Relevant bibliographies by topics / Experimental ischemic stroke

Contents

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

Academic literature on the topic 'Experimental ischemic stroke'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Experimental ischemic stroke"

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Meadows, Kristy L. "Experimental models of focal and multifocal cerebral ischemia: a review." Reviews in the Neurosciences 29, no. 6 (2018): 661–74. http://dx.doi.org/10.1515/revneuro-2017-0076.

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AbstractRodent and rabbit stroke models have been instrumental in our current understanding of stroke pathophysiology; however, translational failure is a significant problem in preclinical ischemic stroke research today. There are a number of different focal cerebral ischemia models that vary in their utility, pathophysiology of causing disease, and their response to treatments. Unfortunately, despite active preclinical research using these models, treatment options for ischemic stroke have not significantly advanced since the food and drug administration approval of tissue plasminogen activa
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Yang, Fan, Ziying Wang, Xinbing Wei, et al. "NLRP3 Deficiency Ameliorates Neurovascular Damage in Experimental Ischemic Stroke." Journal of Cerebral Blood Flow & Metabolism 34, no. 4 (2014): 660–67. http://dx.doi.org/10.1038/jcbfm.2013.242.

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Although the innate immune response to induce postischemic inflammation is considered as an essential step in the progression of cerebral ischemia injury, the role of innate immunity mediator NLRP3 in the pathogenesis of ischemic stroke is unknown. In this study, focal ischemia was induced by middle cerebral artery occlusion in NLRP3−/−, NOX2−/−, or wild-type (WT) mice. By magnetic resonance imaging (MRI), Evans blue permeability, and electron microscopic analyses, we found that NLRP3 deficiency ameliorated cerebral injury in mice after ischemic stroke by reducing infarcts and blood–brain barr
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Vannucci, Susan J., Lisa B. Willing, Shozo Goto, et al. "Experimental Stroke in the Female Diabetic, db/db, Mouse." Journal of Cerebral Blood Flow & Metabolism 21, no. 1 (2001): 52–60. http://dx.doi.org/10.1097/00004647-200101000-00007.

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Diabetic hyperglycemia increases brain damage after cerebral ischemia in animals and humans, although the underlying mechanisms remain unclear. Gender-linked differences in ischemic tolerance have been described but have not been studied in the context of diabetes. In the current study, we used a model of unilateral common carotid artery ligation, combined with systemic hypoxia, to study the effects of diabetes and gender on hypoxic–ischemic (HI) brain damage in the genetic model of Type II diabetes, the db/db, mouse. Male and female, control and db/db, mice were subjected to right common caro
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Sommer, Clemens J. "Ischemic stroke: experimental models and reality." Acta Neuropathologica 133, no. 2 (2017): 245–61. http://dx.doi.org/10.1007/s00401-017-1667-0.

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Li, Xiao-Qiu, Lin Tao, Zhong-He Zhou, Yu Cui, and Hui-Sheng Chen. "Remote ischemic conditioning for acute moderate ischemic stroke (RICAMIS): Rationale and design." International Journal of Stroke 15, no. 4 (2019): 454–60. http://dx.doi.org/10.1177/1747493019879651.

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Rationale A large number of basic and clinical studies have proved that remote ischemic conditioning has neuroprotective effect. For example, remote ischemic conditioning showed a neuroprotective role in cerebral ischemia-reperfusion injury model. Recent clinical studies suggested that remote ischemic conditioning may improve neurological function and reduce the risk of recurrence in ischemic stroke patients. However, there is a lack of convincing evidence for the neuroprotective effect of remote ischemic conditioning on ischemic stroke, which deserves further study. Aim To explore the efficac
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Zhou, Yuan, Shanshan Zhang, and Xiang Fan. "Role of Polyphenols as Antioxidant Supplementation in Ischemic Stroke." Oxidative Medicine and Cellular Longevity 2021 (June 25, 2021): 1–19. http://dx.doi.org/10.1155/2021/5471347.

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Stroke is the second most common cause of death globally and the leading cause of death in China. The pathogenesis of cerebral ischemia injury is complex, and oxidative stress plays an important role in the fundamental pathologic progression of cerebral damage in ischemic stroke. Previous studies have preliminarily confirmed that oxidative stress should be a potential therapeutic target and antioxidant as a treatment strategy for ischemic stroke. Emerging experimental studies have demonstrated that polyphenols exert the antioxidant potential to play the neuroprotection role after ischemic stro
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Safari, Anahid, Rasool Safari, and Afshin Borhani-Haghighi. "Immunology of stroke." Galen Medical Journal 5 (May 24, 2016): 10–17. http://dx.doi.org/10.31661/gmj.v5is1.592.

