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Biomedical subjects

A Ueno

Publications and source records attributed to A Ueno.

At least 109 records · Page 6Linked to original sources
PubMed1997

The role of lymphadenectomy in the treatment of transitional cell carcinoma of the upper urinary tract.

PURPOSE: We evaluated the efficacy of lymphadenectomy in conjunction with nephroureterectomy in patients with transitional cell carcinoma of the upper urinary tract. MATERIALS AND METHODS: Data were evaluated retrospectively in 21 consecutive men and 15 women (mean age 67 years) who underwent total nephroureterectomy with lymphadenectomy between January 1985 and December 1993. RESULTS: Of the 36 patients 11 (31%) had lymph node metastases. Of 20 patients with stages pT3 to 4 or pN+ tumors 12 received cisplatin based chemotherapy (11 postoperatively and 1 preoperatively). Followup ranged from 3 to 135 months (mean 55). Among 13 patients who died by May 1996 tumor was the cause of death in 8, while 5 died of unrelated causes. The probability of a cause specific survival at 5 years was 100% in patients with stages pTa to 1, 80% with stage pT2, 59% with stage pT3 and 0% with stage pT4 cancer. The probability of a cause specific survival at 5 years in patients with nodal metastasis was 21%. No patient without nodal metastasis died of tumor related causes. CONCLUSIONS: Lymphadenectomy may provide therapeutic benefit in select patients with lymph node metastasis. It also may be a useful indicator of candidates for adjuvant chemotherapy if an effective regimen is established because lymph node metastasis is common in patients with carcinoma of the upper urinary tract and is critical in establishing the prognosis.

Adult↗
PubMed1997

[Intraocular neovascularization].

To investigate the mechanism of intraocular neovascularization, we studied how vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) are expressed in the ocular tissues under hypoxic conditions. Prior to proliferation of vascular endothelial cells resulting in neovascularization, the retinal tissues such as pericytes, retinal glial cells, ganglion cells, and ciliary epithelium react directly to hypoxia expressing VEGF and/or IL-8 and stimulate endothelial cell proliferation in a paracrine manner. We demonstrated that transcription factor activator protein-1 (AP-1) is activated for expression of VEGF messenger ribonuculeic acid (mRNA) and in a similar way nuclear factor kappa B (NF-kappa B) is activated for expression of IL-8 mRNA. However, hypoxia-induced expression of VEGF and/ or IL-8 is only one aspect of the complicated processes in intraocular neovascularization. We hope that further detailed analysis of the mechanism will make it possible to inhibit and treat clinically intraocular neovascularization in the near future.

Adult↗
PubMed1996

Osteotropic factor-stimulated synthesis of thrombospondin in rat dental pulp cells.

The amount of thrombospondin (TSP) mRNA in confluent clonal rat dental pulp cells was increased by transforming growth factor-beta (TGF-beta), 1 alpha-25-dihydroxyvitamin D3 (1,25(OH)2D3), and phorbol 12,13-didecanoate (PDD), with maximal levels 6, 36 and 2 h, respectively, after stimulation. These increases were accompanied by enhanced syntheses of TSP proteins which were found in the different forms in cell layer/matrix fraction (198 and 165 kDa TSP) and the culture medium (180 kDa TSP). These three factors also raised the mRNA level of osteopontin, which is thought to play an important role in mineralization in dentin and bone. The order of effectiveness of these factors was PDD > TGF-beta > 1,25(OH)2D3 for all the stimulations described above. These results suggest that the osteotropic factors enhance TSP synthesis at the pretranslational level and that TSP produced by dental pulp cells participates in formation of reparative dentin.

Animals↗
PubMed1996

Protein tyrosine kinase inhibitors promote amylase secretion and inhibit ornithine decarboxylase induction in sialagogue-stimulated rat parotid explants.

Three sialagogues, isoproterenol (IPR), carbachol, and methoxamine, caused induction of ornithine decarboxylase (ODC) in cultured rat parotid explants. All the protein tyrosine kinase inhibitors tested suppressed this ODC induction but enhanced sialagogue-dependent amylase secretion. Sodium orthovanadate showed the reverse effects as the kinase inhibitors. Immunoblot analysis with anti-phosphotyrosine antibody revealed that herbimycin A depresses IPR-stimulated tyrosine phosphorylation of parotid proteins. Herbimycin A did not affect the IPR- or dibutyryl cAMP-induced surge of the parotid cAMP level but inhibited these agonist-dependent ODC inductions. These results suggest that sialagogue-induced ODC induction and amylase secretion are mediated by different signal transduction pathways and that protein tyrosine kinase participates in IPR-dependent ODC induction and amylase secretion in the process subsequent to the cAMP surge.

