Relevant bibliographies by topics / Cerebral ischemia – Animal models

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
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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 reduced infarct size by 20% and improved neurological score by 12% compared with control; a second therapy improved efficacy by an additional 18% and 25%, respectively. Publication bias may affect combination efficacy for infarct size but not neurological score. Combining thrombolysis with other therapies may extend the time window from 4.4 to 8 hours in animal models, although testing beyond 6 hours is required to confirm this. Benefits of additional therapy decreased as the efficacy of the primary treatment increased, with combination efficacy reaching a ceiling at 60% to 80% protection. Combining treatments may bring benefits and extend the time window for treatment. More evidence is needed due to potential publication bias and heterogeneity.
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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 modifiers can exert influence on all known pathways involved in the complex course of ischemic disease development. Beneficial transcriptional effects range from attenuation of cell death, suppression of inflammatory processes, and enhanced blood flow, to the stimulation of repair mechanisms and increased plasticity. Most striking are the results obtained from pharmacological inhibition of histone deacetylation in animal models of stroke. Multiple studies suggest high remedial qualities even upon late administration of histone deacetylase inhibitors (HDACi). In this review, the role of epigenetic mechanisms, including histone modifications as well as DNA methylation, is discussed in the context of known ischemic pathways of damage, protection, and regeneration.
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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 ischemia after 24 hours reperfusion.Method: This study uses post-test only study group design. The subjects are 20 female and 20 male Wistar rat that being divided into 8 groups which are male rat with occlusion duration of 5 minutes, 10 minutes and 20 minute, also the female rat with occlusion duration of 5 minutes, 10 minutes, 20 minutes respectively. BCCAO occlusion then followed by 24 hour reperfusion. Rat decapitation and brain extraction are done after reperfusion. Brain tissue sliced into 2 mm size and stained with 0.05% TTC solution for 30 minutes. Ischemic brain volume are being observed using Cavalieri method. Statistical data are being analyzed using One Way Anova.Result: There are significant difference in male rat cerebral ischemia volume between 5 minutes and 10 minutes occlusion (p<0.006). Meanwhile, there are no significant difference at cerebral ischemia volume between 10 and 20 minutes occlusion group (p=0.377). There are significant differences in the volume of brain ischemia between the 5, 10 and 20 minutes ischemia group (p<0.05). Post-hoc test showed no significant differences between the male and female rat (p>0.05).Conclusion: Duration of the bilateral common carotid artery occlusion for 5 and 10 minutes affect the volume of cerebral ischemia in male rat after 24 hour reperfusion. The occlusion of bilateral common carotid artery for 5,10 and 20 minutes also affect the volume of cerebral ischemia in female rat after 24 hour reperfusion. No significant differences of cerebral ischemia volume between the sexes after 5, 10 and 20 minutes occlusion.Bangladesh Journal of Medical Science Vol.17(1) 2018 p.129-137
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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 understanding of cerebral plasticity is pivotal to design effective therapeutic strategies. Experimental models and clinical studies have fueled the current understanding of the cellular and molecular processes responsible for plastic remodeling. In this review, we describe the known mechanisms, in patients and animal models, underlying cerebral reorganization and contributing to functional recovery after ischemic stroke. We also discuss the manipulations and therapies that can stimulate neural plasticity. We finally explore a new topic in the field of ischemic stroke pathophysiology, namely the brain-gut axis.