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Stroke, a multifactorial disease, has distinct pathophysiologic mechanisms, among which inflammation plays a pivotal role. Various types of inflammatory cells, substances, and molecules emerge in the ischemic stroke. Neutrophils, Tcell subtypes, macrophages, microglial cells, dendritic cell, mast cells, asrocytes, as influential cell, tumor necrosis factor_α, interleukin-17, interleukin-10, as released substances, and vascular cell adhesion molecule-1 (VCAM-1), leukocyte very late antigen-4 (VLA-4), and glial fibrillary acidic protein (GFAP), as cellular adhesion molecules. Lymphocytes' invasi
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Gafarova, M. E., G. M. Naumova, M. V. Gulyaev, V. B. Koshelev, I. A. Sokolova, and M. A. Domashenko. "Erythrocyte (dis)aggregation in stroke model in rats." Regional blood circulation and microcirculation 14, no. 2 (2015): 63–69. http://dx.doi.org/10.24884/1682-6655-2015-14-2-63-69.

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Introduction and aim of the study. Ischemic stroke develops in conjunction with interruption of blood flow in microvessels that depends on rheological blood properties. There is a lack of knowledge in hemorheological features of experimental stroke making more difficult to value the relevance of stroke models. The study aims investigation of microhemorheological parameters in two experimental stroke models - thromboembolic model and middle cerebral artery (MCA) ligation model. Methods. Male Wistar rats were subjected to focal brain ischemia in MCA ligation stroke model or thromboembolic stroke
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Sheng, Siyuan P., Beilei Lei, Michael L. James, et al. "Xenon Neuroprotection in Experimental Stroke." Anesthesiology 117, no. 6 (2012): 1262–75. http://dx.doi.org/10.1097/aln.0b013e3182746b81.

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Background Xenon has been proven to be neuroprotective in experimental brain injury. The authors hypothesized that xenon would improve outcome from focal cerebral ischemia with a delayed treatment onset and prolonged recovery interval. Methods Rats were subjected to 70 min temporary focal ischemia. Ninety minutes later, rats were treated with 0, 15, 30, or 45% Xe for 20 h or 0 or 30% Xe for 8, 20, or 44 h. Outcome was measured after 7 days. In another experiment, after ischemia, rats were maintained at 37.5° or 36.0°C for 20 h with or without 30% Xe. Outcome was assessed 28 days later. Finally
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Xie, Luokun, Wenjun Li, Jessica Hersh, Ran Liu, and Shao-Hua Yang. "Experimental ischemic stroke induces long-term T cell activation in the brain." Journal of Cerebral Blood Flow & Metabolism 39, no. 11 (2018): 2268–76. http://dx.doi.org/10.1177/0271678x18792372.

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Mounting evidence has demonstrated that both innate and adaptive immune cells infiltrate into the brain after ischemic stroke. T cell invasion has been found in the ischemic region up to one month post experimental ischemic stroke and has been shown to persist for years in stroke patients. However, the function and phenotypic characteristics of the brain invading T cells after ischemic stroke have not been investigated. In the current study, we determined the function of brain invading T cells in the acute and chronic phase following experimental ischemic stroke induced by transient middle cer
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Dissertations / Theses on the topic "Experimental ischemic stroke"

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Salmeron, Kathleen Elizabeth. "INVESTIGATIONS OF INTERLEUKIN-1 ALPHA AS A NOVEL STROKE THERAPY IN EXPERIMENTAL ISCHEMIC STROKE." UKnowledge, 2018. https://uknowledge.uky.edu/neurobio_etds/20.

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Stroke is a leading cause of death and disability worldwide. Although rapid recognition and prompt treatment have dropped mortality rates, most stroke survivors are left with permanent disability. Approximately 87% of all strokes result from the thromboembolic occlusion of the cerebrovasculature (ischemic strokes). Potential stroke therapeutics have included anti-inflammatory drugs, as well as many other targets with the goal of mitigating the acute and chronic inflammatory responses typically seen in an ischemic stroke. While these approaches have had great success in preclinical studies, the
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CUCCIONE, ELISA. "Cerebral collateral circulation in experimental ischemic stroke: from molecular penumbra to collateral therapeutics." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/94446.

