Apoptosis and Necrosis in Brain: Contribution of Glycerophospholipid, Sphingolipid, and Cholesterol-Derived Lipid Mediators
Reference231 articles.
1. Adayev T., Estephan R., Meserole S., Mazza B., Yurkow E. J., and Banerjee P. (1998). Externalization of phosphatidylserine may not be an early signal of apoptosis in neuronal cells, but only the phosphatidylserine-displaying apoptotic cells are phagocytosed by microglia. J. Neurochem. 71:1854–1864.
2. Adibhatla R. M., Hatcher J. F., and Dempsey R. J. (2002). Citicoline: neuroprotective mechanisms in cerebral ischemia. J. Neurochem. 80:12–23.
3. Adibhatla R. M., Hatcher J. F., and Dempsey R. J. (2003). Phospholipase A2, hydroxyl radicals, and lipid peroxidation in transient cerebral ischemia. Antioxid. Redox Sign. 5:647–654.
4. Ahn M. J., Sherwood E. R., Prough D. S., Lin C. Y., and DeWitt D. S. (2004). The effects of traumatic brain injury on cerebral blood flow and brain tissue nitric oxide levels and cytokine expression. J. Neurotrauma 21:1431–1442.
5. Ajmone-Cat M. A., Nicolini A., and Minghetti L. (2003). Prolonged exposure of microglia to lipopolysaccharide modifies the intracellular signaling pathways and selectively promotes prostaglandin E2 synthesis. J. Neurochem. 87:1193–1203.