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Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 1,243 records · Page 69Linked to original sources
PubMed1984

Modulation of cell surface antigens induced by 12-O-tetradecanoyl-phorbol 13-acetate in two myeloblastic cell lines, a promyelocytic cell line, and a monoblastic cell line: detection with five monoclonal antibodies.

The modulation of cell surface antigens in 2 myeloblastic cell lines (ML-1 and KG-1), a promyelocytic cell line (HL-60), and a monoblastic cell line (THP-1-0) by the presence of 12-O-tetradecanoyl-phorbol 13-acetate [(TPA) CAS: 16561-29-8] was investigated by indirect membrane immunofluorescence with the use of three monoclonal antibodies (MoAb) (OKM-1, 63D3, and MCS-2) reacting with myeloid-monocyte antigens (expressed by cells of both granulocyte and monocyte lineages) and two MoAb (1/12/13 and MCS-1) reacting with myeloid antigens (expressed by cells of the granulocyte lineage). Functionally mature macrophage properties, such as adherence, morphologic character, and phagocytosis, were induced by the presence of TPA in each of the cell lines except for adherence in the HL-60 cells. After 3 days in culture, the expression of the OKM-1-defined antigen was markedly augmented in all 4 cell lines. The expression of the 63D3-defined antigen was also markedly augmented in the ML-1, KG-1, and THP-1-0 cells, but it was not significantly altered in the HL-60 cells. The MCS-2-defined antigen was amplified in expression in the ML-1 and HL-60 cells, but it showed minimum decrease in the KG-1 and THP-1-0 cells. The MCS-1-defined antigen expression was suppressed in ML-1, HL-60, and THP-1-0 but was enhanced in KG-1. The suppressed expression of My-1 antigen (detected by the MoAb 1/12/13) was noted in all 4 cell lines. Thus in the ML-1 cells, expression of the myeloid-monocyte antigens was augmented, whereas myeloid antigen expression was inhibited in the presence of TPA, a result that parallels antigenic expression in terminal macrophage differentiation. The trend was true, except for the 4 cell line-antigen combinations (MCS-2-defined antigen and MCS-1-defined antigen in KG-1, 63D3-defined antigen in HL-60, and MCS-2-defined antigen in THP-1-0). The heterogeneous attitude of some antigens to TPA found in these cell lines may result from the fact that they represent different points in the myeloid-monocyte differentiation scheme.

Antibodies, Monoclonal↗
PubMed1984

Mutagenicity of alpha-hydroxy N-nitrosamines in V79 Chinese hamster cells.

N-Nitrosodialkylamines are activated metabolically by alpha-hydroxylation. Chemical properties and bacterial mutagenicity of alpha-hydroxy N-nitrosamines have been reported previously. This paper describes potent and direct mutagenicity of four N-nitroso-N-(hydroxymethyl)alkylamines in V79 Chinese hamster cells, using ouabain resistance as an indicator. The mutagenic potency depended on the alkyl group, decreasing in the following order: methyl greater than ethyl greater than propyl, butyl. A similar order was observed for cytotoxicity. Mutagenic and cytotoxic potencies of these alpha-hydroxy N-nitrosamines in V79 cells were well correlated not only with those of model compounds (alpha-acetoxy and alpha-hydroperoxy N-nitrosamines), but also with their alkylating ability, measured by alkylation of thiophenol. The mutagenic activity of the alpha-hydroxy N-nitrosamines in V79 cells was shown to be parallel to that in Salmonella typhimurium TA1535 and to that of N-nitrosodialkylamines in V79 cells, after metabolic activation by rat hepatocytes. The results obtained here further support the conclusion that the alpha-hydroxy N-nitrosamine is the active species in the metabolic activation of carcinogenic and mutagenic N-nitrosodialkylamines.

Animals↗
PubMed1984

Acute and chronic hypotensive effects of nifedipine and niludipine in hypertensive patients with chronic renal failure.

