Hiroshi Itokawa

Astrocytes co-express aquaporin-1, -4, and vascular endothelial growth factor in brain edema tissue associated with brain contusion

INTRODUCTION Brain edema may be life threatening. The mechanisms underlying the development of traumatic brain edema are still unclear; however, mixed mechanisms including vasogenic, ischemic, and neurotoxic types of edema may be contributors. Recent studies indicate that astrocytes, aquaporins (AQPs; a protein family of water channels), and vascular endothelial growth factor (VEGF) may have important roles in the formation and resolution of brain edema. We studied the expression of AQPs and VEGF in the edematous brain. METHODS We investigated the expression of AQP1, AQP4, and vascular endothelial growth factor (VEGF) in contusional brain tissue surgically obtained from 6 patients. Glial fibrillary acidic protein (GFAP) was also stained to detect astrocytes and to clarify the location of those proteins. The specimens received immunohistological staining and 3-color immunofluorescent staining, and were observed using confocal laser scanning microscopy. RESULTS AQP1, AQP4, and VEGF were co-expressed in GFAP-positive astrocytes. AQP1 and AQP4 were expressed strongly in astrocytic end-feet. The astrocytes were located in the edematous tissue, and some cells surrounded cerebral capillaries. CONCLUSION Our results suggest that AQP1, AQP4, and VEGF are induced in astrocytes located in and surrounding edematous tissue. Those astrocytes may regulate the water in- and out-flow in the injured tissue.

Dural invasion of meningioma: a histological and immunohistochemical study

Meningioma usually grows and expands into the brain, but invasion into the brain parenchyma is relatively rare. Meningioma arises from arachnoid cap cells, and infiltration into dura mater is the main growth pattern of meningiomas. However, little is known about the mechanism of meningioma invasion into the dura mater. In this study, seven specimens, including dural attachments, from seven cases of meningioma were used for immunohistochemical analysis. Matrix metalloproteinase (MMP)-1, -2, -9, urokinase-type plasminogen activator (uPA), vascular endothelial growth factors (VEGF), flt-1, E-cadherin, estrogen receptor (EgR), progesterone receptor (PgR), and aquaporin (AQP)-1, -4 were used as primary antibodies. There were several patterns of meningioma invasion into the dura mater: papillary-shaped invasion with destruction of dural structure, infiltration along the fibers of the dura mater, and invasion of several tumor cell units with fibroblast infiltration. Strong immunostaining was obtained with MMP-1, followed by AQP-1 and uPA, within the invading tumor cells. Neovasculature and extravasated erythrocytes, which stained with AQP-1, were also occasionally observed around the invading tumor cells. Simpson grade II removal of meningiomas results in high recurrence rates, and the inhibition of meningioma growth via dural invasion will facilitate improved remission in many cases with meningioma. In this study, MMP-1, AQP-1, and uPA are considered to have some role in the dural infiltration of meningioma cells. The fact that AQP-1 was highly expressed at the dural attachment and invading front of meningioma may indicate that dural invasion of the meningioma may be facilitated by AQP-1-induced water flow and neovascularization.

Very early expression of vascular endothelial growth factor in brain oedema tissue associated with brain contusion

BACKGROUND Brain oedema associated with cerebral contusion can be life-threatening. Mechanisms of the development of brain oedema are still unclear. METHOD We investigated the expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2 (KDR/Flk-1) in the contusional brain tissue obtained during neurosurgery from 5 patients. FINDINGS VEGF is expressed in some but not all the astrocytes, and KDR/Flk-1 is expressed in vascular endothelial cells in the con-tusional tissue as early as 3 hours after onset. CONCLUSION The results suggested that the VEGF is induced in the contusional tissue in the very early period after onset, and that it increases capillary permeability via KDR/Flk-1 resulting in vasogenic type brain oedema.

Persistent primitive first cervical intersegmental artery (proatlantal artery II) associated with subarachnoid hemorrhage of unknown origin

Proatlantal intersegmental artery is a persistent arotid–vertebral embryonic anastomosis. This artery is very are, and 2 types have been described, proatlantal artery types and II. Persistent primitive proatlantal intersegmental artery proatlantal artery type I) arises from the internal carotid artery nd transverses rostrally to enter the foramen magnum where t joins the vertebral artery. Persistent primitive first cervical ntersegmental artery (proatlantal artery type II) arises from the xternal carotid artery, runs posteriorly to join the vertebral rtery and then passes through the transverse foramen of the C1 ertebra segment. The purpose of this paper is to present a case ith proatlantal artery type II without an ipsilateral vertebral rtery. This anomaly was an incidental finding in a patient with ubarachnoid hemorrhage (SAH) of unknown origin.

A case of prolactin-secreting pituitary carcinoma and its histological findings.

Pituitary carcinomas are very rare. The diagnosis of pituitary carcinoma is defined by evidence of craniospinal and/or systemic metastasis, rather than by histological malignancies. We report a case of prolactin-secreting pituitary macroadenoma invading the cavernous sinuses at the time of initial treatment, which later metastasized to the cerebellum, medulla oblongata, and spinal axis. The patient survived approximately nine years following the initial diagnosis of a pituitary tumor and two years following the diagnosis of metastatic disease. Histological examination of the metastatic cerebellar tumor showed an adenoma with high cellularity and hyperchromasia, but no mitoses.