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H Ueda

Publications and source records attributed to H Ueda.

At least 487 records · Page 27Linked to original sources

WS75624 A and B, new endothelin converting enzyme inhibitors isolated from Saccharothrix sp. No. 75624. I. Taxonomy, fermentation, isolation, physico-chemical properties and biological activities.

Novel endothelin converting enzyme (ECE) inhibitors, WS75624 A and B, have been isolated from the fermentation broth of Saccharothrix sp. No. 75624. These inhibitors were purified from an acetone extract of whole culture broth followed by HP-20 column chromatography, silica gel column chromatography and HPLC. WS75624 A and B showed highly potent ECE inhibitory activity, and both had IC50 values of 0.03 microgram/ml. WS75624 A and B also showed other metalloprotease (collagenase and neutral endopeptidase) inhibitory activity with IC50 values of 1 microgram/ml. Since large amount of WS75624 B was isolated, we tried in vivo evaluation using WS75624 B. WS75624 B inhibited big endothelin-induced pressor effect when administered to SD rat intravenously with big ET-1.

Animals↗

Protein kinase C involvement in homologous desensitization of delta-opioid receptor coupled to Gi1-phospholipase C activation in Xenopus oocytes.

We have developed the coexpression system of both delta-opioid receptor (DOR1) and M2-muscarinic receptor (M2) which mediate agonist-evoked currents due to common post-receptor mechanisms including Gi1 and phospholipase C (PLC) activation in Xenopus oocytes reconstituted with Gi1 alpha. The DOR1-currents by 100 nM D-Ser2-leu-enkephalin-Thr6 (DSLET) were selectively desensitized by 10 nM phorbol 12-myristate 13-acetate (PMA). The PMA-desensitization of DSLET-currents was abolished in the presence of calphostin C, a protein kinase C inhibitor, or reversed by an intracellular injection of calcineurin, a protein phosphatase 2B. When a higher concentration (3 microM) of DSLET was used, DSLET-currents were rapidly desensitized by repeated challenges of DSLET itself. However, repeated challenges of 10 microM ACh caused no influence on such DSLET- or M2-currents. The desensitization of DSLET-currents was selectively reversed by protein kinase C inhibitors. Similar results were also obtained with various delta-opioid agonists. These results suggest that protein kinase C is involved in the homologous desensitization of delta-opioid receptors.

Animals↗

Dystrophin localization at presynapse in rat retina revealed by immunoelectron microscopy.

PURPOSE: It has been accepted that retinal dystrophin is localized in the outer plexiform layer (OPL) of the retina, but no electron microscopic evidence has been reported until now. Using immunoelectron microscopy, the authors investigate whether retinal dystrophin localizes at the presynaptic or postsynaptic membrane of synaptic regions. METHODS: Monoclonal antibody raised against human dystrophin C-terminus was used. Immunoblotting analysis was used for testing dystrophin protein in retinal tissues. Tissue preparations were stained with the immunofluorescence or immunoperoxidase method and were observed with light and electron microscopy. RESULTS: Immunoblotting analysis showed a molecular weight of band 420 kDa in the sodium dodecyl sulfate--polyacrylamide gel electrophoresis of the retinal tissues. Immunoelectron microscopy disclosed that retinal dystrophin was localized at the presynaptic membrane of synaptic regions in the OPL. CONCLUSIONS: Rat retinal dystrophin localizes at the presynaptic membrane in the OPL, suggesting that it may play some role in the neurotransmitter release of the photoreceptor cell.

Amino Acid Sequence↗

Effect of cilazapril on vascular restenosis after percutaneous transluminal coronary angioplasty.

BACKGROUND: In experimental studies using cilazapril, the strongest inhibition of neointima formation was obtained when treatment was initiated 6 days before injury. The MERCATOR trial showed no reduction in restenosis with cilazapril given after percutaneous transluminal coronary angioplasty (PTCA). The purpose of this study is to determine whether previous administration of cilazapril could prevent restenosis. METHODS: A total of 167 patients were randomly and prospectively assigned to the cilazapril group or the control group. In the cilazapril group, 78 patients received a 2 mg dose of cilazparil daily, starting 7 days before PTCA and continuing for 6 months. Only 128 patients (cilazapril 56, control 72) completed the study because 39 dropped out. Coronary angiograms were evaluated by the quantitative coronary angiogram (QCA) system. RESULTS: There were no differences between the two groups of patients with regard to baseline clinical and angiographic characteristics. QCA analysis (cilazapril 66 lesions, control 101 lesions): the loss at follow-up in minimal lumen diameter was 0.36 +/- 0.57 mm in the cilazapril group and 0.57 +/- 0.75 mm in the control group (P < 0.05). Restenosis rate: in the cilazapril group, 16 of 56 patients (28.6%) had restenosis in contrast to 36 of 72 patients (50.0%) in the control group (P < 0.02). When vessel restenosis was evaluated, 16 of 63 vessels (25.4%) demonstrated restenosis in the cilazapril group, in contrast to 41 of 82 vessels (50.0%) in the control group (P < 0.01). CONCLUSIONS: Treatment using cilazapril 7 days before PTCA significantly reduced the rate of restenosis. These data suggest that previous administration of cilazapril might be important for preventing restenosis.

