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Our composite-mediated, sequential delivery of EGF-PEG and EPO leads to tissue repair in a mouse stroke model and minimizes damage compared to ICV infusion.
Dietary Cr pre-treatment in an experimental mouse stroke model was reported to mitigate ischemic neuronal cell death in part by inhibiting cytochrome c release and subsequent caspse-3 activation, possibly via primary buffering of ATP levels [80].
CDK5 activity was next evaluated in our permanent mouse stroke model.
In addition, in a mouse stroke model in which human TG2 was expressed in neurons, translocation of TG2 into the nucleus was observed [20].
In a mouse stroke model using middle cerebral artery occlusion (MCAO), Vitamin C has been shown to be cerebroprotective [11], [12].
Recently, we demonstrated in a mouse stroke model that infections and mortality can effectively be reduced, and neurological outcome improved by preventive antibacterial therapy with the fluoroquinolone antibiotic moxifloxacin [11].
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To understand how successful recovery occurs, dissect candidate molecular pathways, and test new therapies, there is a need for multiple distinct mouse stroke models, in which the parameters of recovery after stroke are well defined.
Following brain transplantation in mouse ICH stroke model, B10 human MSCs integrate into host brain, survive, differentiate into neurons and astrocytes and induce behavioral improvement in the ICH animals.
Considering evidence of functional recovery in stroke animals following brain transplantation of human NSCs and Akt1 protein as a general mediator of survival signals, the present study is designed to investigate whether human NSCs overexpressing Akt1 can lead to the prolonged cell survival of grafted human NSCs and functional recovery in the mouse ICH stroke model.
Preconditioning with IL-6 protected the grafted NSCs from ischaemic reperfusion injury in a mouse ischemic stroke model [ 172].
Most recently, inhibition of phosphoinositide 3-kinase delta, a molecule that controls intracellular TNF trafficking in macrophages, was shown to reduce TNF secretion and neuroinflammation and confer protection in a mouse cerebral stroke model [ 130].
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