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T Hasegawa

Publications and source records attributed to T Hasegawa.

At least 19 recordsLinked to original sources
PubMed1996

Morphological and functional factors predicting bladder deterioration after spinal cord injury.

PURPOSE: We investigated factors predictive of morphological and functional deterioration of the bladder in patients with spinal cord injury. MATERIALS AND METHODS: Urological evaluation, including excretory urography and urodynamic studies, was performed once a year in 66 patients. Bladder compliance was used as an index of bladder function. RESULTS: Mean age of the patients with worsening bladder form and function was significantly greater than that of those with no change. In patients with worsening bladder function intermittent catheterization was performed less frequently and mean catheterization volume was greater compared to those with improvement and no change. Catheterization was less frequent and at long intervals in patients with a high urethral closure pressure. CONCLUSIONS: High storage pressure due to a high urethral closure pressure is believed to cause deterioration of bladder form and function.

Adult↗
PubMed1995

The first observation of O2- generation at real time in vivo from non-Kupffer sinusoidal cells in perfused rat liver during acute ethanol intoxication.

Infusion of ethanol or phorbol myristate acetate (PMA) into the perfused rat liver immediately produces O2- which was detected directly by infusion of a Cypridina luciferin analogue, MCLA as a chemiluminescence reagent. The MCLA photon emission was inhibitable by SOD. Generation of O2- in the liver was further verified by nitroblue tetrazolium, formazan precipitate formation. Ethanol-induced O2- generation was unaffected by gadolinium chloride (GdCl3), an inhibitor of kupffer cells, while PMA induced O2- generation was completely abolished by GdCl3. Since PMA is a known stimulator of phagocytic cells including Kupffer cells, the results indicate, for the first time that ethanol stimulates a non-Kupffer cell population, probably liver sinusoid endothelial cell to produce O2-.

Animals↗
PubMed1995

Recognition of sialosaccharide chains of glycophorin on damaged erythrocytes by macrophage scavenger receptors.

Binding of mouse erythrocytes oxidized in vitro mildly with diamide, periodate or ADP/Fe3+, and the erythrocytes incubated in vitro in a serum-free medium for 12 h (in vitro aged erythrocytes) to mouse peritoneal macrophages was effectively inhibited by isolated glycophorin A, a major sialoglycoprotein of human erythrocyte membrane existing as oligomers in solution, and some of known ligands for macrophage scavenger receptors such as maleyl-BSA, dextran sulfate, fucoidan and polyinosinic acid. Binding of oxidized low density lipoprotein (ox-LDL) to macrophages was inhibited by glycophorin A as well as the known ligands. When the sialyl residues of the saccharide chains of glycophorin A were cleaved by neuraminidase, or the polypeptide of glycophorin A was digested by Pronase, which would destroy its oligomeric forms, the inhibitory effect of glycophorin A was decreased, suggesting that isolated glycophorin A binds to scavenger receptors depending on its sialyl residues and oligomeric structure. Glycopeptides prepared from the N-terminal region of glycophorin A containing most of the sialosaccharide chains of the molecule inhibited the binding of ox-LDL although the potency was lower than that of glycophorin A. N-Acetylneuraminic acid at a high concentration also inhibited the ox-LDL binding. Uptake and degradation of 125I-labeled ox-LDL by macrophages was inhibited by glycophorin A, N-acetylneuramin lactose, as well as the known ligands. 125I-labeled glycophorin A bound to macrophages, and the binding was inhibited by the unlabeled glycophorin A and the known ligands. Inhibitory activity of the unlabeled glycophorin A against the labeled glycophorin A-binding was lowered by neuraminidase and Pronase treatment. These results suggest that oxidized and in vitro aged mouse erythrocytes are recognized by scavenger receptors of mouse peritoneal macrophages, and the cell surface components recognized are sialosaccharide chains of glycophorin, possibly glycophorin A counterpart of mouse erythrocytes which clustered or aggregated in the membrane. The finding indicates that the cell surface sialosaccharides can be ligands for scavenger receptors when cells undergo denaturation by oxidative stress or other damaging effects.

Adenosine Diphosphate↗
PubMed1995

Regulation of early T cell development by the engagement of TCR-beta complex expressed on fetal thymocytes from TCR-beta-transgenic scid mice.

