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Biomedical subjects

T Endo

Publications and source records attributed to T Endo.

At least 433 records · Page 24Linked to original sources
PubMed1997

[Hemodynamic effects of right ventricular outflow pacing].

The effects of right ventricular outflow pacing were studied in 13 patients (mean [+/-SD] 69.8 +/- 8.2 years old). All patients received DDD pacemakers except two patients with implanted VVI pacemakers who had chronic atrial fibrillation. Cardiac output and pulmonary capillary wedge pressure were measured by Swan-Ganz catheter. Pacing rate was fixed at 70-80/min and atrioventricular delay was fixed at 165 msec. When the pacing site was changed from the right ventricular apex to the right ventricular outflow during right ventricular pacing in 11 patients, cardiac output increased from 3.3 +/- 0.6 to 3.4 +/- 0.5 l/min (p < 0.001), and wedge pressure decreased from 9.3 +/- 1.9 to 8.8 +/- 2.0 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow during atrioventricular pacing in eight patients, cardiac output increased from 3.9 +/- 0.4 to 4.0 +/- 0.4 l/min (p < 0.05), and wedge pressure decreased from 7.1 +/- 2.3 to 6.6 +/- 2.1 mmHg (p < 0.05). When the pacing site was changed from the right ventricular apex to the right ventricular outflow in seven patients with ejection fraction (EF) greater than 55%, cardiac output increased from 3.6 +/- 0.5 to 3.7 +/- 0.4 l/min (p < 0.05), and in four patients with EF less than 55%, it increased from 2.9 +/- 0.4 to 3.0 +/- 0.4 l/min (p < 0.01). Cardiac function was improved by right ventricular outflow pacing compared to right ventricular apex pacing regardless of the pacing mode or cardiac function.

Aged↗
PubMed1997

Pharmacokinetic and pharmacodynamic evaluation of central effect of the novel antiallergic agent betotastine besilate.

Betotastine besilate (betotastine CAS 125602-71-3, TAU-284) is a novel antiallergic agent with histamine H1 receptor antagonistic activity. As the classical antihistamines are known to produce drowsiness, the present study was conducted to assess a possible influence of betotastine on the central nervous system (CNS). Measurement of the drug concentration in brain and plasma after i.v. administration revealed that betotastine, as well as cetirizine and epinastine, poorly penetrate into the CNS, while terfenadine do so slightly more and ketotifen remarkably more. In vitro receptor binding assays demonstrated that betotastine is a highly specific histamine H1 receptor ligand, having no significant binding affinity for histamine H3, adrenergic alpha 1, alpha 2, beta, dopamine D2L, serotonin 5-HT2, muscarinic, and benzodiazepine receptors. On global behavior of mice, oral administration of betotastine did not produce any marked changes at the doses of 100-1000 mg/kg, but suppressed huddling behavior at 1000 mg/kg and caused slight mydriasis at 300 mg/kg and more. Betotastine did not significantly affect spontaneous motor activity (SMA) and hexobarbital-induced anesthesia in mice up to 300 mg/kg p.o. In the sleep-wakefulness pattern of cats, it reduced the total duration of sleep at 10 mg/kg p.o., but did not show significant effect at 30 and 100 mg/ kg p.o. Cetirizine showed a similar profile as betotastine in these experiments, whereas ketotifen and epinastine induced sedative signs or toxic symptoms in lower doses, and terfenadine affected SMA and the anesthesia at a high dose. These results suggest the very low liability of betotastine to produce sedative side-effect in a therapeutic dose range.

Animals↗
PubMed1997

Thrombin stimulates platelet-derived growth factor release by alveolar macrophages in rats--significance in bleomycin-induced pulmonary fibrosis.

