Academic literature on the topic 'Stroke, mice, recovery, biomarker'
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Journal articles on the topic "Stroke, mice, recovery, biomarker"
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Cecchini, Gloria, Alessandro Scaglione, Anna Letizia Allegra Mascaro, Curzio Checcucci, Emilia Conti, Ihusan Adam, Duccio Fanelli, Roberto Livi, Francesco Saverio Pavone, and Thomas Kreuz. "Cortical propagation tracks functional recovery after stroke." PLOS Computational Biology 17, no. 5 (May 17, 2021): e1008963. http://dx.doi.org/10.1371/journal.pcbi.1008963.
Full textAbstract:
Stroke is a debilitating condition affecting millions of people worldwide. The development of improved rehabilitation therapies rests on finding biomarkers suitable for tracking functional damage and recovery. To achieve this goal, we perform a spatiotemporal analysis of cortical activity obtained by wide-field calcium images in mice before and after stroke. We compare spontaneous recovery with three different post-stroke rehabilitation paradigms, motor training alone, pharmacological contralesional inactivation and both combined. We identify three novel indicators that are able to track how movement-evoked global activation patterns are impaired by stroke and evolve during rehabilitation: the duration, the smoothness, and the angle of individual propagation events. Results show that, compared to pre-stroke conditions, propagation of cortical activity in the subacute phase right after stroke is slowed down and more irregular. When comparing rehabilitation paradigms, we find that mice treated with both motor training and pharmacological intervention, the only group associated with generalized recovery, manifest new propagation patterns, that are even faster and smoother than before the stroke. In conclusion, our new spatiotemporal propagation indicators could represent promising biomarkers that are able to uncover neural correlates not only of motor deficits caused by stroke but also of functional recovery during rehabilitation. In turn, these insights could pave the way towards more targeted post-stroke therapies.
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Zaidi, Syed Kashif, Md Nasrul Hoda, Shams Tabrez, and Mohammad Imran Khan. "Pharmacological Inhibition of Class III Alcohol Dehydrogenase 5: Turning Remote Ischemic Conditioning Effective in a Diabetic Stroke Model." Antioxidants 11, no. 10 (October 18, 2022): 2051. http://dx.doi.org/10.3390/antiox11102051.
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The restoration of cerebral blood flow (CBF) to achieve brain tissue oxygenation (PbtO2) is the primary treatment for ischemic stroke, a significant cause of adult mortality and disability worldwide. Nitric oxide (NO) and its bioactive s-nitrosylated (SNO) reservoirs, such as s-nitrosoglutathione (GSNO), induce hypoxic vasodilation to enhance CBF during ischemia. The endogenous pool of SNOs/GSNO is enhanced via the activation of endothelial NO synthase (eNOS/NOS3) and by the suppression of class III alcohol dehydrogenase 5 (ADH5), also known as GSNO reductase (GSNOR). Remote ischemic conditioning (RIC), which augments NOS3 activity and SNO, is an emerging therapy in acute stroke. However, RIC has so far shown neutral effects in stroke clinical trials. As the majority of stroke patients are presented with endothelial dysfunctions and comorbidities, we tested the hypothesis that NOS3 dysfunction and diabetes will abolish the protective effects of RIC therapy in stroke, and the prior inhibition of GSNOR will turn RIC protective. Our data demonstrate that RIC during thrombotic stroke failed to enhance the CBF and the benefits of thrombolysis in NOS3 mutant (NOS3+/−) mice, a genetic model of NOS3 dysfunction. Interestingly, thrombotic stroke in diabetic mice enhanced the activity of GSNOR as early as 3 h post-stroke without decreasing the plasma nitrite (NO2−). In thrombotic stroke, neither a pharmacological inhibitor of GSNOR (GRI) nor RIC therapy alone was protective in diabetic mice. However, prior treatment with GRI followed by RIC enhanced the CBF and improved recovery. In a reperfused stroke model, the GRI–RIC combination therapy in diabetic mice augmented PbtO2, a translatory signature of successful microvascular reflow. In addition, RIC therapy unexpectedly increased the inflammatory markers at 6 h post-stroke in diabetic stroke that were downregulated in combination with GRI while improving the outcomes. Thus, we conclude that preexisting NOS3 dysfunctions due to comorbidities may neutralize the benefits of RIC in stroke, which can be turned protective in combination with GRI. Our findings may support the future clinical trial of RIC in comorbid stroke. Further studies are warranted to test and develop SNO reservoirs as the blood-associated biomarker to monitor the response and efficacy of RIC therapy in stroke.
