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Biomedical subjects

T Endo

Publications and source records attributed to T Endo.

At least 379 records · Page 21Linked to original sources
PubMed1997

Inhibition of NMDA-induced increase in brain temperature by N-omega-nitro-L-arginine and indomethacin in rats.

Intracerebroventricular administration of N-methyl-D-aspartate (NMDA) caused an increase in brain temperature, which appeared rapidly and preceded that in rectal temperature, in urethane-anesthetized rats. The increase in brain temperature was divided into two phases, an early increase and a late increase. Intracerebroventricular indomethacin, a cyclooxygenase inhibitor, completely abolished the NMDA-induced late increase, but not the early increase, in brain temperature. On the other hand, intracerebroventricular N-omega-nitro-L-arginine, a potent inhibitor of nitric oxide synthase, strongly suppressed both the early and the late increases. These findings suggest that both nitric oxide and prostaglandins may be involved in the increase in brain temperature after NMDA receptor activation.

Animals↗
PubMed1997

Value of cardiac ultrafast computed tomography for detecting right atrial thrombi in chronic atrial fibrillation.

We evaluated the accuracy of cardiac ultrafast computed tomography in diagnosing atrial thrombi in 70 patients with chronic atrial fibrillation, and identified the predictors of atrial thrombi from among clinical, echocardiographic, and ultrafast computed tomographic features. Ultrafast computed tomography identified 11 atrial thrombi in 9 patients: 4 patients had thrombi in the left atrium, 3 in the right, and 2 in both. Transthoracic echocardiography detected only 4 left atrial thrombi, and enlargement of the left or right atrium was associated with atrial thrombi (p <0.05).

Aged↗
PubMed1997

Effects of zinc and copper on cadmium uptake by brush border membrane vesicles.

The effects of essential metals, zinc (Zn) and copper (Cu), on cadmium (Cd) uptake were investigated in brush border membrane vesicles (BBMV) isolated from the rat renal cortex and LLC-PK1 cells. BBMV were incubated with Cd in the presence or absence of Zn or Cu, and then washed with a chelating agent, EGTA, to remove Cd bound to the outer surface of BBMV. Co-incubation with Zn or Cu decreased Cd accumulation in these BBMV in a concentration-dependent manner. Kinetic analysis of the initial accumulation of Cd suggested that Cd is taken up into rat BBMV via an unsaturable component and a saturable component (K(m) = 13.8 microM, V(max) = 1.44 nmol/mg protein/min), and co-incubation with Zn significantly increased the K(m) of the saturable component without affecting the V(max), whereas Cu significantly increased the K(m)-value and decreased the V(max)-value. Increasing the osmolarity of the incubation medium slightly decreased Cd accumulation in the absence of Zn or Cu, whereas it did not decrease Cd accumulation in the presence of these metals. These results suggest the possibility that, in addition to passive diffusion, Cd is also taken up from the renal brush border membrane via carrier-mediated mechanisms that are inhibited by Zn competitively and by Cu non-competitively. Furthermore, these results suggest that: (1) Cd binds externally and internally to BBMV, (2) little Cd is transported into the intravesicular space, and (3) both Zn and Cu decrease the binding and transport of Cd.

Animals↗
PubMed1997

Simultaneous determination of glycyl-L-histidyl-L-lysine and its metabolite, L-histidyl-L-lysine, in rat plasma by high-performance liquid chromatography with post-column derivatization.

A selective and sensitive high-performance liquid chromatographic (HPLC) method was developed for the determination of glycyl-L-histidyl-L-lysine (GHK), a liver-cell growth factor isolated from human plasma, and its metabolite, L-histidyl-L-lysine (HK), in rat plasma. Both high selectivity and sensitivity were achieved by the use of solid-phase extraction with a Bond-Elut Certify cartridge, ion-pair chromatography with 1-pentanesulfonate on a 5-microm Capcell Pak C18 UG120 column (250x4.6 mm I.D.) with a guard column, and by post-column derivatization with o-phthalaldehyde (OPA). GHK and HK were extracted from 0.1 ml of rat plasma after addition of o-phenanthroline to protect against degradation. The limit of detection for GHK and HK were 50 and 15 ng/ml, respectively, and the calibration curves were linear in the range 0.1-5.0 microg/ml. The developed method was applied to the pharmacokinetic study of GHK after a single dose was administered intravenously to rats. GHK was rapidly degraded to HK, which was eliminated rapidly.