Thrombin is a multifunctional enzyme generated at sites of vascular injury, and is known to be increased in the lungs in some types of fibrotic lung disease. In this study, to determine whether thrombin is associated with fibroblast growth and pulmonary fibrosis in these disorders, we examined whether a growth factor for fibroblasts (platelet-derived growth factor, PDGF) was released by thrombin-stimulated alveolar macrophages (AM). The culture supernatants of rat AM stimulated with 1 or 10 U/ml of thrombin showed a significant increase in fibroblast growth-stimulating activity (FGA). Pretreatment of the AM supernatant with anti-PDGF-AA antibody significantly decreased the FGA, but pretreatment with anti-PDGF-BB antibody did not. The supernatants of AM stimulated with thrombin also increased the growth of fibroblasts from the lungs of rats with bleomycin-induced lung injury. These results indicate that thrombin stimulates AM to release PDGF-AA, which is responsible, at least in part, for fibroblast growth and the development of pulmonary fibrosis in some types of fibrotic lung disease.

Animals↗
PubMed1997

[Adhalin(alpha-sarcoglycan) gene mutations in patients with malignant limb-girdle muscular dystrophy (MLGMD) (Miyoshi)].

Malignant limb-girdle muscular dystrophy (MLGMD) (Miyoshi) is considered to be roughly the same as SCARMD (Ben Hamida) in its clinical features and mode of inheritance. Adhalin(alpha-Sarcoglycan) gene mutations have been reported in 51 families with MLGMD/SCARMD including our 8 families. The mutations were found through the adhalin gene, most of which (97%) were, however, found in the region encoding the extracellular domain. The mutations included missense mutation, insertion, and deletion. Half of the families carried C229T mutation which results in the amino acid replacement of Arg77Cys. Mutations were homozygous in 26 of 51 families (51%) and compound heterozygous in 25 families (49%). The heterogeneity of clinical course in MLGMD/SCARMD might be explained mainly by the variety of the mutations.

Cytoskeletal Proteins↗
PubMed1997

[Relationship between the morphological changes of Japanese cedar (Cryptomeria japonica) pollen grains and the release of major allergens from the pollen].

Release of major allergens (Cry j 1, Cry j 2) from Japanese cedar (C. japonica) pollen grains treated with high pressure was investigated. C. japonica pollen grains crushed by high pressure treatment using FRENCH Pressure Cell Press released greater amounts of major allergens, particularly Cry j 2, compared to those without crush. This suggests that the cytoplasm of C. japonica pollen grains contains more Cry j 2 than previously reported. The effect of nasal fluid on the release of major allergens from C. japonica pollen grains was analyzed in vitro. Nasal fluid from patients with nasal allergy remarkably increased the release of major allergens from pollen grains, compared to controls, and the amount of Cry j 1 was greater than Cry j 2. Further studies revealed that nasal fluid affects the outer wall of pollen grains, where Cry j 1 is located, to a greater extent than its effect on the cytoplasm, where Cry j 2 is located.

Allergens↗
PubMed1997

Cyclophosphamide increases 5-hydroxytryptamine release from the isolated ileum of the rat.

We recently reported that chronic administration of cyclophosphamide significantly increased urinary 5-hydroxyindole acetic acid (5-HIAA) excretion in rats indicative of a release of 5-hydroxytryptamine (5-HT) from intestinal enterochromaffin (EC) cells. Cyclophosphamide is considered to be an inactive prodrug and require conversion to active emetic metabolities (e.g. phosphoramide mustard) by hepatic metabolism. However the presence of cytochrome P450 in the intestine raises the possibility of cyclophosphamide metabolism in the wall of the intestine, a site which would have considerable significance for 5-HT release and the emetic effects of cyclophosphamide. The aim of this study was to investigate whether cyclophosphamide could induce the release of 5-HT from the isolated ileum and to examine its mechanism of action. Cyclophosphamide (10(-6)M and 10(-7)M) induced a concentration dependent increase of 5-HT from rat isolated ileum. This cyclophosphamide-induced 5-HT release was significantly reduced by granisetron (10(-6)M and 10(-7)M) or atropine (10(-7)M and 10(-6)M). Tetrodotoxin (10(-6)M completely inhibited the increased 5-HT release induced by cyclophosphamide. These results suggest that cyclophosphamide has the capacity to induce 5-HT release via activation of enteric cholinergic neurons. In addition the in vitro study demonstrate for the first time that cyclophosphamide may be activated to emetic metabolites at extra-hepatic sites (e.g. intestine) and that conversion at these sites could contribute to the mechanism of cyclophosphamide induced emesis.

Animals↗
PubMed1997

Effects of TNF-alpha injection into the ovary on blood progesterone concentration in pseudopregnant rabbits.

