Relevant bibliographies by topics / Experimental ischemic stroke

Academic literature on the topic 'Experimental ischemic stroke'

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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 (August 28, 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 activator in 1996. This review aims to summarize current stroke therapies, the preclinical experimental models used to help develop stroke therapies, as well as their advantages and limitations. In addition, this review discusses the potential for naturally occurring canine ischemic stroke models to compliment current preclinical models and to help bridge the translational gap between small mammal models and human clinical trials.
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Yang, Fan, Ziying Wang, Xinbing Wei, Huirong Han, Xianfang Meng, Yan Zhang, Weichen Shi, et al. "NLRP3 Deficiency Ameliorates Neurovascular Damage in Experimental Ischemic Stroke." Journal of Cerebral Blood Flow & Metabolism 34, no. 4 (January 15, 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 barrier (BBB) damage. We further showed that the contribution of NLRP3 to neurovascular damage was associated with an autocrine/paracrine pattern of NLRP3-mediated interleukin-1 β (IL-1 β) release as evidenced by increased brain microvessel endothelial cell permeability and microglia-mediated neurotoxicity. Finally, we found that NOX2 deficiency improved outcomes after ischemic stroke by mediating NLRP3 signaling. This study for the first time shows the contribution of NLRP3 to neurovascular damage and provides direct evidence that NLRP3 as an important target molecule links NOX2-mediated oxidative stress to neurovascular damage in ischemic stroke. Pharmacological targeting of NLRP3-mediated inflammatory response at multiple levels may help design a new approach to develop therapeutic strategies for prevention of deterioration of cerebral function and for the treatment of stroke.
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Vannucci, Susan J., Lisa B. Willing, Shozo Goto, Nabil J. Alkayed, Robert M. Brucklacher, Teresa L. Wood, Javad Towfighi, Patricia D. Hurn, and Ian A. Simpson. "Experimental Stroke in the Female Diabetic, db/db, Mouse." Journal of Cerebral Blood Flow & Metabolism 21, no. 1 (January 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 carotid artery ligation followed by varying periods of hypoxia (8% oxygen/92% nitrogen) to assess mortality, infarct volume, and tissue damage by light microscopic techniques. End-ischemic regional cerebral blood flow (CBF) was determined using [14C] iodoantipyrine autoradiography. Glycolytic and high energy phosphate compounds were measured in blood and brain by enzymatic and fluorometric techniques. Gender and diabetes had significant effects on mortality from HI and extent of brain damage in the survivors. Female mice were more resistant than their male counterparts, such that the severity (mortality and infarction size) in the male diabetics > female diabetics ~ male controls > female controls. End-ischemic CBF and depletion of cerebral high energy reserves were comparable among all groups. Surprisingly, female diabetic mice were more hyperglycemic and demonstrated a greater prolonged lactacidosis than the males; however, they were more resistant to damage. The results suggest a unique pathophysiology of hypoxia–ischemia in the female diabetic brain.
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Sommer, Clemens J. "Ischemic stroke: experimental models and reality." Acta Neuropathologica 133, no. 2 (January 7, 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 (October 3, 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 efficacy and safety of remote ischemic conditioning for acute moderate ischemic stroke. Sample size estimates A maximum of 1800 subjects are required to test the superiority hypothesis with 80% power according to a one-sided 0.025 level of significance, stratified by gender, age, time from onset to treatment, National Institutes of Health Stroke Scale (6–10 vs. 11–16), degree of responsible vessel stenosis, location of stenosis, and stroke etiology. Methods and design Remote Ischemic Conditioning for Acute Moderate Ischemic Stroke is a prospective, random, open label, blinded endpoint and multi-center study. The subjects are divided into experimental group and control group randomly. The experimental group was treated with remote ischemic conditioning twice daily with 200 mmHg pressure for 10–14 days besides guideline-based therapy. The control group was treated according to the guidelines. Study outcome The primary efficacy endpoint is favorable functional outcome, defined as modified Rankin Scale 0–1 at 90 days post-randomization.
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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 stroke. This comprehensive review summarizes antioxidant effects of some polyphenols, which have the most inhibition effects on reactive oxygen species generation and oxidative stress after ischemic stroke.