Animals↗
PubMed1997

Oxidative injury of synapse and alteration of antioxidative defense systems in rats, and its prevention by vitamin E.

In order to define whether active oxygen species actually induce oxidative damage to the nervous system, and how antioxidative defense systems are changed by oxidative stress, morphological and functional changes in the nervous system and antioxidant status were investigated. When rats were exposed to 100% oxygen in a chamber, many morphological changes, e.g. swollen astrocytes around vessels, deformed nuclei in nerve cells, pigmentation, swollen mitochondria, and abnormal accumulation of synaptic vesicles in swollen nerve terminals, were observed by electron microscopy. When synaptosomes isolated from oxygen-exposed rats were stimulated by KCl, acetylcholine release from the terminal was decreased more significantly than in synaptosomes from unexposed rats (P < 0.01). Synaptic plasma membrane fluidity decreased in response to oxygen exposure, and plasma membrane permeability to sucrose was increased significantly (P < 0.05). The cholesterol/phospholipid ratio of the plasma membranes was increased by oxidative stress and the content of unsaturated fatty acids, especially arachidonic acid and docosahexaenoic acid, decreased. The levels of thiobarbituric-acid-reactive substances in the plasma membranes of oxygen-exposed rats were significantly higher than in unexposed rats (P < 0.01). These results suggest that free radicals derived from oxygen may attack nerve terminals and peroxidize the plasma membrane. It was found that in response to the oxidative stress, the status of the defense system in synapse, i.e. the concentration of vitamin E, activities of superoxide dismutase and glutathione peroxidase changed, and that many of the changes observed were reduced remarkably by the intraperitoneal administration of vitamin E prior to stress. Data support the idea that vitamin E contributes to the protection against nerve dysfunction caused by oxidative stress.

Acetylcholine↗
PubMed1997

STAT5 activation correlates with erythropoietin receptor-mediated erythroid differentiation of an erythroleukemia cell line.

Interaction between erythropoietin (EPO) and its membrane receptor induces the proliferation and differentiation of erythroid progenitors. EPO has been shown to activate the JAK2-STAT5 pathway in various hematopoietic cell lines, although the physiological role of this pathway is unclear. We have previously shown that epidermal growth factor activates a chimeric receptor bearing the extracellular domain of the epidermal growth factor receptor linked to the cytoplasmic domain of the EPO receptor, resulting in proliferation of interleukin-3-dependent hematopoietic cells and erythroid differentiation (globin synthesis) of EPO-responsive erythroleukemia cells. In the present study, we introduced various deletion and tyrosine to phenylalanine substitution in the cytoplasmic domain of the chimeric receptor and expressed these mutant chimeras in an EPO-responsive erythroleukemia cell line, ELM-I-1. Mutant chimeric receptors retaining either Tyr343 or Tyr401 could activate STAT5, judged by tyrosine-phosphorylation of STAT5 and induction of CIS, a target gene of STAT5. These mutants were able to induce erythroid differentiation. However, a chimeric receptor containing both Y343F and Y401F mutations could not activate STAT5 nor induce erythroid differentiation. Thus, Tyr343 or Tyr401 of the EPO receptor are independently necessary for erythroid differentiation as well as STAT5 activation. Moreover, exogenous expression of dominant-negative STAT5 suppressed EPO-dependent erythroid differentiation. These findings suggest that STAT5 plays an important role in erythroid differentiation through the EPO receptor cytoplasmic domain.

