Restenosis following carotid endarterectomy is not a rare condition. Among 122 endarterectomies we experienced, five restenoses (4.1%) were encountered and treated by the second surgery. The present report clarifies the clinical profiles and pathological findings of restenosis following carotid endarterec-tomy. Mean age of restenosis group (59 years old) was not significantly different from the group without restenosis (62 years old). Average duration between the first endarterectomy and the second surgery was 17 months (8-30 months). Initial symptoms were transient ischemic attack in three sides, minor stroke in one side, and asymptomatic in one. Degree of stenosis was tight (≥90%) in two and moderate (70-89%) in three. It is interesting to note that no ulcer was noted in the first endarterectomy specimen. At surgery for restenosis, two cases had symptoms and another two cases were asymptomatic, though all had neck bruits. Four of five lesions were treated by short venous graft from common carotid artery to distal internal carotid artery and another lesion was treated by second endarterectomy and Dacron patch graft. Pathology was studied in four and all showed myointimal hyperplasia. Three of four reste-nosis tissues showed mutant form p53 by immunohistochemistry. The present study indicates that reste-nosis following carotid endarterectomy is not a rare status. Short venous bypass across the stenotic por-tion is the treatment of choice. Monoclonal growth of smooth muscle with mutant form p53 might be related to the restenosis.
Hemodynamic changes are of importance while removing large and high-flow arteriovenous malformations (AVM), because a phenomenon called "normal perfusion pressure breakthrough" may occur. In this report, we evaluated hemodynamic changes in 14 cases of high-flow AVM with cerebral angiogram and intraoperative monitoring of cortical-surface blood flow. The criteria we used for high-flow AVM are; nidus larger than 4 cm, a few large feeders, high-flow shunt in the nidus, and reduced circulation or dilated arteries in the adjacent brain tissue. For last 2 years, we experienced 14 cases of high-flow AVM which fulfilled the criteria, and 9 of these were operated on for total removal of AVM. Of those, 2 cases evolved postoperative local edema and hemorrhage and was thought to be due to "normal perfusion pressure breakthrough." Intraoperative monitoring of cortical-surface blood flow was useful to predict occurrence of "perfusion breakthrough", because blood flow in the adjacent brain tissue increased markedly with feeder clipping. Intraoperative barbiturate protection and postoperative controlled hypotension were thought to be useful for prevention of "normal perfusion pressure breakthrough", though the details of mechanisms are unknown.
We investigated zinc protoporphyrin (ZnPP) formation in pork at pH 5.5, identified the contributors to ZnPP formation, and verified the involvement of myoglobin in this process. When pork homogenate was separated into two water-soluble fractions (>10 and <10 kDa) and an insoluble fraction, ZnPP formation was suppressed. ZnPP formation was rescued after mixing of all three fractions. Heating of the soluble <10 kDa fraction did not suppress the formation of ZnPP as opposed to heating of the soluble >10 kDa fraction, suggesting that protein(s) presents in the >10 kDa fraction contributed to ZnPP formation. Components of the soluble 10-30 kDa fractions separated by ultrafiltration were important in ZnPP formation. Exogenous myoglobin was not essential for ZnPP formation. A gel filtration study showed that soluble protein(s) with molecular weight higher than that of myoglobin was involved. Therefore, it was suggested that the soluble <10 kDa fraction, the insoluble fraction, and the soluble 10-30 kDa fraction (excluding myoglobin) are essential for ZnPP formation in pork at pH 5.5.
To investigate the role of phosphatase in O2- generation, the effects of the potent phosphoprotein phosphatase inhibitors, Calyculin A and FK506, were analyzed during phagocytosis using rat peritoneal macrophages. O2- generation was continuously measured after addition of opsonized zymosan (op. ZY) or IgG-coated zymosan (IgG-ZY). The rate of O2- generation was directly proportional to the number of macrophages, up to 1-2 x 10(6) cells/ml. It was found that the rate and duration of O2- generation were markedly inhibited by Calyculin A. The addition of 100 nM of Calyculin A reduced O2- generation to about one-tenth of the control value. In contrast, FK506 did not inhibit O2- generation, suggesting that calcium calmodulin phosphatase is not involved in the activation of NADPH oxidase. This result indicates that the process of dephosphorylation might involve activation of NADPH oxidase as a control mechanism in phagocytosis by rat peritoneal macrophages. Furthermore, since Calyculin A is an inhibitor of phosphatase 1 and 2A, it is suggested that dephosphorylation may be evoked by these phosphatases.