Transgenic expression of the beta-chain of T cell antigen-receptor (TCR) is known to induce the generation of CD4+ CD8+ thymocytes in the immunodeficient scid mouse, in which thymocyte development is otherwise arrested at CD4- CD8- cells. It is not clear, however, whether or not the thymocyte development is controlled by ligand engagement of the TCR-beta complex on the cell surface. In the present study, we have examined how the engagement by Ab of the TCR-beta complex expressed on the TCR-beta-transgenic scid fetal thymocytes can regulate the generation of CD4+ CD8+ thymocytes. Organ cultures of CD4- CD8- day 14 fetal thymocytes from the TCR-beta-transgenic scid mice resulted in the generation of CD4- CD8+ and then CD4+ CD8+ cells. The initial step from CD40- CD8- cells to CD4- CD8+ cells was enhanced by the addition of anti-TCR-beta Ab, whereas the subsequent step from CD4- CD8+ cells to CD4+ CD8+ cells was markedly inhibited by anti-TCR-beta Ab. These results indicate that ligand engagement of the TCR-beta complex can positively and negatively regulate the early thymocyte development. Moreover, the finding that engagement of TCR-beta complex inhibits the generation of CD4+ CD8+ cells suggests that the induction of CD4+ CD8+ thymocytes by the TCR-beta transgene is not an immediate consequence of cell-surface engagement of the TCR-beta complex but requires liberation from the continued TCR-beta signaling.

Animals↗
PubMed1995

Adenosine kinase-deficient mutant of Saccharomyces cerevisiae.

A cordycepin-resistant mutant strain of Saccharomyces cerevisiae (CD-R2) was found to be deficient in adenosine kinase. This mutant accumulated S-adenosylhomocysteine during growth in the presence of exogenous adenosine and it grew in a pseudohyphal manner in the presence of this nucleotide.

Adenosine↗
PubMed1995

Neuronal mechanism of the inhibitory effect of calcitonin on N-methyl-D-aspartate-induced aversive behavior.

To elucidate the mechanism of antinociceptive effects of calcitonin, we investigated whether receptor antagonists for various neurotransmitter receptors alter the inhibitory effect of calcitonin on intrathecally injected N-methyl-D-aspartate-induced aversive behavior in mice. Neither naloxone, an opioid receptor antagonist, phentolamine and benextramine, alpha-adrenoceptor antagonists, nor ritanserin, a 5-HT2A receptor antagonist, inhibited the calcitonin-induced anti-aversive effects. Pindolol and (--)-propranolol, non-selective antagonists of beta-adrenoceptors and 5-HT1 receptors, 1-(2-methoxyphenyl)-4-[4-(2-phethalimido) butyl]-piperazine hydrobromide (NAN-190), a 5-HT1A receptor antagonist, 3-tropanyl-3,5-dichlorobenzoate (MDL72222) and metoclopramide, 5-HT3 receptor antagonists, significantly inhibited the calcitonin-induced anti-aversive effects. (--)-Bicuculline, a GABAA receptor antagonist, phaclofen and 5-aminovaleric acid, GABAB receptor antagonists, also attenuated the calcitonin-induced anti-aversive effects. These results suggest that beta-adrenoceptor, 5-HT1A, 5-HT3, GABAA and GABAB receptors, but not alpha-adrenoceptor, opioid nor 5-HT2A receptors, are involved in the inhibitory effect of calcitonin on intrathecally injected N-methyl-D-aspartate-induced aversive behavior in mice.

Adrenergic alpha-Antagonists↗
PubMed1995

Participation of peroxynitrite in acetylcholine release induced by nitric oxide generators.

Peroxynitrite is a product produced by spontaneous reaction of nitric oxide (NO) with superoxide. Functional roles of peroxynitrite in the release of endogenous acetylcholine evoked by NO generators has been examined using primary-cultured cerebral cortical neurons. NO generators, such as sodium nitroprusside and S-nitroso-N-acetylpenicillamine, dose-dependently increased the release of acetylcholine (ACh); such increase of the release was significantly suppressed by hemoglobin which has the capacity to abolish biological effects of NO. Two types of superoxide scavengers, Cu2+, Zn2+ superoxide dismutase and ceruloplasmin, significantly reduced the NO-evoked ACh release. These results indicate that NO requires superoxide to evoke the release of ACh. Synthesized peroxynitrite evoked the release of ACh from cerebral cortical neurons in a dose-dependent manner. Thus, it is indicated that the NO-evoked ACh release is mediated, at least in part, by peroxynitrite produced by the reaction of NO with superoxide.

