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H Nukui

Publications and source records attributed to H Nukui.

At least 55 records · Page 3Linked to original sources
PubMed1997

Effect of irradiation on transforming growth factor-beta secretion by malignant glioma cells.

Glioblastoma cells secrete transforming growth factor-beta (TGF-beta), which has a variety of immunosuppressive properties. We investigated the effect of irradiation TGF-beta secretion by malignant glioma cells. Three malignant glioma cell lines (T98G, A172, KG-1-C) were cultured and irradiated using 10 and 50 Gy Linac radiation. After further culture for 36 hours in serum-free culture medium, the supernatants were collected. The TGF-beta activity in the culture supernatants was determined using a specific bioassay. The levels of the active form and total TGF-beta in the supernatants from irradiated malignant glioma cells decreased compared to those from un-irradiated cells. However, since irradiation inhibited the growth of tumor cells, the amount of TGF-beta secretion per cell in irradiated cells tended to increase after irradiation. These results suggest that malignant glioma cells can still secrete TGF-beta and activate latent TGF-beta even after large dose irradiation, despite the inhibition of tumor growth.

Animals↗
PubMed1996

The time course of glucose metabolism in rat cerebral ischemia with middle cerebral artery occlusion-reperfusion model and the effect of MK-801.

Following cerebral ischemia, the extracellular concentration of excitatory amino acids increases, and the excitatory cell death may play an important role contributing to ischemic neuronal damage. Although sequential metabolic changes in permanent local cerebral ischemia have been reported, the effect of reperfusion in local cerebral ischemia on glucose metabolism is less clear. In order to investigate the time course change of glucose metabolism in a middle cerebral artery occlusion-reperfusion model and the effect of dizocilpin (MK-801) on glucose metabolism, the 14C-Deoxyglucose method was used. Hypermetabolism occurred at 30 min after the middle cerebral artery (MCA) occlusion, and reached a peak at 60 min after ischemia in both ischemic core and penumbra. The shift from hyper- to hypometabolism was observed after the ischemia. The reperfusion facilitated the decrease of cerebral glucose metabolism in the ischemic region following 2 h of MCA occlusion. The pretreatment of MK-801 (0.4 mg kg-1) inhibited both increased glucose metabolism during ischemia and decreased glucose metabolism during reperfusion. These findings support the hypothesis that excitation-induced hyper-metabolism plays a major role in the ischemic insult following focal cerebral vascular occlusion.

Animals↗
PubMed1996

Modulation of transforming growth factor-beta secretion from malignant glioma cells by interleukin-1 beta.

Malignant glioma cells secrete transforming growth factor-beta (TGF-beta) which has potent immunosuppressive properties. We investigated the effect of interleukin-1 beta (IL-1 beta) on TGF-beta secretion from malignant glioma cells in vitro. T98G glioblastoma cells were treated with various doses of IL-1 beta and the TGF-beta activity in the supernatant was determined using a specific bioassay. Six other human malignant glioma cell lines were also treated with 1000 U/ml of IL-1 beta, and the TGF-beta activity in the supernatants was determined. The effect of IL-1 beta on the growth of tumor cells was also assessed by a bioassay using crystal violet which reflects the actual cell number in the plate wells. IL-1 beta treatment resulted in inhibition of TGF-beta secretion in two malignant glioma cell lines. TGF-beta secretion from T98G cells was suppressed by IL-1 beta in a dose-related manner. However, IL-1 beta treatment resulted in an obvious increase (> 20%) of TGF-beta secretion in two tumor lines, and a slight increase (< 20%) in three tumor lines. IL-1 beta did not affect the growth of four malignant glioma cell lines, and only slightly affected the growth of the other three cell lines. IL-1 beta modulates TGF-beta secretion from malignant glioma cells, but not in a consistent way.

Cell Division↗
PubMed1996

Transforming growth factor-beta inhibits interferon-gamma secretion by lymphokine-activated killer cells stimulated with tumor cells.

