Relevant bibliographies by topics / Cerebral ischemia – Animal models

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cerebral ischemia – Animal models'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Cerebral ischemia – Animal models"

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Umemura, Kazuo. "Experimental animal models of cerebral ischemia." Japanese Journal of Pharmacology 76 (1998): 39. http://dx.doi.org/10.1016/s0021-5198(19)40286-2.

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Takizawa, Shunya, and Antoine M. Hakim. "Animal Models of Cerebral Ischemia. 2. Rat Models." Cerebrovascular Diseases 1, no. 1 (1991): 16–21. http://dx.doi.org/10.1159/000108876.

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Ma, Rong, Qian Xie, Yong Li, Zhuoping Chen, Mihong Ren, Hai Chen, Hongyan Li, Jinxiu Li, and Jian Wang. "Animal models of cerebral ischemia: A review." Biomedicine & Pharmacotherapy 131 (November 2020): 110686. http://dx.doi.org/10.1016/j.biopha.2020.110686.

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Bacigaluppi, Marco. "Animal Models of Ischemic Stroke. Part Two: Modeling Cerebral Ischemia." Open Neurology Journal 4, no. 1 (August 31, 2010): 34–38. http://dx.doi.org/10.2174/1874205x01004010034.

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Traystman, R. J. "Animal Models of Focal and Global Cerebral Ischemia." ILAR Journal 44, no. 2 (January 1, 2003): 85–95. http://dx.doi.org/10.1093/ilar.44.2.85.

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O'Collins, Victoria E., Malcolm R. Macleod, Geoffrey A. Donnan, and David W. Howells. "Evaluation of Combination Therapy in Animal Models of Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 32, no. 4 (February 1, 2012): 585–97. http://dx.doi.org/10.1038/jcbfm.2011.203.

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Combination therapy has been identified as a promising strategy to improve stroke management. We conducted a systematic review and meta-analysis of evidence from animal models of ischemic stroke to determine whether combining treatments improved efficacy. Multiple databases were searched and data were extracted from focal ischemia experiments comparing control groups, single treatments, and combination treatments. Of 11,430 papers identified, 142 met the inclusion criteria; these tested 126 treatments in 373 experiments using 8,037 animals ( I2 = 85 to 96%). Taken together, single treatments r
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Schweizer, Sophie, Andreas Meisel, and Stefanie Märschenz. "Epigenetic Mechanisms in Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 9 (June 12, 2013): 1335–46. http://dx.doi.org/10.1038/jcbfm.2013.93.

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Treatment efficacy for ischemic stroke represents a major challenge. Despite fundamental advances in the understanding of stroke etiology, therapeutic options to improve functional recovery remain limited. However, growing knowledge in the field of epigenetics has dramatically changed our understanding of gene regulation in the last few decades. According to the knowledge gained from animal models, the manipulation of epigenetic players emerges as a highly promising possibility to target diverse neurologic pathologies, including ischemia. By altering transcriptional regulation, epigenetic modi
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Handayani, Ety S., Titis Nurmasitoh, Syaefudin Ali Akhmad, Afifah Nur Fauziah, Rizky Rizani, Rika Yulita Rahmawati, and Angga Afriandi. "Effect of BCCAO Duration and Animal Models Sex on Brain Ischemic Volume After 24 Hours Reperfusion." Bangladesh Journal of Medical Science 17, no. 1 (January 11, 2018): 129–37. http://dx.doi.org/10.3329/bjms.v17i1.35293.

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Background: Literature study shows, there are several variations regarding BCCAO duration and duration of reperfusion after BCCAO that can cause cerebral ischemia. Duration of BCCAO techniques varies between 10 to 30 minutes, while the duration of reperfusion period ranging between 45 minutes to 72 hours. Differences in the duration of occlusion, duration of BCCAO reperfusion and the sex of animal model could lead to different responses to ischemia conditions.Objective. This study aims to determine whether the duration BCCAO and sex of the animal models influences the volume of cerebral ischem
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Cirillo, Carla, Nabila Brihmat, Evelyne Castel-Lacanal, Alice Le Friec, Marianne Barbieux-Guillot, Nicolas Raposo, Jérémie Pariente, et al. "Post-stroke remodeling processes in animal models and humans." Journal of Cerebral Blood Flow & Metabolism 40, no. 1 (October 23, 2019): 3–22. http://dx.doi.org/10.1177/0271678x19882788.