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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' invasion to the ischemic brain tissue occurs as the result of VLA-4 ̶ VCAM-1 interaction. Regarding Tcell subtypes, CD4+ cells have known detrimental effects in the ischemic area, while natural killer T cells (NKT cells) and γδ T cells have minor importance in the early stage of ischemia. While some studies proved the cerebroprotective impact of T regulatory cells, others refuted this by presenting a prominent harmful role of them. Bcells have important protective function by releasing IL-10. Neutrophils along with microglial cell, appearing as the first inflammatory cell in the ischemic tissue, and also macrophages deteriorate ischemia. Mast cells and dendritic cells are of great value in stroke progression. The resting astrocytes are neuroprotective, whereas the activated ones present detrimental function in the ischemic region by expression of GFAP. Hence, stroke consequences occur as the result of systemic inflammatory response. The more activation of this system, the poorer neurological outcomes would be observed. As expected, anti-inflammatory interventions in the experimental stroke in animals, have revealed successful results as less infarct size and attenuated neurological damages.
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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 (June 30, 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 model. The neurological deficit, the size of ischemic brain lesion and hemorheological parameters (hematocrit, kinetics of red blood cells (RBC) (dis)aggregation and RBC deformability) were evaluated. Results. The neurological deficit was correlated with the size of brain ischemic lesion. The increased rate of RBC aggregate formation was detected in both stroke models. At the same time, the strength of RBC aggregates changed in a model-dependent manner, namely, it raised sharply in the MCA ligation stroke model, but was somewhat decreased in thromboembolic stroke model. Conclusion. The focal stroke models produce repeatable and neurologically significant lesions of brain followed with fundamental changes in the hemorheological parameters. The way of ischemia producing can be crucial for the direction of hemorheological changes.
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Sheng, Siyuan P., Beilei Lei, Michael L. James, Christopher D. Lascola, Talaignair N. Venkatraman, Jin Yong Jung, Mervyn Maze, et al. "Xenon Neuroprotection in Experimental Stroke." Anesthesiology 117, no. 6 (December 1, 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, mice were subjected to intracerebral hemorrhage with or without 30% Xe for 20 h. Brain water content, hematoma volume, rotarod function, and microglial activation were measured. Results Cerebral infarct sizes (mean±SD) for 0, 15, 30, and 45% Xe were 212±27, 176±55, 160±32, and 198±54 mm, respectively (P=0.023). Neurologic scores (median±interquartile range) followed a similar pattern (P=0.002). Infarct size did not vary with treatment duration, but neurologic score improved (P=0.002) at all xenon exposure durations (8, 20, and 44 h). Postischemic treatment with either 30% Xe or subtherapeutic hypothermia (36°C) had no effect on 28-day outcome. Combination of these interventions provided long-term benefit. Xenon improved intracerebral hemorrhage outcome measures. Conclusion Xenon improved focal ischemic outcome at 7, but not 28 days postischemia. Xenon combined with subtherapeutic hypothermia produced sustained recovery benefit. Xenon improved intracerebral hemorrhage outcome. Xenon may have potential for clinical stroke therapy under carefully defined conditions.
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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 (August 10, 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 cerebral artery occlusion. We observed a significant increase of CD4+ and CD8+ T cells presented in the peri-infarct area at up to one month after experimental ischemic stroke. The brain invading T cells after ischemic stroke demonstrated close interaction with active astrocytes and a progressive proinflammatory phenotype as evidenced by the increased expression of T cell activation markers CD44 and CD25, proinflammatory cytokines INF-γ, IL-17, IL-10, TNF-α, and perforin, with corresponding transcriptional factors T-bet and RORc. Our results indicated a prolonged activation of brain invading CD4+ and CD8+ T cells after ischemic stroke which may play a role in the neural repair process after stroke.
