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Postconditioning promotes recovery in the neurovascular unit after stroke.
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Systemic macrophage depletion attenuates infarct size in an experimental mouse model of stroke.
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Systematic Study of the Immune Components after Ischemic Stroke Using CyTOF Techniques.
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JLX001 Modulated the Inflammatory Reaction and Oxidative Stress in pMCAO Rats via Inhibiting the TLR2/4-NF-κB Signaling Pathway.
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Silencing the lncRNA in pro-inflammatory macrophages attenuates acute experimental ischemic stroke via LCP1 in mice.
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The protective effects of T cell deficiency against brain injury are ischemic model-dependent in rats.
Neurochem Int. 2013 Feb;62(3):265-70. doi: 10.1016/j.neuint.2012.11.016. Epub 2012 Dec 8.
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Macrophages prevent hemorrhagic infarct transformation in murine stroke models.
Ann Neurol. 2012 Jun;71(6):743-52. doi: 10.1002/ana.23529.
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Intrastriatal B-cell administration limits infarct size after stroke in B-cell deficient mice.
Metab Brain Dis. 2012 Dec;27(4):487-93. doi: 10.1007/s11011-012-9317-7. Epub 2012 May 18.
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The immunology of stroke: from mechanisms to translation.
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Chemokine receptor Ccr2 is critical for monocyte accumulation and survival in West Nile virus encephalitis.
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Post-stroke inhibition of induced NADPH oxidase type 4 prevents oxidative stress and neurodegeneration.
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Inflammatory mechanisms in ischemic stroke: role of inflammatory cells.
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Infarct volume is a major determiner of post-stroke immune cell function and susceptibility to infection.
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Delayed hypoxic postconditioning protects against cerebral ischemia in the mouse.
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