whole brain coverage of 160mm from skull base to vertex. In this thesis, I presented a series of studies aiming to evaluate the utility of whole-brain CTP in acute ischemic stroke. The first study was to derive the optimal penumbra measurement on whole-brain CTP with the reference of ischemic tissue outcome, and the second study was to test the penumbra measurement of whole-brain CTP in predicting clinical patient outcome. The two studies found that only with the threshold setting at Tmax>6s or DT>3s, did the whole-brain CTP achieve high accuracy (>99%) in delineating acute ischemic penumbra and good sensitivity (>80%) in predicting favourable clinical outcome. It was also confirmed that the accuracy of penumbra measurement was comprised when the brain coverage of CTP decreased from 160mm to 20mm. Following two studies examined the utility of whole-brain CTP in the clinical setting. Firstly, CTP was compared to MRP, the perfusion modality that has already been well used in clinic. This work demonstrated that with whole brain coverage, CTP was as effective as MPR in measuring the acute penumbra and in selecting patients for reperfusion treatment. Secondly, a case by case review was carried out to assist clinicians in the interpretation CTP output. In conclusion, findings of this thesis support the usage of whole-brain CTP in acute ischemic stroke. Noticeably, the conclusion only applies to patients with anterior circulation stroke. Whole-brain CTP might also have advantage in detecting ischemic lesions in posterior circulation territory, which require studies to prove it in the future.

Advisors/Committee Members: University of Newcastle. Faculty of Health & Medicine, School of Medicine and Public Health.

Subjects/Keywords: CT perfusion; ischemic stroke; penumbra; reperfusion

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lin, L. (2015). Whole-brain CTP in acute ischemic stroke. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1310399

Chicago Manual of Style (16^th Edition):

Lin, Longting. “Whole-brain CTP in acute ischemic stroke.” 2015. Doctoral Dissertation, University of Newcastle. Accessed March 07, 2021. http://hdl.handle.net/1959.13/1310399.

MLA Handbook (7^th Edition):

Lin, Longting. “Whole-brain CTP in acute ischemic stroke.” 2015. Web. 07 Mar 2021.

Vancouver:

Lin L. Whole-brain CTP in acute ischemic stroke. [Internet] [Doctoral dissertation]. University of Newcastle; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1959.13/1310399.

Council of Science Editors:

Lin L. Whole-brain CTP in acute ischemic stroke. [Doctoral Dissertation]. University of Newcastle; 2015. Available from: http://hdl.handle.net/1959.13/1310399

University of Toronto

24. Chaturvedi, Swasti. SLIT2 Prevents Renal Ischemia Reperfusion Injury in Mice.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/42902

►

The Slit family of secreted proteins act as axonal repellents during embryogenesis. Slit2 via its receptor, Roundabout-1, also inhibits chemotaxis of multiple leukocyte subsets. Using… (more)

Subjects/Keywords: acute kidney injury; ischaemia-reperfusion injury; 0379

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chaturvedi, S. (2012). SLIT2 Prevents Renal Ischemia Reperfusion Injury in Mice. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/42902

Chicago Manual of Style (16^th Edition):

Chaturvedi, Swasti. “SLIT2 Prevents Renal Ischemia Reperfusion Injury in Mice.” 2012. Masters Thesis, University of Toronto. Accessed March 07, 2021. http://hdl.handle.net/1807/42902.

MLA Handbook (7^th Edition):

Chaturvedi, Swasti. “SLIT2 Prevents Renal Ischemia Reperfusion Injury in Mice.” 2012. Web. 07 Mar 2021.

Vancouver:

Chaturvedi S. SLIT2 Prevents Renal Ischemia Reperfusion Injury in Mice. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1807/42902.