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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, their clinical translation has been less successful. Master inflammatory cytokines, such as IL-1, are of particular interest. IL-1’s isoforms, IL-1α and IL-1β, were long thought to have similar function. While IL-1β has been extensively studied in stroke, the role of IL-1α during post stroke inflammation has been overlooked. Because IL-1 inhibitors have been unsuccessful in clinical application, we reasoned that IL-1α may provide previously unknown benefits to the brain after injury. We hypothesized that IL-1α could be protective or even accelerate reparative processes in the brain such as producing new blood vessels (angiogenesis) or neurons (neurogenesis). To test that IL-1α is protective after stroke, we tested IL-1α’s protective effects on primary cortical neurons in in vitro models of stroke. We showed that IL-1α was directly protective on primary cortical neurons in a dose-dependent fashion. We then performed mouse middle cerebral artery occlusion stroke studies to determine the safety of giving IL-1α in vivo. These studies showed that administering IL-1α acutely was neuroprotective. However, intravenous (IV) administration of IL-1α resulted in transient, hemodynamic changes following drug delivery. To minimize these systemic effects, we administered IL-1α intra-arterially (IA) directly into the stroke affected brain tissue, allowing us to significantly lower the concentration of administered IL-1α. In comparison to IV, IA IL-1α showed greater histological protection from ischemic injury as well as improved functional recovery following stroke, all without systemic side effects. To test that IL-1α could aid in neurorepair following stroke, we tested IL-1α’s ability to help damaged blood vessels repair in vitro. We found that IL-1α significantly increased brain endothelial cell activation, proliferation, migration, and capillary formation. We tested IL-1α’s proangiogenic properties in vivo by administering IL-1α three days following stroke. Delayed administration allowed us to separate IL-1α’s acute neuroprotective effects from potential subacute angiogenic effects. We found that mice receiving IL-1α performed significantly better on behavioral tests and also showed greater vascularization within the penumbra two weeks following stroke. We also found that IL-1α treated animals showed more endothelial activation than vehicle treated animals. Finally, our studies showed that IL-1α treated animals showed increased early-phase neurogenesis with evidence of increased proliferation at the subventricular zone suggesting that IL-1α’s beneficial effects are even more far-reaching than previously thought. In conclusion, our experiments suggest that the inflammatory cytokine IL-1α is neuroprotective and neuroreparative in experimental ischemic stroke and worthy of further study as a novel stroke therapy.
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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-minutes transient occlusion of the middle cerebral artery (MCA) in Wistar rats, followed by 24 hours of reperfusion. During surgery, multi-site laser Doppler flowmetry (LDF) was used for real-time monitoring of cerebral blood flow both in the lateral MCA territory and in the borderzone between the MCA and anterior cerebral artery territories, where the collateral circulation is connecting these two different vascular territories. The relationship between collateral flow, evaluated by multi-site LDF in the collaterals territory, and the post-reperfusion molecular penumbra, defined by protein expression of Heat Shock Protein 70kDa (HSP70), was investigated. Good collateral flow was associated with reduced extent of both molecular penumbra and ischemic core and increased extent of intact tissue, suggesting a complete protection from ischemic injury in variable areas of the cortex and striatum, if reperfusion is achieved. Conversely, poor collateral status was associated with a greater extent of both ischemic core and molecular penumbra. High variability in infarct size is common in experimental stroke models and highly affects statistical power and validity of preclinical neuroprotection trials. Cerebral collateral flow was explored as a stratification factor for the prediction of ischemic outcome, using magnetic resonance imaging (MRI) as a reference. Multi-site LDF monitoring for collateral flow assessment was able to predict ischemic outcome and infarct typology and reflected perfusion deficit in good agreement with acute MRI. These results support the additional value of cerebral collateral flow monitoring for outcome prediction in experimental ischemic stroke, especially when acute MRI facilities are not available. Modulating collateral blood flow in order to augment or maintain perfusion to the ischemic penumbra could represent a new therapeutic strategy for the hyperacute (even pre-hospital) phase, particularly if applied before recanalization therapies. Four therapeutic strategies were administered 30 minutes after ischemia onset: acetazolamide (selective cerebral vasodilation), polygeline (intravascular volume load), phenylephrine (induced hypertension) and head-down tilt (cerebral flow diversion). Globally, the treated animals showed better outcomes at 24 hours post reperfusion and an augmentation of cerebral perfusion, especially in the collaterals territory, after treatment administration. These results prompt further study of strategies aiming at modulating the cerebral collateral circulation. In conclusion, the cerebral collateral circulation and its functional performance determined both ischemic outcome and penumbra in the experimental model considered. Monitoring collateral flow while testing therapeutic strategies provides insight about their mechanism of action.