To examine the effects of TNF-alpha on luteal functions, TNF-alpha was injected into the ovary of rabbits on the 7th day of pseudopregnancy (Day 7). The animals were laparotomized under general anesthesia, and 1 x 10(4) IU TNF-alpha dissolved in PBS was injected into the ovary. On Days 8 and 10, the blood progesterone (P) concentration was determined. The mean blood P level was 10.31 ng before the administration of TNF-alpha on Day 7. On Day 8, the mean blood P level was 11.22 ng in the control group, while it was markedly reduced to 1.29 ng in the TNF-alpha administration group. On Day 10, the mean blood P level was 6.80 ng in the control group and 5.49 ng in the TNF-alpha group. These results suggest that the capacity for P secretion of the corpus luteum, which reached a degenerative stage by TNF-alpha administration, can be recovered.

Animals↗
PubMed1996

MR lmaging of the Primary Breast Lymphoma: A Case Report.

Recently magnetic resonance (MR) imaging has been investigated for the detection and differentiation of benign and malignant breast lesions. Dynamic scan using the contrast material has been shown to increase the specificity of breast MR imaging. Primary breast lymphoma (PBL) is a rare disease and its MR imaging finding has not been described before. We recently experienced a case of PBL that was demonstrated on MR imaging as an early enhancing mass similar to common carcinomas. Other imaging findings including sonography, mammography were also non-specific. Furthermore, lymphoma cells had spread beyond the early enhanced area. Thus the precise delineation of the tumor extent was impossible. However, features such as a quite unclear border on pre-contrast T2-weighted image, and increased uptake of gallium-67-citrate may allow diagnosis of such lesions as malignant lymphoma.

Journal Article↗
PubMed1996

ATF site of human RB gene promoter is a responsive element of myogenic differentiation.

RB mRNA increases during terminal differentiation of C2 myoblasts. We demonstrate that RB promoter activity increases about 4-fold during differentiation. The increase of RB promoter activity was reduced when a point mutation was designed in the ATF site. In a gel shift assay of the ATF site, two specific bands were observed. One of them, with the lower mobility, disappeared during differentiation. This band reacted with an antibody against ATF-1. We cotransfected an RB promoter-luciferase plasmid with the TREB36/ATF-1 plasmid. ATF-l suppressed the activity of the wild-type RB promoter but not of that with a point mutation at the ATF site. These results suggest that the ATF site of the RB promoter is a responsive element during myogenic differentiation of C2 cells. We hypothesize that RB promoter activity is stimulated partially due to the dissociation of ATF-1, which suppresses the promoter activity through the ATF site in C2 myoblasts.

Activating Transcription Factor 1↗
PubMed1996

Autoantibody against thyroid iodide transporter in the sera from patients with Hashimoto's thyroiditis possesses iodide transport inhibitory activity.

Recently we have newly identified an autoantibody against thyroid iodide transporter (TIT) in the sera from patients with autoimmune thyroid disease. In order to study the function of these autoantibodies, we established CHO-KI cells stably expressing recombinant rat TIT (CHO-TIT cells), and the effect of IgGs from the patients with Hashimoto's thyroiditis on iodide uptake activity of CHO-TIT cells was investigated. We found that 4 out of 34 sera from patients with Hashimoto's thyroiditis strongly recognized TIT by Western blot analysis. These 4 IgGs, purified by protein A column chromatography, caused 14 to 62% inhibition of I- accumulation in CHO-TIT cells. Next, using synthetic peptides, we determined the recognition site of the autoantibody on the TIT molecule. The autoantibody reacted with the synthetic peptide corresponding to the 6th extracellular loop of the TIT molecule. These results suggest that autoantibody against TIT in the sera from patients with Hashimoto's thyroiditis binds to the 6th extracellular loop of TIT protein and inhibits I- transport into the thyrocytes. Anti-TIT autoantibody might participate in the pathogenesis of Hashimoto's thyroiditis and modulate thyroid function of patients with the disease.

Animals↗
PubMed1996

Distinct troponin T genes are expressed in embryonic/larval tail striated muscle and adult body wall smooth muscle of ascidian.

