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Biomedical subjects

Y Takeda

Publications and source records attributed to Y Takeda.

At least 631 records · Page 35Linked to original sources
PubMed1994

Angiotensin II up-regulates the expression of type A endothelin receptor in human vascular smooth muscle cells.

Using vascular smooth muscle cells, the effect of angiotensin II on endothelin receptor regulation was examined. Vascular smooth muscle cells cultivated from human pulmonary artery exhibited high affinity receptors for endothelin-1. When the cells were exposed to angiotensin II, the number of receptors was found to be increased without any change in their affinity. The ligand binding was effectively displaced by BQ123, a selective antagonist for type A endothelin receptor, but not by S6c, a selective ligand for type B receptor, in both control and angiotensin II-treated cells. The level of mRNA coding for the type A receptor was elevated in the latter. These results indicate that angiotensin II up-regulates type A endothelin receptors in human vascular smooth muscle cells through an increase in their corresponding mRNA, suggesting a link between the renin-angiotensin and the endothelin systems.

Angiotensin II↗
PubMed1994

[S antigen in retinas of royal college of surgeons rats: time course and retinal pigment epithelium transplant study].

Retinas of Royal College of Surgeons (RCS) rats were investigated immunocytochemically for the distribution of S antigen prior to and during the retinal disease process. RCS retinas onto which retinal pigment epithelium (RPE) had been transplanted were also immunostained with antibody for S antigen. At P2, weak immunostaining for S antigen was seen in neuroepithelium. At P22, the staining pattern outlined the entire photoreceptor layer. At P30, at the beginning of retinal degeneration, immunostaining for S antigen was considerably reduced in the degenerating photoreceptor outer segment. In the RCS retina at P90, immunostaining for S antigen was completely lost. However, retinas with transplanted RPE showed preserved immunocytochemical staining for S antigen at this late stage. These results suggest a loss of production of S antigen in degenerated retinal tissue, and that RPE transplantation helps to preserve S antigen in the RCS rat retina.

Animals↗
PubMed1994

[Cooley operation for hypertrophic obstructive cardiomyopathy associated with Noonan Syndrome following Morrow operation--a case report].

A 21-year-old female underwent ventricular septoplasty (Cooley operation) for severe left ventricular outflow tract obstruction (LVOTO), which had developed after performance of a Morrow operation at the age of 14. Diagnosis of Noonan syndrome and hypertrophic obstructive cardiomyopathy had been already established by clinical manifestations and a myocardial biopsy. The septoplasty technique and valve replacement could be successfully used to repair the residual LVOTO and aortic regurgitation. We found that this approach was one of the most convenient and provided effective management of LVOTO. Post-operative course has been uneventful and the patient remains completely well as of the 18th months after surgery.

Adult↗
PubMed1994

[Studies on the stability of ferrous ion in the feeds added iron lactate during storage].

Studies on the stability of ferrous ion in the feeds added iron lactate were conducted for a chronic toxicity test. No significant changes in contents of ferrous ion were observed in all samples when feeds containing 0.2 and 5% of iron lactate were stored in the dark at room temperature (25 +/- 2 degrees C) for 72 hours, or feeds containing 1 and 2% iron lactate stored at 4 degrees C for 90 days.

Animal Feed↗
PubMed1993

Human T cell clones reactive against U-small nuclear ribonucleoprotein autoantigens from connective tissue disease patients and healthy individuals.

SLE and mixed connective tissue disease (MCTD) are characterized by the presence of high titers of autoantibodies against uridine-rich RNA-small nuclear ribonucleoprotein (snRNP) Ag. Because the presence of such snRNP-reactive autoantibodies has recently been shown to be associated with polymorphisms of HLA, this study was undertaken to determine whether snRNP-reactive T cells could be identified and characterized from patients. PBMC were stimulated with affinity-purified snRNP Ag and cloned by limiting dilution in the presence of rIL-2 and rIL-4, snRNP-reactive human T cell clones were generated from three patients and two healthy blood donors who possessed disease-associated HLA genotypes. The cell surface phenotype of clones determined by flow cytometry was CD3+, CD4+, CD45RO+, TCR V alpha beta+. TCR V beta analysis, performed using V beta-specific primers and polymerase chain reaction, revealed that the T cell lines generated were clonal; a limited number of TCR V beta genes were expressed among the clones tested. All clones tested by mAb blocking of Ag-induced proliferation were restricted by HLA-DR. Several T cell clones were identified that were specific for B'/B or D polypeptides. These results demonstrate that snRNP-reactive T cells can be isolated from SLE and MCTD patients in vitro, and that Ag-driven expansion of such T cells could play a role in the immunopathogenesis of these diseases in vivo.

Adult↗
PubMed1993

Voltage-dependent modulation of L-type Ca2+ current by manidipine in guinea-pig heart cells.

Effects of manidipine, a dihydropyridine derivative, on L-type Ca2+ currents were examined in guinea-pig ventricular cells, using the whole-cell patch-clamp method. At a holding potential of -37 mV, manidipine decreased the Ca2+ current at concentrations above 0.1 nM, and abolished it at 100 nM (IC50 = 2.6 nM). At a holding potential of -78 mV, manidipine did not suppress the Ca2+ current at concentrations less than 100 nM, but increased the Ca2+ current slightly at a concentration of 10 nM. The antagonistic effect of manidipine was significant at concentrations above 100 nM (IC50 = 400 nM). The voltage-dependent effect of manidipine on the Ca2+ current may explain the weak negative inotropism of manidipine in ventricular muscles, and provide an electrophysiological basis for its vascular selectivity.

