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Biomedical subjects

T Takeda

Publications and source records attributed to T Takeda.

At least 955 records · Page 53Linked to original sources
PubMed1989

Mother's attitudes towards the mass screening of neuroblastoma.

Two hundred and two mothers whose infants participated in mass screening of neuroblastoma in Sapporo City, and 200 mothers whose infants did not, were interviewed about their attitudes towards the mass screening. Only a few non-participants (3.5%) thought the mass screening was unnecessary. More than half of non-participations (56.0%) were due to mothers' forgetfulness or to loss of the "Neuroblastoma Screening Examination Set" during the two months' interval between the delivery of the set and the sample submission. Mailing of the set at six months for the purpose of eliminating this interval would greatly reduce such neglect of the mass screening. On the other hand, not many infants would participate in re-screening for detection of false negative cases, since the percentage of mothers who were willing to make their children take part in re-screening for a fee of 1,000 yen (about 7 U.S. dollars, which would be administratively necessary) was less than 60%.

Attitude to Health↗
PubMed1989

Possible involvement of interferon alfa in the pathogenesis of fever in systemic lupus erythematosus.

Serum concentrations of interferon alfa, interleukin 1, and tumour necrosis factor alpha were measured in 25 untreated patients with systemic lupus erythematosus (SLE). A close correlation was found between serum concentrations of interferon alfa and the degree of fever, while no significant correlations were found between fever and interleukin 1 or tumour necrosis factor alpha. These results suggest the possible involvement of interferon alfa in the pathogenesis of fever in SLE.

Fever↗
PubMed1989

Putative mechanisms involved in excitatory and inhibitory effects of somatostatin on intestinal motility.

The mechanism of action of somatostatin on the motility of intestine was examined in the entire preparation and the longitudinal muscle attached with Auerbach's plexus (LA) preparation of guinea pig ileum, in relation to the cholinergic neuron and gamma-aminobutyric acid (GABA)ergic neuron. Somatostatin produced a transient potentiation of electrical stimulation-induced twitch contractions followed by an inhibition. The excitatory effect of somatostatin was associated with an increase in the release of [3H]acetylcholine (ACh) from the preparations preloaded with [3H]choline. Bicuculline, a GABAA antagonist, inhibited the somatostatin-induced excitatory effect. Somatostatin inhibited the electrical stimulation-induced twitch contraction and release of [3H]ACh, and the inhibition was greater in the entire preparation than in the LA. Phaclofen, a GABAB antagonist, prevented the inhibitory effects of somatostatin. Somatostatin induced a Ca2+ -dependent, tetrodotoxin-sensitive release of [3H]GABA from the preparations preloaded with [3H]GABA. Therefore somatostatin exerts excitatory and inhibitory effects on the cholinergic neuron due to the stimulation of the GABAergic neuron, and the motility of the intestine is regulated.

Acetylcholine↗
PubMed1989

Glucocorticoids and dopamine-1 receptors on vascular smooth muscle cells.

The effect of glucocorticoids on the dopamine (DA)-mediated cyclic adenosine monophosphate (cAMP) by intact vascular smooth muscle cells (VSMC) was studied in rats. Cultured VSMC were obtained from renal arteries of 14-week-old Wistar-Kyoto rats by explant method. Micromolar concentrations of dexamethasone (DEX) pretreatment for 48 hours potentiated DA-mediated response without any change of affinity constant. However, micromolar concentrations of aldosterone pretreatment for 48 hours had almost no effect on DA-mediated response. The DEX-induced facilitation began at 6 hours and reached maximum at 24 hours after DEX administration in a dose-dependent manner. Inhibitors of protein and RNA synthesis blocked this glucocorticoid effect. The basal activity of adenylate cyclase in DEX-treated cells was twofold higher than that in control cells. Treatment of VSMC with DEX increased cholera toxin-stimulated and forskolin-stimulated adenylate cyclase activity. However, pertussis toxin treatment did not augment or reduce the effect of DEX treatment. These results suggest that glucocorticoids increase DA-mediated cAMP formation by VSMC through glucocorticoid type II receptors and the induction of protein synthesis and that the activation of the catalytic unit may play some role in this facilitation.