Animals↗
PubMed1997

Increased expression of highly branched N-glycans at cell surface is correlated with the malignant phenotypes of mouse tumor cells.

Three NIH3T3 transformants, MTAg, MTPy, and MT1, which grow similarly in soft agar media, showed remarkable differences in athymic mice: MTAg grew more rapidly than MTPy, whereas MT1 and NIH3T3 did not, and only MTAg metastasized in lung. Structural analysis of N-glycans from plasma membrane glycoproteins revealed that each sample contains similar amounts of N-glycans, but the relative amounts of 2,6-branched tri- and tetra-antennary oligosaccharides prominently increase and the relative amounts of biantennary oligosaccharides prominently decrease in the order of NIH3T3, MT1, MTPy, and MTAg, whereas those of others remained constant. Western blot analysis revealed that binding of Datura stramonium agglutinin, which interacts with 2,6-branched tri- and tetra-antennary oligosaccharides, is significantly increased in several bands from MTAg compared with NIH3T3, two of which are tentatively identified as lysosome-associated membrane protein-1 and fibronectin (FN)-receptor. It was also shown that the spreading of MTAg on FN-coated plates is dramatically inhibited with the anti-FN-receptor antiserum when compared with NIH3T3. These results indicate that the increased expression of highly branched N-glycans at cell surface is correlated with the rapidness of tumor formation and altered adhesive properties of tumor cells in vivo.

3T3 Cells↗
PubMed1997

Antiemetic effects of N-3389, a newly synthesized 5-HT3 and 5-HT4 receptor antagonist, in ferrets.

The antiemetic activity of N-3389 (endo-3,9-dimethyl-3,9-diazabicyclo[3,3,1]non-7-yl-1 H-indazole-3-carboxamide dihydrochloride), a new 5-HT3 and 5-HT4 receptor antagonist, against cisplatin-, cyclophosphamide- and copper sulfate-induced emesis was investigated using ferrets. We also examined the effects of these agents on abdominal afferent vagus nerve activity in anesthetized ferrets. Both intraperitoneal (0.1-1.0 mg/kg) and oral (0.1-1.0 mg/kg) administration of N-3389 produced dose-dependent antiemetic effects. The time-course of cisplatin (10 mg/kg, i.p.)-induced emesis in another group of ferrets paralleled the increase in abdominal afferent vagus nerve activity induced by cisplatin (10 mg/kg, i.p.) and was inhibited by pretreatment with N-3389 (1.0 mg/kg, i.v.). Furthermore, the cisplatin (10 mg/kg, i.p.)-induced increase in abdominal afferent vagus nerve activity was markedly reduced by an additional injection of N-3389 (0.1-1.0 mg/kg, i.v.) in a dose-dependent manner. The antiemetic effects exhibited by N-3389 are probably due to the inhibition of 5-HT3 and 5-HT4 receptors on the abdominal afferent vagus nerves.

5-Methoxytryptamine↗
PubMed1997

Selective and total sleep deprivation: effect on the sleep EEG in the rat.

Although sleep deprivation is known to exert an antidepressant effect in depressed patients, the involvement of sleep regulation is still unknown. Selective sleep deprivation experiments were performed in the rat to investigate the interactions between non-REM sleep (NREMS) and REM sleep (REMS) in an animal model. A12-h total sleep deprivation (TD) period ending at lights on was followed by one of the following protocols: (1) recovery sleep (TD12); (2) 4-h total sleep deprivation (TD16); (3) 4-h slow-wave deprivation (SWD); (4) 4-h REMS deprivation (RD). In the SWD protocol, the reduction of EEG slow-wave activity (SWA; power density in the 0.75-4.0 Hz band) was obtained by curtailing NREMS episodes to 20 s. During RD the number of interventions required to prevent REMS increased during the first 2 h and then remained constant. While RD caused only a minor reduction of NREMS, it increasingly suppressed SWA in NREMS. The rebound of SWA occurred later and was less prominent after RD than after SWD. Whereas an REMS rebound occurred after all three 4-h sleep deprivation protocols, a persistent increase in the dark period was present only after TD16. It is concluded that (a) SWA in NREMS is inhibited by an increased level of REMS propensity; (b) the hypothesis that REMS propensity increases only during NREMS is not supported; and (c) the results are compatible with the hypothesis that the suppression of NREMS intensity is the common denominator of different antidepressive sleep manipulations in depressive patients.