Aged↗

[Peripheral T-cell lymphoma with abundant ATL-like cells in the blood].

A 69-year-old woman was admitted to our hospital because of leucocytosis and systemic lymphadenopathy. On admission, white blood cell count was 163,000/microliters, most of which consisted of flower-like cells with convoluted nuclei in the peripheral blood. In the abnormal lymphocyte cells surface-marker test by flow cytometry showed that they expressed CD2, CD3, CD4, CD29, CD45RA, and CD38, but not CD8, CD16, and CD25. Serum anti-Human T-lymphotropic virus type-I (HTLV-I) antibody was negative in particle agglutination, enzyme-linked immunosorbent assay (ELISA) and western-blotting assay. HTLV-I proviral DNA in the abnormal lymphocyte cells was not detected by southern blotting hybridization technique. Moreover, HTLV-I provirus was not detected using a polymerase-chain-reaction (PCR). A monoclonal rearrangement of the TCR-beta chain gene was evident by using DNA probe in southern blot hybridization. Because of the rapid progress of the disease, chemotherapy was started immediately after admission. Though, this patient became refractory, and she died about 1 year after admission.

Aged↗

The Comprehensive Assessment List for Affective Disorders (COALA): a polydiagnostic, comprehensive, and serial semistructured interview system for affective and related disorders.

This supplement describes the development and structure of the Comprehensive Assessment List of Affective Disorders (COALA) system, which was recently developed for a collaborative follow-up study of a broad spectrum of affective disorders in Japan and which consists of a series of semistructured interviews for affective and related disorders. The COALA distinguishes itself from the extant semistructured interviews by being able to provide polydiagnostic, comprehensive and serial assessments. It is polydiagnostic because it derives diagnoses according to 29 historical and modern diagnostic systems through computer algorithms. It is comprehensive because it not only depicts the symptoms profile and rates their severity according to various endogenicity indices and severity rating scales but also measures, in the psychosocial domain, the life events and their characteristics. In addition, it has sections for past illnesses and family history. It is serial because the system includes follow-up semistructured interviews that can be administered monthly and that monitor changes in the psychopathological and psychosocial features. The theoretical underpinnings of the COALA system, especially its polydiagnostic approach to a broad spectrum of affective disorders and its treatment of psychosocial factors, are discussed in view of recent proposals for the future nosological research. The findings of the interrater reliability study (n = 107) are also presented, with satisfactory to excellent results for almost all of the psychopathological and psychosocial variables, all of the composite severity ratings and most of the polydiagnostic evaluations.

Female↗

[The Quick Return Service of electroencephalogram].

Because electroencephalography (EEG) examinations take time and numerous channels are used, they generate an enormous volume of data. Vast amounts of space would be required to store the data on shelves and in storage rooms, and a great deal of time and labor would be needed to retrieve the data and use it again. We developed an EEG optical disk filing system to solve such problems. With this system display terminals are set up in the various outpatient departments which often request EEG examinations, i.e., the neurology department, psychiatry department, and pediatric department, making it possible to search and display EEG waveforms, the content of EEG reports, etc., stored on the optical disks at any time. Using such functions patients can be examined without having to send for charts and EEG paper-output waveforms, which is troublesome and time-consuming, and contributes to shortening examination time.

Electroencephalography↗

[A case of testicular tumor associated with the contralateral undescended testis].

A 36-year-old man visited the hospital complaining of painless swelling of the right scrotal contents. His left scrotal contents were absent in the scrotum. Right inguinal orchiectomy was performed on May 17, 1993 under the diagnosis of testicular tumor. The pathological diagnosis of the tumor was pure seminoma. Abdominal computed tomography (CT) and magnetic resonance imaging (MRI) revealed the enlargement of para-aortic lymph nodes and there was a soft tissue signal in the left inguinal region which seemed to be the left testis in MRI. His serum testosterone level was low and gonadotropin level was high. The left orchiopexy was performed on June 24, 1993, but the left testis was finally removed because of methicillin-resistant Staphylococcus aureus (MRSA) infections. Radiation therapy was done against the metastatic lesion in the retroperitoneal lymph nodes and complete remission was obtained. The left undescended testis pathologically showed atrophy of germ cells but there was no appearance of atypia of Leydig cells or germ cells.