The present study was aimed to evaluate the acute and chronic hypotensive effects of nifedipine (Bay a 1040, Adalat) and niludipine (Bay a 7168) in hypertensive patients with chronic renal failure. 1. The decrease of blood pressure lasted for at least 3 h and maximum decrement was achieved in 60 min (26% decrement, p less than 0.05) after oral administration of nifedipine (10 mg). On the other hand, niludipine (20 mg) caused decrease of blood pressure for at least 4 h and attained maximum decrement in 90 min (13% decrement, p less than 0.05) after oral administration. 2. In chronic studies of both drugs, the maximum decrease of blood pressure (p less than 0.05) was attained after one week and lasted at least 4 weeks. There were no significant changes of pulse rate, body weight and urine volume in both nifedipine and niludipine groups. 3. Nifedipine caused great diurnal or day-to-day fluctuations of blood pressures after chronic administrations. On the other hand niludipine did not cause any significant fluctuations. Any serious complications could not be seen during these studies. In conclusion, these results provide clinical evidence that niludipine could be usefused great diurnal or day-to-day fluctuations of blood pressures after chronic administrations. On the other hand niludipine did not cause any significant fluctuations. Any serious complications could not be seen during these studies. In conclusion, these results provide clinical evidence that niludipine could be useful for treatment of hypertension associated with chronic renal failure. Results also suggest that the optimal efficacy of nifedipine and niludipine in part depends on the specific clinical situation at hand. For example, nifedipine seems to be the drug of choice in hypertensive emergencies when there is a need for rapid lowering of blood pressure.

Adolescent↗
PubMed1984

[Comparative study of two-dimensional echocardiography and left ventriculography in detecting interventricular septal asynergy in myocardial infarction].

We investigated the reasons for discrepancies between two-dimensional echocardiography (2DE) and left ventriculography (LVG) in detecting interventricular septal asynergy in anterior or inferior myocardial infarction. Twenty-six patients with anterior infarctions due to proximal lesions of the left anterior descending artery and 20 patients with inferior infarctions due to proximal lesions of the right coronary artery were studied by 2DE and LVG. A 2DE long-axis view, a short-axis view at the papillary muscle level, an apical four-chamber view (AP-4CV), and right and left anterior oblique left ventriculograms (RAO-LVG and LAO-LVG) were recorded. The interventricular septum (IVS) on LAO 60 degree-LVG was divided into the basal and apical portions. 2DE and LVG were independently evaluated individually by the same readers, and the interventricular septal asynergy was classified as hypokinesis, akinesis and dyskinesis. Anterior infarction About 80% of the patients with akinesis of the apical third of the IVS in a long-axis view or of the apical half of the IVS in an AP-4CV were assessed as having akinesis of the entire septum by LAO-LVG. Inferior infarction Asynergy was echocardiographically detected in the posterior IVS in a short-axis view at the papillary muscle level. LAO-LVG showed asynergy in the apical third of the posterolateral segment (segment 7) in all cases and akinesis in the apical IVS in six of 20 patients (30%). In conclusion, the extent of asynergy of the IVS in anterior infarction is overestimated by LAO-LVG compared to 2DE, and asynergy of the apex assessed by LAO-LVG in inferior infarction will correspond to that of the inferior segment by 2DE. This discrepancy is attributed to the different planes between a long-axis view and an LVG projection. We conclude both LVG and 2DE are mandatory for estimating accurately the extent of asynergy in the infarcted IVS.

Echocardiography↗
PubMed1984

[Correlation between left ventricular wall thickness and the depth of negative T waves in apical hypertrophic cardiomyopathy].

Electrocardiographic features of apical hypertrophic cardiomyopathy are high QRS voltage and giant negative T waves greater than 10 mm in left precordial leads. We analyzed thirty patients with apical hypertrophic cardiomyopathy to clarify the correlation between left ventricular (LV) wall thickness and the depth of negative T waves. LV anterior wall thickness was measured by the left ventriculogram (LVG) in the RAO projection. LV posterior wall and septal thickness were measured by echocardiograms recorded from the left sternal border. THA and THM were defined as apical thickness and mid ventricular wall thickness, respectively. The results were as follows: LVG disclosed that the depth of negative T waves in apical hypertrophic cardiomyopathy was significantly related to the absolute thickness of apical segment itself rather than the difference in the distribution of thickness from the basal to apical segment of the left ventricle. This results support the clinical observation that giant negative T waves in some cases are associated with diffuse hypertrophy of the LV without a spade like configuration in LVG. Results of the echocardiographic analysis, however, revealed that the depth of negative T waves had no relation to the distribution of left ventricular hypertrophy. This is partly because of unsatisfied and difficult recordings and measurements of the true LV apical segment by echocardiography. The presence of both high QRS voltage and giant negative T waves is indispensable for the diagnosis of apical hypertrophy.

Cardiomyopathy, Hypertrophic↗
PubMed1984

Macromolecular and cell cycle effects of different classes of agents inducing the maturation of human myeloblastic leukemia (ML-1) cells.