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After cerebral ischemia, events like neural plasticity and tissue reorganization intervene in lesioned and non-lesioned areas of the brain. These processes are tightly related to functional improvement and successful rehabilitation in patients. Plastic remodeling in the brain is associated with limited spontaneous functional recovery in patients. Improvement depends on the initial deficit, size, nature and localization of the infarction, together with the sex and age of the patient, all of them affecting the favorable outcome of reorganization and repair of damaged areas. A better understandin
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Hossmann, Konstantin-A. "Animal Models of Cerebral Ischemia. 1. Review of Literature." Cerebrovascular Diseases 1, no. 1 (1991): 2–15. http://dx.doi.org/10.1159/000108875.

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Dissertations / Theses on the topic "Cerebral ischemia – Animal models"

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Ng, Kit-ying, and 吳潔瑩. "Neuroprotective effects of adiponectin in focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634371.

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Tsang, Hing-wai, and 曾慶威. "In vitro studies of hypoxic ischemic down-regulated 1 (HID-1) protein encoded by a novel gene down-regulated in neonatal hypoxic-ischemicencephalopathy in different cell death paradigms." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45608192.

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Mullins, Paul Gerald Mark. "Magnetic resonance imaging in the study of animal models of cerebral ischaemia /." [St. Lucia, Qld.], 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16186.pdf.

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Liu, Lingguang, and 刘灵光. "Neuroprotection of melatonin and/or electro-acupuncture in a rat model of focal cerebral ischemia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/198928.

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Stroke is a serious cerebral vascular event and a leading cause of death and disability worldwide, and ischemic stroke is the most common type. Evidence from animal research in acute cerebral ischemia shows that a combination of neuroprotectants might be more efficacious than the single agent given individually. Both melatonin and electro-acupuncture (EA) have been suggested to be effective treatments against cerebral ischemia. However, it is unknown whether a combination of these two therapies could be beneficial against focal cerebral ischemia. In the first study, the effect of post-tr
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Chan, Chu-fung, and 陳柱峰. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40687284.

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Wang, Yanxin, and 王燕欣. "Hypoxic-ischemic injury in the neonatal rat model: prediction of irreversible infarction size by DiffusionWeighted MR Imaging." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B35757577.

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Sicard, Kenneth M. "Multimodal MRI, Behavioral Testing, and Histology in a Rat Model of Transient Focal Cerebral Ischemia : A Dissertation." eScholarship@UMMS, 2006. http://escholarship.umassmed.edu/gsbs_diss/318.

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Cerebral ischemia is defined as a decrease in blood flow to the brain. It is most often caused by obstruction of a cerebral blood vessel, and is recognized by the World Health Organization as the leading cause of serious adult disability and one of the top three causes of adult death worldwide. Most survivors demonstrate partial restitution of function over time, but the underlying recovery mechanism(s) remain unclear especially in a subset of patients with persistent neurological morbidities despite normal-appearing brain on neuroimaging. The optimal way to understand any human disease state
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Jeffs, Graham J. "The effect of sodium/calcium exchanger 3 (NCX3) knockout on neuronal survival following global cerebral ischaemia in mice." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0063.

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Cerebral ischaemia is a leading cause of disability and death world-wide. The only effective treatments are thrombolytic therapy (plasminogen activator; tPA) and hypothermia (33?C). However, tPA has limited clinical application due to its short therapeutic time window and its specific application in thrombo-embolic stroke. Moderate hypothermia (33?C) is only being used following cardiac arrest in comatose survivors. Hence more treatments are urgently required. The first step in developing new treatments is the identification and characterisation of a potential therapeutic target. Since brain d
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Brodin, Camille. "De la paillasse au lit du patient, surmonter les problèmes de translation dans le domaine de l'AVC ischémique Single- and two- chain tissue plasminogen activator treatment differentially influence cerebral recovery after stroke Single- and two- chain tissue plasminogen activator treatment differentially influence cerebral recovery after stroke Cerebral blood flow correlates with ischemic brain lesion only when Stroke occurs awake: a preclinical model to bypass the translational roadblocks to clinic." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMC427.