Council of Science Editors:

Chaturvedi S. SLIT2 Prevents Renal Ischemia Reperfusion Injury in Mice. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/42902

University of Toronto

25. Rohailla, Sagar. A Langendorff-perfused Mouse Heart Model for Delayed Remote Limb Ischemic Preconditioning Studies.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/33511

►

Remote ischemic preconditioning (rIPC) through transient limb ischemia induces potent cardioprotection against ischemia reperfusion (IR) injury. I examined the delayed phase of protection that appears… (more)

Subjects/Keywords: Ischemia Reperfusion; Myocardial Infarction; Cardiology; Preconditioning; 0719

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rohailla, S. (2012). A Langendorff-perfused Mouse Heart Model for Delayed Remote Limb Ischemic Preconditioning Studies. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/33511

Chicago Manual of Style (16^th Edition):

Rohailla, Sagar. “A Langendorff-perfused Mouse Heart Model for Delayed Remote Limb Ischemic Preconditioning Studies.” 2012. Masters Thesis, University of Toronto. Accessed March 07, 2021. http://hdl.handle.net/1807/33511.

MLA Handbook (7^th Edition):

Rohailla, Sagar. “A Langendorff-perfused Mouse Heart Model for Delayed Remote Limb Ischemic Preconditioning Studies.” 2012. Web. 07 Mar 2021.

Vancouver:

Rohailla S. A Langendorff-perfused Mouse Heart Model for Delayed Remote Limb Ischemic Preconditioning Studies. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1807/33511.

Council of Science Editors:

Rohailla S. A Langendorff-perfused Mouse Heart Model for Delayed Remote Limb Ischemic Preconditioning Studies. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/33511

University of Toronto

26. Kwong, Wilson. Effect of Selective/Non-selective COX Inhibition on Rosuvastatin-Mediated Protection from Ischemia-reperfusion Induced Endothelial Dysfunction in the Human Forearm Vasculature.

Degree: 2011, University of Toronto

URL: http://hdl.handle.net/1807/29586

►

Statins can act as preconditioning agents against ischemia reperfusion (IR)-injury through a mechanism involving cyclooxygenase (COX)-2 and the upregulation of prostaglandin synthesis. The following study… (more)

Subjects/Keywords: statin; ischemia reperfusion injury; preconditioning; cox; 0419

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kwong, W. (2011). Effect of Selective/Non-selective COX Inhibition on Rosuvastatin-Mediated Protection from Ischemia-reperfusion Induced Endothelial Dysfunction in the Human Forearm Vasculature. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/29586

Chicago Manual of Style (16^th Edition):

Kwong, Wilson. “Effect of Selective/Non-selective COX Inhibition on Rosuvastatin-Mediated Protection from Ischemia-reperfusion Induced Endothelial Dysfunction in the Human Forearm Vasculature.” 2011. Masters Thesis, University of Toronto. Accessed March 07, 2021. http://hdl.handle.net/1807/29586.

MLA Handbook (7^th Edition):

Kwong, Wilson. “Effect of Selective/Non-selective COX Inhibition on Rosuvastatin-Mediated Protection from Ischemia-reperfusion Induced Endothelial Dysfunction in the Human Forearm Vasculature.” 2011. Web. 07 Mar 2021.

Vancouver:

Kwong W. Effect of Selective/Non-selective COX Inhibition on Rosuvastatin-Mediated Protection from Ischemia-reperfusion Induced Endothelial Dysfunction in the Human Forearm Vasculature. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/1807/29586.

Council of Science Editors:

Kwong W. Effect of Selective/Non-selective COX Inhibition on Rosuvastatin-Mediated Protection from Ischemia-reperfusion Induced Endothelial Dysfunction in the Human Forearm Vasculature. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/29586

27. Benhabbouche, Souhila. Protection du cœur ischémique au cours de la reperfusion par le post-conditionnement et la basse pression : Protection of ischemic heart at reperfusion by post conditioning and low pressure reperfusion.