The effect of transforming growth factor-beta (TGF-beta) secreted by glioblastoma (T98G) cells on the secretion of interferon-gamma (IFN-gamma) by lymphokine-activated killer (LAK) cells stimulated with tumor cells was investigated in cocultures of LAK and Daudi cells supplemented with T98G culture supernatant, T98G culture supernatant preincubated with anti-TGF-beta 1 and anti-TGF-beta 2 neutralizing antibodies, anti-TGF-beta 1 and anti-TGF-beta 2 antibodies, or natural human TGF-beta 1 or recombinant human TGF-beta 2. LAK cells were incubated with anti-TGF-beta 1 and anti-TGF-beta 2 antibodies, and with T98G cells of which the supernatant contained both active and latent forms of TGF-beta 1 and TGF-beta 2, with or without neutralizing antibodies. Addition of the supernatant from T98G cells to LAK/Daudi culture caused inhibition of IFN-gamma secretion by LAK cells. The inhibition was abolished by pretreatment of the supernatants with anti-TGF-beta antibodies. Addition of TGF-beta 1 and TGF-beta 2 to the LAK/Daudi culture inhibited IFN-gamma secretion by LAK cells in a dose-dependent manner. Addition of anti-TGF-beta antibodies to the LAK culture resulted in increased IFN-gamma secretion. T98G cells failed to stimulate LAK cells to secrete more IFN-gamma. Addition of anti-TGF-beta antibodies to the LAK-T98G culture resulted in increased IFN-gamma secretion by LAK cells. These results suggest that most malignant glioma cells which secrete high levels of TGF-beta can inhibit IFN-gamma secretion by LAK cells even after tumor cell stimulation.

Brain Neoplasms↗
PubMed1995

Secretion of transforming growth factor-beta 1 and -beta 2 by malignant glioma cells.

The secretion of transforming growth factor-beta (TGF-beta), a growth inhibitory factor with immunosuppressive properties, was investigated in one glioblastoma cell line and seven surgically resected malignant glioma cells. Cultured cells from surgically resected tumors were examined immunohistochemically for glial fibrillary acidic protein (GFAP) and S-100 protein. The levels of TGF-beta 1 and TGF-beta 2 in culture supernatants from malignant glioma cells were determined by a specific bioassay using anti-TGF-beta 1 and anti-TGF-beta 2 antibodies. Two glioblastoma cell lines were cultured in the presence of TGF-beta 1 or TGF-beta 2 to assess the effect of TGF-beta on the growth of glioblastoma cells. Cultured cells from surgically resected tumors were positive for both GFAP and S-100 protein. Both active and latent forms of TGF-beta 1 and TGF-beta 2 were detected in the culture supernatants from malignant gliomas, except in one patient with anaplastic astrocytoma which secreted only latent forms of TGF-beta 1 and TGF-beta 2. There was no statistical difference in the levels of TGF-beta 1 and TGF-beta 2 in glioblastomas and anaplastic astrocytomas. Neither TGF-beta 1 nor TGF-beta 2 affected the growth of glioblastoma cells. These findings suggest that most malignant glioma cells secrete both TGF-beta 1 and TGF-beta 2, can convert TGF-beta from a latent to active form, and may suppress cytokine secretion by activated lymphocytes in vivo as well as in vitro.

Astrocytoma↗
PubMed1994

Inhibition of tumor necrosis factor-alpha and -beta secretion by lymphokine activated killer cells by transforming growth factor-beta.

Transforming growth factor-beta (TGF-beta) has a variety of immunosuppressive properties. We investigated the effect of TGF-beta secreted by glioblastoma (T98G) cells on the secretion of tumor necrosis factor-alpha and -beta (TNFs) by lymphokine activated killer (LAK) cells stimulated with tumor cells. The supernatant from T98G cells was preincubated with anti-TGF-beta 1 and -beta 2 neutralizing antibodies or untreated, and added to a coculture of LAK and Daudi cells. The neutralizing antibodies were added to LAK/Daudi and LAK culture, and natural human TGF-beta 1 and recombinant human TGF-beta 2 were also added to the LAK/Daudi culture. LAK cells were also cultured with T98G cells, of which the supernatant contained both active and latent forms of TGF-beta 1 and TGF-beta 2, and the neutralizing antibodies were added to the coculture. TNFs activity in the supernatants from LAK/Daudi cultures was examined by a specific bioassay. Addition of the supernatant from T98G cells to LAK/Daudi culture resulted in the inhibition of TNFs secretion by LAK cells. The inhibition was abrogated by the pretreatment of the supernatants with the anti-TGF-beta antibodies. Addition of TGF-beta 1 and TGF-beta 2 to LAK/Daudi culture inhibited TNFs secretion by LAK cells in a dose-dependent manner. Addition of anti-TGF-beta antibodies to LAK culture resulted in an increase of TNFs secretion. These results suggest that, if tumor cells have the capacity to convert TGF-beta from a latent to an active form, the active TGF-beta suppresses TNFs secretion by LAK cells stimulated with the tumor cells, and that TGF-beta secreted and activated by glioblastoma cells suppresses the propagation of immune reaction by inhibiting TNFs secretion by activated lymphocytes adjacent to tumor cells.