Animals↗
PubMed1993

Antithrombin III producing hepatocellular carcinoma.

A case of primary hepatocellular carcinoma with an abnormal increase in the antigenic quantity and activity of Antithrombin III (AT-III) is reported. The patient was a 53-year-old man. The liver was palpated for a five fingerbreadths, but no jaundice or ascites was noted. Computed tomogram (CT) revealed the presence of many nodules of various sizes in the right hepatic lobe. Both viral markers of HBV and HCV were negative. For tumor markers, PIVKA-II was high (27.7 AU/ml) but AFP was normal. Among coagulation and fibrinolytic factors, the activity and antigenic levels of AT-III were abnormally high (290% and 81.6 mg/dl). An US guided needle biopsy of the tumor revealed hepatocellular carcinoma, Edmondson I. The cellularity was high and the tumor cells were small, well differentiated. The tumor cells were positively stained in immunohistochemical staining using the anti-AT-III antibody. It was believed that AT-III produced by the tumor cells was responsible for this exaggerated level.

Antigens, Neoplasm↗
PubMed1993

Cis-diamminedichloroplatinum(II) inhibits p34cdc2 protein kinase in human lung-cancer cells.

cis-Diamminedichloroplatinum(II) (CDDP) induced G2-phase arrest in PC-9 human cancer cells. To elucidate how CDDP acts on cell-cycle regulation, we analyzed the effect of CDDP on cell-cycle regulators such as p34cdc2 protein kinase. p34cdc2 protein kinase activity was maximum in G2 phase and decreased after G2/M transition in synchronized PC-9 human lung cancer cells. Evidence for a phosphorylated p34cdc2 protein kinase complexed with cyclin B was obtained from cells in G2 phase and the p34cdc2 protein kinase appeared to be dephosphorylated at M phase. After exposure to CDDP in G1 phase, PC-9 cells were arrested in G2 phase. The activation of p34cdc2 protein kinase was inhibited by CDDP. Cyclin A and wee-I kinase were not affected by the exposure to CDDP. Cyclin B was degraded in M phase in PC-9 cells. Exposure to CDDP did not affect the degradation of cyclin B. Our data suggest that the effect of CDDP on cell-cycle phase might be regulated by the dephosphorylation of p34cdc2 protein kinase. To determine whether the p34cdc2 protein kinase is a primary target for CDDP, we examined the direct effect of CDDP on tyrosine dephosphorylation of p34cdc2 protein kinase in cellular extracts. Cell lysates from synchronized PC-9 in G2 phase were immunoprecipitated with p13-Sepharose beads. In vitro dephosphorylation of phosphotyrosine of p34cdc2 protein kinase was observed after exposure to okadaic acid in a concentration-dependent manner. The dephosphorylation of p34cdc2 protein kinase by okadaic acid was inhibited by CDDP. We hypothesize that inhibition of p34cdc2 dephorphorylation by CDDP is important for its growth-inhibiting properties.

CDC2 Protein Kinase↗
PubMed1993

Detection of serum cytokine levels in experimental cancer cachexia of colon 26 adenocarcinoma-bearing mice.

The aim of this study was to evaluate the correlations between tumor size and cachexia parameters including cytokine levels in serum. In transplantable colon 26 adenocarcinoma-bearing mice, parameters having negative correlations with tumor size were host weight changes, epididymal adipose tissue weight, glucose and interleukin 3 (IL-3) concentration in serum. Parameters having a positive correlation with tumor size were the number of circulating white blood cells and immunosuppressive acidic protein (IAP), interleukin 6 (IL-6) and transforming growth factor beta (TGF-beta) concentration in serum.

Adenocarcinoma↗
PubMed1993

Modulation of cisplatin sensitivity and accumulation by amphotericin B in cisplatin-resistant human lung cancer cell lines.

To ascertain whether resistance to cis-diamminedichloroplatinum(II) (cisplatin) could be overcome, we determined the effects of amphotericin B (AmB), an antifungal agent, on cisplatin cytotoxicity, cisplatin-induced DNA interstrand cross-links formation, and cellular accumulation of cisplatin in human lung cancer cell lines, PC-9, PC-14, PC-7, and H69 and their corresponding respective cisplatin-resistant sublines PC-9/CDDP, PC-14/CDDP, PC-7/CDDP, and H69/CDDP in vitro. In PC-9/CDDP but not PC-9 cells, augmentation of cytotoxicity was observed when a nontoxic concentration (10 micrograms/ml) of AmB was combined with cisplatin, cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II), and cis-diammine(glycolato)platinum(II). Sensitizing effects of AmB of varying magnitudes on cisplatin cytotoxicity also were observed in all the other cell lines except PC-14. AmB-induced increases in cisplatin-induced interstrand cross-links formation were observed, the magnitudes of which corresponded to the magnitudes of AmB-augmented cisplatin cytotoxicity. Increased intracellular cisplatin accumulation was observed in the presence of AmB in all the cells that were sensitized to cisplatin by AmB. Therefore, the increases in cisplatin accumulation were considered to be responsible, at least in part, for the mechanism of the sensitizing effect. Further experiments using other human lung cancer cell lines showed that cells that were more resistant to cisplatin were more sensitized to cisplatin by AmB than cells that were cisplatin-sensitive.

Amphotericin B↗