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Biomedical subjects

T Furui

Publications and source records attributed to T Furui.

At least 37 records · Page 2Linked to original sources

Effects of the conventional anticonvulsants, phenytoin, carbamazepine, and valproic acid, on sodium-potassium-adenosine triphosphatase in acute ischemic brain.

The effects of phenytoin, carbamazepine and valproic acid on alterations in sodium-potassium-adenosine triphosphatase activity during ischemia were studied in the rat brain. Pretreatment with phenytoin and carbamazepine prevented a reduction of this activity, which, without either treatment, was observed in the cerebral hemisphere exposed to 30-minute ischemia resulting from unilateral middle cerebral artery occlusion. Valproic acid, on the other hand, did not principally affect the ischemic impairment of this membrane-bound enzyme activity. These results lend support to the previously proposed use of phenytoin in cerebral ischemia, but also suggest the therapeutic availability of another common anticonvulsant, carbamazepine, for treatment of the insult.

Animals↗

Inhibition by prolactin of membrane-associated phosphatidylinositol kinase of human endometrial fibroblast.

Certain malignant tumors synthesize and secrete a putative peptide mitogen, which elicits a potent proliferative response in their supporting stromal cells. We recently demonstrated that prolactin (PRL) binds to human endometrial fibroblasts and inhibits mitogenicity of an endometrial carcinoma extract (Imai A, et al. Proc Soc Exp Biol Med 203:117-122, 1993). In this report, we have studied inhibitory regulation by PRL of phosphatidylinositol (PtdIns) kinase activity associated with plasma membranes isolated from human endometrial fibroblasts. Incubation of the isolated plasma membrane with [gamma-32P]ATP and exogenous PtdIns caused [32P]phosphate incorporation into PtdIns phosphate (PtdInsP); 95% of the 32P-labeled PtnInsP was accounted for by PtdIns 4-P. The PtdIns phosphorylation by membrane preparations was selectively stimulated in a dose-dependent manner by vanadate, in parallel with an elevated autophosphorylation of endogenous membrane proteins. Concomitant exposure of the membrane preparations to PRL led to a remarkable inhibition of the vanadate-responsive PtdIns phosphorylation and protein autophosphorylation. This inhibition was dependent on PRL dose, and half-maximal effect occurred at a concentration 1-10 nM of PRL. Degradation of the produced PtdInsP in the plasma membranes was not affected by PRL. Similar inhibition of PtdIns kinase activities were observed in membranes prepared from cells that had been pretreated in vivo with PRL prior to assay in vitro. These findings demonstrate that PtdIns kinase activity associated with protein autophosphorylation is suppressed by PRL in plasma membrane isolated from endometrial fibroblasts. The inhibition of vanadate-responsive PtdIns kinase by PRL suggests an involvement of this enzyme in the antimitogenic action of the hormone on human endometrial fibroblasts.

1-Phosphatidylinositol 4-Kinase↗

Decrease in cytochrome c oxidase and cytochrome oxidase subunit I messenger RNA levels in preeclamptic pregnancies.

OBJECTIVE: To elucidate the possible relation between mitochondrial gene expression and placental dysfunction. METHODS: We measured the activity of cytochrome c oxidase and the expression of cytochrome oxidase subunit I in mitochondria from human placentas of women whose gestations were appropriate for gestational age (AGA) and those with preeclampsia. In addition, the amounts of normal mtDNA and deleted mitochondrial DNA were examined in the two groups by Southern blot analysis and polymerase chain reaction, respectively. RESULTS: Cytochrome c oxidase activity and expression of cytochrome oxidase subunit I were significantly lower in the preeclamptic group than in the AGA group. There were no differences between the groups in the amounts of mitochondrial DNA. In addition, no mutant mitochondrial DNA with a 4977-base pair deletion was detected in the two groups. CONCLUSION: These results suggest that reduced expression of the mitochondrial gene is involved in placental dysfunction in preeclamptic pregnancy.

Actins↗

Endodermal sinus tumor of the vagina in an infant: magnetic resonance imaging evaluation.

