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Biomedical subjects

T Takano

Publications and source records attributed to T Takano.

At least 469 records · Page 26Linked to original sources
PubMed1991

Family involvement for improving the abstinence rate in the rehabilitation process of female alcoholics.

We investigated the effect of family involvement on abstention of 90 female alcoholics in recovery processes by multivariate analysis. The abstinence rate of the family-involved group was significantly higher than that of the group not involved (p less than .05). The logistic regression model in which family involvement, age, marital status, eligibility for welfare assistance, and history of previous psychiatric inpatient care were used as independent variables indicated that family involvement was the only variable having a significant effect on abstention (p less than .05).

Adult↗
PubMed1991

Platelet adhesion to a biomimetic prosthesis prepared from canine arterial wall.

A biomimetic prosthesis was prepared from canine arterial wall by extraction with 70% formic acid. Under these conditions, the arterial architecture consisting of elastic lamella was conserved and the tensile strength was retained. Attachment of 51Cr-endothelial cells to the surface of the prosthesis was enhanced in the presence of collagen (50 micrograms/ml), fibronectin (20 micrograms/ml), and fibrinogen (500 micrograms/ml). These agents also enhanced the adhesion of 51Cr-platelets. However, preattachment of endothelial cells to prostheses prevented platelet adhesion.

Acetates↗
PubMed1991

[Acute hemodynamic effect of cigarette smoking and its relationship with nicotine content].

We studied the acute effects of cigarette smoking on the cardiovascular system, especially regarding nicotine-related hemodynamic effects using cigarettes with low and high nicotine contents. 40 healthy men who were habitual smokers were divided into two groups: 20 subjects smoked cigarettes of low nicotine content [0.4 mg/cigarette; group 1 (G1)] and another 20 tested cigarettes containing high nicotine [2 mg/cigarette; group 2 (G2)]. All of the subjects were requested to abstain from cigarette smoking for at least 12 hours prior to study, and to rest in the supine position for 30 minutes just prior to the test. They smoked two consecutive cigarettes for 10 minutes, inhaling every 30 seconds by drawing on the cigarette for two seconds, and holding the smoke for three seconds before exhaling. Blood pressure (BP), heart rate (HR) and cardiac output (CO) were measured and blood samples were taken before, and 5, 10 and 30 minutes after the start of smoking. Smoking with a high nicotine content (G2) produced a significant increase in both systolic and diastolic BP (124 +/- 14/78 +/- 8----138 +/- 21/90 +/- 10 mm Hg), but no significant changes in BP were observed in the low nicotine group. HR and CO increased predominantly in both groups (HR: G1; 62 +/- 7----66 +/- 7, G2; 64 +/- 7----76 +/- 9/min, CO: G1; 4.85 +/- 1.36----5.31 +/- 1.37, G2; 4.95 +/- 1.58----5.63 +/- 2.01 l/min), but the present increases were significantly less in G1 than in G2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

[Modification of the smoking-induced hemodynamic effect by nifedipine].

Effects of nifedipine, a Ca(++)-channel blocker, on smoking-induced hemodynamic changes were studied in 35 habitual male smokers. They were divided into three groups: 20 healthy persons (G1), 11 patients with essential hypertension (G2) who were under nifedipine treatment, and 4 patients (G3) with essential hypertension but who were receiving no medication. After abstaining from smoking for more than 12 hours, they smoked, within 10 minutes, two filtered cigarettes each containing 2 mg of nicotine. Hemodynamic parameters were measured and blood samples were taken before and 5, 10, and 30 minutes after beginning to smoke. In each group, smoking produced significant increases in blood pressure, heart rate and cardiac output. Plasma adrenaline increased significantly in 3 groups, and tended to be highest in G2. Plasma noradrenaline was the highest in G2 predominantly, but did not change after smoking. These results indicate that a smoking-induced hyperdynamic state including vasoconstriction due to catecholamine release might not depend on the calcium channel which is blocked by nifedipine, and the reflex activation of the sympathetic nerve system would develop in the presence of nifedipine.

Calcium Channel Blockers↗
PubMed1990

Monoclonal antibody EMR1a/212D recognizing site of deposition of extracellular lipid in atherosclerosis. Isolation and characterization of a cDNA clone for the antigen.