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Cerebral collateral circulation is a subsidiary vascular network which is dynamically recruited after acute ischemic stroke and may provide residual blood flow to the affected areas, slowing down the progression of ischemic penumbra to irreversible ischemic damage. The anatomy and functional performance of the collateral circulation varies among individuals, both humans and rodents, and is emerging as a strong prognostic factor in patients. Nonetheless, collateral circulation in experimental ischemic stroke is frequently neglected. In the present work, ischemic stroke was modelled by 90-minute
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Khansari, Parto S. "An investigation of the neuroprotective properties of fenamate NSAIDs, against experimental models of ischemic stroke." Scholarly Commons, 2007. https://scholarlycommons.pacific.edu/uop_etds/2745.

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Stroke is a devastating neurological disease with limited treatment opportunities. Recent advances in understanding the underlying pathogenesis of cerebral ischemia support the involvement of multiple biochemical pathways in the development of the ischemic injury. The work reported in this thesis was undertaken to investigate the hypothesis that fenamate NSAIDs have neuroprotective properties against ischemic stroke and to explore the underlying mechanisms for any efficacy. Fenamates are non-selective inhibitors of cyclooxygenases. In addition, fenamates are antagonists of non-selective cation
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Khanasari, Parto S. "An investigation of the neuroprotective properties of fenamate NSAIDs, against experimental model of ischemic stroke." Scholarly Commons, 2007. https://scholarlycommons.pacific.edu/uop_etds/671.

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Stroke is a devastating neurological disease with limited treatment opportunities. Recent advances in understanding the underlying pathogenesis of cerebral ischemia support the involvement of multiple biochemical pathways in the development of the ischemic injury. The work reported in this thesis was undertaken to investigate the hypothesis that fenamate NSAIDs have neuroprotective properties against ischemic stroke and to explore the underlying mechanisms for any efficacy. Fenamates are non-selective inhibitors of cyclooxygenases. In addition, fenamates are antagonists of non-selective cation
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Strand, Magnus. "Estrogen signaling in stroke : genetic and experimental studies." Doctoral thesis, Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1397.

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Sun, Ping. "Study of the role of SSAO/VAP-1 in OGD conditions using SSAO/VAP-1-expressing HUVEC and human brain endothelial cells (hCMEC/D3) as experimental models of ischemic stroke, and its possible nexus with Alzheimer´s disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/308325.

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La proteína de adhesión vascular 1 (VAP-1) es una proteína pro-inflamatoria que facilita el reclutamiento leucocitario a través de su actividad amino oxidasa sensible a semicarbazida (SSAO, E.C 1.4.3.21). La SSAO plasmática incrementa en pacientes con infarto cerebral o “stroke” isquémico y hemorrágico, y su actividad predice la aparición de hemorragias después del tratamiento con tPA. Además, la SSAO/VAP-1 se encuentra incrementada en plasma y tejido cerebral de pacientes con enfermedad de Alzheimer (EA). Así pues, creemos que la SSAO/VAP-1 puede contribuir al daño vascular en stroke y EA. Si
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Kostulas, Nikolaos. "Studies on cytokines and chemokines in cerebrovascular diseases and experimental cerebral ischemia /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4701-5/.

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Kuric, Enida. "The Impact of Enriched environment on Lipid metaboilsm after Experimental Stroke." Thesis, Mälardalen University, Mälardalen University, Department of Biology and Chemical Engineering, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-6530.

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<p>Stroke is the major cause of serious long-term disability with a sufficient acute treatment for only a very limited number of patients. Limited recovery of neurological functions occurs and can be elevated by a permissive post-stroke milieu. Housing animals in an enriched environment modulates regenerative mechanisms in the nonischemic peri-infarct area which might be an attractive target for pharmacological treatments to promote recovery.</p><p>Upon ischemia, cellular lipids are released due to massive cell damage and free lipids significantly contribute to the progression of acute and del
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Atefi, Seyed Reza. "Electrical Bioimpedance Cerebral Monitoring : From Hypothesis and Simulation to First Experimental Evidence in Stroke Patients." Doctoral thesis, KTH, Medicinska sensorer, signaler och system, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-176634.