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Zhao, Haiping, Guangwen Li, Sijia Zhang, Fangfang Li, Rongliang Wang, Zhen Tao, Qingfeng Ma, et al. "Inhibition of histone deacetylase 3 by MiR-494 alleviates neuronal loss and improves neurological recovery in experimental stroke." Journal of Cerebral Blood Flow & Metabolism 39, no. 12 (September 11, 2019): 2392–405. http://dx.doi.org/10.1177/0271678x19875201.
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HDAC3 is an essential negative regulator of neuronal plasticity and memory formation. Although a chemical inhibitor has been invented, little is known about its endogenous modulators. We explored whether miR-494 affects HDAC3-mediated neuronal injury following acute ischemic stroke. A substantial increase in plasma miR-494 was detected in AIS patients and was positively associated with the mRS at one year after symptom onset. The miR-494 levels were transiently increased in the infarcted brain tissue of mice. In contrast, miR-494 levels were reduced in neurons but increased in the medium after OGD. Intracerebroventricular injection of miR-494 agomir reduced neuronal apoptosis and infarct volume at the acute stage of MCAO, promoted axonal plasticity and long-term outcomes at the recovery stage, suppressed neuronal ataxin-3 and HDAC3 expression and increased acetyl-H3K9 levels in the ipsilateral hemisphere. In vitro studies confirmed that miR-494 posttranslationally inhibited HDAC3 in neurons and prevented OGD-induced neuronal axonal injury. The HDAC3 inhibitor increased acetyl-H3K9 levels and reversed miR-494 antagomir-aggravated acute cerebral ischemic injury, as well as brain atrophy and long-term functional recovery. These results suggest that miR-494 may serve as a predictive biomarker of functional outcomes in AIS patients and a potential therapeutic target for the treatment of ischemic stroke.
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Leon, Lisa R., David A. DuBose, and Clifford W. Mason. "Heat stress induces a biphasic thermoregulatory response in mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 1 (January 2005): R197—R204. http://dx.doi.org/10.1152/ajpregu.00046.2004.
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Previous animal models of heat stress have been compromised by methodologies, such as restraint and anesthesia, that have confounded our understanding of the core temperature (Tc) responses elicited by heat stress. Using biotelemetry, we developed a heat stress model to examine Tcresponses in conscious, unrestrained C57BL/6J male mice. Before heat stress, mice were acclimated for >4 wk to an ambient temperature (Ta) of 25°C. Mice were exposed to Taof 39.5 ± 0.2°C, in the absence of food and water, until they reached maximum Tcof 42.4 ( n = 11), 42.7 ( n = 12), or 43.0°C ( n = 11), defined as mild, moderate, and extreme heat stress, respectively. Heat stress induced an ∼13% body weight loss that did not differ by final group Tc; however, survival rate was affected by final Tc(100% at 42.4°C, 92% at 42.7°C, and 46% at 43°C). Hypothermia (Tc< 34.5°C) developed after heat stress, with the depth and duration of hypothermia significantly enhanced in the moderate and extreme compared with the mild group. Regardless of heat stress severity, every mouse that transitioned out of hypothermia (survivors only) developed a virtually identical elevation in Tcthe next day, but not night, compared with nonheated controls. To test the effect of the recovery Ta, a group of mice ( n = 5) were acclimated for >4 wk and recovered at Taof 30°C after moderate heat stress. Recovery at 30°C resulted in 0% survival within ∼2 h after cessation of heat stress. Using biotelemetry to monitor Tcin the unrestrained mouse, we show that recovery from acute heat stress is associated with prolonged hypothermia followed by an elevation in daytime Tcthat is dependent on Ta. These thermoregulatory responses to heat stress are key biomarkers that may provide insight into heat stroke pathophysiology.