The effect of various classes of differentiation-inducing agents on macromolecular synthesis was studied in a human myeloblastic leukemia cell line (ML-1). Antineoplastic drugs such as 1-beta-D-arabinofuranosylcytosine, daunorubicin, and actinomycin D caused early inhibition of DNA synthesis, which generally preceded the accrual of differentiation markers. In contrast, retinoic acid and conditioned medium from mitogen-stimulated leukocytes caused a delayed decline in DNA synthesis, which accompanied the appearance of maturing morphology. With 12-O-tetradecanoylphorbol-13-acetate, the decline in DNA synthesis was temporally linked to the onset of maturation, and this agent evidenced some properties of both the antineoplastic agents and the more physiological inducers, retinoic acid and conditioned medium. Antineoplastic agents and conditioned medium, when applied simultaneously, induced differentiation in an additive or synergistic manner, simulating the effects of 12-O-tetradecanoylphorbol-13-acetate. RNA and protein synthesis continued during maturation induced with all these agents, although a partial reduction in RNA synthesis was observed at later time points (greater than or equal to 24 hr). Agents incapable of inducing differentiation, such as cordycepin and cycloheximide, were characterized by a lack of sustained inhibition of DNA synthesis and/or by early (3 hr) inhibition of RNA or protein synthesis. The decline in DNA synthesis caused by the inducing agents was accompanied by decreased cell cycle progression, cells accumulating largely in G1 phase. With daunorubicin and actinomycin D, block of the G1-S transition was evident at 24 hr, whereas with conditioned medium and retinoic acid, accumulation in G1 occurred in a progressive fashion, greater than 77% of cells residing in this phase on Day 6. Maximal inducing doses of 12-O-tetradecanoylphorbol-13-acetate (greater than 80% differentiation) caused an accumulation of cells in G1, as well as an accumulation of cells with a G2-M-phase DNA content (approximately 40%). These observations indicate that early inhibition of DNA synthesis, with sparing of RNA and protein synthesis, is characteristic of the differentiation-inducing antineoplastic drugs examined. These agents may induce differentiation by inhibition of the proliferation path, whereas conditioned medium and retinoic acid may act by the stimulation of differentiation paths. Differentiation can be enhanced by the simultaneous application of agents targeting both of these paths.

Cell Cycle↗
PubMed1984

Changes in biliary and fecal bile acids in mice after treatments with diosgenin and beta-sitosterol.

Diosgenin and beta-sitosterol (1% in diet) were administered to CRJ:CD-1 male mice for 15 days, in order to examine the changes in bile acid metabolism. There were some differences between diosgenin and beta-sitosterol in their effects on diet intake, liver weight, and plasma cholesterol level. However, both phytosterols caused no statistically significant changes in body weight gain, decreased cholesterol absorption to about one-third that observed in control mice, decreased liver cholesterol level, increased fecal excretion of cholesterol, and decreased fecal excretion of bile acids. Most of the increase in fecal excretion of cholesterol occurred 2 days after the start of feeding of phytosterols and gradually declined thereafter, but the levels on day 15 were nevertheless higher than those in the control mice. The fecal excretion of bile acids decreased progressively after the treatment with phytosterols. The decrease of bile acid derived from chenodeoxycholic acid was more predominant than the decrease of those derived from cholic acid, resulting in an increase of the cholic acid/chenodeoxycholic acid ratio. The biliary cholesterol, phospholipid, and bile acid mole % ratios and the lithogenic index were not changed, but the percentages of cholic acid and its related bile acids (the cholic acid group) to the total bile acids increased and those of the chenodeoxycholic acid group decreased after the treatments. The pool size of bile acids decreased in the mice given diosgenin but not in those given beta-sitosterol. Distribution of bile acids between the gallbladder and intestine was not altered by either phytosterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

[Clinical effect of human lymphoblastoid interferon in patients with multiple myeloma].

Five patients with multiple myeloma were treated with human lymphoblastoid interferon (HLBI). HLBI, 3 X 10(6) IU/day, was administered daily for more than two weeks by intramuscular injection. Out of four evaluable patients, a minor response was obtained in 3 patients. In these responders, one patient developed pleural effusion due to the infiltration of myeloma cells during the administration of HLBI, and drug resistance was observed in another patient during the re-administration of HLBI. Therefore, out of six evaluable courses, a minor response was obtained in 3 courses of HLBI treatment. No severe side effects were observed. Thrombocytopenia, general malaise, liver dysfunction and anorexia were the main reasons for discontinuation of HLBI administration. On the basis of the preliminary study, it is concluded that HLBI is worth trying in the management of refractory multiple myeloma.