Adenylyl Cyclases↗
PubMed1989

Evaluation of myocardial perfusion abnormality by profile analysis for digital subtraction angiogram.

For quantitative estimation of ischemia, ECG-synchronized digital subtraction angiography was performed for selective coronary arteriography. The authors obtained sequential myocardial perfusion images at the arterial, capillary, and venous phases. Profile densitometry was performed along the cross section perpendicular to the long axis of the left ventricle to assess regional myocardial perfusion at the capillary phase quantitatively. By this densitometry, the volumes of vascular bed perfused by the left coronary artery could be estimated, and further, nontransmural myocardial infarction could be differentiated from transmural myocardial infarction through the profile of its density curve. This method appears to be useful for the analysis of myocardial perfusion of ischemic heart disease.

Adult↗
PubMed1989

Cases of neuroblastoma missed by the mass screening programs.

Twenty-two reported cases of neuroblastoma missed by the mass screening programs were reviewed (six cases in Sapporo City where a quantitative measurement for both vanillylmandelic acid (VMA) and homovanillic acid (HVA) is used and 16 cases in the districts of qualitative judgment only for VMA), and some potential factors for missing a patient were discussed. Most of the 22 patients were diagnosed over 12 mo and had advanced clinical stages at diagnosis (III or IV). Of the 17 cases whose outcome in prognosis was available, nine cases were dead and only three cases were alive without any trace of tumor. Fluctuation in the amounts of urinary VMA and HVA seemed to be one of the causes for missing a patient, especially with a small tumor. The comparison about tumor wt, VMA and HVA amounts, and clinical stage between the 22 true positive cases in Sapporo City and 46 ones in the districts of qualitative methods, and the difference in detection rate between the two groups suggested that the qualitative methods missed more patients with a small tumor. The patients who had abnormally high amounts of HVA with low amounts of VMA accounted for a fairly large part of the missed cases in Sapporo City as well as in the districts of qualitative methods. To the contrary, no patient of this type was found even among the 22 true positive cases in Sapporo City.

Child, Preschool↗
PubMed1989

Cytosolic 3,5,3'-triiodo-L-thyronine (T3)-binding protein (CTBP) regulation of nuclear T3 binding: evidence for the presence of T3-CTBP complex-binding sites in nuclei.

Effect of cytosolic 3,5,3'-triiodo-L-thyronine (T3)-binding protein (CTBP) on [125I]T3 binding to nuclei was investigated in vitro. CTBP and nuclei were prepared from rat kidney. CTBP was inactivated by incubating with charcoal and activated by incubating with NADPH or with NADP and dithiothreitol. Two complexes of CTBP and T3 [CTBP-T3(NADPH) and CTBP-T3(NADP)] were separately prepared, and the functions of these complexes were estimated. [125I]T3 binding to nuclei was not influenced by the inactive form of CTBP. NADP or NADPH alone did not modify [125I]T3 binding to the nuclei. However, the binding was markedly inhibited by NADPH in the presence of the inactive form of CTBP, but it was not inhibited by NADP in the presence of the inactive form of CTBP. The ability of nuclei to bind [125I]T3 was markedly diminished by pretreatment of the nuclei with 10(-8) M unlabeled T3. The diminished activity was not modified by adding NADPH or NADP. However, [125I]T3 bound to these nuclei in the presence of NADP and the inactive form of CTBP. Binding of [125I]T3 to these nuclei was not observed in the presence of NADPH and the inactive form of CTBP. When the nuclei that had previously been saturated with 10(-6) M unlabeled T3 were incubated with [125I]T3-CTBP(NADP) complex, radioactivity bound to the nuclei. The binding of radioactivity, however, was not observed when these nuclei were incubated with [125I]T3. The [125I]T3-CTBP(NADPH) complex did not bind to these nuclei. When the nuclei that had previously been treated with T3-CTBP(NADP) complex were incubated with [125I]T3, radioactivity bound to the nuclei. The binding of radioactivity, however, was not observed when these nuclei were incubated with [125I] T3-CTBP(NADP) complex. The [125I]T3-CTBP(NADPH) complex did not bind to these nuclei. These results suggested that 1) CTBP activated by NADP plays a role as a carrier protein for T3 from cytoplasm to nucleus; 2) there are binding sites for T3-CTBP(NADP) complex in rat kidney nuclei; and 3) these binding sites are different from nuclear T3 receptors.