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Les défauts de translation des études précliniques vers les essais cliniques dans le domaine des AVC ischémiques et l'échec des développements thérapeutiques pourraient être expliqués par trois aspects : (1) le manque de compréhension des mécanismes des deux formes de rtPA, le traitement pharmacologique de l'AVC; (2) le manque d'outils adaptés d'imagerie de perfusion chez le petit animal et (3) l'influence de l'anesthésie sur l’effet des traitements testés dans les modèles animaux.Le tPA utilisé en clinique (Actilyse®) est un mélange de deux formes de tPA: une forme chaîne simple (sc-rtPA) et
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Chaparro-Buitrago, Rafael Eduardo. "Neuroprotection with Anesthetics in Two Models of Cerebral Ischemia." Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/3521.

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Neuroprotection with anesthetics has been studied for many decades; important advances in this field have modified the way Anesthesiologists treat patients in the operating room. Animal models have played an important role in the study of ischemia in the operating room. Recent studies have demonstrated that the effect of anesthetics seems to be different in different animal models. We decided to evaluate anesthetics in a well-known model of cerebral ischemia and also in hypotensive models designed by us. We used a model of cerebral ischemia (MCAO) to test anesthetics neuroprotective effect in
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Books on the topic "Cerebral ischemia – Animal models"

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N, Maĭorov V., ed. Reakt͡s︡ii neĭronov mozga na gipoksii͡u︡. Leningrad: Izd-vo "Nauka," Leningradskoe otd-nie, 1985.

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Rodent models of stroke. New York, N.Y: Humana Press, 2010.

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The intelligent movement machine: An ethological perspective on the primate motor system. New York: Oxford University Press, 2009.

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Schaller, B. Cerebral Ischemic Tolerance: From Animal Models To Clinical Relevance. Nova Science Publishers, 2004.

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Pluta, Ryszard. Ischemia-Reperfusion Pathways in Alzheimer's Disease. Nova Science Pub Inc, 2007.

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Felling, Ryan J. Targets for Neuroprotection in Ischemic Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0111.

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Cerebral ischemia or hypoxia-ischemia initiate a cascade of biochemical events including impaired reuptake of glutamate into perisynaptic glia causing glutamate flooding, calcium fluxing through NMDA glutamate channels, activation of neuronal nitric oxide synthetase, and impaired mitochondrial ATP production. In animal models it is possible to block these steps and protect the brain but the temporal window of protection after the insult lasts only a few hours. Recombinant TPA is clinically protective if given within 3 hours of stroke, but other agents have not been shown to protect brain tissu
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Murine models of cerebral ischemia: Development of a mouse model of global cerebral ischemia ; response of GluR2 knockout mice in a model of permanent focal cerebral ischemia. Ottawa: National Library of Canada, 2000.

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Ohta, Hitomi. Effects of NK-4, a Cyanine Dye with Antioxidant Activities: Attenuation of Neuronal Deficits in Animal Models of Oxidative Stress-Mediated Brain Ischemia and Neurodegenerative Diseases. INTECH Open Access Publisher, 2012.

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(Foreword), Thomas Woolsey, ed. Barrel Cortex. Cambridge University Press, 2008.

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D, Rosen Glenn, ed. The dyslexic brain: New pathways in neuroscience discovery. Mahwah, N.J: L. Erlbaum Associates, Publishers, 2006.

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Book chapters on the topic "Cerebral ischemia – Animal models"

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Borlongan, Cesario V., Toru Shimizu, John Q. Trojanowski, Shigeru Watanabe, Virginia M. Y. Lee, Yasuo Tajima, Thomas B. Freeman, Hitoo Nishino, and Paul R. Sanberg. "Animal Models of Cerebral Ischemia." In Cell Transplantation for Neurological Disorders, 211–30. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-476-4_11.

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Tamura, Akira, Kensuke Kawai, and Kiyoshi Takagi. "Animal Models Used in Cerebral Ischemia and Stroke Research." In Clinical Pharmacology of Cerebral Ischemia, 265–94. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-59259-472-6_11.

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Raval, Ami P., and Bingren Hu. "Histopathological Assessments of Animal Models of Cerebral Ischemia." In Springer Protocols Handbooks, 3–11. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-576-3_1.

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Zivin, Justin A. "Animal Models of Ischemia." In Emerging Strategies in Neuroprotection, 57–75. Boston, MA: Birkhäuser Boston, 1992. http://dx.doi.org/10.1007/978-1-4684-6796-3_4.