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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-treatment with a combination of melatonin and EA on regional cerebral blood flow (rCBF), neurological deficit score and infarct volume was investigated in both permanent and transient middle cerebral artery occlusion (MCAO) models in rats. When compared with the single treatment of melatonin or EA, the combination therapy resulted in a significant improvement of neurological function and a dramatic reduction of infarct volume at 72 hr after transient MCAO. A significant upregulatory effect on rCBF has been exerted by the combined treatment. The effect of a combination of melatonin and EA on inflammatory reaction was investigated in the second study. Post-treatment of the combination therapy effectively inhibited neutrophil infiltration as well as the expression of some pro-inflammatory mediators, and increased the anti-inflammatory protein expression at 72 hr after transient MCAO. This beneficial effect may be due to the respective anti-inflammatory effects of melatonin and EA. In the third study, the effect of a combination of melatonin and EA on apoptosis was examined. When compared with the EA treatment alone, post-treatment of the combination therapy exerted a greater inhibitory effect on tissue apoptosis and expression of the pro-apoptotic proteins as well as an upregulatory effect on the anti-apoptotic protein expression. In the fourth study, the effect of continuous post-treatment of a combination of melatonin and EA on transient MCAO was investigated. The combination treatment significantly improved neurological function and decreased infarct volume at 7 days after transient MCAO. Cell proliferation and expression of the neurotrophic factor were increased by the combined treatment. The effect of pretreatment with a combination of melatonin and EA was examined in the fifth study. Neurological function was improved and infarct volume was reduced by the combination pretreatment at 24 hr after transient MCAO. The inflammatory and apoptotic reaction were inhibited by the combined pretreatment through the modulatory effect of the related proteins. In summary, our results show that, when compared with the single treatment of either melatonin or EA, post-treatment with a combination of melatonin and EA induced a complementary neuroprotective effect on improvement of neurological function and a dramatic reduction of infarct volume after transient MCAO. The complementary protection may be partially mediated via anti-inflammation and anti-apoptosis after transient cerebral ischemia. Pretreatment with a combination of melatonin and EA may be more effective in preventing ischemic brain injury after transient focal cerebral ischemia.
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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 is via clinical studies. Unfortunately, well-controlled experiments in humans are difficult due to small patient populations, the presence of numerous confounding variables, and ethical issues associated with invasive or discomforting experimental procedures. Anesthetized animal models of cerebral ischemia afford a means of avoiding the above difficulties. However, anesthesia and physiological perturbations that occasionally follow brain ischemia may affect the reliability of certain tools used to study this disease, such as functional magnetic resonance imaging (fMRI). Therefore, the central goals of this thesis were: 1) to evaluate the feasibility of performing fMRI in anesthetized and awake animals, 2) to assess fMRI responses under various perturbations of cerebral perfusion and tissue oxygenation in order to identify key factors that may modulate functional signal changes following ischemia, and 3) to utilize fMRI, behavioral tests and histology in an anesthetized animal model of transient focal cerebral ischemia to explore postischemic changes in brain pathology/function and how they relate to changes in behavior. In the first study of this dissertation, I report the evaluation of fMRI responses in anesthetized and awake animals. Anesthesia is frequently used in animal models of cerebral ischemia, but is known to alter brain perfusion and metabolism which may, in turn, affect fMRI responsivity. Perfusion-based fMRI was used to evaluate cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) responses to hypercapnia in awake and isoflurane-anesthetized rats. Hypercapnia produced significant CBF and BOLD fMRI signal changes throughout the cerebrum in awake and isoflurane-anesthetized groups. These results show that perfusion-based fMRI can successfully detect stimulus-evoked hemodynamic changes in the brains of both conscious and isoflurane-anesthetized animals. The second study of this dissertation: 1) investigates the effects of alterations in cerebral perfusion and oxygenation