Correlation between scalp-recorded electroencephalographic and electrocorticographic activities during ictal period.

OBJECTIVE: To investigate the correlation between scalp-recorded electroencephalographic (EEG) and electrocorticographic (ECoG) activities during ictal periods. METHODS: Simultaneous EEG and ECoG recordings with chronic subdural electrodes were performed in eight patients with partial epilepsy. RESULTS: In two cases where the ictal ECoG discharges originated in deep brain structures such as the hippocampus and interhemispheric surface of the frontal lobe, ictal discharges could not be detected on EEG until they expanded to the cortex of convexity. In four cases, the ictal onset zones were located in the lateral convexity. When synchronous or near synchronous ictal ECoG discharges with amplitudes of 200-2000muV were recorded on more than 8-15cm(2) of cortex, corresponding discharges were recorded on EEG in these four cases. However, in a case of frontal lobe epilepsy, asynchronous ictal ECoG discharges were recorded on 10 electrodes of convexity but no ictal EEG activity was recorded. Furthermore, in two frontal lobe epilepsy cases, ictal EEG discharges did not always reflect the ictal ECoG spike, but occasionally reflected slow background ECoG activity around the ictal discharges. CONCLUSIONS: Multiple factors such as the width of the cortical area involved, amplitude of ictal discharges and degree of synchronization of electrical potentials play important roles in the appearance of ictal EEG recordings, and the relationship between ictal EEG and ECoG is not straightforward.     

The enhanced expression of the matrix metalloproteinase 9 in nasal NK/T-cell lymphoma

Background  

Nasal NK/T cell lymphoma is an aggressive disease and has a poor prognosis. Nasal NK/T cell lymphoma is refractory to conventional chemotherapy and has strong tendency of widespread relapse or dissemination into distant sites.     

Malignant schwannoma of acoustic nerve: a case report

During a routine physical examination in 1976, a 54-year-old man was noted to suffer from hearing difficulty and continuing tinnitus of his right ear. He had, however, no further consultations for the next five years, although the symptom persisted and gradually worsened. In May 1981, he experienced complete hearing loss in his right ear. A computed tomography disclosed no abnormalities, and other laboratory tests were unremarkable. In September 1981, the patient began to complain of paresthesia of the right angle of the mouth and tongue, right-sided facial paralysis, and walking difficulty. A repeated computed tomography showed a tumor at the right cerebellopontine angle region. A clinical diagnosis of acoustic schwannoma was made. The first operation was performed in December 1981. Complete removal of the tumor was impossible because of its unexpected, unusual hardness. The pathologic diagnosis was a malignant mesenchymal tumor, compatible with a malignant nerve sheath tumor of the acoustic nerve. A second operation was performed in January 1982, but the rapid postoperative regrowth of the tumor necessitated a third operation in March 1982. The patient died in the next month. Family histories did not show any evidence of von Recklinghausen's disease, and neither did the patient have any clinical stigmata of this disease.     

Enhancement of bradykinin-induced prostacyclin synthesis in porcine aortic endothelial cells by pertussis toxin Possible implication of lipocortin I

Bradykinin-stimulated prostacyclin synthesis in porcine aortic endothelial cells was enhanced by pretreatment of the cells with pertussis toxin or islet-activating protein (IAP) for 5 hr or longer. Although ADP-ribosylation of a protein with a molecular weight of 41–42 kD in the cell membranes was completed by 3 hr after the addition of IAP into the incubation medium, there was good correlation between enhancement of bradykinin-induced prostacyclin synthesis and ADP-ribosylation of the IAP substrate over a wide range of IAP concentrations. Furthermore, even if IAP was removed from the incubation medium at 3 hr, bradykinin-induced prostaglandin synthesis at 24 hr was still potentiated. Cycloheximide and actinomycin D enhanced bradykinin-induced prostacyclin synthesis and apparently blocked the effect of IAP. Since this result suggested the involvement of an inhibitor protein(s) of prostacyclin synthesis in the IAP effect, we studied the effect of IAP on the level of lipocortin I which is known to inhibit phospholipase A₂. Western and Northern blot analyses revealed that IAP decreased the amounts of protein and mRNA of lipocortin I. These results suggest that the enhancement of bradykinin-induced prostacyclin synthesis by IAP is associated with a decrease in the level of lipocortin I.     