Adult↗

[Motilin].

Explore the source record for details and available documents.

Humans↗

Protein kinase inhibitor potentiates opioid delta-receptor currents in Xenopus oocytes.

In Xenopus oocytes injected with RNA coding for the delta-opioid receptor a small chloride current was evoked by [D-Ala2,Ser5]leucine-enkephaline-Thr6 (DSLET), a delta 2-opioid agonist. The evoked currents were rapidly reduced upon repeated challenges of DSLET. When Gil alpha RNA was co-injected into the oocyte, the evoked currents were increased 3.8-fold and became constant after at least three repeated challenges. In oocytes injected with RNAs coding for delta-receptor and Gil alpha, pretreatment with K-252a, a potent inhibitor of protein kinases, further potentiated the delta-receptor-mediated current responses, compared with those without the inhibitor. These results suggest that signalling involving the delta-opioid receptor is inactivated through in vivo phosphorylation in the Xenopus oocyte.

Analgesics↗

6-OHDA-induced lesion of the nigrostriatal dopaminergic neurons potentiates the inhibitory effect of 7-OHDPAT, a selective D3 agonist, on acetylcholine release during striatal microdialysis in conscious rats.

Using striatal microdialysis, we attempted to clarify whether or not locally infused 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OHDPAT), a selective D3 agonist, modulates the basal acetylcholine (ACh) release in conscious rats sham-operated and lesioned with 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. In the sham-operated rats, 7-OHDPAT at 1 microM decreased ACh release by 19% of control. In the 6-OHDA-lesioned rats, 7-OHDPAT (0.1-10 microM) decreased ACh release in a concentration-dependent manner. The decrease of 37% of control was seen at 1 microM 2 weeks after the lesion. The 7-OHDPAT (1 microM)-induced decrease was completely antagonized by 1 microM (-)-sulpiride, a D2 and D3 antagonist, while (-)-sulpiride at 1 microM alone failed to alter ACh release. There may exist intrastriatal D3 receptors to inhibit ACh release, and supersensitization is evident in a 6-OHDA-lesioned rat Parkinson's model.

Acetylcholine↗

1-Phosphatidylinositol 3-kinase activity is required for insulin-stimulated glucose transport but not for RAS activation in CHO cells.

Insulin stimulation drives the formation of a complex between tyrosine-phosphorylated insulin receptor substrate 1 (IRS-1) and 1-phosphatidylinositol 3-kinase (PI 3-kinase; ATP:1-phosphatidyl-1D-myo-inositol 3-phosphotransferase, EC 2.7.1.137), a heterodimer consisting of regulatory 85-kDa (p85) and catalytic 110-kDa (p110) subunits. This interaction takes place via the phosphorylated YMXM motifs of IRS-1 and the Src homology region 2 (SH2) domains of p85. In this study, the stable overexpression in a Chinese hamster ovary (CHO) cell line of a mutant p85 alpha (delta p85) protein, which lacks a binding site for p110, disrupted the complex formation between IRS-1 and the catalytic subunit of PI 3-kinase in intact cells during insulin stimulation. Activation of insulin receptor kinase and the tyrosine phosphorylation of IRS-1 remained unaffected. In this cell line, both insulin-stimulated accumulation of phosphatidylinositol 3,4,5-trisphosphate and the insulin-stimulated glucose uptake due to the translocation of GLUT1 glucose transporters were markedly impaired, whereas neither phorbol 12-myristate 13-acetate-stimulated glucose uptake nor the insulin-stimulated activation of RAS was impaired. These results suggest that PI 3-kinase is required for glucose transport in insulin signaling in CHO cells.

Animals↗

Species and age-dependent differences of functional coupling between opioid delta-receptor and G-proteins and possible involvement of protein kinase C in striatal membranes.

[D-Ser2,Leu5]-enkephalin-Thr6 (DSLET) and [D-Pen2,5]-enkephalin (DPDPE), both delta-agonists, stimulated the high affinity GTPase in the rat striatal membranes in a naltrindole-reversible manner. Similar stimulation was also observed in the striatal membrane preparations of 16-week-old guinea pigs, while not in those preparations of 4-week-old ones. When calphostin C, a protein kinase C inhibitor, was added to the reaction mixture, DSLET showed a marked stimulation in this activity in 4-week guinea pig striatal membranes. There was no effect of KT5720, a cyclic AMP-dependent protein kinase inhibitor, on such delta-opioid-mediated responses. These findings suggest that protein kinase C is locally involved in the functional uncoupling of delta-receptors to G-proteins in the striatum of young guinea pigs.