on fMRI signal changes, and 2) examines the self-consistency of an imaging-based formalism for the calculation of the cerebral metabolic rate of oxygen (CMRO2). Functional MRI responses to a stimulus can be described in terms of relative or absolute signal change. A relative fMRI response is defined as a percent-change relative to its own respective baseline value. An absolute fMRI response is defined as a quantitative change relative to a single fixed baseline value that serves as a control. Thus, an absolute fMRI signal change is largely independent of the baseline state and may more accurately index brain activity when baseline fMRI signals change significantly over time due to, for example, hemodynamic-metabolic disturbances that occur during and/or after brain ischemia. To address these issues, the effects of inspired hypoxic, normoxic, hyperoxic, and hypercapnic gases on baseline and forepaw stimulation-evoked changes in BOLD and CBF fMRI signals were examined in isoflurane-anesthetized rats. Relative fMRI responses to forepaw stimulation varied-whereas. absolute responses were similar--across gas conditions. These results demonstrate that absolute measurements of fMRI signal change may lend a more accurate measure of brain activity during states of altered basal physiology as well as support the self-consistency of the imaging-based CMRO2 formalism under these conditions. The third and last study of this dissertation utilized multimodal MRI, behavioral tests, and histology at acute to chronic periods following transient middle cerebral artery occlusion (tMCAO) in the rat to examine the evolution of pathological, functional, and behavioral parameters following transient focal cerebral ischemia. MRI was used to track the evolution of brain pathology and function following cerebral ischemia, and it was found that the cerebral sensorimotor network, critical for sensory and motor behavioral functions, showed profoundly abnormal signal changes that required up to one day to normalize. Adhesive removal, forepaw placement and beam-walk behavioral tests demonstrated sensorimotor dysfunctions that gradually improved but remained long after the recovery of MRI parameters. Postmortem histology confirmed the presence of selective neural cell death within the sensorimotor network at time points when behavior was abnormal. These results suggest that subtle postischemic pathological changes in the brain undetectable by MRI may be responsible for persistent behavioral deficits-a finding which may be relevant to a clinical subset of patients with persistent neurological morbidities despite negative MRI results following cerebral ischemia.
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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 damage following cerebral ischaemia is associated with disturbances in intracellular calcium homeostasis, the sodium-calcium exchanger (NCX) is a potential therapeutic target due to its ability to regulate intracellular calcium. Currently, however there is uncertainty as to whether the plasma membrane NCX has a neuroprotective or neurodamaging role following cerebral ischemia. To address this issue I compared hippocampal neuronal injury in NCX3 knockout mice (Ncx3-/-) and wild-type mice (Ncx3+/+) following global cerebral ischaemia. In order to perform this study I first established a bilateral common carotid occlusion (BCCAO) model of global ischaemia in wild-type C57/BlHsnD mice using controlled ventilation. After trials of several ischaemic time points, 17 minutes was established as the optimum duration of ischaemia to produce selective hippocampal CA1 neuronal loss in the wild-type mice. I then subjected NCX3 knockout and wild-type mice to 17 minutes of ischaemia. Following the 17 minute period of ischaemia, wild-type mice exhibited 80% CA1 neuronal loss and 40% CA2 neuronal loss. In contrast, NCX3 knockout mice displayed > 95% CA1 neuronal loss and 95% CA2 neuronal loss. Following experiments using a 17 minute duration of global ischaemia, a 15 minute duration of ischaemia was also evaluated. Wild-type mice exposed to a 15 minute period of ischaemia, did not exhibit any significant hippocampal neuronal loss. In contrast, NCX3 knockout mice displayed 45% CA1 neuronal loss and 25% CA2 neuronal loss. The results clearly demonstrate that mice deficient for the NCX3 protein are more susceptible to global cerebral ischaemia than wild-type mice. My findings showing a neuroprotective role for NCX3 following ischaemia, suggest that the exchanger has a positive role in maintaining neuronal intracellular calcium homeostasis. When this function is disrupted, neurons are more susceptible to calcium deregulation, with resultant cell death via calcium mediated pathways. Therefore, improving NCX activity following cerebral ischaemia may provide a therapeutic strategy to reduce neuronal death.