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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 channels, subtype-selective modulators of GABA A receptors, weak inhibitors of glutamate receptors and activators of some potassium channels, all potentially important in the pathogenesis of ischemic stroke. Mefenamic acid, a prototype fenamate, administered by intracerebroventricular (ICV) infusion, reduced the ischemic brain damage and edema volume in the middle cerebral artery occlusion model in male rats. Consistent with these results, systemic administration of mefenamic acid, by multiple intravenous injections, also reduced the ischemic damage and edema volume measured by morphometric analysis and as a function of brain water content. These are the first set of experiments to demonstrate a significant neuroprotective effect of a fenamate against an in vivo model of ischemic stroke. In vitro , mefenamic acid was also shown to reduce glutamate-evoked cell death ( excitotoxicity ) in a concentration-dependent manner in cultured embryonic rat hippocampal neurons. Similarly, selected other fenamates also reduced excitotoxicity in the rank order (from highest): mefenamic acid > flufenamic acid ≥ meclofenamic acid > niflumic acid supporting the idea that this is a drug class action. Three pharmacological properties of fenamates, cyclooxygenase inhibition, GABA A receptor modulation and potassium channel activation were investigated as the potential mechanism(s) for the neuroprotective effects of mefenamic acid against excitotoxicity. The experimental results suggest that these are not the primary mechanisms for neuroprotective effects of mefenamic acid against glutamate-evoked cell death. Collectively, these data support the hypothesis that fenamate NSAIDs are neuroprotective against experimental models of cerebral ischemia and suggest they should be further investigated as potential pharmacological treatments for stroke.
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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 channels, subtype-selective modutators of GABAA receptors, weak inhibitors of glutaniate receptors and activators of some potassium channels, all potentially important in the pathogenesis of ischemic stroke, Mefenamic acid, a prototype fenamate, administered by intracerebroventricular (ICV) infusion, reduced the ischemic brain damage and edema volume in the middle cerebral artery occlusion model in male rats. Consistent with these results; systemic administration of mefenamic acid, by multiple intravenous injections, also reduced the ischemic damage and edema volume measured by morphometric analysis and as a function of brain water content. These are the first set of experiments to demonstrate a significant neuroprotective effect of a fenamate against an in vivo model of ischemic stroke. In vitro, mefenamic acid was also shown to reduce glutamate-evoked cell death (excitotoxicity) in a concentration-dependent manner in cultured embryonic rat hippocampal neurons. Similarly, selected other fenamates also reduced excitotoxicity in the rank order (from highest): mefenamic acid > flufenamic acid ≥ meclofenamic acid > niflumic acid supporting the idea that this is a drug class action. Three pharmacological properties of fenamates, cyclooxygenase inhibition, GABAA receptor modulation and potassium channel activation were investigated as the potential mechanism(s} for the neuroprotective effects of mefenamic acid against excitotoxicity. The experimental results suggest that these are not the primary mechanisms for neuroprotective effects of mefenamic acid against glutamate-evoked cell death. Collectively, these data support the hypothesis that fenamate NSAIDs are neuroprotective against experimental models of cerebral ischemia and suggest they should be further investigated as potential pharmacological treatments for stroke.
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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. Sin embargo, los mecanismos moleculares y su posible contribución al nexo stroke-EA se desconocen. En este trabajo hemos establecido un modelo de isquemia sencillo usando células endoteliales periféricas que expresan la SSAO/VAP-1 humana (HUVEC hSSAO/VAP-1) en condiciones de deprivación de oxígeno y glucosa (OGD). Mediante este modelo encontramos que la expresión de SSAO/VAP-1 incrementa la susceptibilidad de las células endoteliales a la OGD, y la oxidación de sus sustratos aumenta el daño vascular. Las caspasas 3 y 8 se activan durante esta muerte celular. Además, la OGD constituye un estímulo para la liberación de SSAO/VAP-1 soluble. También, una OGD corta induce la unión de leucocitos al endotelio dependiente de SSAO/VAP-1, parcialmente mediada por su actividad enzimática. Para evaluar mejor los efectos beneficiosos de nuevos compuestos inhibidores de la actividad SSAO/VAP-1 en isquemia cerebral generamos una línea celular endotelial cerebral humana que expresa la SSAO/VAP-1 (hCMEC/D3 hSSAO/VAP-1), como