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Biomedical subjects

A Ueno

Publications and source records attributed to A Ueno.

At least 127 records · Page 7Linked to original sources

Gigantic aneurysm in the thoraco-abdominal aorta of an infant.

We report the case of a boy with a gigantic aneurysm in the thoraco-abdominal region which was detected by a chest X-ray taken prior to surgical correction of ptosis of the eyelids at 11 months of age. At 18 months, he successfully underwent aneurysm exclusion and bypass grafting. A biopsy from the thoracic aorta revealed medial degeneration with conspicuous smooth muscle cell involvement. Laboratory examination showed altered elastase activity in the granulocytes and whole blood. The present case may represent a unique form of aneurysm in infancy.

Aortic Aneurysm, Abdominal↗

Thoracoabdominal aortic aneurysm in an infant treated by thromboexclusion with thoracoabdominal aortic bypass. A case report.

A case of a huge thoracoabdominal aortic aneurysm in an eighteen-month-old boy is reported. Surgical treatment was successfully performed by thromboexclusion of the aneurysm with thoracoabdominal aortic bypass using a low-porosity woven Dacron graft 10 mm in diameter and of sufficient surplus length. During the early postoperative period, he developed moderate hydronephrosis, owing to compression of the left ureter by the graft, but no further deterioration was seen. Follow-up angiographies performed four and six years after surgery revealed straightening of the graft and slight stretching of the aorta at the distal anastomosis, but no stenosis was found. Now, seven and a half years after surgery, he has no pressure gradient between upper and lower extremities.

Angiography, Digital Subtraction↗

Studies on differentiation inducers. VI. Lignan derivatives from Arctium fructus. (2).

In the previous paper, we reported the differentiation inducing activities of lignoids from Arctium Fructus (the fruits of Arctium lappa L., Compositae) against mouse myeloid leukemia cells (M1). We reinvestigated the active components of this extract and isolated three new dilignans. Furthermore, structure modifications were carried out using the most active lignan (arctigenin, 1) and its structure-activity relationship was investigated. Its aliphatic esters were more effective in inducing the differentiation of M1 cells than its aromatic esters. Especially, n-decanoate, which was the most active derivative, induced more than half of the M1 cells into phagocytic cells at a concentration of 2 microM.

Animals↗

Five new triterpene saponins, polygalasaponins XXVIII-XXXII from the root of Polygala japonica Houtt.

Five new oleanane-type saponins, polygalasaponins XXVIII-XXXII, along with one known saponin, polygalasaponin XXIV, and one known acylated sucrose, tenuifoliside C, were isolated from the root of Polygala japonica. The structures of these new compounds were elucidated as 3-O-beta-D-glucopyranosyl pesenegenin 28-O-beta-D-xylopyranosyl (1-->4)-alpha-L-rhamnopyranosyl (1-->2)-beta-D-fucopyranosyl ester, 3-O-beta-D-glucopyranosyl presenegenin 28-O-beta-D-galactopyranosyl (1-->5)-beta-D-apiofuranosyl (1-->4)-beta-D-xylopyranosyl (1-->4)-alpha-L-rhamno-pyranosyl (1-->2)-beta-D-fucopyranosyl ester, 3-O-beta-D-glucopyranosyl presenegenin 28-O-beta-D-galactopyranosyl (1-->4)-beta-D-xylopyranosyl (1-->4)-alpha-L-rhamnopyranosyl (1-->2)-[4-O-p-methoxycinnamoyl]-[beta-D-glucopyranosyl (1-->3)]-beta-D-fucopyranosyl ester, 3-O-beta-D-glucopyranosyl presenegenin 28-O-alpha-L-arabinopyranosyl (1-->3)-beta-D-xylopyranosyl (1-->4)-[beta-D-apiofuranosyl (1-->3)]-alpha-L-rhamnopyranosyl (1-->2)-[4-O-3,4,5-trimethoxycinnamoyl]-beta-D-fucopyranosyl ester, 3-O-beta-D-glucopyranosyl persenegenin 28-O-alpha-L-arabinopyranosyl (1-->3)-beta-D-xylopyranosyl (1-->4)-[beta-D-apiofuranosyl (1-->3)-alpha-L-rhamnopyranosyl (1-->2)-[4-O-p-methoxycinnamoyl]-[alpha-L-rhamnopyranosyl (1-->3)-beta-D-fucopyranosyl ester, respectively, on the basis of spectroscopic and chemical evidence.

Carbohydrate Sequence↗

The mediators involved in endotoxin-induced vascular permeability increase in the rat skin and their interactions.