Glioblastoma↗
PubMed1994

Improved bioassay for the detection of transforming growth factor-beta 1 and beta 2 in malignant gliomas.

Growth inhibition assays using radioisotope or dye are used to detect transforming growth factor-beta (TGF-beta). Here, we describe a modified bioassay using crystal violet for the quantitative detection of TGF-beta 1 and TGF-beta 2. The procedure is based on staining Mv1Lu mink lung epithelial cells with crystal violet, followed by measurement of the absorbance at 570 nm in individual wells of a 96-well microtiter plate. The number of Mv1Lu cells correlated with the eluted dye intensity. The sensitivity of the bioassay to recombinant TGF-beta 1 and TGF-beta 2 increased approximately twofold by using only 500 Mv1Lu cells in microtiter wells. The bioassay was used to measure TGF-beta activity in the culture supernatant from glioblastoma cells. Culture supernatants were untreated or acid-activated to quantify the active or total TGF-beta, and neutralized with anti-TGF-beta 1 and/or anti-TGF-beta 2 antibody to measure the activity. Both TGF-beta 1 and TGF-beta 2 were detected in the untreated and acid-activated supernatants, and the amounts were calculated by extrapolating from the known recombinant TGF-beta 1 or TGF-beta 2 dilution curve. Our results show that the modified bioassay using crystal violet can measure the levels of TGF-beta 1 and TGF-beta 2 in culture supernatants from malignant glioma cells.

Biological Assay↗
PubMed1993

Granulomatous angiitis of the central nervous system--case report.

A 22-year-old male presented with granulomatous angiitis manifesting as headache. Computed tomography (CT) demonstrated a low-density area and ring-like enhancement in the right frontoparietal region. Steroid therapy caused rapid improvement in the signs and symptoms. Withdrawal of steroid was followed by recurrence of the headache and low-density area. The steroid treatment was resumed until he became asymptomatic 3 months after admission. He was followed up as an outpatient once every 2 weeks. One month after discharge, he complained of mild headache, and CT again demonstrated a mild increase in the low-density area. He was followed up continuously without steroid treatment. Two months after discharge, he suddenly lost consciousness, and CT demonstrated multiple intracerebral hematomas in the bilateral parietal regions. Removal of an intracerebral hematoma in the right parietal region and external decompression were carried out, but he died 3 days later. Histological examination of tissues from the right parietal cortex and leptomeninges demonstrated granulomatous inflammation with several giant cells in the vessels of the cerebral cortex and leptomeninges.

Adult↗
PubMed1993

[Speech disturbance in acute stage of putaminal hemorrhage].

Speech disturbance was evaluated in the acute stage of 34 patients with left putaminal hemorrhage. Twenty-two patients were surgically treated and 12 were medically treated. Word cognition, naming, and obedience to verbal command were evaluated according to the STLA severity grade, and speech disturbance in the acute stage was classified as 10 severe cases, 13 moderate cases and 9 mild cases. Severity of speech disturbance was correlated to severity of hemiparesis, volume of hematoma and extension of hematoma. The cases with hematomas extending to the corona radiata showed severe speech disturbance. At the time of re-evaluation about one month after the initial evaluation, 13 cases showed improvement of the disturbance to some extent, but 19 cases showed no improvement. The improvement was related to severity of initial speech disturbance, type of hematoma and volume of hematoma. The hematomas whose volumes were over 30ml were related to poor recovery. However, the cases with hematomas extending to the posterior part of the corona radiata showed poor improvement even though the volume was less than 30 ml. In conclusion, these clinical factors, especially the degree of hematoma extension shown on CT scan, are useful for diagnosis and evaluation of speech disturbance in putaminal hematoma.