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Stroke is amongthe leading causes of death worldwide and requires immediate care to prevent death or permanent disability. Unfortunately, the current stateof stroke diagnosis is limited to fixed neuroimaging facilities that do not allow rapid stroke diagnosis. Hence, a portable stroke-diagnosis device could assist in the pre-hospital triage of patients. Moreover, such a portable device could also be useful for bedside stroke monitoring of patients in the Neuro Intensive Care Unit (Neuro-ICU) to avoid unnecessary neuroimaging. Recent animal studies and numerical simulations have supported the i
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Sánchez, Opazo Guillem. "Estudi dels mecanismes de mort cel·lular induïts per un model d’isquèmia cerebral in vitro: implicació dels antagonistes dels receptors de mortJosé Rodríguez Álvarez." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/284058.

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L’ictus o accident cerebrovascular és la segona causa de mort en els països industrialitzats i constitueix la primera causa de discapacitat en adults. L’únic tractament aprovat en l’actualitat és el trombolític activador del plasminògen tissular (tPA), el qual només es pot aplicar en un nombre molt reduït de pacients i dintre d’una estreta finestra terapèutica. Els mecanismes de mort cel·lular en la isquèmia cerebral són amplis i venen provocats per l’interrupció del flux sanguini al cervell, el qual provoca una mort ràpida i eminentment necròtica en el nucli de la zona afectada i una mort de
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Books on the topic "Experimental ischemic stroke"

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Chauveau, Fabien. MRI Assessment of Post-Ischemic Neuroinflammation in Stroke: Experimental and Clinical Studies. INTECH Open Access Publisher, 2012.

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Stocchetti, Nino, and Marco Carbonara. Pharmacologic Neuroprotection. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0002.

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Acute cerebral injury sets into motion a cascade of deleterious biochemical events that cause further neuronal damage and amplify deleterious effects. This cascade develops over time and potentially may be attenuated or limited by pharmacologic manipulation. The neuroprotective properties of several molecules have been clearly demonstrated in experimental models of various pathologies. Based on these findings, many promising compounds have been tested in clinical trials. Large randomized controlled trials, however, have repeatedly failed to provide evidence of clinical efficacy. The authors pr
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Book chapters on the topic "Experimental ischemic stroke"

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Dalkara, Turgay, Luis Alarcon-Martinez, and Muge Yemisci. "Pericytes in Ischemic Stroke." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-16908-4_9.

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Back, Tobias. "Insights from Experimental Studies." In Magnetic Resonance Imaging in Ischemic Stroke. Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-27738-2_4.

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Garcia, J. H., Z. R. Ye, K. F. Liu, and J. A. Gutierrez. "Delayed Neuronal Death in Experimental Ischemic Stroke." In Maturation Phenomenon in Cerebral Ischemia III. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-58602-6_32.

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Yang, Jian, Mengli Chen, Richard Y. Cao, Qing Li, and Fu Zhu. "The Role of Circular RNAs in Cerebral Ischemic Diseases: Ischemic Stroke and Cerebral Ischemia/Reperfusion Injury." In Advances in Experimental Medicine and Biology. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1426-1_25.

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Fern, Robert. "Focal Ischemic White Matter Injury in Experimental Models." In White Matter Injury in Stroke and CNS Disease. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9123-1_8.

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Zhao, Heng. "The Protective Effects of Ischemic Postconditioning in Experimental Stroke." In Innate Tolerance in the CNS. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9695-4_16.

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Leonardo, Christopher C., Hilary Seifert, and Keith R. Pennypacker. "The Splenic Response to Ischemic Stroke: Neuroinflammation, Immune Cell Migration, and Experimental Approaches to Defining Cellular Mechanisms." In Translational Stroke Research. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9530-8_23.

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Zheng, Yi, Yu Liu, Hulya Karatas, Kazim Yigitkanli, Theodore R. Holman, and Klaus van Leyen. "Contributions of 12/15-Lipoxygenase to Bleeding in the Brain Following Ischemic Stroke." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21735-8_12.

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Kuroda, Satoshi, Masaki Koh, Emiko Hori, Yumiko Hayakawa, and Takuya Akai. "Muse Cell: A New Paradigm for Cell Therapy and Regenerative Homeostasis in Ischemic Stroke." In Advances in Experimental Medicine and Biology. Springer Japan, 2018. http://dx.doi.org/10.1007/978-4-431-56847-6_10.

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Awano, Takayuki, Kaoru Sakatani, Noriaki Yokose, et al. "EC-IC Bypass Function in Moyamoya Disease and Non-Moyamoya Ischemic Stroke Evaluated by Intraoperative Indocyanine Green Fluorescence Angiography." In Advances in Experimental Medicine and Biology. Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1241-1_75.