✓ Cyclophosphamide and 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) were found to have an equivalent cytostatic effect in rats with subcutaneous transplants of Walker 256 carcinosarcoma. Rats with meningeal carcinomatosis received a single intravenous dose of cyclophosphamide (30 mg/kg) or ACNU (15 mg/kg) at various times after intracisternal inoculation of 1 × 10 4 Walker 256 carcinosarcoma cells. Cyclophosphamide, administered 1 day after tumor inoculation, failed to prevent tumor growth in the subarachnoid space. The survival time of these rats was prolonged only 10% to 14% compared to the controls, while ACNU produced a maximum increased survival time of 180%. If administered 2, 3, 4, and 5 days after tumor inoculation, both drugs were effective; cyclophosphamide yielded a maximum increase in median survival time of 109%, 94%, 90%, and 52%, and ACNU 127%, 139%, 240%, and 100%, respectively. These results indicate that the blood-cerebrospinal fluid (CSF) barrier was circumvented in the early stage of subarachnoid tumor growth, although some areas remained where the infiltrating tumor cells were protected from systemically administered drugs by the intact barrier.
We compared the functional and anatomical alterations of somatosensory circuits in the acute (1-3 days after infarct) and chronic (3 months after infarct) stage after subcortical striatal infarct in Wistar rats. Occlusion of the left middle cerebral artery produced subcortical striatal infarct in approximately 69% of the rats. The others developed cortical infarct. The function of the somatosensory circuits was evaluated by [14C]2-deoxyglucose autoradiography during physiological stimulation of the right vibrissae and face. In rats with subcortical infarct, the areas activated by sensory stimulation of the right vibrissae and face, applied 1 and 3 days after occlusion, were reduced compared to sham-operated controls (P < 0.05). In the chronic stage of subcortical infarct, the areas of metabolic activation of the left anterior vibrissal and facial sensory area were increased compared to rats with acute subcortical infarct (P < 0.05). To evaluate the anatomical changes in the somatosensory pathway, at 1 day and 3 months after occlusion, we injected wheat germ agglutinin-horseradish peroxidase solution as an axonal transport substance bilaterally into the anterior vibrissal and facial sensory area. Tract tracing studies in both the acute and chronic stage of subcortical infarct showed a reduction in the peroxidase-positive area in the left thalamus compared to the control hemispheres (P < 0.01). The functional disturbance and recovery of the somatosensory circuits after subcortical infarct are discussed.
To assess immunohistochemically whether the neural cell adhesion molecule L1, which is a member of the immunoglobulin superfamily and has been shown recently to be a stimulating factor for glioma migration, is expressed in glioma tissues, and to investigate factors that can regulate this expression.Twenty seven glioma tissue specimens including 13 glioblastomas, seven anaplastic astrocytomas, and seven astrocytomas were examined. Immunohistochemical analyses of L1, p53, and transforming growth cell factor beta (TGF-beta) were performed on each tumour using both polyclonal and monoclonal antibodies.Nine (33%) specimens (six glioblastomas and three anaplastic astrocytomas) had L1 positive immunostaining. p53 positive staining was detected in 10 (43%) of 23 glioma specimens (seven glioblastomas and three anaplastic astrocytomas). TGF-beta positive immunostaining was observed in 12 (52%) of the 23 glioma specimens (six glioblastomas, four anaplastic astrocytomas, and two astrocytomas). There was a statistical correlation between both p53 and L1 expression and TGF-beta and L1 expression. No such correlation was found between p53 and TGF-beta expression.These results suggest that mutation of the p53 gene or expression of TGF-beta may upregulate the expression of the L1 gene, thus resulting in high grade migration of glioma cells.