Amylases↗
PubMed1996

Inhibitory effect of arachidonic acid on platelet-activating factor production in rat neutrophils.

Platelet-activating factor production in rat neutrophils in response to opsonized zymosan was suppressed dose dependently in the presence of 10-100 microM arachidonic acid. The amount of lyso-PAF was also reduced by these doses of arachidonic acid. Phospholipase A2 activity was not changed by addition of arachidonic acid up to 100 microM, but acetyltransferase activity was slightly reduced at a 100 microM concentration of arachidonic acid. Pretreatment with indomethacin did not alter the inhibitory effect of arachidonic acid on PAF production, indicating no involvement of cyclooxgenase products. Triacsin C, an acyl-CoA synthetase inhibitor, reversed the arachidonic acid-induced suppression of lyso-PAF and PAF production, suggesting that arachidonic acid might exert its inhibition via the acylation pathway of lyso-PAF to reduce the availability of lyso-PAF.

Acetyl-CoA C-Acetyltransferase↗
PubMed1996

Role of synergistic action of PAF and kinin in bacterial endotoxin-induced hypotension in rats.

Involvement of PAF and kinin in the endotoxin (LPS)-induced hypotension was examined in the rat strains, Brown Norway (B/N);Kitasato (Normal) and B/N-Kitasato rats, intravenous injection of 10 mg/kg LPS caused a hypotension composed on two phases (15 min and 70 min after LPS injection). However in the kininogen-deficient B/N-Katholiek rats. LPS induced only the second phase. Pretreatment with bradykinin (BK) antagonist. Hoe 140 suppressed LPS-induced hypotension of normal rats to the level of Katholiek rats. TCV 309, a PAF-antagonist, suppressed the LPS-hypotension almost completely in the both strains. The reason why the PAF-antagonist showed almost complete inhibition, could be explained by a synergism. Because concomitant injection of a small amount of BK with PAF caused potentiation of the effect of the PAF action. These results suggest that formation of endogenous BK contributes mainly to the 1st phase of LPS-hypotension, and PAF contributes to both phases, by either direct and synergistic actions.

Animals↗
PubMed1996

Araliasaponins I-XI, triterpene saponins from the roots of Aralia decaisneana.

Seven new oleanane-type and four new ursane-type triterpene saponins, named araliasaponins I-XI were isolated from the roots of Aralia decaisneana, together with four known triterpene saponins. On the basis of the chemical and spectroscopic evidence, the structures of these new saponins were elucidated as follows: 3-O-beta-D-xylopyranosyl-(1-->3)-beta-D- glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-alpha-L- arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-alpha-L- arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D- glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D- xylopyranosyl-(1-->2)]-alpha-L-arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-beta-D- glucopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-beta-D- galactopyranosyl oleanolic acid, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D- xylopyranosyl-(1-->2)]-beta-D-galactopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-beta-D- galactopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]- alpha-L-arabinopyranosyl ursolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]-alpha-L - arabinopyranosyl ursolic acid, 3-O-beta-D-glucopyranosyl-(1-->3)-alpha-L-arabinopyranosyl ursolic acid 28- O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester and 3-O-beta-D-glucopyranosyl-(1-->3)-[beta-D-xylopyranosyl-(1-->2)]- beta-D-glucopyranosyl ursolic acid 28-O-beta-D-glucopyranosyl ester.

Carbohydrate Conformation↗
PubMed1996

Araliasaponins XII-XVIII, triterpene saponins from the roots of Aralia chinensis.

Seven new oleanane-type saponins, named araliasaponins XII-XVIII, were isolated from the roots of Aralia chinensis, together with 14 known triterpene saponins. On the basis of the chemical and spectroscopic evidence, the structures of these new saponins were elucidated as follows: 3-O-beta-D-glucopyranosyl(1-->3)-[beta-D -glucopyranosyl(1-->2)]-alpha-L-arabinopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl(1-->3)-[beta-D-xylopyranosyl (1-->2)]-alpha-L-arabinopyranosyl oleanolic acid 28-O-alpha-L-rhamnopyranosyl(1-->4)-beta-D-glucopyranosyl (1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D -glucopyranosyl(1-->3)-[beta-D-galactopyranosyl(1-->2)] -beta-D-glucopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-beta-D-glucopyranosyl(1-->3)-[beta-D -xylopyranosyl(1-->2)]-beta-D-glucopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl (1-->6)-beta-D-glucopyranosyl ester, 3-O-beta-D -glucopyranosyl(1-->3)-[beta-D-galactopyranosyl (1-->2)]-beta-D-galactopyranosyl oleanolic acid 28-O-beta-D-glucopyranosyl ester, 3-O-alpha-L -arabinofuranosyl(1-->4)-[beta-D-glucopyranosyl (1-->2)]-beta-D-glucuronopyranosyl oleanolic acid dimethyl ester and 3-O-alpha-L-arabinofuranosyl (1-->4)-[beta-D-glucopyranosyl(1-->2)]-beta-D -glucuronopyranosyl oleanolic acid 28-O-beta-D -glucopyranosyl(1-->6)-beta-D-glucopyranosyl methyl ester, respectively.