Acute Disease↗
PubMed1992

Proliferating cell nuclear antigen (PCNA) immunostaining as an alternative to bromodeoxyuridine (BrdU) immunostaining for brain tumours in paraffin embedded sections.

Immunohistochemical staining for proliferating cell nuclear antigen (PCNA) and BrdU using anti-PCNA and anti-BrdU monoclonal antibodies, respectively, was performed in 16 human brain tumours, including 3 glioblastomas multiforme, 2 anaplastic astrocytomas, 1 cerebellar astrocytoma, 2 recurrent meningiomas, 4 non-recurrent meningiomas, 3 neurinomas and 1 medulloblastoma. Patients with brain tumours received an injection of bromodeoxyuridine (BrdU) intravenously during surgery, and tumour specimens were fixed in 70% ethanol and embedded in paraffin. The percentage of positive cells for PCNA was compared with a BrdU labelling index using adjacent paraffin-embedded sections. The percentage of PCNA-positive cells was correlated with the BrdU labelling index and the histological malignancy of the brain tumours. The correlation coefficient was 0.84. This suggests that the immunohistochemical staining for PCNA in paraffin sections is a good alternative to the BrdU labelling index.

Antigens, Neoplasm↗
PubMed1992

Partial resection of the gyrus rectus in pterional approach to anterior communicating artery aneurysms.

The effect of partial resection of the gyrus rectus during the unilateral pterional approach on surgical outcome was evaluated in 194 consecutive patients with ruptured anterior communicating artery aneurysms. Resection was performed more frequently in cases with poor clinical grade, in the acute stage, with superiorly directed aneurysms, and with high-positioned aneurysms. The surgical results were graded into three stages, and the follow-up results into five stages using the Glasgow Outcome Scale. Outcomes for 52 patients receiving gyrus rectus resection were compared with those for 142 patients without resection. There were no apparent effects caused by gyrus rectus resection on outcome.

Adolescent↗
PubMed1992

Analysis of tumor necrosis factor and lymphotoxin secreted by incubation of lymphokine-activated killer cells with tumor cells.

This study investigated the secretion of a tumor necrosis factor (TNF) and lymphotoxin (LT) from lymphokine-activated killer (LAK) cells during co-culture with glioblastoma cell lines, autologous glioma cells, and other non-gliomatous tumor cell lines (K562 and Daudi). Cytokine secretion from peripheral blood mononuclear cells (PBMC) was also examined. The TNF activity of culture supernatants was measured by L cell cytotoxic assay, and a neutralization test using anti-TNF and/or anti-LT antibodies determined whether the cytotoxic activity was due to TNF or LT. The results show that LAK cells secrete both TNF and LT during monoculture and release increased amounts of TNF and LT with non-gliomatous tumor cell stimulation, but PBMC secrete only TNF with tumor cell stimulation. Glioblastoma or anaplastic astrocytoma cells, however, did not stimulate cytokine secretion from either LAK cells or PBMC. This indicates a discrepancy between the capability of LAK cells to lyse malignant glioma cells and cytokine secretion from LAK cells, and suggests that malignant glioma cells may produce some factors which inhibit cytokine secretion from LAK cells.

Astrocytoma↗
PubMed1992

Giant aneurysm of the azygos anterior cerebral artery associated with acute subdural hematoma--case report.

A ruptured giant aneurysm of the azygos anterior cerebral artery (ACA) associated with an acute subdural hematoma (SDH) occurred in a 67-year-old male with two episodes of sudden severe headache and transient loss of consciousness. Neurologically, he had mild weakness of the left lower extremity. Computed tomography showed an elliptical heterogeneous hyperdense mass in the interhemispheric fissure in front of the corpus callosum and an acute SDH on the right. Angiography disclosed a giant aneurysm (2.8 x 2.0 cm) at the distal end of the azygos ACA. Removal of the SDH and aneurysmal neck clipping achieved a good outcome. Successive small bleedings may allow the aneurysmal dome to develop adhesions to the arachnoid membrane, and the final rupture will occur into the subdural space, resulting in a SDH.

Acute Disease↗
PubMed1992

Oblique sagittal magnetic resonance imaging visualizing vascular compression of the trigeminal or facial nerve.