modelo de barrera hematoencefálica (BHE), y establecimos también las condiciones óptimas de OGD. Mediante el uso de las células HUVEC y hCMEC/D3 que expresan SSAO/VAP-1 probamos que el DPH-4, un nuevo compuesto multidiana diseñado para la EA, es capaz de proteger ambas células y disminuir la adhesión leucocitaria dependiente de SSAO en OGD con reoxigenación (OGD-Reox). El DPH-4 también fue efectivo contra el daño inducido por OGD-Reox en presencia de beta amiloide, como modelo de patología de EA. Para determinar los mecanismos moleculares subyacentes a los efectos beneficiosos de la simvastatina en el stroke, utilizamos las células hCMEC/D3 que expresan SSAO/VAP-1 en OGD, así como dos modelos animales de oclusión de la arteria cerebral media (MCAO). Los resultados revelaron que la simvastatina impide la liberación de SSAO/VAP-1 soluble al plasma o medio de cultivo, la cual induce la expresión de E-selectina y VCAM-1, y amplifica la inflamación y el daño subsiguiente en el cerebro infartado. Finalmente, se estudió del posible papel de la SSAO/VAP-1 en el nexo existente entre el stroke y la EA con las células hCMEC/D3. Resultados preliminares mostraron que en las células que expresan SSAO/VAP-1, la OGD-Reox induce la expresión de BACE1 y la disminución de LRP-1, y que su sustrato es capaz de incrementar los niveles de APP. Además, el metabolismo de la metilamina por la SSAO/VAP-1 induce una muerte celular adicional cuando se co-trata con Aβ1-40D, en OGD-Reox. De estos resultados concluimos que la expresión de SSAO/VAP-1 en endotelio puede incrementar el daño asociado a la OGD, y que la OGD induce la liberación de SSAO/VAP-1 soluble. También, que la oxidación de su sustrato media parte del daño vascular y que la adhesión leucocitaria dependiente de la SSAO/VAP-1 agrava la progresión de la patología aumentando la inflamación en isquemia. La inhibición de SSAO/VAP-1 por el DPH-4 puede aportar un beneficio terapéutico para el retraso y/o prevención del stroke, así como para su progresión a EA. La modulación de los niveles de SSAO/VAP-1 media parte de los efectos beneficiosos de la simvastatina en isquemia cerebral. Además, la presencia de SSAO/VAP-1 en el endotelio cerebral puede facilitar la generación de β-amiloide, incrementando el riesgo y el empeoramiento neurológico de la EA.
Vascular adhesion protein 1 (VAP-1) is a pro-inflammatory protein that mediates leukocyte recruitment through its semicarbazide-sensitive amine oxidase (SSAO, E.C 1.4.3.21) activity. Plasmatic SSAO increases in ischemic and in hemorrhagic stroke patients, and its activity predicts the appearance of parenchymal hemorrhages after tPA treatment in ischemic stroke patients. Moreover, SSAO/VAP-1 is also increased in AD patients’ plasma and brain tissue. Hence, we believe that SSAO/VAP-1 could contribute to the vascular damage in both stroke and AD. However, the molecular mechanisms of SSAO/VAP-1 in stroke and its possible contribution to the nexus of ischemic stroke and AD have not been studied in detail. In this work, an easy ischemic model was set up by using peripheral endothelial cells expressing the human SSAO/VAP-1 protein (HUVEC hSSAO/VAP-1) under oxygen-glucose deprivation (OGD) conditions. Based on this model, it was found that SSAO/VAP-1 expression increases the susceptibility of endothelial cells to OGD, and that its substrates oxidation through its enzymatic activity increases the vascular cell damage. Caspase-3 and caspase-8 are activated during the death process. In addition, OGD constitutes a stimulus for the soluble SSAO/VAP-1 release, partly mediated by metalloproteinase-2-dependent shedding. Also, short-time OGD induces SSAO/VAP-1-dependent leukocyte binding on endothelial cells, which is partly dependent on its enzymatic activity. In order to better evaluate the beneficial effects of new pharmaceutical compounds by SSAO/VAP-1 activity inhibition under cerebral ischemia conditions, a human brain endothelial cell line expressing the human SSAO/VAP-1 (hCMEC/D3 hSSAO/VAP-1) was further generated as a model of the brain blood barrier (BBB). OGD conditions were established with these cells as well. By using hSSAO/VAP-1 HUVEC and hCMEC/D3 cells, a novel multitarget-directed ligand (MTDL) DPH-4, designed for AD therapy, was proved able to protect both endothelial cells, as well as to decrease the SSAO-dependent leukocyte adhesion under OGD with reoxygenation. DPH-4 was also effective against the damage induced by OGD and reoxygenation in the presence of beta amyloid as a model of AD pathology. With regard to determine the molecular mechanisms underlying the beneficial effect of simvastatin on ischemic stroke, hCMEC/D3 hSSAO/VAP-1 cells subjected to OGD conditions and two middle cerebral arterial occlusion (MCAO) rat models were used. Results revealed that simvastatin could suppress the release of soluble SSAO/VAP-1 into the plasma or cell culture media, which induces the expression of the adhesion molecules E-selectin and VCAM-1, and amplifies the inflammation and the