Carbohydrate Conformation↗
PubMed1996

Phenylethanoid glycosides from Stachys officinalis.

From the aerial parts of Stachys officinalis, six new phenylethanoid glycosides, named betonyosides A-F, and six known phenylethanoid glycosides, acetoside, acetoside isomer, campneosides II, forsythoside B and leucosceptoside B, were isolated and their structures were elucidated from spectroscopic and chemical evidence. Campneosides II were separated into two epimers.

Carbohydrate Conformation↗
PubMed1996

Induction of a B1-receptor mediating hypotensive response in young brown Norway rats.

A hypotensive response to intravenously injected des-Arg9-bradykinin was elicited in young male Brown Norway rats (8-12 weeks-old), when the rats were intravenously injected with endotoxin (30 micrograms/kg) 24 h before they were repeatedly injected with bradykinin or des-Arg9-bradykinin. The potency of this inducible dose-dependent hypotensive response to des-Arg9-bradykinin was comparable to that induced by bradykinin on a molar base (3-30 nmol/kg). A hypotensive response to des-Arg9-bradykinin could also be induced when the rats were pretreated with endotoxin 6 h before. However, the potency of the response was less than that induced by 24-h pretreatment. This inducible response to des-Arg9-bradykinin did not occur in old rats (8-10 months old). Intravenous infusion of a B1-receptor antagonist, des-Arg9-[Leu8]-bradykinin, suppressed the hypotensive response of des-Arg9-bradykinin. These results suggest that the B1-receptor, mediating hypotension in rats, was inducible through time-dependent and age-dependent sensitization by endotoxin pretreatment.

Age Factors↗
PubMed1996

Thrombin stimulates production of interleukin-8 in human umbilical vein endothelial cells.

Interleukin-8 (IL-8) is regarded as an important mediator of inflammation because of its potent and specific chemotactic activity on neutrophils. In the present investigation, human umbilical vein endothelial cells (HUVEC) stimulated with thrombin were found to produce IL-8, in a dose- and time-dependent manner. After stimulation with 10 U/ml thrombin for 24 hr, the level of IL-8 in the conditioned medium was 14 ng/ml, or enough to elicit PMN chemotaxis in vitro. Northern blot analysis revealed that thrombin as well as IL-1 beta elevates the level of IL-8 mRNA preceding the formation of IL-8 protein. A synthetic peptide SFLLRN [human thrombin receptor-activating peptide (TRAP)] was found to mimic the action of thrombin. Preincubation with anti-thrombin compounds such as hirudin and antithrombin-III-heparin almost completely suppressed the action of thrombin without affecting the actions of other stimuli including IL-1 beta, phorbol 12-myristate 13-acetate (PMA) and TRAP. Diisopropylfluorophosphate-treated thrombin did not stimulate IL-8 production. Calphostin-C, a protein kinase C (PKC) inhibitor, attenuated the production of IL-8 by thrombin, TRAP and PMA, but left the action of IL-1 beta unchanged. These results strongly suggest that catalytic activation of thrombin receptor by thrombin results in PKC-dependent IL-8 production accompanied by an increase in IL-8 mRNA level.

Blotting, Northern↗
PubMed1996

Relation between distribution of viral RNA and development of histopathological changes in encephalomyocarditis virus-induced orchitis in mice.

The relation between the distribution of viral RNA and the development of histopathological changes was investigated in the early stage of encephalomyocarditis (EMC) virus-induced orchitis in mice. Signals of viral RNA were first detected by in situ hybridization in a few Sertoli cells in almost intact germinal epithelia at 2 days post-inoculation (d.p.i.). The number of Sertoli cells bearing signals of viral RNA increased at 3 d.p.i. when mild degenerative changes were exceptionally found in germinal epithelia. Signals of viral RNA came to be detected not only in Sertoli cells but also in a small number of germinal cells and spermatogonia at 4 d.p.i. when mild to moderate degenerative changes developed in germinal epithelia, resulting in desquamation of degenerated cells. At the same time, virus-like particles were observed by electron-microscopy in the degenerated and desquamated germinal cells. At and after 5 d.p.i., luminal obstruction with cellular debris and inflammatory cells was generally found. These results suggest that EMC virus carried to seminiferous tubules via the blood first attacks Sertoli cells and then damages germinal cells and spermatogonia.

Animals↗