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Garcia, Christian K., Gerard P. Robinson, Bryce J. Gambino, Michael T. Rua, Orlando Laitano, and Thomas L. Clanton. "The impact of castration on physiological responses to exertional heat stroke in mice." PLOS ONE 17, no. 10 (October 13, 2022): e0275715. http://dx.doi.org/10.1371/journal.pone.0275715.
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Introduction The capability of male mice to exercise in hot environments without succumbing to exertional heat stroke (EHS) is markedly blunted compared to females. Epidemiological evidence in humans and other mammals also suggests some degree of greater vulnerability to heat stroke in males compared to females. The origins of these differences are unknown, but testosterone has previously been shown to induce faster elevations in core temperature during acute, passive heat exposure. In this study, we tested the hypothesis that loss of testosterone and related sex hormones through castration would improve the performance and heat tolerance of male mice during EHS exposure. Methods Twenty-four male mice were randomly divided into 3 groups, untreated EHS mice (SHAM-EHS), castrated EHS mice (CAS+EHS) and naïve exercise controls (NAIVE). Exercise performance and physiological responses in the heat were monitored during EHS and early recovery. Two weeks later, blood and tissues were collected and analyzed for biomarkers of cardiac damage and testosterone. Results Core temperature in CAS+EHS rose faster to 39.5°C in the early stages of the EHS trial (P<0.0001). However, both EHS groups ran similar distances, exhibited similar peak core temperatures and achieved similar exercise times in the heat, prior to symptom limitation (unconsciousness). CAS+EHS mice had ~10.5% lower body mass at the time of EHS, but this provided no apparent advantage in performance. There was no evidence of myocardial damage in any group, and testosterone levels were undetectable in CAS+EHS after gonadectomy. Conclusions The results of these experiments exclude the hypothesis that reduced performance of male mice during EHS trials is due to the effects of male sex hormones or intact gonads. However, the results are consistent with a role of male sex hormones or intact gonads in suppressing the early and rapid rise in core temperature during the early stages of exercise in the heat.
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Rodriguez-Grande, Beatriz, Matimba Swana, Loan Nguyen, Pavlos Englezou, Samaneh Maysami, Stuart M. Allan, Nancy J. Rothwell, Cecilia Garlanda, Adam Denes, and Emmanuel Pinteaux. "The Acute-Phase Protein PTX3 is an Essential Mediator of Glial Scar Formation and Resolution of Brain Edema after Ischemic Injury." Journal of Cerebral Blood Flow & Metabolism 34, no. 3 (December 18, 2013): 480–88. http://dx.doi.org/10.1038/jcbfm.2013.224.
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Acute-phase proteins (APPs) are key effectors of the immune response and are routinely used as biomarkers in cerebrovascular diseases, but their role during brain inflammation remains largely unknown. Elevated circulating levels of the acute-phase protein pentraxin-3 (PTX3) are associated with worse outcome in stroke patients. Here we show that PTX3 is expressed in neurons and glia in response to cerebral ischemia, and that the proinflammatory cytokine interleukin-1 (IL-1) is a key driver of PTX3 expression in the brain after experimental stroke. Gene deletion of PTX3 had no significant effects on acute ischemic brain injury. In contrast, the absence of PTX3 strongly compromised blood–brain barrier integrity and resolution of brain edema during recovery after ischemic injury. Compromised resolution of brain edema in PTX3-deficient mice was associated with impaired glial scar formation and alterations in scar-associated extracellular matrix production. Our results suggest that PTX3 expression induced by proinflammatory signals after ischemic brain injury is a critical effector of edema resolution and glial scar formation. This highlights the potential role for inflammatory molecules in brain recovery after injury and identifies APPs, in particular PTX3, as important targets in ischemic stroke and possibly other brain inflammatory disorders.
