About the Book
The immature brain is especially vulnerable to inflammatory factors, before, during and after birth. This publication presents new insights into the detection, pathophysiology and treatment of inflammation-induced injury in the developing brain from both clinical and basic science perspectives. Cellular mechanisms that lead to perinatal brain injury are presented, with specific emphasis on inflammation, brain development and potential treatment strategies. In particular, studies report on inflammatory pathways involved in perinatal brain injury, including caspases, STAT3, toll-like receptors and oxidative stress. Some data demonstrate how different inflammatory cell types may contribute to the injury, such as microglia and mast cells, and how peripheral organs can influence the cerebral inflammatory response. Further, new developments in neuroprotective therapies using human amnion epithelial cells to reduce inflammation-induced brain damage in the fetus are described. This publication is recommended to both clinicians and basic scientists who are interested in the developing nervous system, its vulnerability to inflammation and the short- and long-term consequences for neurologic development.
Table of Contents:
Preface: Mallard, C.; Raghupathi, R.; * Caspases Playing in the Field of Neuroinflammation: Old and New Players: Venero, J.L.; Burguillos, M.A.; Joseph, B.; * Oligodendroglial Alterations and the Role of Microglia in White Matter Injury: Relevance to Schizophrenia: Chew, L.-J.; Fusar-Poli, P.; Schmitz, T.; * Toll-Like Receptor 3 Expression in Glia and Neurons Alters in Response to White Matter Injury in Preterm Infants: Vontell, R.; Supramaniam, V.; Thornton, C.; Wyatt-Ashmead, J.; Mallard, C.; Gressens, P.; Rutherford, M.; Hagberg, H.; * 12/15-Lipoxygenase Expression is Increased in Oligodendrocytes and Microglia of Periventricular Leukomalacia: Haynes, R.L.; van Leyen, K.; * Neonatal Systemic Exposure to Lipopolysaccharide Enhances Susceptibility of Nigrostriatal Dopaminergic Neurons to Rotenone Neurotoxicity in Later Life: Cai, Z.; Fan, L.-W.; Kaizaki, A.; Tien, L.-T.; Ma, T.; Pang, Y.; Lin, S.; Lin, R.C.S.; Simpson, K.L.; * Maternal Exposure to Lipopolysaccharide Leads to Transient Motor Dysfunction in Neonatal Rats: Rousset, C.I.; Kassem, J.; Aubert, A.; Planchenault, D.; Gressens, P.; Chalon, S.; Belzung, C.; Saliba, E.; * Ischemia-Induced Neuroinflammation Is Associated with Disrupted Development of Oligodendrocyte Progenitors in a Model of Periventricular Leukomalacia: Falahati, S.; Breu, M.; Waickman, A.T.; Phillips, A.W.; Arauz, E.J.; Snyder, S.; Porambo, M.; Goeral, K.; Comi, A.M.; Wilson, M.A.; Johnston, M.V.; Fatemi, A.; * Cerebral and Hepatic Inflammatory Response after Neonatal Hypoxia-Ischemia in Newborn Rats: Bonestroo, H.J.C.; Nijboer, C.H.A.; van Velthoven, C.T.J.; Kavelaars, A.; Hack, C.E.; van Bel, F.; Heijnen, C.J.; * Temporal Expression of Cytokines and Signal Transducer and Activator of Transcription Factor 3 Activation after Neonatal Hypoxia/Ischemia in Mice: Shrivastava, K.; Llovera, G.; Recasens, M.; Chertoff, M.; Gimenez-Llort, L.; Gonzalez, B.; Acarin, L.; * CEACAM1 Expression in Oligodendrocytes of the Developing Rat Brain Shows a Spatiotemporal Relation to Myelination and Is Altered in a Model of Encephalopathy of Prematurity: Prager, S.; Singer, B.B.; Bendix, I.; Schlager, G.W.; Bertling, F.; Ceylan, B.; Keller, M.; Felderhoff-Mueser, U.; Ergun, S.; * Phenotype and Secretory Responses to Oxidative Stress in Microglia: Pathipati, P.; Muller, S.; Jiang, X.; Ferriero, D.; * Oxygen Toxicity Is Reduced by Acetylcholinesterase Inhibition in the Developing Rat Brain: Sifringer, M.; Bendix, I.; von Haefen, C.; Endesfelder, S.; Kalb, A.; Buhrer, C.; Felderhoff-Mueser, U.; Spies, C.D.; * Mast Cell Isolation from the Immature Rat Brain: Patel, S.D.; Brennan, G.; Brazin, J.; Ciardiello, A.J.; Silver, R.B.; Vannucci, S.J.; * Human Amnion Epithelial Cells Reduce Fetal Brain Injury in Response to Intrauterine Inflammation: Yawno, T.; Schuilwerve, J.; Moss, T.J.M.; Vosdoganes, P.; Westover, A.J.; Afandi, E.; Jenkin, G.; Wallace, E.M.; Miller, S.L.
