Acute Ischemic Stroke Management Review for the Hospitalist

Haldal, Shilpa; Beary, Jonathan M.; Nattanmai, Premkumar; George, Pravin; Newey, Christopher R.

doi:10.24150/ajhm/2018.001

Cited by 2 publications

(3 citation statements)

References 78 publications

(105 reference statements)

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“…The methods for quantifying transport measurements using membrane vesicles from brain capillary endothelial cells have been published by us [8,9,[24][25][26]. Rates of substrate uptake by luminal and abluminal membrane vesicles were determined using radiolabeled tracers and a rapid filtration technique [27,28].…”

Section: Transport Measurements In Membrane Vesiclesmentioning

confidence: 99%

“…85%) are due to interrupted blood flow to the brain, resulting in hypoxia [2]. Thus, the treatment for cerebral ischemia accompanying stroke includes therapies to re-establish blood flow using a thrombolytic agent [3][4][5][6][7][8]. Delayed reperfusion following cerebral ischemia (>3-4.5 hours) may cause damage to brain capillary endothelial cells [9][10][11] that can lead to cerebral bleeding and death [12,13], a process called reperfusion injury leading to hemorrhagic transformation [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Prevention of Oxidative Injury Associated with Thrombolysis for Ischemic Stroke

Peterson¹,

Sukowski²

2019

Antioxidants

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Although treatment of ischemic stroke focuses on re-establishing blood flow to the brain (e.g., thrombolysis), delayed reperfusion may be associated with oxidative damage to brain capillary endothelial cells, resulting in cerebral bleeding and death (hemorrhagic transformation). The goal of this study was to define cellular mechanisms responsible for reperfusion injury to brain capillaries, and to provide a rationale for more effective treatment of stroke. Mechanisms of oxidative injury to cerebral capillary endothelial cells were measured in the presence and absence of experimental inhibitors to define the roles of transport and metabolic pathways. In vitro experiments provided evidence that: (1) intracellular calcium is elevated in brain capillary endothelial cells following simulated transient ischemia and reperfusion, due to reverse movement of Na/Ca exchange; (2) a simultaneous increase of calcium and reactive oxygen species (ROS) during re-oxygenation causes mitochondrial dysfunction, thus initiating apoptosis and loss of brain capillary integrity. In vivo studies showed that γ-glutamylcysteine (an antioxidant precursor of glutathione) and the experimental compound KB-R7943 (inhibits reverse movement of Na/Ca exchange) protect brain capillary endothelial cells when co-administered just before reperfusion following transient ischemia. The data indicate that these agents may be useful in preventing oxidative injury associated with thrombolysis for ischemic stroke.

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Section: Transport Measurements In Membrane Vesiclesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Prevention of Oxidative Injury Associated with Thrombolysis for Ischemic Stroke

Peterson¹,

Sukowski²

2019

Antioxidants

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“…CP is a disorder that affects muscle tone and motor skills, inducing uncoordinated movements [1]. For CA, this disease causes death or spasticity due to low blood flow to brain cells [2]. Spasticity is an exaggerated contraction of the antagonist muscle, which generates an opposition couple or even an inversion of the desired movement [3].…”

Section: Introductionmentioning

confidence: 99%

Neuromotor Strategy of Gait Rehabilitation for Lower-Limb Spasticity

Charafeddine

Pradon

Chevallier

et al. 2019

2019 Fifth International Conference on Advances in Biomedical Engineering (ICABME)

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Assisting users and restoring human locomotion for patients with lower limb spasticity is a challenging task. Studies focusing on patients with abnormal walking behavior are scarce because there is an important variability from one patient to another. Those patients could benefit the most from rehabilitation and assistive mechatronic devices, there is no generic controlling scheme or any dynamical gain indicator. This contribution introduces a bio-kinematic index which is called Neuro-motor index (NMI), based on electromyographic (EMG) and joint angles measurements. NMI is derived from the nonlinear regression with a combination of two co-contraction indices (CCI), which allows addressing the variability of walking situations. This new index is evaluated on patients with cerebral palsy and a stroke. Then, the estimation error was calculated in comparison with the other co-contraction indices. This estimation shows that this index has the highest signification of joint angles prediction. Thus it can be suitable in adaptive rehabilitation control for spasticity cases.

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Acute Ischemic Stroke Management Review for the Hospitalist

Cited by 2 publications

References 78 publications

Prevention of Oxidative Injury Associated with Thrombolysis for Ischemic Stroke

Prevention of Oxidative Injury Associated with Thrombolysis for Ischemic Stroke

Neuromotor Strategy of Gait Rehabilitation for Lower-Limb Spasticity

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