Endodermal sinus tumor is a rare and highly malignant lesion. This report documents the clinical findings and magnetic resonance imaging (MRI) of an uncommon case of the endodermal sinus tumor arising in the vagina of a 6-month-old infant. MRI was extremely accurate in delineating the possible extent and location of the vaginal lesion. This is the first report to demonstrate MRI of vaginal endodermal sinus tumor.

Antineoplastic Combined Chemotherapy Protocols↗

Studies on transmission of hepatitis C virus from mother-to-child in the perinatal period.

To elucidate whether breast milk, vaginal discharge and contamination with maternal blood at birth are possible routes of mother-to-child transmission of hepatitis C virus (HCV), we examined HCV RNA in the cord and peripheral blood of infants, and in the blood, vaginal discharge, and breast milk of anti-HCV seropositive mothers. From July 1991 to July 1992, we studied 20 healthy pregnant women, who were seropositive with the Ortho anti-HCV EIA, and their infants. Using a sensitive nested polymerase chain reaction (nested PCR), we investigated the presence or absence of hepatitis C virus in the above-mentioned specimens. Moderate elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) was observed in only one woman in the first and third trimesters. The nested PCR and subsequent Southern hybridization detected 0.5-5.5 copies of HCV c-DNA. HCV RNA was detected in 17/20 blood samples (85%), 7/14 vaginal discharge samples (50%) and 4/10 cord blood samples (40%). However, no HCV RNA was identified in the peripheral blood of infants or breast milk. The mother-to-child transmission of HCV at delivery or via breast milk does not appear to contribute much to maintaining the global HCV reservoir.

Adult↗

Presence of gonadotropin-releasing hormone and its messenger ribonucleic acid in human ovarian epithelial carcinoma.

OBJECTIVE: The purpose of this study was to investigate the expression of gonadotropin-releasing hormone messenger ribonucleic acid and the presence of gonadotropin-releasing hormone in human ovarian carcinoma known to have gonadotropin-releasing hormone binding sites and to be affected by gonadotropin-releasing hormone analog. STUDY DESIGN: Human ovarian carcinomas surgically removed and human ovarian carcinoma cell lines were examined. Gonadotropin-releasing hormone was determined by a radioimmunoassay and a bioassay. Gonadotropin-releasing hormone messenger ribonucleic acid was determined by reverse transcription polymerase chain reaction using oligonucleotide primers synthesized according to the published human gonadotropin-releasing hormone sequence. RESULTS: Gonadotropin-releasing hormone was shown to be present in extracts of ovarian mucinous cystadenocarcinoma sample (0.8 +/- 0.12 pg/mg of protein) and ovarian adenocarcinoma cell line SK-OV3 (0.92 +/- 0.17 pg/mg of protein) but not in the normal ovary and placenta. Two of two extract samples from individual cases evoked dose-dependent phosphoinositide breakdown in rat granulosa cells similar to that caused by authentic gonadotropin-releasing hormone. Gonadotropin-releasing hormone messenger ribonucleic acid was detected in two of two mucinous cystadenocarcinoma specimens, one of one serous cystadenocarcinoma, and SK-OV3 cells but not in the dysgerminoma, mucinous cystadenoma, and normal ovary and placenta. CONCLUSION: The demonstration of gonadotropin-releasing hormone and its messenger ribonucleic acid raises the possibility that gonadotropin-releasing hormone may play an autocrine regulatory role in the growth of ovarian carcinoma.

Adenocarcinoma↗

Pregnancy and successful delivery in a patient with triple heart valve prosthesis.

A 42-year-old patient had a history of rheumatic fever in childhood. At 37 years of age, she underwent a triple heart valve replacement; thereafter, she was followed with the administration of warfarin and methyldigoxin. Her third pregnancy occurred with the last menstruation on 12 March 1990. At the 30th gestational week, she was admitted to the Nagoya University Hospital for the control of anticoagulation and rest. She delivered by cesarean section a healthy male infant weighing 2070 g at 34 weeks of gestation. The post-operative course was uneventful. This report shows that a patient with a three heart valve prosthesis tolerated pregnancy well under intense medical supervision.