Acetylcholine↗
PubMed1995

Del(12)(p11.21p12.2) associated with an asphyxiating thoracic dystrophy or chondroectodermal dysplasia-like syndrome.

We describe a 5-year-old Japanese boy who has some radiographic findings characteristic of asphyxiating thoracic dystrophy (ATD)-chondroectodermal dysplasia with a de novo chromosome abnormality. He also has mild mental retardation, short stature, hypoplastic hair and skin, oligodontia, small thoracic cage, hypoplastic pelvis and cone-shaped epiphyses of hands. On cytogenetic studies he was found to have a de novo del(12)(p11.21p12.2). These results suggest that the locus of the gene associated with ATD-chondroectodermal dysplasia may be situated at 12p11.21p12.2.

Child, Preschool↗
PubMed1995

Measurement of apolipoprotein A1 in cholesterol gallstones and gallbladder bile of patients with gallstones.

Biliary apolipoprotein A1 in bile inhibits the nucleation of cholesterol crystals from bile super-saturated with cholesterol. In the present study, using an enzyme-linked immunosorbent assay of apolipoprotein A1, we determined the content of apolipoprotein A1 in cholesterol gallstones and samples of gallbladder bile collected simultaneously from 23 patients during cholecystectomy. Protein content in cholesterol gallstones ranged from 50 to 5700 micrograms/g, with median, quartile, and three quartile values being 250, 111, and 740; apolipoprotein A1 content ranged from 9 to 9000 ng/g (200, 41, 647). The gallbladder bile samples contained protein at concentrations of 0.4-9.0 mg/ml (2.0, 1.1, 3.2), while apolipoprotein A1 was present at concentrations of 2.0-136.0 micrograms/ml (30.0, 10.0, 90.0). A notable finding was that the A1/total protein (TP) values for gallbladder bile, which ranged from 0.13% to 6.80% (1.62, 0.89, 3.34), were several times higher than those determined for gallstone samples, which ranged from 0.01% to 1.2%, 2% (0.06, 0.02, 0.25). The results of sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis showed that the protein profile in cholesterol gallstones was similar to that in gallbladder bile. It was concluded that: (1) the protein contained in gallstones may originate from bile, (2) the content of apolipoprotein A1 in cholesterol gallstones is only a trace amount, compared with that in gallbladder bile, and (3) biliary apolipoprotein A1 may be retained in a soluble phase in gallbladder bile, with minimal precipitation onto the surfaces of gallstones.

Apolipoprotein A-I↗
PubMed1995

Is CIS of the ureter responsible for skipped lymph node metastasis? A case report.

A case of skipped lesion of lymph node metastasis of left ureteral tumour with concurrent carcinoma in situ in the affected ureter is presented. Postoperatively, lymph node metastasis was de novo detected in the left retrocrural and renal hilar regions on CT scan, although only the obturator lymph node was histologically metastatic among the regional lymph nodes completely dissected. The possible explanations of this rare metastatic mode are discussed.

Carcinoma in Situ↗
PubMed1995

Chemical form of selenium-containing metabolite in small intestine and liver of mice following orally administered selenocystine.

The chemical form of a selenium-containing metabolite in the small intestine following a single oral administration of selenocystine was investigated with ICR male mice. Selenium content in the small intestine of animals treated with 50 mg/kg selenocystine significantly increased 15 min, 1 h and 6 h after treatment. In contrast, selenocystine significantly depressed the intestinal reduced glutathione (GSH) level at 1 h after administration. A significant negative correlation between the selenium level and the level of GSH in the small intestine was observed (r = -0.83, p < 0.001). Analysis of the intestinal metabolite of selenocystine showed that selenium-containing metabolites elute in two fractions from a Sephadex G-25 column: the low-molecular fraction (peak I) contained the selenocystine, while the high-molecular fraction (peak II) contained selenocysteine-containing metabolite. An in vitro experiment was performed to gain insight into the mechanism for selenocysteine-containing metabolite production in the intestinal cytosol. When selenocystine or selenocysteine reacted with excess GSH in the presence of intestinal homogenate, the peak II fraction which involved the selenocysteine-containing metabolite was recognized in the Sephadex G-25 chromatogram. From an examination of the distribution of the selenocysteine-containing metabolite, it was recognized that this metabolite exists in plasma and liver cytosol of mice after oral administration of selenocystine. These results suggested that the mice treated with selenocystine produce selenocysteine-containing metabolite by reaction of selenocystine with excess GSH in the small intestine, and the metabolite is then transported to the liver through blood plasma.