The injection of lipopolysaccharide (LPS) from E. Coli into the dorsal skin of rats caused a dose-dependent increase in vascular permeability as measured by the extravasation over a 40-min period of intravenously injected dye. This increase caused by LPS was attenuated by pretreatment with the bradykinin (BK) receptor antagonist HOE140, the selective platelet-activating factor (PAF) antagonist TCV309, and by combined treatment with mepyramine and methysergide. Combined treatment with HOE140 and TCV309 resulted in further suppression than that achieved with a single treatment alone. By the simultaneous pretreatment with all antagonists, the response was almost totally abolished. On the other hand, indomethacin also inhibited the response induced by LPS, but not those induced by BK and PAF itself. A small dose of BK or histamine synergistically potentiated the effect of PAF when simultaneously injected. These results suggest that BK, PAF, histamine/serotonin and prostaglandins are involved in the LPS-induced increase in vascular permeability, where PAF, in addition to its direct action, potentiates the response to BK and histamine, and prostaglandins potentiate the actions of other mediators without its direct action.

Animals↗

[Comparison of hormone therapy alone and in combination with chemotherapy of cisplatin and methotrexate in newly diagnosed patients with stage D2 prostatic cancer].

BACKGROUND: Prognosis of hormone-refractory prostatic cancer is dismal. We evaluated the efficacy of cytotoxic chemotherapy in combination with hormone therapy in patients with newly diagnosed metastatic prostatic cancer. METHODS: From February 1984 to March 1992, 39 newly diagnosed patients with stage D2 prostatic cancer were randomized to orchiectomy plus diethylistilbestrol diphosphate or orchiectomy plus diethylstilbestrol diphosphate plus combination chemotherapy with cisplatin and methotrexate. RESULTS: There was not significant difference in survival or progression-free survival between the two groups. CONCLUSION: Chemotherapy has not been proved to prolong survival or progression-free survival in patients who received hormone therapy.

Adenocarcinoma↗

[89Sr Therapy for pain relief in patients with bone metastases].

Radioactive strontium chloride (89Sr) was administered for pain relief in 6 patients with bone metastases (4 prostate cancer and 2 breast cancer patients). Out of 6 patients, 2 showed apparent relief of bone pain and improvement of QOL, and 3 showed slight relief of the pain with or without improvement of QOL; that is, 83% was effective. Side effects were seen in 2 patients; transient deterioration of bone pain in one patient and bone marrow suppression in the other patient. The patient who showed bone marrow suppression had rather more lesions of bone metastasis (diffuse metastasis) and least urinary excretion of the radioactivity. Urinary excretion for 2 days varied 5 to 40% of the administered dose and was less in the patients with more metastatic lesions.

Bone Marrow↗

Involvement of bradykinin in endotoxin-induced vascular permeability increase in the skin of rats.

The aim of the present study was to investigate the role of bradykinin as well as that of platelet-activating factor in the endotoxin-induced acute vascular permeability increase in the dorsal skin of rats by use of kininogen-deficient and normal Brown-Norway rats. In the kininogen-deficient rats, the dose-dependent dye exudation induced by endotoxin was about one half of that in the normal rats at any doses of endotoxin tested (0.1-1.0 mg per site), whereas the dose-response curves obtained by bradykinin (1-100 nmol per site), platelet-activating factor (0.1-1 nmol per site) or histamine (50-500 nmol per site) were the same in both rats. This effect induced by endotoxin in the kininogen-deficient rats was not changed by pretreatment with a bradykinin B2 receptor antagonist, HOE140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin, 1 mg kg-1 i.v.), whereas the endotoxin-induced response in the normal rats was attenuated by the receptor antagonist. These responses in both kininogen-deficient and normal rats were significantly inhibited by a selective platelet-activating factor antagonist, TCV309 (3-bromo-5-[N-phenyl-N-[2-[[2-(1,2,3,4,-tetrahydro-2- isoquinolylcarbonyl-oxy)-ethyl]-carbamoyl]-ethyl]carbamoyl]-1-prop yl- pyridinium nitrate, 0.1 mg kg-1 i.v.). These results suggest that bradykinin could be one of the major mediators in the endotoxin-induced vascular permeability increase in rat skin in addition to platelet-activating factor.

Animals↗

Thrombin induces GRO alpha/MGSA production in human umbilical vein endothelial cells.

