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2015 Apoptotic Cell Recognition & Clearance (GRS)

Responses to Apoptotic Cells Leading to Inflammatory Resolution solution and Pathogenesis
Jun 13-14 University of New England Goutham Pattabiraman

2013 Apoptotic Cell Recognition & Clearance (GRS) Jun 22-23 University of New England Lucia Cottone

2011 Apoptotic Cell Recognition & Clearance (GRS)

Removal, Resolution and Regeneration
Jul 16-17 Bates College Helena Paidassi

https://www.grc.org/conferences.aspx?id=0000622
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"This information is current as of September 12, 2015.
Complement C1q Is Dramatically Up-Regulated in Brain Microglia in Response to Transient Global Cerebral Ischemia
Martin K.-H. Scha¨fer, Wilhelm J. Schwaeble, Claes Post, Patricia Salvati, Marcello Calabresi, Robert B. Sim, Franz "


"Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS.
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It has recently been suggested that local activation of complement in the CNS is of pathophysiological significance in both degenerative and inflammatory neurological diseases including Alzheimer’s (2, 5, 6, 7, 8, 9) and Parkinson’s dementia (10), supranuclear palsy (11), Pick’s disease (12), multiple sclerosis (13, 14), cerebral malaria (15), meningoencephalitis (16), scrapie (17, 18), and cerebrovascular disorders (19). Increased biosynthesis of various complement factors in the CNS has also been reported in experimental animal models of neurodegeneration or neuroinflammation such as peripheral or central axotomy (20, 21, 22, 23, 24), excitotoxic kainic acid lesions (21, 25), exposure to neurotoxins (26), and experimental allergic and virus-induced encephalitis (27) and in cultured microglial cells (28, 29, 30, 31, 32). By using a combination of techniques to monitor and localize biosynthesis in vivo, we provide evidence that experimentally induced cerebral ischemia causes a dramatic increase of C1q in brain microglia resulting in markedly enhanced levels of C1q functional activity in cerebrospinal fluid (CSF). "