Aging↗

Supersensitivity of quinpirole-evoked GTPase activation without changes in gene expression of D2 and Gi protein in the striatum of hemi-dopaminergic lesioned rats.

Quinpirole with D2 agonist activity showed a two-fold increase in the GTPase activity in the 6-hydroxydopamine-lesioned side of the striatum, compared with that in the control side. However, neither qualitative nor quantitative changes were observed in the gene expression of two alternative splicing products derived from dopamine D2 receptor gene or of Gil alpha, in the RNAase protection assay. These results suggest that D2 receptor-mediated supersensitization does not come from the D2 receptor upregulation.

Animals↗

A complex of GRB2-dynamin binds to tyrosine-phosphorylated insulin receptor substrate-1 after insulin treatment.

Insulin drives the formation of a complex between tyrosine-phosphorylated IRS-1 and SH2-containing proteins. The SH2-containing protein Grb2 also possesses adjacent SH3 domains, which bind the Ras guanine nucleotide exchange factor Sos. In this report, we examined the involvement of another SH3 binding protein, dynamin, in insulin signal transduction. SH3 domains of Grb2 as GST fusion proteins bound dynamin from lysates of CHO cells expressing wild-type insulin receptor (IR) (CHO-IR cells) in a cell-free system (in vitro). Immunoprecipitation studies using specific antibodies against Grb2 revealed that Grb2 was co-immunoprecipitated with dynamin from unstimulated CHO-IR cells. After insulin treatment of CHO-IR cells, anti-dynamin antibodies co-immunoprecipitated the IR beta-subunit and IRS-1, as tyrosine-phosphorylated proteins and PI 3-kinase activity. However, purified rat brain dynamin did not bind directly to either the IR, IRS-1 or the p85 subunit of PI 3-kinase in vitro. Together, these results suggest that in CHO-IR cells, insulin stimulates the binding of dynamin to tyrosine-phosphorylated IRS-1 via Grb2 and that IRS-1 also associates with PI 3-kinase in response to insulin. This complex formation was reconstituted in vitro using recombinant baculovirus-expressed IRS-1, GST-Grb2 fusion proteins and dynamin peptides containing proline-rich sequences. Furthermore, dynamin GTPase activity was found to be stimulated when an IRS-1-derived phosphopeptide, containing the Grb2 binding site, was added to the dynamin-Grb2 complex in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptor Proteins, Signal Transducing↗

Supersensitization of intrastriatal dopamine receptors involved in opposite regulation of acetylcholine release in Parkinson's model rats.

Using striatal microdialysis, we studied effects of SKF 38393, a D1 agonist, and quinpirole, a D2 agonist, on the acetylcholine (ACh) release from the striatum of 6-hydroxydopamine (6-OHDA)-lesioned rats by local infusion into the striatum. The present experiments clearly demonstrated evidence for the existence of intrastriatal D1 and D2 receptors regulating ACh release and for supersensitization of the striatal stimulatory D1 and inhibitory D2 receptor mechanisms in 6-OHDA lesioned rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Involvement of phosphoinositide 3-kinase in insulin- or IGF-1-induced membrane ruffling.

Insulin, IGF-1 or EGF induce membrane ruffling through their respective tyrosine kinase receptors. To elucidate the molecular link between receptor activation and membrane ruffling, we microinjected phosphorylated peptides containing YMXM motifs or a mutant 85 kDa subunit of phosphoinositide (PI) 3-kinase (delta p85) which lacks a binding site for the catalytic 110 kDa subunit of PI 3-kinase into the cytoplasm of human epidermoid carcinoma KB cells. Both inhibited the association of insulin receptor substrate-1 (IRS-1) with PI 3-kinase in a cell-free system and also inhibited insulin- or IGF-1-induced, but not EGF-induced, membrane ruffling in KB cells. Microinjection of nonphosphorylated analogues, phosphorylated peptides containing the EYYE motif or wild-type 85 kDa subunit (Wp85), all of which did not inhibit the association of IRS-1 with PI 3-kinase in a cell-free system, did not inhibit membrane ruffling in KB cells. In addition, wortmannin, an inhibitor of PI 3-kinase activity, inhibited insulin- or IGF-1-induced membrane ruffling. These results suggest that the association of IRS-1 with PI 3-kinase followed by the activation of PI 3-kinase are required for insulin- or IGF-1-induced, but not for EGF-induced, membrane ruffling.

Amino Acid Sequence↗