In order to assess the role of circulating blood in early microglial activation after traumatic brain injury (TBI), controlled cortical impact injury was applied to adult rat brain slices (400 microm in thickness) and the microglial response was examined. The complement receptor (CR3) expression and morphological transformation of the microglia were evaluated by OX42 immunohistochemistry. At 5 min following injury, activated microglia with intense CR3 expression appeared throughout the hemisphere on the injured side. In contrast, the morphology and CR3 expression of the microglia on the contralateral side were indistinguishable from those of the resident ramified microglia seen in normal brains. At 30 min following injury, microglial activation was more pronounced on the injured side, while the microglia on the contralateral side still retained a ramified morphology. These results are consistent with our previous observations made in in vivo experiments, which indicate that, as the brain slice paradigm excludes variables arising from the circulating blood, the rapid and widespread microglial activation observed following TBI can not be attributed exclusively to the infiltration of blood-borne macrophages or molecules. Rather this activation is most likely caused by intrinsic mechanisms within the brain tissue, such as traumatic depolarization.
Chordomas that are entirely extraosseous and intradural are extremely rare. The tumors described in the literature were observed mostly in the prepontine region. This is the first case reported of an intradural extraosseous chordoma occurring in the foramen magnum region. The tumor was totally excised. The distinction between an intradural extraosseous chordoma and a classic chordoma is important from a clinical viewpoint because of the potential for complete surgical excision and a more benign growth pattern.
Intracranial ectopic pituitary adenoma occurs most frequently in the suprasellar cistern, usually in continuity with the pituitary stalk. Such tumors probably originate from cells of the pars tuberalis located above the diaphragma sellae or from aberrant anterior pituitary cells of the pituitary stalk. The authors report the case of a 37-year-old woman with Cushing's syndrome caused by an ectopic pituitary adenoma of unique location: the tumor was separate form the pituitary stalk and confined within the interpeduncular cistern. After surgical removal of the tumor, continued improvement in the patient's laboratory results and disappearance of her endocrine symptoms strongly indicated the absence of adenoma cells in the pituitary gland or stalk. The tumor in the present case appears to have arisen from aberrant pituitary cells that were present in the leptomeninges of the basal surface of the hypothalamus.
Enteral nutrition of MA may be useful for the inhibition of intestinal mucosal atrophy and the prevention of multiple organ dysfunction syndrome caused by the inhibition of BT and subsequent overproduction of cytokines.
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