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Grosman, Benyamin, Osman S. Shaik, Bryan G. Helwig, Lisa R. Leon, and Francis J. Doyle. "A physiological systems approach to modeling and resetting of mouse thermoregulation under heat stress." Journal of Applied Physiology 111, no. 3 (September 2011): 938–45. http://dx.doi.org/10.1152/japplphysiol.00519.2010.
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Heat stroke (HS) is a serious civilian and military health issue. Due to the limited amount of experimental data available in humans, this study was conducted on a mouse mathematical model fitted on experimental data collected from mice under HS conditions, with the assumption there is good agreement among mammals. Core temperature (Tc) recovery responses in a mouse model consist of hypothermia and delayed fever during 24 h of recovery that represent potential biomarkers of HS severity. The objective of this study was to develop a simulation model of mouse Tc responses and identify optimal treatment windows for HS recovery using a three-dimensional predictive heat transfer simulation model. Several bioenergetic simulation variables, including nonlinear metabolic heat production (W/m3), temperature-dependent convective heat transfer through blood mass perfusion (W/m3), and activity-related changes in circadian Tc were used for model simulation. The simulation results predicted the experimental data with few disparities. Using this simulation model, we tested a series of ambient temperature treatment strategies to minimize hypothermia and delayed fever to accelerate HS recovery. Using a genetic algorithm, we identified eight time segments (ambient temperature = 27, 30, 31, 29, 28, 28, 27, 26°C) of 110 min total duration that optimized HS recovery in our model simulation.
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Vaibhav, Kumar, Molly Braun, Mohammad Badruzzaman Khan, Sumbul Fatima, Nancy Saad, Adarsh Shankar, Zenab T. Khan, et al. "Remote ischemic post-conditioning promotes hematoma resolution via AMPK-dependent immune regulation." Journal of Experimental Medicine 215, no. 10 (September 6, 2018): 2636–54. http://dx.doi.org/10.1084/jem.20171905.
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Spontaneous intracerebral hemorrhage (ICH) produces the highest acute mortality and worst outcomes of all stroke subtypes. Hematoma volume is an independent determinant of ICH patient outcomes, making clot resolution a primary goal of clinical management. Herein, remote-limb ischemic post-conditioning (RIC), the repetitive inflation–deflation of a blood pressure cuff on a limb, accelerated hematoma resolution and improved neurological outcomes after ICH in mice. Parabiosis studies revealed RIC accelerated clot resolution via a humoral-mediated mechanism. Whereas RIC increased anti-inflammatory macrophage activation, myeloid cell depletion eliminated the beneficial effects of RIC after ICH. Myeloid-specific inactivation of the metabolic regulator, AMPKα1, attenuated RIC-induced anti-inflammatory macrophage polarization and delayed hematoma resolution, providing a molecular link between RIC and immune activation. Finally, chimera studies implicated myeloid CD36 expression in RIC-mediated neurological recovery after ICH. Thus, RIC, a clinically well-tolerated therapy, noninvasively modulates innate immune responses to improve ICH outcomes. Moreover, immunometabolic changes may provide pharmacodynamic blood biomarkers to clinically monitor the therapeutic efficacy of RIC.
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Lee, Jungsoo, Heegoo Kim, Jinuk Kim, Won Hyuk Chang, and Yun-Hee Kim. "Multimodal Imaging Biomarker-Based Model Using Stratification Strategies for Predicting Upper Extremity Motor Recovery in Severe Stroke Patients." Neurorehabilitation and Neural Repair 36, no. 3 (December 31, 2021): 217–26. http://dx.doi.org/10.1177/15459683211070278.