Degree: Docteur es, Physiologie cardiovasculaire, 2011, Université Claude Bernard – Lyon I

URL: http://www.theses.fr/2011LYO10263

►

Bien qu’il ait prouvé son efficacité dans différentes espèces (lapin, porc, souris,…) ainsi que dans différents organes (rein, foie coeur, poumon,…), le Postconditionnement (PostC) peut… (more)

▼

Bien qu’il ait prouvé son efficacité dans différentes espèces (lapin, porc, souris,…) ainsi que dans différents organes (rein, foie coeur, poumon,…), le Postconditionnement (PostC) peut être limité par plusieurs facteurs. Parmi les limites du Post C, on note la nécessité de son application à l’initiation de la reperfusion. L’objectif de notre travail était d’évaluer la protection induite par la Basse pression de reperfusion (BP) après un décalage temporel de son application et d’étudier les principales fonctions mitochondriales connues pour être impliquées dans la cardioprotection. Nos résultats nous ont permis de démontrer que, contrairement au PostC, la BP pouvait s’appliquer avec succès même après un décalage temporel de 10 minutes après le début de la reperfusion. Cette protection décalée est en lien avec les fonctions mitochondriales, en particulier, l’inhibition du pore de transition de perméabilité mitochondriale (PTPm). L’utilisation de la cyclosporine A (CsA), puissant inhibiteur de l’ouverture du PTPm, permet également de décaler de 10 minutes la manœuvre de protection à la reperfusion dans le modèle de coeur isolé perfusé de rat. Le PostC, comme la BP, utilise deux sources de production de NO (NOS et Xanthine oxydase reductase) pour induire la cardioprotection. Ces résultats nous semblent importants dans le sens où ils proposent une nouvelle fenêtre thérapeutique pour combattre les dégâts liés à l’ischémie/reperfusion, la BP

Although its efficacy in various species (rabbit, pig, mouse,…) and various organs (kidney, liver heart, lung), Postconditioning (PostC) can be limited by many factors such as the necessity of its application in the initiation of the reperfusion. The objective of our work was to evaluate the protection by low pressure reperfusion (LPR) with delayed intervention at reperfusion and to study the mitochondrial functions which are known to be involved in the cardioprotection. Our results showed that, contrary to PostC, LPR can protect until 10 minutes of its delayed intervention at reperfusion. This delayed protection is in correlation with mitochondrial functions, particularly, inhibition of mitochondrial transition pore (PTPm). Cyclosporine, inhibitor of PTPm, has also shown protection until 10 minutes of delayed intervention, on isolated heart rat model. PostC, like LPR, use tow sources of prodution of NO (NOS and Xanthine oxydase reductase). These results seem, to us, very important because they propose LPR as a new therapeutic window to reduce ischemia/reperfusion injury

Advisors/Committee Members: Ferrera, René (thesis director).

Subjects/Keywords: Ischémie-reperfusion; Cardioprotection; Basse pression de reperfusion; Postconditionnement; Mitochondrie; PTPm; Cœur isolé de rat; Ischemia-reperfusion; Cardioprotection; Low pressure of reperfusion; Postconditioning; Mitochondria; PTPm; Isolated heart rat; 616.123

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Benhabbouche, S. (2011). Protection du cœur ischémique au cours de la reperfusion par le post-conditionnement et la basse pression : Protection of ischemic heart at reperfusion by post conditioning and low pressure reperfusion. (Doctoral Dissertation). Université Claude Bernard – Lyon I. Retrieved from http://www.theses.fr/2011LYO10263

Chicago Manual of Style (16^th Edition):

Benhabbouche, Souhila. “Protection du cœur ischémique au cours de la reperfusion par le post-conditionnement et la basse pression : Protection of ischemic heart at reperfusion by post conditioning and low pressure reperfusion.” 2011. Doctoral Dissertation, Université Claude Bernard – Lyon I. Accessed March 07, 2021. http://www.theses.fr/2011LYO10263.

MLA Handbook (7^th Edition):

Benhabbouche, Souhila. “Protection du cœur ischémique au cours de la reperfusion par le post-conditionnement et la basse pression : Protection of ischemic heart at reperfusion by post conditioning and low pressure reperfusion.” 2011. Web. 07 Mar 2021.