We have isolated from a rabbit liver cDNA library, clones coding for the 66-kDa glycoprotein (GP66) characterized previously by EMR1a/212D monoclonal antibody (Nakagami, K., Shimasaki, O., Sato, R., Komine, Y., Ohkuma, S. and Takano, T. (1989) Am. J. Pathol. 135, 93-100), which recognizes the extracellular regions of atherosclerotic arterial wall. The clone spans the sequence coding for the entire GP66 (456 amino acids) and 19 amino acids of signal peptide. GP66 deduced from nucleotide sequence contained an Arg-Gly-Asp cell attachment sequence and had a 76% amino acid sequence homology with human vitronectin. Furthermore, EMR1a/212D recognized rabbit vitronectin purified by heparin-affinity chromatography. RNA blot hybridization detected one transcript of the same size in normal and Watanabe-heritable hyperlipidemic rabbit liver. The levels of plasma GP66 and liver GP66 mRNA were not altered, whereas 9-fold greater accumulation of GP66 was observed in thoracic aorta of Watanabe-heritable hyperlipidemic rabbit. These results suggest that GP66 is rabbit vitronectin and that it is vitronectin which selectively accumulates in thoracic aorta with the development of atherosclerosis.

Amino Acid Sequence↗
PubMed1990

Degradation of newly synthesized apolipoprotein B-100 in a pre-Golgi compartment.

The synthesis and secretion of apolipoprotein (apo) B-100 have been studied in a human hepatoblastoma cell line, the Hep G2 cells. Pulse-chase analysis showed that apoB-100 was not quantitatively recovered in the culture medium. To reveal the intracellular degradation of apoB-100 prior to secretion, cells were incubated with 1 microgram/ml Brefeldin A (BFA) which impeded protein transport from the endoplasmic reticulum (ER) to the Golgi apparatus and the fate of apoB-100 retained in the cells was traced at 37 degrees C. A significant amount of intracellular apoB-100 (40-60%/h) was degraded during the chase period, whereas apoA-1 remained intact. ApoB-100 degradation was temperature dependent, no degradation was observed below 20 degrees C. This degradation process was not inhibited by chloroquine, leupeptin, pepstatin, and chymostatin, suggesting that lysosomal proteases were not involved and that apoB-100 was degraded in a pre-Golgi compartment which is either part of, or closely related to, the ER. Preincubation of cells with low density lipoproteins (LDL) induced a 22-32% increase in the degradation of apoB-100. This result raised the possibility that secretion of apoB-100 might be regulated through the intracellular degradation of apoB-100. These results suggest the existence of the degradation pathway for apoB-100 in a pre-Golgi compartment and an unique regulatory mechanism for apoB-100 secretion.

Anti-Bacterial Agents↗
PubMed1990

Circadian variations in trichloroethylene toxicity under a 12:12 hr light-dark cycle and their alterations under constant darkness in rats.

In order to investigate the circadian variations in acute toxicity of trichloroethylene (TRI), TRI (1.2 g/kg weight) or saline was injected intraperitoneally in a total of 88 male Wistar rats at four circadian stages (03.00, 09.00, 15.00, and 21.00:hr.min) under two different lighting regimens of a 12:12 hr light-dark cycle (LD; light from 06.00 to 18.00) and of constant darkness (DD). Circadian variations in TRI toxicity were confirmed in both LD and DD. The toxicity of TRI evaluated by the increase in glutamic-pyruvate transaminase activity (GPT) was greatest when injected at 09.00 in LD while at 21.00 in DD. The increases in blood urea nitrogen, serum total cholesterol and triglyceride concentrations reached peaks when injected at 09.00 in LD and 03.00 in DD. The circadian variations in serum trichloroethanol concentration were very similar to those in GPT in both LD and DD, showing a significant correlation (p less than 0.05). The present study revealed that circadian variations in TRI toxicity existed in LD and that these variations persisted in a free-running condition. The peak phase of TRI toxicity was located in a trough phase (09.00) in LD and in a peak phase (21.00 or 03.00) in DD of temperature rhythm. Thus, the phase relationship changed in DD, showing a desynchronization between TRI toxicity rhythm and temperature rhythm, which is an unusual phenomenon. This means that an unexpected potentiation of TRI toxicity during active phase which is not a critical phase in a well-synchronized state could occur in a free-running condition.