Anorexia↗
PubMed1983

[R 1881 binding receptor and DHT concentrations in prostatic cytosol].

R 1881 binding receptor and DHT concentrations in human prostatic cytosol were assayed in surgically removed prostatic tissues of benign prostatic hyperplasia (BPH) and of the normal prostate. The normal prostates were obtained from totally cystectomized male patients with bladder cancer. Cytosols were incubated with 0.25--8.0 nM (6 points) of 3H-R 1881 in the presence or absence of excess radioinert R 1881 at 4 degrees C for 20 hours, thereafter treated with 0.5% dextran coated charcoal. Specific bindings were analysed in the form of scatchard plot analysis. Cytosol DHT levels were determined by radioimmunoassay reported previously. Steroid specificity studies revealed that R 1881 binding receptor was inhibited not only by androgens but also by progesterone, however, an addition of 1000 fold excess triamcinolone acetonide (TCA) reduced the inhibition by progesterone. As R 1881-receptor complex was eluted at the void volume of sephacryl S-200 chromatography, the receptor was considered to be 8-9S protein. Cytosol DHT levels were 35.5 +/- 13.6 pg/mg cytosol protein in BPH and 18.9 +/- 7.1 pg/mg protein in the normal prostates, showing a significantly higher value in the former (p less than 0.01). Kd and NBS of R 1881 receptor in BPH were 0.73 +/- 0.21 nM and 30.1 +/- 9.0 fmol/mg cytosol protein and those in normal prostate were 0.68 +/- 0.28 nM, 10.2 +/- 4.2 fmol/mg protein, respectively. NBS were also higher in BPH compared to the normal prostate (p less than 0.001). Moreover, DHT levels (y) and NBS (x) showed a significant correlation (y = 0.631 X + 15.764, r = 0.506).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1983

Differential ability of mitogen-stimulated human leukocyte-conditioned media to induce Fc receptors in human leukemia cells.

The ability of mitogen-stimulated human leukocyte-conditioned media (M-CM) to induce the in vitro differentiation of various human leukemic cell lines was evaluated by measuring the appearance of Fc receptors (FcR) through their ability to form EA rosettes. Only cells of myeloid lineage were induced by M-CM to express FcR; T-, and B-, and non-T/non-B cells failed to respond. As determined with ML-1, a line of human myeloblastic leukemia cells, pokeweed mitogen-conditioned medium, at concentrations of 1-10%, stimulated the expression of FcR in 70-98% of the cells within 1 day after treatment. Phytohemagglutinin-, concanavalin A-, and lipopolysaccharide-conditioned media were less active. The FcR-inducing activity was partially separated from M-CM by chromatography on Sephadex G-75. It was stable between pH 4 and 10, and lost activity at temperatures above 40 degrees C.

Cell Line↗
PubMed1983

Dysfunction of supramedullary alpha-adrenergic mechanisms following sino-aortic denervation in Kyoto Wistar rats.

Central alpha-adrenergic mechanisms of blood pressure regulation were investigated by injecting norepinephrine or bradykinin into the carotid input of the cross-circulated head preparations of normotensive Wistar Kyoto rats (WKY). Rats were divided into three groups: sham-operated (sham), carotid sinuses denervated (SD) and carotid sinuses and aortic nerves debuffered (SAD). Norepinephrine, 5 micrograms, produced vasodepression in all rats, accompanied by corresponding decreases in sympathetic nerve activity recorded in some rats. Magnitude of vasodepression was largest in SAD rats. In sham rats, bradykinin, 1 micrograms, produced a biphasic response: initial vasodepression followed by a sustained pressor phase. This was accompanied by corresponding changes in peripheral sympathetic nerve activity recorded in some rats. In both SAD and SD rats bradykinin-induced vasodepression was abolished, while the magnitude of the pressor phase became more prominent. The increase in the pressor phase was greater in SAD than in SD rats. In similar studies of spontaneously hypertensive rats (SHR), responses to both alpha-adrenergic agonist and bradykinin are augmented, suggesting a dysfunction of hypothalamic alpha-adrenergic mechanisms. Since in the present study it has been shown that sino-aortic denervation produces effects similar to those seen in SHR, dysfunction of buffer nerves may account for the deficient central alpha-adrenergic mechanisms in SHR.

Animals↗