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Titlebook: Neuroinflammation in Stroke; U. Dirnagl,B. Elger Conference proceedings 2004 Springer-Verlag Berlin Heidelberg 2004 Biomarker.Blood Brain

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Matrix Metalloproteinases in Neuroinflammation and Cerebral Ischemia, al. 1999; Graham and Chen 2000). Neurons and astrocytes are affected early, while blood vessels are more resistant to hypoxia. However, when the vasculature begins to break down, vasogenic edema and hemorrhage result (Klatzo 1967). Since first observed by Fisher and Adams (1951), many investigators
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Involvement of Tight Junctions During Transendothelial Migration of Mononuclear Cells in Experimentted by the blood-brain barrier (BBB). The BBB is formed by highly specialized capillary endothelial cells, which inhibit transendothelial passage of molecules from blood to brain by an extremely low pinocytotic activity and the lack of fenestrae, and the BBB restricts the paracellular diffusion of h
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發(fā)表于 2025-3-24 10:14:09 | 只看該作者
Complement Activation: Beneficial and Detrimental Effects in the CNS,reserving normal “self cell”. The complement system also contributes through its activation to the release of inflammatory mediators, promoting potential tissue injury at sites of inflammation (Frank and Fries 1991).
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Protective Autoimmunity and Prospects for Therapeutic Vaccination Against Self-Perpetuating Neurode. It should be stressed, however, that inflammation is not a single process, but involves cascades of processes mediated by numerous compounds and factors (Hauben et al. 2002; Hauben and Schwartz 2003; Schwartz and Hauben 2003). The function of inflammation in acute or chronic insults to the CNS has
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