Animals↗
PubMed1990

The effect of HMG-CoA reductase inhibitor (CS-514) on the synthesis and secretion of apolipoproteins B and A-1 in the human hepatoblastoma Hep G2.

Human hepaotoblastoma cells (Hep G2) were cultured with a competitive inhibitor of HMG-CoA reductase, CS-514. The synthesis of cholesterol was markedly inhibited after 1 h preincubation with CS-514. The synthesis and secretion of apolipoprotein (apo) B and A-1, however, were not affected. A long-term incubation (21-24 h) of cells with CS-514 did not change apo B synthesis and secretion, although a slight depression of apo A-1 synthesis was observed. Hep G2 cells were found to secrete LDL- and HDL-like lipoproteins which were poor in cholesterol when cells were incubated with the drug. These results suggest that the modulation of cholesterol synthesis affects neither the synthesis and secretion of apo B and A-1 nor the formation of lipoproteins.

Apolipoprotein A-I↗
PubMed1990

Structure of (R)-tetrahydro-2-furancarboxylic acid monohydrate.

C5H10O4, Mr = 134.31, monoclinic, P2(1), a = 11.670 (2), b = 6.177 (3), c = 10.704 (2) A, beta = 115.11 (2) degrees, V = 698.7 (4) A3, Z = 4, Dm = 1.26, Dx = 1.28 g cm-3, Cu K alpha, lambda = 1.54178 A, mu = 9.69 cm-1, F(000) = 288, room temperature, R = 0.046 for 1047 reflections with [Fo[ greater than 3 sigma(F). There are two independent molecules of the title compound in the crystal. No twofold symmetry is observed in the tetrahydrofuran rings. Hydrogen bonds between water molecules and carboxylic acid groups stabilize the crystal structure.

Furans↗
PubMed1990

A selected ion monitoring method for quantifying simvastatin and its acid form in human plasma, using the ferroceneboronate derivative.

Simvastatin, a pro-drug lactone, forms the open carboxylic acid as a major metabolite that inhibits the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Simvastatin and the acid in plasma were quantified by a gas chromatography/mass spectrometry/selected ion monitoring (GC/MS/SIM) method. These drugs were separated by solid-phase extraction and independently converted into a 1,3-diol-type compound. This compound reacted with ferroceneboronic acid to yield the cyclic boronate that gave satisfactory mass spectra for GC/MS/SIM measurements. The serum was dominated by the molecular ion appearing as the base peak, thereby leading to a sensitive and selective assay. The calibration curves for simvastatin and the acid were linear in their concentration range of 0.1-10 ng ml-1, where the values of coefficient of variation for both drugs were below 8%, except for the value of 11% for simvastatin at a concentration of 0.1 ng ml-1. The quantification limit for both drugs was 0.1 ng ml-1 on the basis of a signal-to-noise ratio of 4:1.

Ferrous Compounds↗
PubMed1990

Osteoarthrosis induced by intra-articular hydrogen peroxide injection and running load.

Osteoarthrosis of the rat knee joint was induced successfully by intra-articular injection of 2% hydrogen peroxide (H2O2) and running load. In the group receiving two injections of physiological saline with running load, no histological osteoarthrotic knees were developed up to 8 weeks after the injection. In the group receiving two 2% H2O2 injections and running load, advanced osteoarthrosis occurred in all knees 8 weeks after the first injection, and the Mankin's score of osteoarthrotic knees appeared to be higher than the group receiving two 2% H2O2 injections without running load (p less than 0.004, Kruskal-Wallis H test). In the rats receiving a single 2% H2O2 injection with running load and a vitamin E-enriched diet, the inhibitory effect of vitamin E on the development of osteoarthrosis was statistically significant compared to the regular diet group (p less than 0.05, Wilcoxon rank test).

Animals↗
PubMed1990

Transcellular transport of angiotensin II through a cultured arterial endothelial monolayer.