Vancouver:

Benhabbouche S. Protection du cœur ischémique au cours de la reperfusion par le post-conditionnement et la basse pression : Protection of ischemic heart at reperfusion by post conditioning and low pressure reperfusion. [Internet] [Doctoral dissertation]. Université Claude Bernard – Lyon I; 2011. [cited 2021 Mar 07]. Available from: http://www.theses.fr/2011LYO10263.

Council of Science Editors:

Benhabbouche S. Protection du cœur ischémique au cours de la reperfusion par le post-conditionnement et la basse pression : Protection of ischemic heart at reperfusion by post conditioning and low pressure reperfusion. [Doctoral Dissertation]. Université Claude Bernard – Lyon I; 2011. Available from: http://www.theses.fr/2011LYO10263

Robert Gordon University

28. Hair, Steven C. Determining the role of the LPI/GPR55 system in the development of obesity and associated cardiovascular consequences.

Degree: PhD, 2018, Robert Gordon University

URL: https://rgu-repository.worktribe.com/output/248960 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.758179

► Obesity has reached worldwide epidemic proportions and with this increased incidence of obesity, comes an increase in incidence of the comorbidities associated with obesity such… (more)

▼ Obesity has reached worldwide epidemic proportions and with this increased incidence of obesity, comes an increase in incidence of the comorbidities associated with obesity such as diabetes and cardiovascular disease (CVD). The underlying mechanisms which connect these diseases are still poorly understood. One system which has been shown to be up-regulated in the setting of obesity and diabetes is that of the G-protein coupled receptor-55/Lysophosphatidylinositol (GPR55/LPI). Despite being upregulated in the setting of obesity, the function of GPR55 in obesity and other disease states remains elusive. Therefore, the present study aimed to 1) investigate the role of GPR55 in obesity by characterising the phenotype of the GPR55 knockout (GPR55-/-) mouse when challenged with a high fat diet (HFD) intervention, 2) elucidate any effect of the GPR55 knockout and HFD intervention on the myocardial infarct size sustained following a period of ischaemia/reperfusion (I/R) and 3) make use of an in vitro model to elucidate the mechanisms by which changes occur in the adipose tissue of mice fed a HFD. GPR55-/- mice fed a HFD for 12-weeks gained significantly more weight in the form of fat mass, compared to wild-type (WT) controls and consequently become obese. Obese GPR55-/- mice displayed hypertrophic adipose tissue concurrent with the significant dysregulation of plasma lipids, increases in specific circulating LPI species, increased lipid deposition within the liver and a change in adipose tissue gene expression profile. These changes were not observed in GPR55-/- mice fed a standard diet or WT mice fed a HFD. Following a period of I/R, the myocardial infarct size in hearts from WT HFD fed mice was significantly smaller than in hearts from WT standard diet fed mice. This reduction in infarct size due to HFD intervention was not dependent on RISK-pathway activation and was not observed in hearts from GPR55-/- mice, therefore demonstrating that the cardio-protective effect of a HFD on infarct size is dependent on GPR55. In vitro studies using 3T3-L1 cells determined that the changes in adipose tissue gene expression of HFD fed mice was not due to enhanced stimulation with LPI or via hypoxic mechanisms. The results of these studies demonstrate that GPR55 has an anti-obesity function in vivo and also mediates the cardio-protective effect of a HFD on myocardial infarct size, through currently unknown mechanisms.

Subjects/Keywords: 610; Myocardial ischaemia; Reperfusion; Lysophosphatidylinositol; Obesity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hair, S. C. (2018). Determining the role of the LPI/GPR55 system in the development of obesity and associated cardiovascular consequences. (Doctoral Dissertation). Robert Gordon University. Retrieved from https://rgu-repository.worktribe.com/output/248960 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.758179

Chicago Manual of Style (16^th Edition):

Hair, Steven C. “Determining the role of the LPI/GPR55 system in the development of obesity and associated cardiovascular consequences.” 2018. Doctoral Dissertation, Robert Gordon University. Accessed March 07, 2021. https://rgu-repository.worktribe.com/output/248960 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.758179.

MLA Handbook (7^th Edition):

Hair, Steven C. “Determining the role of the LPI/GPR55 system in the development of obesity and associated cardiovascular consequences.” 2018. Web. 07 Mar 2021.