During development of the ascidian Halocynthia roretzi, the tadpole larva hatched from the tailbud embryo metamorphoses to the sessile adult with a body wall muscle. Although the adult body wall muscle is morphologically nonsarcomeric smooth muscle, it contains troponin complex consisting of three subunits (T, I, and C) as do vertebrate striated muscles. Different from vertebrate troponins, however, the smooth muscle troponin promotes actomyosin Mg2+-ATPase activity in the presence of high concentration of Ca2+, and this promoting property is attributable to troponin T. To address whether the embryonic/larval tail striated muscle and the adult smooth muscle utilize identical or different regulatory machinery, we cloned troponin T cDNAs from each cDNA library. The embryonic and the adult troponin Ts were encoded by distinct genes and shared only <60% identity with each other. Northern blotting and whole mount in situ hybridization revealed that these isoforms were specifically expressed in the embryonic/larval tail striated muscle and the adult smooth muscle, respectively. These results may imply that these isoforms regulate actin-myosin interaction in different manners. The adult troponin T under forced expression in mouse fibroblasts was unexpectedly located in the nuclei. However, a truncated protein with a deletion including a cluster of basic amino acids colocalized with tropomyosin on actin filaments. Thus, complex formation with troponin I and C immediately after the synthesis is likely to be essential for the protein to properly localize on the thin filaments.

Actomyosin↗
PubMed1996

Local changes in oxygen tension and blood flow in the brain under hyperthermia induced by intracerebroventricular NMDA in rats.

Intracerebroventricular administration of N-methyl-D-aspartate (NMDA; 100 nmol) to rats increased oxygen tension and blood flow of the caudate putamen and the ventral hippocampus. The regional differences in the increase in oxygen tension could not be explained in terms of those in the blood flow. NMDA also increased the temperature of the two brain regions to a similar extent, and these increases preceded that in the rectum. These findings suggest that NMDA receptor stimulation leads to exposure of the brain to a higher oxygen level and higher temperature, which might be involved in NMDA neurotoxicity.

Animals↗
PubMed1996

Pharmacological profile of T-0632, a novel potent and selective CCKA receptor antagonist, in vivo.

The pharmacological profile of a new CCKA receptor antagonist, T-0632 [sodium (S)-1-(2-fluorophenyl)-2,3-dihydro-3-[(3-isoquinolinylcarbonyl) amino]-6-methoxy-2-oxo-1H-indole-3-propanoate], was examined in in vivo studies and compared with those of L-364, 718 [3S(-)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1, 4-benzodiazepine-3-yl)-1 H-indole-2-carboxamide] and loxiglumide [D.L-4-(3,4-dichlorobenzoylamino)-5-(N-3-methoxypropyl-pentylam ino)-5- oxopentanoic acid]. In rats, intravenously administered T-0632, L-364,718 and loxiglumide dose dependently inhibited cholecystokinin octapeptide (CCK-8)-stimulated pancreatic exocrine secretion with estimated ED50 values of 0.025, 0.016 and 1.8 mg/kg, respectively. The ED50 values for intraduodenal administration of these compounds were 0.040, 0.26 and 3.0 mg/kg, respectively. In mice, orally administered T-0632 prevented caerulein-induced pancreatitis, CCK-8-induced inhibition of gastric emptying and CCK-8-induced gallbladder emptying in dose-dependent manners with ED50 values of 0.028, 0.04, and 0.12 mg/kg, respectively. The effect of T-0632 for caerulein-induced pancreatitis was 4-fold more potent than that for gallbladder emptying. In contrast, the effects of L-364,718 and loxiglumide for caerulein-induced pancreatitis were 2-4-fold weaker than those for gallbladder emptying. In dogs, T-0632 and loxiglumide maximally inhibited CCK-8-stimulated pancreatic amylase secretion at doses of 0.01 and 10 mg/kg, respectively. At these doses, the effect of T-0632 on CCK-8-induced increase in the gallbladder intraluminal pressure was weaker than that of loxiglumide. These results suggest that T-0632 has a potent antagonistic action on CCKA receptors in several animal species and the effects of T-0632 are more selective for the pancreas over the gallbladder compared with L-364,718 and loxiglumide.

Animals↗