We have studied the mechanisms of angiotensin II (A-II) transport through a cultured arterial endothelial cell monolayer. The transport of 125I-labeled A-II was inhibited by excess unlabeled A-II (50 microM) and [Sar1, Ile8]-A-II (50 microM), but was not inhibited by bradykinin (50 microM). The transport process was shown to be temperature dependent and was inhibited by 10 mM NaN3 plus 50 mM 2-deoxyglucose. Monensin (50 microM), an inhibitor of endocytotic trafficking, reduced the rate of transport of 125I-A-II. It is also shown that the specific pathway for A-II transport was unidirectional from the apical to the basolateral surface of the endothelial cell monolayer.

Adenosine Triphosphate↗
PubMed1990

Peroxidized lipoproteins recognized by a new monoclonal antibody (DLR1a/104G) in atherosclerotic lesions.

Monoclonal DLR1a/104G antibody, which recognizes peroxidized lipoproteins, was raised. Mice were immunized with the float-up fraction of the atherosclerotic arterial homogenate from WHHL rabbits. Sensitized spleen cells were fused with myeloma cells (3P/U1). Hybridoma clones were selected using peroxidized LDL prepared by CuSO4-catalyzed peroxidation and native LDL as positive and negative standards, respectively. The monoclonal DLR1a/104G antibody was highly reactive with peroxidized LDL, slightly with LDL modified with malondialdehyde, but not significantly with acetyl- or native LDL. The antigenicity in the case of peroxidized LDL did not decrease on extraction with hexane/isopropanol (3:2). The antigenicity coincided with the fluorescence (E350, F430) of the protein fraction of LDL peroxidized with CuSO4. These results suggest that an antigenic determinant exists in atherosclerotic lesions, which is the same as that for lipoproteins peroxidized with CuSO4.

Animals↗
PubMed1990

Atherosclerosis and molecular pathology: mechanisms of cholesteryl ester accumulation in foam cells and extracellular space of atherosclerotic lesions.

This article reviews aspects of the molecular pathology of cholesteryl ester accumulation in atherosclerotic lesions. 1. Transcytosis of lipoproteins through cultured endothelial monolayer. 2. Transformation to foam cell from macrophage. 3. Cholesteryl ester deposition in the extracellular space of atherosclerotic lesions. We also discuss the development and use of novel monoclonal antibodies recognizing atherosclerotic lesions and peroxidized lipoproteins prepared from atherosclerotic lesions.

Animals↗
PubMed1990

Preparations of 5-alkylmethylidene-3-carboxymethylrhodanine derivatives and their aldose reductase inhibitory activity.

Reactions of 3-carboxymethylrhodanine (1) with aldehydes (2a-u) afforded stereoselectively the 5-mono-alkylmethylidene-3-carboxymethylrhodanines (3a-u). The configuration of the 5-monoalkylmethylidene-3-carboxymethylrhodanine (3k) were examined by X-ray structure analysis and confirmed to be Z-configuration. The stereoselective reaction path was discussed. Several 5-dialkylmethylidene-3-carboxymethylrhodanines (15a-f) and alkylamino derivatives of 3-carboxymethylrhodanines (18a-o) were also prepared. These products were evaluated for aldose reductase-inhibitory potency and half of them exhibited valuable inhibitory potency.

Aldehyde Reductase↗
PubMed1990

Localization of chromogranin A-immunoreactivity in bovine gastrointestinal endocrine cells with special reference to Grimelius silver stain.

Immunohistochemical studies of the gastrointestinal tract were carried out to characterize the cells exhibiting immunoreactivity for chromogranin A (CGA), a glycosylated protein primarily found in secretory granules of the adrenal medulla. Double immunostaining for gastrointestinal hormones and CGA revealed that in the bovine gastrointestinal tract CGA immunoreactivity occurs in mucosal epithelial cells containing gastrin, glucagon, substance P or motilin, but not in those containing somatostatin. Combined staining with anti-CGA serum and Grimelius' silver demonstrated frequent association of the two stains in a variety of endocrine cells. However, intracellular distribution of the two stains was different: CGA-immunoreactivity was detected in both supra- and infranuclear cytoplasm, whereas Grimelius' silver was mostly localized in the infranuclear region. These results suggest that CGA is the target of Grimelius' silver, as postulated recently (Rindi et al., 1986), but that some subcellular structure-related modification of molecules such as sialation is necessary for the positive Grimelius reaction.

Animals↗