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Background. Various prognostic biomarkers for upper extremity (UE) motor recovery after stroke have been reported. However, most have relatively low predictive accuracy in severe stroke patients. Objective. This study suggests an imaging biomarker-based model for effectively predicting UE recovery in severe stroke patients. Methods. Of 104 ischemic stroke patients screened, 42 with severe motor impairment were included. All patients underwent structural, diffusion, and functional magnetic resonance imaging at 2 weeks and underwent motor function assessments at 2 weeks and 3 months after stroke onset. According to motor function recovery at 3 months, patients were divided into good and poor subgroups. The value of multimodal imaging biomarkers of lesion load, lesion volume, white matter integrity, and cortical functional connectivity for motor recovery prediction was investigated in each subgroup. Results. Imaging biomarkers varied depending on recovery pattern. The integrity of the cerebellar tract ( P = .005, R 2 = .432) was the primary biomarker in the good recovery group. In contrast, the sensory-related corpus callosum tract ( P = .026, R 2 = .332) and sensory-related functional connectivity ( P = .001, R 2 = .531) were primary biomarkers in the poor recovery group. A prediction model was proposed by applying each biomarker in the subgroup to patients with different motor evoked potential responses ( P < .001, R 2 = .853, root mean square error = 5.28). Conclusions. Our results suggest an optimized imaging biomarker model for predicting UE motor recovery after stroke. This model can contribute to individualized management of severe stroke in a clinical setting.
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Malkki, Hemi. "Gut microbiota influence stroke recovery in mice." Nature Reviews Neurology 12, no. 5 (April 15, 2016): 252. http://dx.doi.org/10.1038/nrneurol.2016.52.
Full textDissertations / Theses on the topic "Stroke, mice, recovery, biomarker"
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Gower, Annette. "The Efficacy of Specific Activation of D1-class Dopamine Receptors to Enhance Motor Recovery in Mice Following Cortical Photothrombotic Stroke." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37619.
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Stroke is a widespread condition, which often leaves survivors with lasting deficits in motor function, however, physical rehabilitation is the only treatment available after the acute period. A large body of preclinical literature suggests dopamine-augmenting drugs, could enhance motor recovery following stroke. Unfortunately, mixed clinical results have prevented the implementation of such treatments, possibly due to the wide variety of G protein-coupled receptors these drugs can activate. Using a mouse photothrombosis stroke model and a battery of motor and sensorimotor behavioural tests, the current study aims to demonstrate proof of principle for the use of D1-class dopamine receptor agonists to enhance poststroke motor recovery and to evaluate the role of aerobic exercise rehabilitation in an asynchronous study design. The effect of light-dark cycle on behavioural outcome (horizontal ladder test, adhesive removal test, cylinder test) and histological outcome (infarct size) in photothrombotic stroke was evaluated in order to optimize the stroke model, but no there was no evidence of differences between strokes occurring during the light or dark period of a mouse’s circadian rhythm. A bioactive, suboptimal dose of D1-agonist dihydrexidine, was determined by evaluating its effect on locomotor activity and its ability to increase expression of immediate early gene c-fos. Using the determined dose, studies evaluating the efficacy of 7-days and 2-days of dihydrexidine administration on poststroke motor recovery, were performed, indicating efficacy of a 7-days, but not of a 2-days, course of treatment. The 7-days dihydrexidine treatment resulted in accelerated recovery as compared to a control group receiving saline. This work demonstrates, for the first time, proof of principle for the use of specific activation of D1-class dopamine receptors to enhance motor recovery following stroke.
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Hazime, Mahmoud. "Etude de l’effet de l’octadécaneuropeptide sur l’activité du cortex cérébral : intérêt pour la récupération fonctionnelle post-ischémique The gliopeptide ODN, a ligand for the benzodiazepine site of GABAA receptors, boosts functional recovery after stroke Prolonged deficit of gamma oscillations in the peri-infarct cortex of mice after stroke Bi-directional effect of the endozepine ODN on neuronal activity in vivo." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR127.
