Titlebook: Brain Hypothermia; Pathology, Pharmacol Nariyuki Hayashi (Professor) Conference proceedings 2000 Springer-Verlag Tokyo 2000 Trauma.brain.br

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Local Cooling: Limits on Secondary Injury and Neuronal Death Following Spinal Cord Injurywas complete destruction of neural tissue at the crush site, the area was filled in by other cells including neutrophils and connective tissue elements in both the hypothermia-treated and the untreated groups. These was a striking reduction in the progressive necrosis and cavitation that is characte

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mia, Basic Research of Hypothermia Treatment, and Clinical Studies of Brain Hypothermia. The book is a valuable source for practitioners and researchers in neurosurgery and neurology and in critical care and emergency medicine.978-4-431-70277-1978-4-431-66882-4

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Enhanced Neuronal Damage in Severely Brain-Injured Patients by Hypothalamus, Pituitary, and Adrenal e these pathophysiological changes, such as hypotension, hypoxia, free radicals, blood-brain barrier dysfunction, excitatory amino acid, and increased intracellular Ca., have been considered targets of treatment. This concept of brain injury mechanism has long been supported by many animal studies.

Conscientious

Molecular System Controlling Mammalian Hibernation with Circannual Rhythm. Such adaptation has been suggested to be due to readjustment of cells and organs to a new physiological state. As hibernation occurs with circannual rhythm, this physiological readjustment has been suggested to be under the control of a circannual rhythm. Recently, a novel protein complex (HP), fo

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Mild Hypothermia Amelioration of Damage During Rat Spinal Cord Injury: Inhibition of Pathological Minal cord injury, the rat spinal cord was exposed at the 11th vertebra and compressed using 20 g of weight for 20 min. The temperature of the animals was fixed for 1 h from the beginning of the compression period at 33°C and 37°C for the mild hypothermic treatment and the control, respectively. At 24

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Effect of Intraischemic Hypothermia on Expression of c-Fos, c-Jun, and HSP72 After Transient Focal Cto either a normothermic (NT) or a hypothermic (HT) group. In the NT group the animals were left at ambient temperature (21°C), and the brain temperature was elevated to 40°C during ischemia. In the HT group the animals were put into a cold room (1°C), and the brain temperature was decreased to 30°C