Vancouver:

Hair SC. Determining the role of the LPI/GPR55 system in the development of obesity and associated cardiovascular consequences. [Internet] [Doctoral dissertation]. Robert Gordon University; 2018. [cited 2021 Mar 07]. Available from: https://rgu-repository.worktribe.com/output/248960 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.758179.

Council of Science Editors:

Hair SC. Determining the role of the LPI/GPR55 system in the development of obesity and associated cardiovascular consequences. [Doctoral Dissertation]. Robert Gordon University; 2018. Available from: https://rgu-repository.worktribe.com/output/248960 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.758179

Grand Valley State University

29. Hake, Benjamin Matthew. Changes in Vascular Reactivity of Mesenteric Arteries Following Hyperbaric Oxygen Treatment.

Degree: 2013, Grand Valley State University

URL: https://scholarworks.gvsu.edu/theses/304

► The objective of this study was to evaluate the changes in vascular reactivity of mesenteric arteries resulting from hyperbaric oxygen treatment. It was hypothesized that… (more)

▼ The objective of this study was to evaluate the changes in vascular reactivity of mesenteric arteries resulting from hyperbaric oxygen treatment. It was hypothesized that hyperbaric oxygen treatment alters vascular reactivity in mesenteric arteries due to enhanced production of ATP resulting in significantly larger responses to vasoactive stimuli. All arteries were dissected from porcine mesenteries and placed in Krebs- Henseleit solution. Arteries were initially mounted in isolated organ baths and passively loaded with tensions ranging from 1 to 25 grams at odd intervals to ascertain the optimal passive tension for studying mesenteric arteries. Following a 1-hour equilibration in Krebs-Henseleit solution, arteries were treated with potassium chloride (a nonreceptormediated vasoconstrictor; KCl; 15 – 60 mM) to assess vascular reactivity. Following determination of the optimal passive tension, additional arteries were dissected and tested for viability with KCl. Viable arteries were then subjected to a 2-hour hyperbaric treatment in 100% oxygen, 100% nitrogen, or ambient air at 1.00 or 1.75 ATA. Immediately following treatments, arteries were again mounted in isolated organ baths and passively loaded with 7 grams of tension. Following a 1-hour equilibration in Krebs- Henseleit solution, arteries were treated with KCl (15 – 60 mM). Arteries were then treated with increasing concentrations of phenylephrine (a receptor-mediated vasoconstrictor; 10-7 – 10-4 M) followed by increasing concentrations of sodium nitroprusside (a potent vasodilator; 10-7 – 10-4 M) to measure changes in vascular reactivity. Additional arteries were subjected to the 2-hour hyperbaric regiment involving 5 different gas/ pressure exposures. Arteries were then processed for determination of protein concentration and measurement of ATP concentration using commercially available assay kits. When compared to the 1 ATA room air control, KCl-induced constriction was significantly increased for the hyperbaric oxygen exposure. Treatment with hyperbaric oxygen also augmented vascular responses to phenylephrine and sodium nitroprusside relative to nitrogen, but not ambient air. There was no significant difference in ATP concentrations found among treatments. The results from these studies provide insight into the vascular effects of hyperbaric oxygen treatment.

Subjects/Keywords: Hyperbaric; Ischemic Reperfusion; Vascular Reactivity; ATP

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hake, B. M. (2013). Changes in Vascular Reactivity of Mesenteric Arteries Following Hyperbaric Oxygen Treatment. (Thesis). Grand Valley State University. Retrieved from https://scholarworks.gvsu.edu/theses/304

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hake, Benjamin Matthew. “Changes in Vascular Reactivity of Mesenteric Arteries Following Hyperbaric Oxygen Treatment.” 2013. Thesis, Grand Valley State University. Accessed March 07, 2021. https://scholarworks.gvsu.edu/theses/304.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hake, Benjamin Matthew. “Changes in Vascular Reactivity of Mesenteric Arteries Following Hyperbaric Oxygen Treatment.” 2013. Web. 07 Mar 2021.