consequent damage in the infarcted brain. At last, hCMEC/D3 hSSAO/VAP-1 cells were used so as to study the possible role of SSAO/VAP-1 in the nexus between ischemic stroke and AD. Preliminary results showed that in SSAO/VAP-1-expressing cells, OGD with reoxygenation induces the expression of BACE1 and decreases the expression of LRP-1, and that the substrate of SSAO/VAP-1 can further up-regulate the levels of APP under OGD with reoxygenation. Furthermore, the metabolism of methylamine by SSAO/VAP-1 activity induces additional cell death when co-treated with Aβ1-40D under OGD with reoxygenation. In summary, these results conclude that the expression of SSAO/VAP-1 in endothelial cells can increase the OGD-associated cell damage. OGD induces soluble SSAO/VAP-1 release. The oxidation of its substrate mediates part of the tissue damage. SSAO/VAP-1 activity-dependent leukocyte binding further exacerbates the disease progression by augmenting inflammation in cerebral ischemia. The inhibition of SSAO/VAP-1 activity by DPH-4 can provide a therapeutic benefit to the delay and/or prevention of ischemic stroke as well as its progression to AD. The modulation of the SSAO/VAP-1 levels mediates part of the beneficial effect of simvastatin on cerebral ischemia. In addition of ischemic condition, the presence of SSAO/VAP-1 in brain endothelium may facilitate the generation of β-amyloid, hence increasing the risk and neurological worsening of AD.
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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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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.

Upon ischemia, cellular lipids are released due to massive cell damage and free lipids significantly contribute to the progression of acute and delayed cell death. The aim of this study was to evalute the effect of enriched environment on lipid metabolism. In particular we characterize the activation of the transcription factor liver X receptor (LXR) in glial scar formation and regulation of cholesterol balance of relevance for functional recovery following stroke.                                      Brain tissues from animals subjected to permanent occlusion of middle cerebral artery (pMCAo) were analysed for LXRα and β protein expression. We found an upregulation and an increased transcriptional activity of LXRβ in the peri-infarct area of rats housing in an enriched environment following pMCAO. Our data anticipate that enriched environment may have positive effects on lipid recycling in the ischemic hemisphere following experimental stroke.

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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 idea of implementing Electrical Bioimpedance (EBI) in a portable device, allowing non-invasive assessment as a useful tool for the pre-hospital triage of stroke and Traumatic Brain Injury (TBI) patients. Unfortunately, these studies have not reported any results from human subjects in the acute phase of the stroke. The numerical simulations are also based on simple models that sometimes lack necessary details. Finite Element Method (FEM) simulations on a realistic numerical head model as well as experimental Bioimpedance Spectroscopy (BIS) measurements from human subjectsin the acute, subacute and chronic phasesof stroke were used to answer the following research questions: (i) Does stroke modify the electrical properties of brain tissue in a way that is detectable via EBI? (ii) Would it be possible to detect stroke via EBI as early as in the acute and sub-acute phase?(iii) Is EBI sensitive enough to monitor changes caused by stroke pathogenesis? Using FEM to simulate electrical current injection on the head and study the resulting distribution of electrical potential on the scalp, it was shown that Intra-Cranial Hemorrhage (ICH) affects the quasi-symmetric scalp potential distribution,creating larger left-right potential asymmetry when compared to the healthy head model. Proof-of-concept FEM simulations were also tested in a small cohort of 6ICH patients and 10 healthy controls, showing that the left-right potential difference in the patients is significantly (p<0.05) larger than in the controls. Using bioimpedance measurements in the acute,  subacute and chronic phasesof stroke and examining simple features, it was also shown that the head EBI measurements of patients suffering stroke are different from controls, enabling the discrimination of healthy controls and stroke patients at any stage of the stroke. The absolute change in test-retest resistance measurements of the control group (~5.33%) was also found to be significantly (p<0.05) smaller than the EBI measurements of patients obtained 24 hours and 72 hours after stroke onset (20.44%). These results suggested that scalp EBI is sensitive to stroke pathogenesis changesand thususeful for bedside monitoring in the Neuro-ICU. These results suggested that EBI is a potentially useful tool for stroke diagnosis and