Administration, Oral↗
PubMed1995

Orthotopic liver transplantation for ornithine transcarbamylase deficiency with hyperammonemic encephalopathy.

Ornithine transcarbamylase (OTC) deficiency is an X chromosome-linked disorder causing hyperammonemic encephalopathy with a very poor prognosis. We describe here two patients with OTC deficiency, one a late on-set female patient (case 1) and the other a neonatal-onset male patient (case 2), who were successfully treated with orthotopic liver transplantation (OLTx). The OTC activity in the excised liver was 10% and 0% of control, respectively. Hyperammonemic encephalopathy was controlled with medical therapy in case 1 until the of 5 years, but the complicated course in case 2 in which hyperammonemia required peritoneal dialysis and hemodialysis in the neonatal period necessitated OLTx with a reduced-size liver at the age of 80 days. Both patients had restoration of serum ammonia level to normal in 2 and 3 days after liver replacement, and both patients have normal neurological and developmental status after 2 and 0.5 years of postoperative follow-up. These cases illustrate not only the metabolic cure of this disorder, but also the need to preserve neurological integrity by aggressive medical management of the hyperammonemia preoperatively and early surgical intervention when indicated, even if this is required very early in life.

Ammonia↗
PubMed1995

Risperidone prevents the development of supersensitivity, but not tolerance, to phencyclidine in rats treated with subacute phencyclidine.

We investigated whether risperidone, a 5-HT2/dopamine-D2 receptor antagonist, inhibits the development of tolerance and supersensitivity to PCP and whether subacute administration of PCP with risperidone affects the [3H]MK-801 binding in rat brain, in comparison with dopamine-D2 receptor antagonist haloperidol and 5-HT2 receptor antagonist ritanserin. In rats treated with PCP (10 mg/kg, i.p.) for 14 days, PCP (10 mg/kg, i.p.)-induced hyperlocomotion, rearing and sniffing were potentiated (supersensitivity), and head-weaving, head-twitch, backpedalling and turning were diminished (tolerance). The development of supersensitivity to PCP was blocked by oral co-administration of risperidone (2.4 mg/kg, p.o.) and haloperidol (1.0 mg/kg, p.o.) for 14 days, but not ritanserin (10 mg/kg, p.o.) and risperidone (0.8 mg/kg, p.o.), while no drugs prevented the development of tolerance to PCP. Both risperidone (2.4 mg/kg, p.o.) and haloperidol (1.0 mg/kg, p.o.) also inhibited the cross-supersensitivity to methamphetamine (MAP; 2.5 mg/kg, i.p.)-induced rearing in rats treated with PCP for 14 days. The profiles of [3H]MK-801 binding in discrete brain areas did not change after subacute administration of PCP alone or in combination with risperidone, haloperidol or ritanserin for 14 days. Therefore, it is suggested that subacute administration of PCP may cause functional changes in the dopaminergic neuronal transmission under conditions where the binding of [3H]MK-801 in discrete brain areas is unchanged, and that co-administration of risperidone may block these PCP-induced changes in neuronal function.

Animals↗
PubMed1995

The attenuation of suppression of motility by triazolam in the conditioned fear stress task is exacerbated by ethanol in mice.