Vancouver:

Hake BM. Changes in Vascular Reactivity of Mesenteric Arteries Following Hyperbaric Oxygen Treatment. [Internet] [Thesis]. Grand Valley State University; 2013. [cited 2021 Mar 07]. Available from: https://scholarworks.gvsu.edu/theses/304.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hake BM. Changes in Vascular Reactivity of Mesenteric Arteries Following Hyperbaric Oxygen Treatment. [Thesis]. Grand Valley State University; 2013. Available from: https://scholarworks.gvsu.edu/theses/304

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cambridge

30. Prag, Hiran Ambelal. Developing drugs to attenuate succinate accumulation and oxidation.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/289443

► Ischaemia-reperfusion (IR) injury is caused by the re-introduction of oxygen to organs, following periods of reduced blood flow (ischaemia). Whilst re-establishing blood flow (reperfusion) to… (more)

▼ Ischaemia-reperfusion (IR) injury is caused by the re-introduction of oxygen to organs, following periods of reduced blood flow (ischaemia). Whilst re-establishing blood flow (reperfusion) to the heart following myocardial infarction is vital for organ survival, this paradoxically leads to tissue damage. Mitochondria are at the heart of IR injury, with succinate dehydrogenase (SDH) a major player in orchestrating the damage. Succinate accumulates during ischaemia and is rapidly oxidised by SDH upon reperfusion, producing reactive oxygen species (ROS), leading to cellular death. I have investigated the development of drugs, aimed at targeting succinate metabolism to ameliorate IR injury. I firstly screened a range of compounds for their ability to inhibit SDH, having been chosen for their similar structures to succinate or the classical SDH inhibitor, malonate. Interestingly, only malonate and oxaloacetate showed potent SDH inhibition, thus were selected for further development. Malonate ester prodrugs with different properties were characterised. Hydrolysis rates of the esters differed greatly, with tuned, labile, malonate esters releasing malonate much more rapidly. Malonate esters were taken up into cells and hydrolysed to release malonate to different extents. Additionally, mitochondria-targetedmalonatemono and diesters were developed, each differing in mitochondrial and cellular uptake andmalonate release. Targeted and nontargeted malonate esters distributed into tissues in vivo, with preliminary in vivo work carried out on IR injury models, to assess for protective effects of the compounds. In addition, the physiological role of the tricarboxylic acid cycle metabolite, itaconate, was investigated. In lipopolysaccharide stimulated macrophages, itaconate has been reported to exert its effects by inhibition of SDH however, I found itaconate was a relatively poor SDH inhibitor, indicating other mechanisms of action. Current prodrugs of itaconate have many non-specific effects, not attributable to itaconate. I therefore characterised a novel itaconate prodrug and found it to be a much better surrogate, which could be subsequently used to elucidate roles for itaconate. Overall, I have shown the importance of ester selection for the prodrug delivery of dicarboxylate molecules and developed methods to improve their biological delivery.

Subjects/Keywords: mitochondria; ischaemia-reperfusion injury; succinate dehydrogenase

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Prag, H. A. (2019). Developing drugs to attenuate succinate accumulation and oxidation. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/289443

Chicago Manual of Style (16^th Edition):

Prag, Hiran Ambelal. “Developing drugs to attenuate succinate accumulation and oxidation.” 2019. Doctoral Dissertation, University of Cambridge. Accessed March 07, 2021. https://www.repository.cam.ac.uk/handle/1810/289443.

MLA Handbook (7^th Edition):

Prag, Hiran Ambelal. “Developing drugs to attenuate succinate accumulation and oxidation.” 2019. Web. 07 Mar 2021.

Vancouver:

Prag HA. Developing drugs to attenuate succinate accumulation and oxidation. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Mar 07]. Available from: https://www.repository.cam.ac.uk/handle/1810/289443.

Council of Science Editors:

Prag HA. Developing drugs to attenuate succinate accumulation and oxidation. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/289443

Open Access Theses and Dissertations