Thrombin, besides being a potent coagulation factor, exerts influence on endothelial and leukocyte functions and may thus be involved in the regulation of inflammatory reactions. The present study investigated whether thrombin stimulates the production of growth-related cytokine/melanoma growth-stimulatory activity (GRO alpha/MGSA) in endothelial cells. Human umbilical vein endothelial cells (HUVEC) stimulated with thrombin were found to product GRO alpha/MGSA in a dose- and time-dependent manner. This action of thrombin was completely suppressed by preincubation with either hirudin or antithrombin-III (AT-III)-heparin. Interestingly, the thrombin receptor-activating peptide SFLLRN mimicked the action of thrombin. In addition, staurosporine, a protein kinase C (PKC) inhibitor, attenuated the production of GRO alpha/MGSA by thrombin, SFLLRN and phorbol 12-myristate 13-acetate (PMA), but left the action of interleukin-1 beta (IL-1 beta) unchanged. These results suggest that catalytic activation of thrombin receptor by thrombin results in GRO alpha/MGSA production, at least in part, via a pathway involving PKC in HUVEC.

Alkaloids↗

A hypotensive response induced by des-Arg9-bradykinin in young brown/Norway rats pretreated with endotoxin.

A hypotensive effect of intravenously injected des-Arg9-bradykinin was found in Brown/Norway strain young male rats which were pretreated with a small amount of endotoxin 24 h before the experiment, whereas the hypotensive effect of bradykinin was unaffected by the endotoxin. The potency of des-Arg9-bradykinin for the hypotensive effect was comparable to that of bradykinin. On the other hand, in endotoxin-pretreated aged rats, this effect of des-Arg9-bradykinin was not observed. Only during the intravenous infusion of des-Arg9[Leu8]bradykinin, a bradykinin B1 receptor antagonist, was the hypotensive effect of des-Arg9-bradykinin inhibited, whereas that of bradykinin was potentiated. After the end of infusion of des-Arg9[Leu8]bradykinin, the response to des-Arg9-bradykinin rapidly recovered. The results suggest the possibility that des-Arg9-bradykinin might play a role in inflammatory diseases.

Amino Acid Sequence↗

Transforming growth factor-beta 1 has both promoting and inhibiting effects on induction of DNA synthesis in human fibroblasts.

Growth-arrested human normal fibroblasts, TIG-1, initiated DNA synthesis following addition of epidermal growth factor (EGF). Transforming growth factor-beta 1 (TGF-beta 1) by itself had no effect on induction of DNA synthesis. When EGF and TGF-beta 1 were added simultaneously to growth-arrested TIG-1 cells, induction of DNA synthesis was enhanced compared with that by EGF alone. Contrarily, when TGF-beta 1 was added earlier than 2 h or later than 2 h of EGF addition, induction of DNA synthesis was prevented. Induction of DNA synthesis by EGF was insensitive to pertussis toxin (PT, an inhibitor of Gi protein) and to staurosporine (a protein kinase inhibitor). The promoting effect of TGF-beta 1 on DNA synthesis was PT-insensitive and staurosporine-insensitive. Contrarily, inhibitory activity of TGF-beta 1 on DNA synthesis was PT-sensitive and staurosporine-insensitive. These studies suggest that the effect of TGF-beta 1 is to promote or to inhibit induction of DNA synthesis by EGF expressed through different signal transduction processes in the same cell.

Alkaloids↗

Heavy ion mutagenesis: linear energy transfer effects and genetic linkage.

We have characterized a series of 69 independent mutants at the endogenous hprt locus of human TK6 lymphoblasts and over 200 independent S1-deficient mutants of the human x hamster hybrid cell line AL arising spontaneously or following low-fluence exposures to densely ionizing Fe ions (600 MeV/amu, linear energy transfer = 190 keV/microns). We find that large deletions are common. The entire hprt gene (> 44 kb) was missing in 19/39 Fe-induced mutants, while only 2/30 spontaneous mutants lost the entire hprt coding sequence. When the gene of interest (S1 locus = M1C1 gene) is located on a nonessential human chromosome 11, multilocus deletions of several million base pairs are observed frequently. The S1 mutation frequency is more than 50-fold greater than the frequency of hprt mutants in the same cells. Taken together, these results suggest that low-fluence exposures to Fe ions are often cytotoxic due to their ability to create multilocus deletions that may often include the loss of essential genes. In addition, the tumorigenic potential of these HZE heavy ions may be due to the high potential for loss of tumor suppressor genes. The relative insensitivity of the hprt locus to mutation is likely due to tight linkage to a gene that is required for viability.

Animals↗

Mazusaponins I-IV, triterpene saponins from Mazus miquelii.