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Kwong, Jacky Man Kwong, and Joseph Caprioli. "Animal Models of Retinal Ischemia." In Neuromethods, 191–206. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-541-5_10.

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Seren, M. S., A. Lazzaro, M. C. Comelli, R. Canella, R. Zanoni, D. Guidolin, and H. Manev. "Monosialoganglioside GM1 in Experimental Models of Stroke." In Cerebral Ischemia and Basic Mechanisms, 125–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78151-3_13.

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Seil, F. J. "Models of Neural Circuit Reorganization After Injury." In Cerebral Ischemia and Basic Mechanisms, 312–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78151-3_32.

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Awad, Hamdy, Haytham Elgharably, and Phillip Popovich. "Animal Models of Spinal Cord Ischemia." In Animal Models of Spinal Cord Repair, 225–54. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-197-4_11.

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Megyesi, J. F., and J. M. Findlay. "In Vivo Animal Models of Cerebral Vasospasm: A Review." In Cerebral Vasospasm, 99–102. Vienna: Springer Vienna, 2001. http://dx.doi.org/10.1007/978-3-7091-6232-3_21.

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Pandian, Natesa G. "Echocardiography During Reversible Ischemia in Animal Models." In Developments in Cardiovascular Medicine, 33–43. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1767-8_3.

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Conference papers on the topic "Cerebral ischemia – Animal models"

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Khodanovich, M. Yu, and A. A. Kisel. "Animal models of cerebral ischemia." In NEW OPERATIONAL TECHNOLOGIES (NEWOT’2015): Proceedings of the 5th International Scientific Conference «New Operational Technologies». AIP Publishing LLC, 2015. http://dx.doi.org/10.1063/1.4936032.

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Zhu, Liang, and Axel J. Rosengart. "Cooling Penetration Surrounding an Intra-Parenchymal Cooling Probe in Hypothermia Treatment for Ischemia or Head Injury Patients: Theoretical Analyses." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61109.

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Inducing hypothermia to brain tissue after brain ischemia or head injury has been demonstrated beneficial to the patients. Clinical studies have shown that even 1 or 2°C temperature reduction in brain tissue can be protective [Dietrich 1992]. On the contrary, fever-induced hyperthermia can worsen the neurological outcome in an animal model after cerebral ischemia. It is of clinical importance to understand the temperature distribution in brain during brain hypothermia.
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Кудабаева, Марина Станиславовна, Андрей Евгеньевич Акулов, Анна Олеговна Пищелко, Михаил Васильевич Светлик, and Марина Юрьевна Ходанович. "SUTURE SIZE OPTIMIZATION IN THE MODEL OF FOCAL ISCHEMIA IN RATS." In Высокие технологии и инновации в науке: сборник избранных статей Международной научной конференции (Санкт-Петербург, Сентябрь 2020). Crossref, 2020. http://dx.doi.org/10.37539/vt187.2020.38.57.004.

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На модели окклюзии срединой церебральной артерии (MCAO) у крыс исследовано влияние параметров монофиламента, используемого для проведения операции, на объем ишемического поражения мозга. Установлена оптимальная длина наконечника филамента, обеспечивающая такой объем ишемического поражения, который позволяет обеспечить хорошую выживаемость животных в сочетании с другими инвазивными процедурами в хроническом эксперименте. In middle cerebral artery occlusion model (MCAO) in rats surgical suture characteristics were analyzed as parameters that can effect on ischemic lesion size. Optimal suture len
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Ludmila, BELAYEV, and BAZAN Nicolas G. "Experimental models of cerebral ischemia: Implications for drug discovery." In I International Symposium in Neuroscience Meeting. Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/isnm-sine35.

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Walsh, Peter W., Craig S. McLachlan, Leigh Ladd, Arie Blitz, R. Mark Gillies, Brett Hambly, Ryan Ocsan, and Glenn Edwards. "Echocardiography Evaluation of a Novel Stable Ovine Heart Failure Model Suitable for Cardiovascular Device Testing." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53824.