monitoring. Finally, the initial observations based on a small number of patients, addressing the proposed future work of this thesis, suggested that the average head resistance amplitude of hemorrhagic stroke patients is smaller than in healthy controls, while ischemic stroke patients show a larger resistance amplitude than the controls. Scalp potential asymmetry analysis of healthy, hemorrhagic and ischemic stroke subjects also suggests that these three groups can be separated. However, these results are based on a small number of patients and need to be validated using a larger cohort. Initial observations also showed that the resistance of the EBI measurements of controls is robust between test and retest measurements, showing no significant difference (less than 2% and p>0.05). Subject position during EBI recording (supine or sitting) did not seem to affect the resistance of the EBI measurements (p>0.05). However, age, sex and head size showed significant effects on the resistance measurements. These initial observations are encouraging for further research on EBI for cerebral monitoring and stroke diagnosis. However, at this stage, considering the uncertainties in stroke type differentiation, EBI cannot replace CT but has the potential to be used as a consultation tool.

QC 20151109

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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 caràcter apoptòtic i més lenta al voltant, en la zona de penombra. El gran impacte socio-econòmic de la malaltia i l’existència d’una mort programada dil·latada en el temps han fet que es posin grans esforços en la búsqueda de mecanismes per salvar la zona de penombra. Tenint en compte aquests fets, el present treball s’ha centrat en l’estudi dels mecanismes de mort cel·lular involucrats en la isquèmia cerebral. Per fer-ho, s’ha utilitzat un model de privació d’oxigen i glucosa (OGD) en cultius corticals mixtes d’embrions de rata. Utilitzant aquest model d’isquèmia s’ha observat neuroprotecció pel bloqueig dels receptors NMDA, principal responsable de l’entrada massiva de calci, i l’activació de la caspasa-3, una proteasa encarregada del desmantellament cel·lular durant l’apoptosis. A més, s’ha estudiat el paper dels antagonistes dels receptors de mort en l’OGD. Aquests receptors són responsables de l’activació de la via apoptòtica extrínseca. S’ha observat que l’OGD indueix la degradació dels antagonistes FLIPL i IAP2 i modula l’expressió de FAIML a través de la via de les MAP cinases. Per altre banda, s’ha observat que el silenciament o la sobrexpressió de FAIML mitjançant vectors lentivirals no afecta la viabilitat dels cultius així com tampoc la morfologia nuclear apoptòtica ni els nivells de caspasa-3 activa en les neurones sotmeses a l’insult isquèmic. En conjunt aquests resultats han servit per aprofundir en els mecanismes moleculars implicats en la isquèmia cerebral i poden servir de base per futurs estudis que ajudin al disseny de noves estrategies terapèutiques.
Stroke is the second cause of death in industrialized countries and is the leading cause of disability in adults. The only currently approved treatment is the thrombolytic tissue plasminogen activator (tPA), which can be applied only in a very small number of patients and within a narrow therapeutic window. The mechanisms of cell death in brain ischemia are numerous and are caused by the interruption of the blood flow to the brain, which causes a quick necrotic death in the core of the affected area and a slow apoptotic-like death around, in the ischemic penumbra. The major socio-economic impact of the disease and the existence of a programmed cell death that stretches through time explain the effort that is being done to find new strategies to save the penumbra. Given these facts, the present work has focused on studying the mechanisms of cell death involved in brain ischemia. To do this, we used a model of oxygen and glucose deprivation (OGD) in mixed cortical cultures from rat embryos. Using this model of ischemia we observed neuroprotection by blocking NMDA receptor, the primarily responsible for the massive influx of calcium during ischemia, and activation of caspase-3, a protease responsible for dismantling the cell during apoptosis. In addition, we studied the role of death receptor antagonists in OGD. These receptors are responsible for the activation of the extrinsic apoptotic pathway. It has been observed that OGD induces degradation of the antagonists FLIPL and IAP2 and modulate the expression of FAIML through the MAP kinase pathway. On the other hand, we observed that the overexpression or silencing of FAIML using lentiviral vectors did not affect the viability of the cultures nor the apoptotic nuclear morphology or the levels of active caspase-3 in the neurons subjected to the ischemic insult. Together these results have served to study the molecular mechanisms involved in brain ischemia and may provide the basis for future studies that will help to design new therapeutic strategies.