Animals↗
PubMed1997

Structures of sialylated O-linked oligosaccharides of bovine peripheral nerve alpha-dystroglycan. The role of a novel O-mannosyl-type oligosaccharide in the binding of alpha-dystroglycan with laminin.

alpha-Dystroglycan is a heavily glycosylated protein, which is localized on the Schwann cell membrane as well as the sarcolemma, and links the transmembrane protein beta-dystroglycan to laminin in the extracellular matrix. We have shown previously that sialidase treatment, but not N-glycanase treatment, of bovine peripheral nerve alpha-dystroglycan greatly reduces its binding activity to laminin, suggesting that the sialic acid of O-glycosidically-linked oligosaccharides may be essential for this binding. In this report, we analyzed the structures of the sialylated O-linked oligosaccharides of bovine peripheral nerve alpha-dystroglycan by two methods. O-Glycosidically-linked oligosaccharides were liberated by alkaline-borotritide treatment or by mild hydrazinolysis followed by 2-aminobenzamide-derivatization. Acidic fractions obtained by anion exchange column chromatography that eluted at a position corresponding to monosialylated oligosaccharides were converted to neutral oligosaccharides by exhaustive sialidase digestion. The sialidases from Arthrobacter ureafaciens and from Newcastle disease virus resulted in the same degree of hydrolysis. The neutral oligosaccharide fraction, thus obtained, gave a major peak with a mobility of 3.8-3.9 glucose units upon gel filtration, and its reducing terminus was identified as a mannose derivative. Based on the results of sequential exoglycosidase digestion, lectin column chromatography, and reversed-phase high-performance liquid chromatography, we concluded that the major sialylated O-glycosidically-linked oligosaccharide of the alpha-dystroglycan was a novel O-mannosyl-type oligosaccharide, the structure of which was Siaalpha2-3Galbeta1-4GlcNAcbeta1-2Man-Ser/Thr (where Sia is sialic acid). This oligosaccharide constituted at least 66% of the sialylated O-linked sugar chains. Furthermore, a laminin binding inhibition study suggested that the sialyl N-acetyllactosamine moiety of this sugar chain was involved in the interaction of the alpha-dystroglycan with laminin.

Animals↗
PubMed1997

Probing the environment along the protein import pathways in yeast mitochondria by site-specific photocrosslinking.

Artificially aminoacylated suppressor tRNAs were used to introduce photoreactive amino acids into model mitochondrial precursor proteins to probe the environment along the protein import pathway. Amino acids with benzophenone side chains of various lengths [DL-2-amino-3-(p-benzoylphenyl)propanoic acid (1) and DL-2-amino-5-(p-benzoylphenyl)pentanoic acid (2)] were incorporated at specific sites throughout the cytochrome b2-dihydrofolate reductase fusion proteins, pb2(220)-DHFR and pb2 delta 19(220)-DHFR, which were destined for the intermembrane space and the matrix in mitochondria, respectively. In vitro import of pb2(220)-DHFR and pb2 delta 19(220)-DHFR bearing 1 or 2 into isolated yeast mitochondria was arrested so that the N terminus reached the intermembrane space or the matrix, respectively, while the DHFR domain remained at the mitochondrial surface. The matrix-targeted pb2 delta 19(220)-DHFR was photocrosslinked to Tom40 in the outer membrane, Tim44 in the inner membrane, and Ssc1p in the matrix, suggesting that the protein has an extended conformation in the import channels. On the other hand, incorporation of 2 at various positions in the 50-residue segment of intermembrane-space-targeted pb2(220)-DHFR gave photocrosslinks only to Tom40, suggesting that the segment is not in an extended conformation, but localized near Tom40. The N-terminal portion of pb2(220)-DHFR, but not pb2 delta 19(220)-DHFR, was photocrosslinked to an as-yet-unidentified mitochondrial component to generate a 95-kDa crosslinked product.