Adult↗

Enhancing effects of estrogens on endometrial carcinogenesis initiated by N-methyl-N-nitrosourea in ICR mice.

The present study was undertaken to examine the effects of estrogens, such as estrone (E1), 17 beta-estradiol (E2) and estriol (E3), on endometrial carcinogenesis initiated by N-methyl-N-nitrosourea (MNU) in mice. A total of 120 female ICR mice received MNU solution (1 mg/100 g body wt.) and normal saline at 10 weeks of age into their left and right uterine corpora, respectively. One week later, they were divided into four groups and treated as follows: Group 1 (30 mice) was given 25 ppm E1-containing diet; and Group 2 (30 mice) was fed 5 ppm E2-containing diet; Group 3 (30 mice) was given 25 ppm E3-containing diet; and Group 4 (30 mice) was fed the basal diet alone. At the termination of the experiment (Week 30), all surviving animals were autopsied and histopathological examinations revealed that endometrial adenocarcinomas had developed in all groups. The incidence of adenocarcinomas in the MNU-treated uterine corpus in Group 1 (25 ppm E1-feeding, 9/23, 39%) was significantly higher than that in Group 4 (basal diet, 3/26, 12%, P < 0.05). Also, the incidences of adenocarcinomas in the MNU-treated uterine corpus in Groups 2 (5 ppm E2-feeding, 8/24, 33%) and 3 (25 ppm E3-feeding, 7/26, 28%) were higher than in Group 4, but the difference was not statistically significant. Feeding of diet containing E1, E2 and E3 increased the incidences of the preneoplastic endometrial lesions (atypical, adenomatous or cystic glandular hyperplasia). In the uterine cervix, small numbers of squamous cell carcinomas, dysplasias or hyperplasias were occasionally found in all groups. These results indicate enhancing effects of the above three types of estrogens on the endometrial carcinogenesis induced by MNU in ICR mice.

Adenocarcinoma↗

Successful outcome of pregnancy complicated with thyroidectomy-induced hypoparathyroidism and sudden dyspnea. A case report.

Total thyroidectomy is often accompanied with airway problem and hypoparathyroidism leading to infertility and pregnancy losses, and its effects are thus rarely reported on delivery. A patient with postoperative hypoparathyroidism carried a pregnancy to successful delivery, but suffered uncontrollable hypocalcemia and sudden respiratory distress at spontaneous labor onset. Both the fetal and maternal outcome were good. The acute deterioration in the hypoparathyroidism and airway problem at labor differed from the complications in previously reported cases.

Adenocarcinoma, Papillary↗

Hematosalpinx and torsion of the fallopian tube in a virgin girl.

Torsion of the fallopian tube is encountered in the diseased tube. The present report describes a hematosalpinx and its tubal torsion in a virgin girl who experienced no prior predisposing factors suggested for tubal obstruction and adhesions. This rare case may highlight a new insight into pathophysiology of tubal torsion associated with hematosalpinx.

Adult↗

Intracerebral hemorrhage associated with migrainous headache--a case report.

A case of intracerebral hemorrhage that developed some time after severe headache is reported in a relatively young woman. It is proposed that hemorrhage may also be included among the causes of so-called migraine-related stroke, which has generally been known to result from infarction.

Cerebral Hemorrhage↗

Potential protection by a specific kappa-opiate agonist U-50488H against membrane failure in acute ischemic brain.

The effects of a novel opioid kappa-receptor agonist U-50488H on Na(+)-K(+)-adenosine triphosphatase (ATPase) activity and regional cerebral blood flow (rCBF) were studied in the acute ischemic brain of rats after middle cerebral artery (MCA) occlusion. Administration of U-50488H 15 minutes prior to MCA occlusion attenuated ischemic reduction in Na(+)-K(+)-ATPase activity 15 minutes after MCA occlusion. The effect was statistically significant at a dosage of 30 mg/kg, but not at lower doses (0.3 and 3 mg/kg). There was no effect on rCBF before MCA occlusion, and the decreased flow after occlusion was enhanced with a significant fall in systemic blood pressure at a dosage of 30 mg/kg. These results indicate that U-50488H has therapeutic potential in cerebral ischemia by mechanisms other than improvement in CBF.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Prolactin binds to human endometrial fibroblasts and inhibits mitogenicity of an endometrial carcinoma extract.