Urinary excretion of glycine.prolile dipeptidile aminopeptidase, N-acetyl-beta-D-glucosaminidase, alanine aminopeptidase and low molecular protein in patients with renal cell carcinoma]

Urinary excretion of glycine.prolile dipeptidile aminopeptidase (GP-DAP), N-acetyl-beta-D-glucosaminidase (NAG), alanine aminopeptidase (AAP) and beta 2-microglobulin (beta 2-M), alpha 1-microglobulin (alpha 1-M) was studied preoperatively in 32 patients with renal cell carcinoma. The excretion indices of GP-DAP, AAP and NAG were significantly higher than those in the healthy control group. The excretion of these enzymes obviously reflected the degree of the tumor progression. However, positive rates were not remarkable (37% for GP-DAP, 37% for AAP and 28% for NAG). The excretion of beta 2-M and alpha 1-M was not increased in renal cell carcinoma patients.     

Difference in the effect of halothane on regional oxygen demand-supply relationship depending on the severity of coronary artery stenosis

We examined the effect of halothane on myocardial oxygen balance and hemodynamics in three groups of canine heart. We measured regional subendocardial oxygen tension before and after 30 minute inhalation of 0.8% and 1.5% halothane in the mixture of nitrogen and oxygen (FIO2 not equal to 0.5). In moderate and severe stenosis group, left circumflex coronary artery flow was reduced to 66% and 31% respectively, at buprenorphine-anesthetized basal condition. In occlusion group, left circumflex coronary artery was ligated at its origin. Both concentrations of halothane decreased heart rate, aortic pressure and LV dp/dt max in all groups. Subendocardial oxygen tension increased in moderate stenosis group. But it was unchanged in severe stenosis group, and it rather decreased in occlusion group with 1.5% halothane inhalation. Halothane might improve endocardial oxygen demand-supply relation in the myocardium with mild to moderate coronary stenosis, while it will possibly deteriorate endocardial oxygen demand-supply balance in ischemic myocardium after coronary artery occlusion.     

Skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) by inhibiting activation of the IGF-I signaling pathways.

We showed that unloading markedly diminished the effects of IGF-I to activate its signaling pathways, and the disintegrin echistatin showed a similar block in osteoprogenitor cells. Furthermore, unloading decreased alphaVbeta3 integrin expression. These results show that skeletal unloading induces resistance to IGF-I by inhibiting activation of the IGF-I signaling pathways at least in part through downregulation of integrin signaling. INTRODUCTION: We have previously reported that skeletal unloading induces resistance to insulin-like growth factor-I (IGF-I) with respect to bone formation. However, the underlying mechanism remains unclear. The aim of this study was to clarify how skeletal unloading induces resistance to the effects of IGF-I administration in vivo and in vitro with respect to bone formation. MATERIALS AND METHODS: We first determined the response of bone to IGF-I administration in vivo during skeletal unloading. We then evaluated the response of osteoprogenitor cells isolated from unloaded bones to IGF-I treatment in vitro with respect to activation of the IGF-I signaling pathways. Finally we examined the potential role of integrins in mediating the responsiveness of osteoprogenitor cells to IGF-I. RESULTS: IGF-I administration in vivo significantly increased proliferation of osteoblasts. Unloading markedly decreased proliferation and blocked the ability of IGF-I to increase proliferation. On a cellular level, IGF-I treatment in vitro stimulated the activation of its receptor, Ras, ERK1/2 (p44/42 MAPK), and Akt in cultured osteoprogenitor cells from normally loaded bones, but these effects were markedly diminished in cells from unloaded bones. These results were not caused by altered phosphatase activity or changes in receptor binding to IGF-I. Inhibition of the Ras/MAPK pathway was more impacted by unloading than that of Akt. The disintegrin echistatin (an antagonist of the alphaVbeta3 integrin) blocked the ability of IGF-I to stimulate its receptor phosphorylation and osteoblast proliferation, similar to that seen in cells from unloaded bone. Furthermore, unloading significantly decreased the mRNA levels both of alphaV and beta3 integrin subunits in osteoprogenitor cells. CONCLUSION: These results indicate that skeletal unloading induces resistance to IGF-I by inhibiting the activation of IGF-I signaling pathways, at least in part, through downregulation of integrin signaling, resulting in decreased proliferation of osteoblasts and their precursors.