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Numerous large animal models of chronic cardiac ischemia have been developed to explore either pathological mechanisms and or device interventions in developed heart failure models. Traditionally chronic heart failure in large animal models such as sheep or pigs has been induced by either coronary ligation with or without reperfusion. Coronary ligation is often attempted in the open chest surgical model or more recently in the closed chest animal via angiography [1]. Both techniques can be challenging and also induce high mortality with the risk of myocardial stunning and resultant shock and o
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Zeng, Zijing, David F. Kallmes, Yong Hong Ding, Ramanathan Kadirvel, Debra A. Lewis, D. Dai, and Anne M. Robertson. "Hemodynamics of Elastase-Induced Aneurysms in Rabbit: A New High Flow Bifurcation Model." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53819.

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An intracranial aneurysm (IA) is a pathological condition of cerebral arteries characterized by local enlargements of the arterial wall, typically into a saccular shape. Rupture of the aneurysm sac can result in devastating cerebral hemorrhage. Hemodynamic factors are believed to play an important role in initiation, development and rupture of IAs [1–3]. However, the coupling between hemodynamics and aneurysm pathophysiology is complex and remains poorly understood. Patient specific diagnostics regarding risk of rupture can be substantially advanced by improving our understanding of the in-viv
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Dolan, Jennifer, Frasier Sim, Hui Meng, and John Kolega. "Positive and Negative Wall Shear Stress Gradients Have Different Effects on Endothelial Phenotype Under High Wall Shear Stress." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53490.

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In both human and animal models, cerebral aneurysms tend to develop at the apices of bifurcations in the cerebral vasculature where the blood vessel wall experiences complex hemodynamics. In vivo studies have recently revealed that the initiation of cerebral aneurysms is confined to a well-defined hemodynamic microenvironment [1,2]. Metaxa et al. [2] found that early aneurysm remodeling initiates where the vessel wall experiences high wall shear stress (WSS) and flow is accelerating, thus creating a positive spatial gradient in WSS (WSSG). Closer examination of such in vivo studies reveals tha
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La Barck, Anthony J., Jennifer E. Akers, and Thomas L. Merrill. "Tissue Oxygen Transfer During Reperfusion and Post-Conditioning." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53064.

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Heart disease is the leading cause of death in the United States. Ischemic heart disease occurs when coronary blood flow to the heart is reduced, limiting the amount of oxygen and nutrients the heart receives. When blood flow is restored after a percutaneous transluminal coronary intervention (PCI), rapid reperfusion from sudden balloon deflation can cause further injury to oxygen-starved tissue, leading to increased cell injury and cell death. Studies in animal models with ischemic heart disease have shown that reperfusion injury may account for up to 50% of the final infarct size [1]. Post-c
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Dolan, Jennifer, Song Liu, Hui Meng, and John Kolega. "Differential Gene Expression of Endothelial Cells Under High Wall Shear Stress and Spatial Gradients." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19662.

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In both human and animal models, cerebral aneurysms tend to develop at the apices of bifurcations in the cerebral vasculature. Due to the focal nature of aneurysm development it has long been speculated that hemodynamics are an important factor in aneurysm susceptibility. The local hemodynamics of bifurcations are complex, being characterized by flow impingement causing a high frictional force on the vessel wall known as wall shear stress (WSS) and significant flow acceleration or deceleration, manifested as the positive or negative spatial gradient of WSS (WSSG). In vivo studies have recently
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Cebral, Juan R., and Christopher M. Putman. "Relating Wall Shear Stress, Bleb Formation and Rupture of Cerebral Aneurysms: Image-Based Modeling and Clinical Observations." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192364.

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Cerebral aneurysms are widely believed to form and grow as a result of the interactions of hemodynamics and wall mechano-biology. Researchers have used a variety of tools to study these complex multi-factorial mechanisms including animal, in vitro, and computational models. The goal of these experiments has been to approximate the in vivo environment so that theories about the natural history of brain aneurysms can be developed and tested in realistic systems. Studying the link between hemodynamics and clinical observations of aneurysm progression is necessary to reach an understanding of the
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Reports on the topic "Cerebral ischemia – Animal models"

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Xu, Fangyuan, Qiqi Yang, Wei Huang, and Zhenzhen Liu. The protective effect of acupuncture at Baihui acupoint (DU 20) for cerebral ischemia-reperfusion injury in rat models: a protocol for a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2021. http://dx.doi.org/10.37766/inplasy2021.3.0114.

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