Uterine endometrial carcinoma has been reported to synthesize and secrete a putative peptide mitogen that elicits a potent proliferative response in endometrial fibroblasts. The extract from endometrial carcinoma stimulated [3H]thymidine incorporation into human endometrial fibroblasts in a dose-dependent manner. Concomitant exposure of the fibroblasts to prolactin (PRL) led to a remarkable inhibition of the extract-stimulated mitogenic activity of the fibroblasts. This inhibition was dependent on PRL dose, and maximal effect occurred at 1 microM of PRL. PRL (10 nM) suppressed an apparent maximal activity of the extract by 50%, and the half-maximal stimulated effect of the extract on thymidine incorporation was observed at the same concentration in the absence or presence of PRL. This noncompetitive manner may imply that PRL acts at a stage after the interaction of the mitogen in the extract with the specific receptor for mitogen. When the fibroblasts were first exposed to the extract for 12 hr and then to PRL, PRL suppressed the mitogenic activity with no lag. The rapid growth-inhibitory effect of PRL was mimicked by prostaglandin E1, but the combination of both types of ligand was not additive in the inhibitory action on growth. PRL and prostaglandin E1 may inhibit a similar mitogenic signaling cascade. Specific receptor sites for PRL were detected in the endometrial fibroblasts, showing high binding affinity (Kd = 16.1 nM) and low binding capacity (Bmax = 1.59 pmol/mg protein). Treatment of the fibroblasts with the endometrial carcinoma extract induced no changes in the level of PRL receptor, excluding the possibility that PRL competes for the binding sites with the mitogen. These findings would suggest that PRL may block the mitogenic activity of the fibroblasts stimulated by the endometrial carcinoma-derived mitogen via a PRL receptor-mediated mechanism, perhaps prostaglandin production.

Binding Sites↗

[Determination of intrauterine pressure using catheter-tip transducer inserted outside fetal membranes].

To determining intrauterine pressure outside fetal membranes, we used a catheter-tip transducer to study 20 women before the occurrence membrane rupture. Their mean age was 28.2 +/- 3.4 years and all women were in weeks 37 to 41 of pregnancy when studied. In the first stage of labor, the peak intrauterine pressure was 60.0 +/- 12.5 mmHg (mean +/- SD) when the external os was dilated 4 to 6 cm, 90.0 +/- 14.8 mmHg, at 7 to 8 cm dilation, and 80.0 +/- 11.5 mmHg at 9 cm or greater dilation. Each pressure wave lasted 45 to 55 sec. The highest baseline pressure (28.0 +/- 4.5 mmHg) was obtained when the subjects were sitting. A baseline pressure of 17.0 +/- 4.0 mmHg was obtained in the supine position, as well as a value of 21.0 +/- 3.5 mmHg in the recumbent position. There were no complications related to the catheter-tip transducer. Our findings indicate that this method is both accurate and reliable in determining the amounts of intrauterine pressure to which fetal membranes are subjected.

Adult↗

[Histopathologic study of carotid artery plaques].

Twenty-six carotid plaques were obtained from endarterectomies in 25 cases and microscopically studied. Ulceration was observed in 11 of the 26 plaques (42%) and more frequently in the plaques from symptomatic cases (TIA, RIND or stroke) (56%) than from asymptomatic cases (13%). Although ulceration occurred more commonly as the degree of plaque stenosis increased, it was also observed in 4 plaques with relatively mild stenosis. The interesting finding in terms of ulcer formation was that 10 of the 11 plaques with ulceration showed intramural hemorrhage, which occurred in 13 of all plaques (50%). Hemorrhage occurred in connection with ulcer in 7 plaques and was exposed into the arterial lumen in 5 of these 7 plaques. Atheromatous debris was found within the ulcer in 4 other plaques with intramural hemorrhage. These results suggest that intraplaque hemorrhage plays an important role in ulceration, through which a clot or atheromatous debris may eventually cause an embolism.