We investigated whether triazolam attenuated the suppression of motility in the conditioned fear stress task in mice and whether ethanol modified the effects of triazolam. When mice were placed 24 hours later (retention test) in the same environment in which they had previously been exposed to an electric foot shock (training), they exhibited a marked suppression of motility (conditioned fear stress). Triazolam (0.01-0.1 mg/kg, s.c.), administered before training, attenuated the suppression of motility in the conditioned fear stress task in a dose-dependent manner, without affecting the sensitivity to an electric foot shock. The doses of triazolam that attenuated the suppression of motility were much lower that those of chlordiazepoxide (5-10 mg/kg, s.c.). Neither drug, administered before the retention test, attenuated the suppression of motility in the conditioned fear stress task. These results suggest that both benzodiazepines may inhibit the process of acquisition, but not the process of recall, of memory. Ethanol (1 g/kg, p.o.), which, by itself, did not affect either the suppression of motility or the sensitivity to an electric foot shock, exacerbated the attenuation of the suppression of motility in the conditioned fear stress task induced by both triazolam (0.01 mg/kg) and chlordiazepoxide (5 mg/kg). These results suggest that ethanol exacerbates the effects of benzodiazepines.

Animals↗
PubMed1995

Differentiation and proliferative activity in benign and malignant cartilage tumors of bone.

To assess the histological grade in benign and malignant cartilage tumors of bone by more objective methods, we examined the differentiation and proliferative activity of tumor cells in six enchondromas, five chondroblastomas, and 13 chondrosarcomas immunohistochemically. A variable number of cells in all tumors showed S-100 protein and vimentin immunoreactivity. In fully differentiated cartilage of enchondromas and low grade chondrosarcomas, tenascin, which is an extracellular matrix glycoprotein, was present in small amounts or absent but was increased at the periphery of tumor lobules and even in the matrix throughout the high grade chondrosarcomas. Higher rate and intensity of proliferating cell nuclear antigen (PCNA) reactivity were found in chondrosarcomas, especially in spindle-shaped cells of high grade tumors, than in enchondromas. The distribution of PCNA-positive cells almost corresponded to the regions with tenascin reactivity. One tumor of high grade chondrosarcoma showed p53 protein immunoreactivity. Aberrant expression of cytokeratin was observed in four chondroblastomas. The expression of desmin was identified in relatively large proportions of enchondromas and chondrosarcomas, regardless of their benign or malignant nature and histological grade. Smooth muscle or muscle-specific actins also were present in a smaller number of tumors. Based on these findings, it is concluded that unusual staining characteristics were present, in addition to those of a chondroblastic nature, in the cartilage tumors of bone. Tenascin and PCNA positivity of various degrees in all chondroblastomas may suggest that they are chondrogenic tumors having a relatively high proliferative activity, albeit their benign clinical course. Proliferative activity of tumor cells in enchondromas and chondrosarcomas correlated well with their histological grade. Tenascin may play a role in promoting tumor cell proliferation of cartilagenous neoplasms and, on the other hand, the alterations of extracellular matrix involving tenascin synthesis seem to be a result of tumor development.

Adolescent↗
PubMed1995

Traumatic basilar impression: case report.

A very rare case of traumatic basilar impression is reported. The patient, a 57-year-old man, was hit on the head vertically in the parietal region. X ray of the cervical spine and computed tomography (CT) scans showed intracranial indentation of the atlas and the odontoid process with a depressed fracture around the foramen magnum. There are no previous reports about this type of fracture.

Cranial Fossa, Posterior↗
PubMed1995

Involvement of peroxynitrite in N-methyl-D-aspartate- and sodium nitroprusside-induced release of acetylcholine from mouse cerebral cortical neurons.

Functional roles of peroxynitrite in N-methyl-D-aspartate (NMDA)- and sodium nitroprusside (SNP)-evoked releases of acetylcholine (ACh) from cerebral cortical neurons in primary culture have been investigated. NMDA increased the release of ACh in a dose-dependent manner, which was significantly suppressed by (+)-5-methyl-10,11-dihydro-5H-dibenzo-[a,d]cycloheptan-5,10-imine (MK-801), a non-competitive antagonist specific for the NMDA receptor complex, and NO synthase inhibitors. SNP also showed a concentration-dependent increase in ACh release. Hemoglobin significantly abolished the stimulatory effects of both NMDA and SNP on ACh release. In addition, superoxide anion scavengers such as superoxide dismutase and ceruloplasmin significantly reduced the increased ACh release evoked by NMDA and SNP. Synthesized peroxynitrite dose-dependently elevated the release of ACh. These results indicate that the increased release of ACh by NMDA and SNP is mediated through peroxynitrite formed in the reaction of superoxide anion with nitric oxide produced by NMDA receptor activation and liberated from SNP rather than nitric oxide itself.

Acetylcholine↗