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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 present an overview of neuroprotective agents studied in traumatic brain injury, subarachnoid hemorrhage, ischemic stroke, and hypoxic-ischemic encephalopathy in adults due to cardiac arrest. They review the molecular mechanisms involved in secondary neuronal injury and how drugs targeting these mechanisms have been evaluated in clinical trials. Finally, the chapter briefly analyzes the possible reasons for repeated failures in translating experimental success into clinical benefit.
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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, 189–213. Cham: 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, 41–73. Berlin, Heidelberg: 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, 267–73. Berlin, Heidelberg: 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, 309–25. Singapore: 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, 169–79. New York, NY: 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, 317–35. New York, NY: 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, 451–68. New York, NY: 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, 125–31. Cham: 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, 187–98. Tokyo: 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, Tatsuya Hoshino, Norio Fujiwara, Shin Nakamura, Yoshihiro Murata, 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, 519–24. Boston, MA: 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, Veronica Revkova, Kirill Sukhinich, Pavel Melnikov, Leonid Gubsky, and Konstantin Yarygin. "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. BMA House, Tavistock Square, London, WC1H 9JR: 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, M. A. Antunes, P. Pelosi, P. R. M. Rocco, and P. L. Silva. "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 significantly post-ischemic regional histopathology [Wass et al., 1995]. Most of the currently used clinical studies have examined only systemic hypothermia by whole body cooling. The major methodological drawback of this approach is slow cooling rate (∼0.5°/hour) due to the large volume of the human body and arteriovenous shunt vasoconstriction [Krieger et al., 2001; Marion et al., 1997; Schwab et al., 1998]. Whole body cooling does induce systemic complications. The systemic risks may outweigh the beneficial effects of neuro-hypothermia in the current clinical practice. Selective brain cooling which keeps the rest of body at normal temperature, on the other hand, can be used to maximize the neuroprotection of hypothermia.
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Heil, L. B., C. L. Braga, R. M. Sacramento, M. A. Antunes, C. D. S. Samary, P. Pelosi, F. F. Cruz, P. L. Silva, and P. R. M. Rocco. "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, N. D. N. Rocha, C. D. S. Samary, R. Fonseca, A. Fernandes, 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 compare the structure and compression behavior of the possible sources of the cerebral emboli extracted from patients and model clots produced in-vitro using human, porcine and bovine donors.
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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:
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 venous thrombolysis. Their advantages and disadvantages in the application will be highlighted Methods: The study was conducted in the period from 2008-2014 in the Neurology Department at the Hospital in Blagoevgrad. The use of specialized kinesitherapy in 15 patients with ischemic stroke treated with venous thrombolysis (experimental group) was compared with the use of standard methods in non-thrombolized (control group) patients. In our study, we used the Barthel Index to verify the data. Statistically significant difference is reported using nonparametric statistics and Mann-Whitney tests. Results: In our study, we examined the activities of daily living using the Barthel index scale. All patients were tested on the day of hospitalization, on the 5th day, and on the 30th day. Of the experimental group, there was a statistically significant difference Asymp. Sig. ≤ .001, which proves that there was a change in the activities of daily living. No sta-tistically significant difference was registered in the control group. Discussion: Through intravenous thrombolysis, a specialized kinesitherapy program, including passive, active move-ments in the uninjured limbs, in mirror therapy and kinesiotaping patients have a better quality of life and faster recovery occurs.
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Vilardo, A., N. D. N. Rocha, R. F. Magalhães, E. B. Carvalho, C. Robba, P. Pelosi, C. D. S. Samary, P. L. Silva, and P. R. M. Rocco. "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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