Biological Transport↗
PubMed1997

Inhalation of diesel exhaust enhances antigen-specific IgE antibody production in mice.

To examine the effects of diesel exhaust (DE) inhalation on IgE antibody production, BALB/c mice were exposed to 0 (control), 3.0 and 6.0 mg/m3 DE inhalation for 3 weeks. Intranasal sensitization with ovalbumin (OA) three times at intervals of 3 weeks was conducted immediately before, immediately after and 3 weeks after DE inhalation. Body weight and thymus weight for the DE-exposed and control mice were essentially the same but spleen weight in mice exposed to 6 mg/m3 significantly increased. Anti-OA IgE antibody titers in the sera of mice exposed to 6 mg/m3 was significantly higher than the control. Total IgE and anti-OA IgG in sera for DE-exposed and control mice remained basically the same. To investigate cytokine production in mice exposed to 6 mg/m3, spleen cells from DE-exposed and control mice were stimulated with OA in vitro and cytokine production in the culture supernatants was measured by ELISA. In vitro antigen-stimulated interleukin-4 (IL-4) and -10 (IL-10) production in spleen cells of exposed mice significantly increased compared to the control. In vitro interferon (IFN)-gamma production in spleen cells of exposed mice markedly decreased. DE inhalation is thus shown to have adverse effect on antigen-specific IgE antibody production in mice through alteration of the cytokine network.

Administration, Inhalation↗
PubMed1997

Shh expression in developing and regenerating limb buds of Xenopus laevis.

The zone of polarizing activity (ZPA) is a specialized region involved in the antero-posterior (A-P) axis formation in chick and mouse limb buds. The existence of ZPA in the posterior margin is suggested in Xenopus hindlimb buds because 180 degree rotation of the distal limb tip induces the supernumerary limb. In this study, we investigated the expression of Sonic hedgehog (shh), a molecular marker for ZPA, in Xenopus developing limb buds and regenerating blastemas by whole-mount in situ hybridization. Although shh was expressed in the posterior margin of the limb bud like in chicks, its expression domain did not correspond to the ZPA map of Xenopus hindlimb buds. shh expression was distant from the ZPA at stage 53 in particular. To clarify the difference between the shh expression domain and ZPA, we examined shh expression in 180 degree rotated limb buds. As a result, ectopic shh expression was newly induced in the proximal region to its original expression domain. These results suggest that ZPA is accompanied by shh expression as in chick limb buds. Furthermore we examined shh expression in regenerating blastemas. shh was reexpressed in the posterior margin of the blastema. This result supports the possibility that ZPA also exists in the regenerating blastema.

Animals↗
PubMed1997

Activated eosinophils stimulate endothelin-1 release from airway epithelial cells by direct adherence via adhesion molecules.

Endothelin-1 (ET-1), synthesized in airway epithelial cells, has a potent constrictive action on airway smooth muscle. In this study, we investigated the effect of eosinophils on ET-1 release from guinea pig cultured tracheal epithelial cells. Eosinophils with or without the activation were directly co-cultured with tracheal epithelial cells. Eosinophils activated by GM/CSF or IL-5 potentiated ET-1 release, but non-activated ones did not. Treatment of activated eosinophils with antibodies against macrophage-1 (Mac-1) and/or very late antigen-4 (VLA-4) suppressed the potentiated ET-1 release. However, inhibition of lipid mediators derived from activated eosinophils could not suppress the potentiated ET-1 release. Moreover, separated co-culture of activated eosinophils with tracheal epithelial cells using Millicell-CM had no effect on ET-1 release. These observations suggest that adherence of activated eosinophils to epithelial cells via adhesion molecules such as Mac-1 and VLA-4 was essential for potentiation of ET-1 release. Since presence of eosinophils in the epithelial layer has been commonly demonstrated in bronchial biopsies and autopsy specimens from patients with asthma, epithelial cells would be activated by adherence of eosinophils via adhesion molecules and potentiate ET-1 release in vivo.