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L’ischémie cérébrale demeure un problème de santé publique majeur pour lequel on manque de solution thérapeutique permettant de favoriser la récupération des fonctions perdues. L’équipe de recherche dans laquelle cette thèse fut menée a mis en évidence que l’octadécaneuropeptide (ODN), un ligand endogène du récepteur GABAA, permet d’améliorer la récupération sensori-motrice après une ischémie cérébrale chez la souris. L’objectif de cette thèse était de caractériser les effets de l’ODN sur l’activité neuronale in vivo afin de mieux comprendre par quel mécanisme ce peptide agit sur la réparation des circuits neuronaux. Dans une première partie, nous avons montré que l’ODN, in vivo, se comporte comme un pro-excitateur à une concentration micromolaire (la concentration à laquelle il permet la récupération fonctionnelle) en revanche, à faible concentration (10-12 M) l’ODN inhibe l’activité des neurones du cortex. Dans ce travail, nous proposons, sur la base d’expériences in vitro, que cette inhibition est induite par une libération astrocytaire de GABA. Dans une deuxième partie, nous avons démontré que le régime oscillatoire du cortex perilésionnel (fluctuations rythmiques de l’excitabilité neuronale) est appauvri en oscillations gamma 7 et 21 jours après une ischémie cérébrale, mais que l’ODN n’a aucun effet sur leur puissance. Ces travaux confirment l’intérêt de renforcer l’excitabilité du cortex après un AVC et montrent qu’à cette fin, l’ODN peut-être un outil pharmacologique efficaceCerebral ischemia remains a major public health problem for which there is a lack of a therapeutic solution to promote the recovery of lost functions. The research team in which this thesis was conducted found that octadecaneuropeptide (ODN), an endogenous ligand of the GABAᴀ receptor, improves sensory-motor recovery after cerebral ischemia in mice. The aim of this thesis was to characterize the effects of ODN in neural activity in vivo in order to better understand by what mechanism this peptide can act on the repair of neural circuits. In a first part, we showed that ODN, in vivo, behaves as an excitability enhancer at micromolar concentration (the concentration at which it improves functional recovery). On the other hand, at low concentrations (10¯¹² M) ODN inhibits the activity of neurons in the cortex. Based on complementary in vitro experiences, we propose that this inhibition is induced by an astrocytic release of GABA. In a second part of the thesis, we demonstrated that the oscillatory regimen of the peri-lesional cortex (rythmic fluctuations of neural excitability) is depressed in gamma oscillation 7 and 21 days after cerebral ischemia. However, ODN has no effect on the oscillatory spectral power. This work confirms the value of enhancing the excitability of the cortex after a stroke and shows that for this purpose ODN can be an effective pharmacological tool
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Busti, Irene. "Identification of prognostic and therapeutic tools for cortical stroke treatment in mice." Doctoral thesis, 2020. http://hdl.handle.net/2158/1190551.
Full textAbstract:
Stroke is one of the main causes of disability worldwide. Around 70-80% of patients survive the ischemic attack, however around three fourths of them do not recover completely. Currently, there are only few effective therapies to treat this pathology in the early phases. Great is therefore the need for (i) reliable biomarkers predictive of spontaneous recovery and (ii) novel approaches to stimulate the recovery of lost functions.
Given this background, the aim of this thesis was to develop novel prognostic and therapeutic tools in preclinical mouse models of stroke.
Book chapters on the topic "Stroke, mice, recovery, biomarker"
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Syeara, Nausheen, Sounak Bagchi, Abdullah Al Shoyaib, Serob T. Karamyan, Faisal F. Alamri, and Vardan T. Karamyan. "The Finer Aspects of Grid-Walking and Cylinder Tests for Experimental Stroke Recovery Studies in Mice." In Methods in Molecular Biology, 345–53. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2926-0_23.
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