Aged↗

Changes of silver-stained nucleolar organizer regions in mouse endometrial carcinogenesis induced by N-methyl-N-nitrosourea and 17 beta-oestradiol.

A high incidence of endometrial adenocarcinoma and pre-neoplastic lesions was induced in ICR mice treated with N-methyl-N-nitrosourea and 17 beta-oestradiol within 23 weeks. The endometrial lesions were histopathologically similar to those of human subjects. To assess the cell proliferative activity of these lesions, a one-step silver colloid staining for nucleolar organizer regions was applied and the numbers of silver-stained nucleolar organizer regions (AgNORs) were counted. The mean numbers +/- SD of AgNORs in each lesion were as follows: simple hyperplasia, 2.07 +/- 0.36; complex hyperplasia without cytological atypia, 2.79 +/- 0.39; complex hyperplasia with cytological atypia, 3.43 +/- 0.38; and well-differentiated adenocarcinoma, 4.17 +/- 0.40. Significant differences were observed in each lesion (P < 0.001). These findings suggest that the mean numbers of Ag-NORs are increased in the progression of neoplastic changes in the mouse endometrium, as in human endometrial lesions. This rapid induction model of endometrial carcinoma in mice is useful in the understanding of the histogenesis of endometrial carcinoma in human subjects.

Adenocarcinoma↗

Juvenile granulosa cell tumor in a 2-year-old infant: report of a case complicated with ascites and acute respiratory distress.

A two-year-old girl with a juvenile granulosa cell tumor (JGCT) and with acutely progressive hydrothorax and ascites is presented. She had precocious pseudopuberty and an elevated level of serum estradiol. Sudden onset of respiratory distress, due to a pleural effusion and severe abdominal distention, led to an emergency laparatomy. Unilateral salpingo-oophorectomy induced a rapidly favorable course. Histological examination showed no evidence of invasion or peritoneal metastasis. This is the first case of JGCT associated with an acute respiratory emergency as a main clinical feature.

Child, Preschool↗

Evidence of a role for phosphatidylinositol synthesis in human amnion cell proliferation.

Phosphatidylinositol (PtdIns) is the key precursor of phosphoinositide-derived intracellular mediators. The effects of changing the rate of PtdIns synthesis on mitogenic activity of human amnion-derived WISH cells were investigated. Incubation of the cells with [3H]inositol caused a time- and dose-dependent PtdIns labeling. Exogenous Ca2+ inhibited [3H]inositol incorporation in a dose-dependent fashion; half-maximal inhibition occurred with 0.3-1.0 mM Ca2+. In contrast, removal of cytosolic Ca2+ by ionophore A23187 and 1 mM EGTA induced enhancement of the PtdIns labeling as a function of A23187 concentration, perhaps through release of inhibitory effects of endogenous Ca2+. The A23187-stimulated PtdIns labeling with [3H]inositol was not abolished by additional unlabeled inositol, suggesting that [3H]inositol labeling of PtdIns occurred mainly through de novo synthesis catalyzed by PtdIns synthase (EC 2.7.8.11). In cells with PtdIns synthase activity decreased by exogenous Ca2+, [3H]thymidine incorporation was also inhibited, while A23187 caused dose-dependent enhancement of thymidine incorporation. The changes in PtdIns synthase activity occurred in parallel with changes in mitogenic activity caused by increasing the dose of exogenous Ca2+ or A23187. A similar lowering of mitogenic activity was observed upon suppression of PtdIns synthase by pemirolast potassium (9-methyl-3-1H-tetrazol-5yl-4H-pyrido[1,2-a]pyridin-4-one potassium) via a Ca(2+)-independent mechanism. These data demonstrate that changes in PtdIns synthase activity by some agents acting via different mechanisms are associated with parallel changes in thymidine incorporation, and suggest that PtdIns production is tightly coupled to cell proliferation in human amnion cells.

Amnion↗