An oblique sagittal magnetic resonance (MR) imaging method was developed to provide better visualization of vascular compression of nerves. The MR images of 12 patients with trigeminal neuralgia and 24 with hemifacial spasm were analyzed. The oblique sagittal views were obtained along the nerve identified by the axial view at an angle of 105 degrees between the line along the dorsal brain stem and the line along the margin of the pontomedullary junction (in patients with hemifacial spasm) or by the midsagittal view through the midpons (in patients with trigeminal neuralgia). The T1- and T2-weighted, proton-density, and/or gradient-echo MR images were evaluated to optimize imaging conditions. The oblique sagittal gradient-echo MR image most clearly visualized vascular compression of the nerves as high-intensity lines in six patients with trigeminal neuralgia, which was confirmed intraoperatively in four. Fifteen (75%) of 20 oblique sagittal gradient-echo MR images demonstrated vascular compression of the facial nerves in patients with hemifacial spasm; 12 of these were confirmed intraoperatively. The control study used 15 oblique sagittal gradient-echo MR images of nonaffected contralateral and normal sites. Four false-positive findings were found. Oblique sagittal gradient-echo MR images are a useful planning aid, allowing differential diagnosis prior to microvascular decompression in trigeminal neuralgia and hemifacial spasm.

Adult↗
PubMed1992

Antiproliferative cytokines secreted by lymphokine-activated killer cells stimulated with tumor cells.

Antiproliferative cytokine secretion by lymphokine-activated killer (LAK) cells during coculture with glioblastoma cell lines, autologous glioma cells, and nongliomatous tumor cell lines (Daudi and K562 cells) was assessed, as was the antiproliferative activity of the culture supernatants against the T98G (glioblastoma) cell line. A neutralization test using agents against interferon-gamma (IFN-gamma), tumor necrosis factor (TNF), and lymphotoxin (LT) showed that antiproliferative activity was due to IFN-gamma, but not to TNF or LT. Nongliomatous tumor cells stimulated LAK cells to secrete cytokines, but gliomatous tumor cells did not. It was found that there is a discrepancy between the LAK cell capability to lyse malignant glioma cells and the ability to secrete cytokines. This may be due to the factors secreted by glioblastoma cells.

Astrocytoma↗
PubMed1991

Effect of recirculation on exacerbation of ischemic vascular lesions in rat brain.

Using electron microscopy, we investigated the small arteries and veins in ischemic lesions induced by occlusion of the ostium of the middle cerebral artery in 42 rats. We observed endothelial denudation in the small arteries of rats receiving occlusion for greater than 6 hours. When the occluding cylinder was removed to allow for reperfusion, however, 2 hours of occlusion was sufficient for endothelial denudation to occur. Medial smooth muscle cells seemed to be more vulnerable to ischemia than endothelial cells because ultrastructural changes in the former cells preceded endothelial denudation. Moreover, endothelial denudation definitely exacerbated vascular changes so that medial necrosis appeared to be complete beneath the denuded areas, allowing erythrocytes, platelets, and exogenous tracers to penetrate into the cytoplasm of smooth muscle cells. These arterial lesions seemed to be repaired 10 days after removal of the occluding cylinder following 2 hours of occlusion. On the other hand, small veins in the ischemic lesion did not show endothelial denudation or medial necrosis. Our study suggests that arterial changes in ischemic lesions play a role in exacerbating the brain edema caused by recirculation after ischemia.

Animals↗
PubMed1991

Giant middle cerebral artery aneurysm with parent artery occlusion--case report.

A 54-year-old female was admitted with consciousness disturbance and right hemiparesis. Computed tomographic (CT) scans and angiograms revealed diffuse subarachnoid hemorrhage, a partially thrombosed, giant middle cerebral artery aneurysm (5 x 5 x 4 cm), and occlusion of the parent artery at the aneurysm site. Despite conservative treatment, a generalized convulsion occurred. Emergency CT scans revealed irregular enlargement of the left temporal high-density mass and severe mass effect due to cerebral infarction. Barbiturate coma therapy was administered, but she did not recover and died 9 days after admission. Only two cases of ruptured aneurysm with simultaneous occlusion of the major cerebral vessels have been reported, both with poor outcome. In this case, the mechanism of parent artery occlusion is unclear, but thrombus protrusion from the giant aneurysm into the parent artery may have been involved.

Arterial Occlusive Diseases↗