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Conference papers on the topic "Experimental ischemic stroke"

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Namestnikova, Daria, Elvira Cherkashova, Ilya Gubskiy, et al. "SYSTEMIC TRANSPLANTATION OF MESENCHYMAL STEM CELLS IN EXPERIMENTAL ISCHEMIC STROKE." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2860.sudak.ns2022-18/244-245.

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Saadat, N., G. Christoforidis, M. Niekrasz, S. Roth, and T. Carroll. "E-081 Susceptibility – Weighted imaging findings in experimental acute ischemic stroke model." In SNIS 18TH ANNUAL MEETING. BMJ Publishing Group Ltd., 2021. http://dx.doi.org/10.1136/neurintsurg-2021-snis.176.

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Sousa, G., C. S. Samary, F. Cruz, et al. "Systemic Infusion of Propofol Better Immunomodulates the Lungs Than Dexmedetomidine in Experimental Focal Ischemic Stroke." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2373.

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Attaluri, Anilchandra, Liang Zhu, and Zhongping Huang. "Targeted Brain Hypothermia Induced by an Interstitial Cooling Device in Human Neck: An Experimental Study." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205558.

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In recent years, mild or moderate hypothermia during which brain temperature is reduced to 30–35°C, has been proposed for clinical use as an adjunct for achieving protection from cerebral ischemia during cardiac bypass injury [Nussmeier 2002], carotid endarterectomy [Jamieson et al., 2003] and resection of extra-cranial aneurysm [Wagner and Zuccarello 2005], as well as stroke and traumatic brain injury [Marion et al., 1996; Marion 1997]. It has been shown that a reduction in brain temperature as small as 2°C substantially reduced ischemic cell damage [Clark et al., 1996], or improved significa
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Heil, L. B., C. L. Braga, R. M. Sacramento, et al. "Comparative Effects of Ketamine and Dexmedetomidine on Brain and Lung Damage in Experimental Acute Ischemic Stroke." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3941.

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Ozertem, Umut, Andras Gruber, and Deniz Erdogmus. "Automatic Brain Image Segmentation for Evaluation of Experimental Ischemic Stroke Using Gradient vector flow and kernel annealing." In 2007 International Joint Conference on Neural Networks. IEEE, 2007. http://dx.doi.org/10.1109/ijcnn.2007.4371162.

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Mendes, R. D. S., G. Martins, M. V. de Oliveira, et al. "Hyperoncotic Albumin Attenuates Brain Damage Compared to Saline and Iso Oncotic Albumin in Experimental Focal Ischemic Stroke." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2727.

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Chueh, Juyu, Christine F. Silva, Ajay K. Wakhloo, and Matthew J. Gounis. "In-Vitro Clot Modeling for the Preclinical Assessment of Mechanical Thrombectomy in Acute Ischemic Stroke." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19230.

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Mechanical thrombectomy devices, such as retrievers or aspiration catheters, have recently received approval from the FDA for the treatment of acute ischemic stroke. There is growing interest in endovascular recanalization procedures due to mounting evidence of favorable clinical outcomes. Several attempts have been made to establish dedicated clot models for in-vitro or in-vivo simulation of thromboembolism [1,2]. However, little is known about the mechanical and structural similarities between experimental clots and human sources of emboli that cause stroke. The goal of this study is to comp
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Filipova, Mariela, Daniela Popova, and Christyan Stoychev. "THE USE OF SPECIALIZED KINESITHERAPY IN PATIENTS WITH ISCHEMIC STROKE WHO ARE TREATED WITH TISSUE PLASMINOGEN ACTIVATOR." In INTERNATIONAL SCIENTIFIC CONGRESS “APPLIED SPORTS SCIENCES”. Scientific Publishing House NSA Press, 2022. http://dx.doi.org/10.37393/icass2022/158.

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ABSTRACT Introduction: In kinesitherapy practice, the challenge is the use of venous thrombolysis with tissue plasminogen activator, due to the relatively severe general condition and the need for kinesitherapy in the first 12 hours of application of tissue plasminogen activator. In our methodology, we introduce the application of passive and active exercises, PNF method, mirror therapy, kinesiotape, etc. Aim and objective: The aim of the study is to compare the methodology proposed by us with standard ones. The subject of the study were 15 patients with ischemic stroke who were treated with v
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Vilardo, A., N. D. N. Rocha, R. F. Magalhães, et al. "Pressure-Support Compared to Pressure-Controlled Ventilation Improves Cardiorespiratory Function and Mitigates Brain Endothelial Cell Damage in Experimental Acute Ischemic Stroke." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3547.

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