From whole plants of Mazus miquelii, four new saponins designated as mazusaponins I-IV and a known saponin, ilexoside VIII, were isolated and the structures of the new compounds elucidated as 3-O-alpha-L-arabinopyranosyl siaresinolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester, 3-O-alpha-L-arabinopyranosyl pomolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester, 3-O-alpha-L-rhamnopyranosyl-(1-->2)-alpha-L-arabinopyranosyl siaresinolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester and 3-O-alpha-L-rhamnopyranosyl-(1-->2)-alpha-L-arabinopyranosyl pomolic acid 28-O-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranosyl ester, respectively, by spectroscopic data and chemical evidence.

Carbohydrate Sequence↗

Linderniosides A and B, oleanane saponins from Lindernia pyxidaria.

Two new oleanane-type triterpene saponins, named linderniosides A and B, were isolated from the whole plants of Lindernia pyxidaria, together with a known triterpene glycoide, medicagenic acid 3-O-glucuronide. The structures of these compounds were determined on the basis of spectral and chemical evidence.

Antifungal Agents↗

cDNA sequence analysis and characterization of a cytokine-inducing monoclonal antibody derived from autoimmune MRL/MP-lpr/lpr mouse.

We have previously reported that a monoclonal antibody 1D11 derived from an autoimmune MRL/Mp-lpr/lpr (MRL/lpr) mouse induced synthesis or increased production of IL-3, IL-6, and TNF-alpha in the IL-3-dependent bone marrow-derived cell line FDC-P2/185-4. In this report, we analyzed a sequence of cDNA encoding the V region of 1D11, and found that VH and VL segments of 1D11 belonged to the J558 and V kappa 21 family, respectively. The nucleotide sequence of 1D11 in the VH segment was highly homologous to that of AM9, a monoclonal RF derived from MRL/lpr mouse, and the only difference was the replacement of 3 nucleotides in the framework region 1 (FR1). However, the deduced amino acid sequence of 1D11 was identical to that of AM9. In contrast with the VH segment, the sequences of the VL regions of these two antibodies were quite different from each other; 1D11 showed a 3 base deletion in the FR2 and a 24 base insertion in the FR3 compared with AM9. At present, the mechanisms of such insertions or deletions in the FRs of autoantibodies are almost unknown. It is generally accepted that the differences in specificity and affinity of these autoantibodies depend on differences of CDR sequence. However, it is possible that not only CDRs but also FRs of autoantibodies play a critical role in pathogenicity and/or specificity in autoimmune diseases.

Amino Acid Sequence↗

Comparative study of endotoxin-induced hypotension in kininogen-deficient rats with that in normal rats.

1. The aim of this study was to clarify the role of endogenous bradykinin (BK) in the hypotensive response induced by lipopolysaccharide (LPS) by comparing the degree of hypotension caused by LPS in a strain of specific pathogen-free (SPF) Brown Norway (B/N), kininogen-deficient mutant Katholiek rats with that of B/N normal Kitasato rats. 2. The dose-dependent hypotensive responses caused by intravenous injection of BK (1-100 nmol kg-1) or platelet-activating factor (PAF, 0.003-1 microgram kg-1), were not different in the two strains of rats used. However, there was a strong difference in the hypotensive response induced by LPS in kininogen-deficient and normal rats; in normal rats the hypotensive response was composed of two phases (15 min and 70-80 min after LPS injection), but in kininogen-deficient rats LPS caused a delayed (second phase), but not an acute (first phase) hypotension. 3. We demonstrate that Hoe 140 (1 mg kg-1, i.v.) is a potent, selective, and long-lasting antagonist of the hypotensive effects of BK. Hoe 140 diminished the hypotension caused by LPS in normal rats to the level observed in kininogen-deficient rats, but had no effect on the hypotension caused by LPS in kininogen-deficient rats. 4. TCV309 (0.1 mg kg-1, i.v.) selectively inhibited the hypotension caused by repetitive injection of PAF for up to 180 min. Pretreatment with TCV309 caused a near complete inhibition of the LPS-induced hypotension in kininogen-deficient and normal B/N rats. 5. In the normal rats, dexamethasone (0.5 mg kg-1, i.p.) inhibited the second phase of the hypotension induced by LPS, but not the first phase of the hypotension. 6. A small amount of BK (0.1 nmol kg-1) potentiated the hypotensive action of PAF (0.01 microg kg-1),when they were injected simultaneously.7. In conclusion, we demonstrate that formation of endogenous BK contributes primarily to the acute,but not to the delayed hypotension afforded by endotoxin in the rat. In contrast, formation of endogenous PAF contributes to both the acute and the delayed hypotension afforded by endotoxin in vivo.

Amino Acid Sequence↗