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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 une double chaîne (tc-rtPA). Malgré des activités fibrinolytiques similaires, ces deux formes de tPA exercent des fonctions cérébrales distinctes influençant différemment la récupération des patients. Ainsi, nous avons décidé d'étudier en détail dans un modèle murin d'AVC thromboembolique les mécanismes pouvant expliquer ces effets divergents. Nous avons confirmé ces observations à savoir que sc-rtPA est bénéfique lorsqu'il est perfusé tôt après le début de l'AVC, alors que le tc-rtPA est délétère en raison d'une altération de la barrière hémato-encéphalique.L'imagerie en temps réel de la perfusion de l'ensemble du cerveau est un atout pour les études cliniques et précliniques. L'émergence des ultrasons ultra-rapides a conduit au développement du Doppler ultra-rapide et de la Microscopie de Localisation à Ultrasons (ULM), deux méthodes avec différents profils de résolutions spatio-temporelles et une excellente sensibilité aux petits flux sanguins. Nous avons combiné ces deux méthodes pour fournir un suivi longitudinal en 3D de la perfusion cérébrale dans un modèle murin d’AVC thromboembolique avec fibrinolyse par rtPA. Nos données montrent que le FUS et l’ULM présentent un intérêt majeur pour le pronostic précoce de l'AVC ischémique et de la réponse au traitement, avec une corrélation étroite entre la reperfusion précoce à 2h et la récupération tissulaire à 24h.Enfin, l’anesthésie utilisée en laboratoire interfère sur la lésion ischémique et les effets des molécules thérapeutiques testées. Nous nous sommes affranchis de ces effets en développant un nouveau modèle d’AVC ischémique chez des souris totalement éveillées. Le débit sanguin cérébral régional a été suivi par laser Doppler avant, pendant et 45min après le début de l’AVC. Le traitement par rtPA (à 20 min) est bénéfique dans les modèles d’AVC vigile et anesthésié, mais l'anesthésie est associée à un manque de corrélation entre la recanalisation et les volumes de lésion post-ischémie. Nous testons actuellement une molécule neuroprotectrice, qui était prometteuse avant d’échouer lors des essais cliniques (NXY-059), afin d’évaluer la pertinence de ce modèle novateur d’AVC pour les futures études pharmacologiques. Dans l’ensemble, ce travail fournit un panel de données précliniques innovantes pour améliorer nos chances de translation en clinique, incluant un modèle pertinent d'AVC thromboembolique chez des animaux vigiles et une méthode d'imagerie du pronostic précoce de réponse aux traitements vasculaires
The lack of translation between preclinical studies and clinical trials in the field of ischemic stroke and the failure of therapeutic developments could be explained by three aspects: (1) the lack of understanding the mechanism of the two forms of tPA, the pharmacological treatment in stroke; (2) the lack of optimized perfusion imaging tools for small animal and (3) the influence of anesthesia on treatment tested in animal models.tPA used in the clinical setting (Actilyse®) is a mix of two forms of tPA: single chain form (sc-rtPA) and two chains form (tc-rtPA). Despite similar fibrinolytic activities, these two forms exert distinct brain functions therefore influencing differentially the outcome patients. We then decided to further investigate in a relevant model of thromboembolic stroke in rodents, the mechanisms that can explain these differential effects. Here, we have confirmed differential outcomes of the two forms: whereas sc-rtPA is clearly beneficial when infused shortly after stroke onset, tc-rtPA is deleterious due to an increased alteration of the blood brain barrier integrity.Live imaging of cerebral perfusion of the whole brain is an asset for both clinical and preclinical studies. The emergence of ultrafast ultrasound led to the development of ultrafast Doppler (fUS) and Ultrasound Localization Microscopy (ULM), two methods with different sets of spatio-temporal resolutions and excellent sensitivity to small blood flows. We combined these two methods to provide a longitudinal monitoring of whole brain perfusion using the thromboembolic stroke model in mice with rtPA-induced reperfusion. Our data show that fUS and ULM are of major interest for early prognosis of ischemic stroke and response to treatment, with a tight correlation between early reperfusion at 2h and tissue recovery at 24h. Finally, we develop a relevant awake ischemic stroke model to test new therapies, avoiding interferences due to anesthesia commonly used during in vivo studies mice. The patern of the MCA was followed using Laser Doppler monitoring before, during and 45 min after the stroke onset. Although rtPA treatment is beneficial in both awake and anesthetized stroke models, anesthesia is associated with a lack of correlation between recanalization and stroke outcome. We are now testing a neuroprotective molecule, which was promising before failing in clinical trials (NXY-059), to assess the relevance of this innovative stroke model for future pharmacological studies. Altogether, we provide here a set of innovative pre-clinical data to improve our chance of translation to clinic, including a relevant model of thromboembolic stroke in awake animals and an early prognosis imaging method of response to vascular treatments