Animals↗
PubMed1997

Mercury uptake by LLC-PK1 cells: dependence on temperature and membrane potential.

The purpose of this study was to investigate the mechanism of inorganic mercury (Hg) uptake in LLC-PK1 cells, a renal tubular epithelial cell line, and to compare the results with those reported previously by us in rat renal cortical epithelial (RCE) cells in primary culture. The LLC-PK1 cells were cultured for 3-12 days, incubated with 1 microM HgCl2 in Hanks' balanced salt solution at 4 or 37 degrees C for 30 min, and washed with phosphate-buffered saline containing BAL to remove the cell membrane-bound Hg. The uptake of Hg was higher in nonconfluent cultures than in confluent cultures and higher at 37 than at 4 degrees C. In confluent culture (Day 8) Hg uptake at 4 degrees C was only 27% of that at 37 degrees C. The initial accumulation of Hg (5 min) from different concentrations of HgCl2 (0.5-50 microM) was linear and did not show a tendency toward saturation, suggesting that a carrier-mediated process was not involved. Pretreatment of cells with 10 microM FCCP, a metabolic inhibitor and a proton ionophore, 0.5 mm DIDS, an anion transport inhibitor, or 0.5 mM ouabain, a Na+/K+-ATPase inhibitor, resulted in 72, 60, and 57% reduction in Hg uptake, respectively. Furthermore, replacement of 137 mm NaCl in the incubation medium with 137 mM KCl or LiCl or 274 mM mannitol caused 30, 45, and 87% reduction in Hg uptake, respectively. These results suggest that in LLC-PK1 cells, as in RCE cells, Hg uptake is inversely related to cell density and is influenced by membrane fluidity, membrane potential, and HCO3-/Cl- transporter.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

Evolutionary motif and its biological and structural significance.

We developed a method for multiple alignment of protein sequences. The main feature of this method is that it takes the evolutionary relationships of the proteins in question into account repeatedly for execution, until the relationships and alignment results are in agreement. We then applied this method to the data of the international DNA sequence databases, which are the most comprehensive and updated DNA databases in the world, in order to estimate the "evolutionary motif" by extensive use of a supercomputer. Though a few problems needed to be solved, we could estimate the length of the motifs in the range of 20 to 200 amino acids, with about 60 the most frequent length. We then discussed their biological and structural significance. We believe that we are now in a position to analyze DNA and protein not only in vivo and in vitro but also in silico.

Amino Acid Sequence↗
PubMed1997

Distinct effects of MK-801 and (+/-)-2-amino-5-phosphonopentanoic acid on N-methyl-D-aspartate-induced rise of brain temperature in rats.

Intracerebroventricular (i.c.v.) administration of N-methyl-D-aspartate (NMDA) caused a biphasic rise of brain temperature, namely, a rapid, early rise and a larger, late rise, in urethane-anesthetized rats. I.c.v. pretreatment with a noncompetitive NMDA receptor antagonist, MK-801, attenuated the late rise of the brain temperature, but had no effect on the early rise, whereas i.c.v. pretreatment with a competitive NMDA receptor antagonist, (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), attenuated both rises. AP-5 per se caused a rise in brain temperature without any rise of rectal temperature, whereas MK-801 per se caused no significant change of the brain or rectal temperature. This rise by AP-5 was suppressed by MK-801, suggesting an agonistic effect of AP-5 on NMDA receptors in rat brain in vivo.

2-Amino-5-phosphonovalerate↗