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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 a two-week period. Then, we used a model of hypotension to characterize the damage caused by this type of insult. Finally we characterized a model of hypotension plus hypoxia that can mimic real situations in the OR. We found that anesthetics alone do not have a neuroprotective effect after two weeks in the MCAO model; but the combination of anesthetics with caspase inhibitors can decrease the damage caused by ischemia. The caspase inhibitor by itself did not show a significant neuroprotective effect. We also found that repetitive periods of profound hypotension can cause important damage in the hippocampus but no memory or neurological changes were seen. The induction of only one episode of hypotension plus hypoxia did not alter the morphology of the hippocampus although induced memory changes that were reverted by the use of anesthetics.
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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 tissue after stroke. However, total body cooling has also been shown to protect the brain of term infants if initiated within 6 hours of perinatal asphyxia, and a similar level of cooling may provide protection for the brain in adults who have been resuscitated after cardiac arrest.
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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 lenght was assigned for inducing ischemic lesion size that facilitates animal survival in long-term experiment, if MCAO and other invasive procedures are combined.
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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 or lethal arrhythmias. There is also difficulty in developing stable heart failure across cases where infarct sizes can be variable. One strategy to over come this variability has been via rapid ventricular pacing, however inducing heart failure does not induce sustained heart failure in many cases if the pacing is switched off, and additionally pacing does not induce some of the underlying pathology seen in the development of heart failure [1].
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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-vivo response of the aneurysm wall to intra-saccular hemodynamic stresses. A mechanism for fundamental studies of the impact of chronically altered WSS on the intact vascular wall is provided by animal models. However, cerebral aneurysms have not been shown to occur naturally in animals. Thus, a number of animal models have been created for studying aneurysm pathogenesis including those in mice, rats, rabbits, canines, swine and primates. To make meaningful use of these models, it is important to evaluate their relevance to human biomechanics and pathophysiology.
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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 that exposure of the vessel wall to equally high WSS in the presence of decelerating flow, that is, negative WSSG, does not result in aneurysm-like destruction.
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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-conditioning (PC) may reduce the amount of reperfusion injury by applying intermittent periods of ischemia during the early moments of reperfusion. This procedure periodically occludes blood vessels during reperfusion by periodically inflating and deflating an angioplasty balloon according to a specific algorithm. Zhao et al. showed that PC reduced reperfusion injury in a canine model by applying 3 cycles of 30 seconds of reperfusion followed by 30 seconds of ischemia (re-occlusion) at the onset of reperfusion. PC in this study reduced tissue AN/AAR (area of necrosis/area at risk) by 48% [2]. In 2008, Gao et al. demonstrated that the effectiveness of PC in rats was dependent on the number of cycles in the PC algorithm, as well as the durations of the ischemia/reperfusion phases [3].
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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 identified that aneurysm initiation occurs at areas of the vessel wall that experience a combination of both high WSS and positive WSSG [1,2]
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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 relative importance of the different mechanisms involved in these processes [1]. The objective of our research is to investigate the possible relationship between wall shear stress (WSS) — which is known to regulate mechano-biological processes at the arterial wall — produced by different blood flow patterns and the evolution and rupture of cerebral aneurysms.
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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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