Animals↗
PubMed1989

Pharmacological characterization of the voltage-dependent calcium channel of pancreatic B-cell.

Pharmacological characteristics of the voltage-dependent calcium channel (VDCC) of the pancreatic B-cell were studied using omega-conotoxin (omega CgTX) and dihydropyridine (DHP) calcium channel blockers. High glucose and potassium (K+) depolarization were employed as the stimulant of insulin release. omega CgTX (greater than 50 nM), a blocker of neural, but not muscular, Ca2+ channels, partially blocked (27%) the second, but not the first, phase of glucose-induced insulin release without a significant effect on K+ depolarization-induced insulin release. The DHP Ca2+ channel blocker nifedipine inhibited both phases of glucose-induced insulin release (ED50 = 200 nM) and completely abolished both phases of response at 10 microM. In contrast, the DHP Ca2+ channel blocker only partially suppressed (75% at 10 microM) K+ depolarization-induced insulin release with an ED50 of 100 nM. We conclude that pancreatic B-cell possesses at least two classes of VDCCs; one is DHP sensitive, and the other DHP insensitive. Partial suppression of the second phase of glucose-induced insulin release by a high concentration of omega CgTX may be due to its toxic effect on the secretory machinery other than VDCC.

Animals↗
PubMed1989

The structure of nephritogenoside.

Nephritogenoside is a minor component of the basement membrane of normal animals (including humans). It is a glycopeptide with the ability to induce chronic progressive glomerulonephritis (end stage kidney) when administered as a single footpad injection, and contains a novel carbohydrate-peptide linkage. The total chemical structure was investigated. It was revealed that nephritogenoside is a simple glycopeptide composed of three glucose residues [alpha-Glc-(1----6)-beta-Glc-(1----6)-Glc] and twenty-one amino acids [1Asn-Pro-Leu-Phe-5Gly-Ile-Ala-Gly-Glu-10Asp-Gly-Pro -Thr-Gly-15Pro-Ser-Gly-Ile-Val-20Gly-21Gln], and that the glucose residues are linked alpha-N-glycosidically to the N-terminal amino acid.

Amino Acid Sequence↗
PubMed1989

[Fractional determination of bile acids bound with protein in serum by high-performance liquid chromatography using dual-column switching system].

A simple and rapid technique for the fractional determination of bile acids bound with protein in the serum was developed by using high performance liquid chromatography with a dual-column switching system. The serum samples were directly injected onto a first column (hydroxyapatite), which was initially flushed with 1 mM phosphate buffer. Serum proteins were strongly retained on a column of hydroxyapatite, but free bile acids were not retained. The bile acids were adsorbed on a second column (Serumout-25) and eluted onto a column of immobilized 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD) with an elution solvent (CH3CN-MeOH-30 mM ammonium acetate, 30:30:40, v/v/v). Reduced nicotinamideadenine dinucleotide was produced on the immobilized 3 alpha-HSD column and then determined fluorometrically. Subsequently, the hydroxyapatite column was flushed with 20 mM phosphate buffer. Bile acids bound with albumin were eluted and condensed on Serumout-25. The phosphate buffer (400 mM) was finally used for the elution of bile acids bound with globulin from the hydroxyapatite column. Each condensed bile acid was eluted onto the immobilized 3 alpha-HSD column as described above.

Bile Acids and Salts↗
PubMed1989

[Non-crystallinity determination by thermal analysis of freeze-dried cephalothin sodium].

Cephalothin sodium (CET-Na) prepared according to the conventional freeze-drying methods is known to easily develop color during storage. Since amorphous CET-Na has been reported to be markedly unstable, the color development is thought to be due to the presence of traces of CET-Na in an amorphous state observed with scanning electron microscopy. Quantitation by use of the powder X-ray diffractometry of such traces of amorphous CET-Na has proved to be of little use. Thermogravimetry (TG) and differential scanning calorimetry (DSC) have demonstrated that the freeze-dried CET-Na by the conventional methods contains three types of CET-Na: amorphous (unstable phase), quasi-crystalline (metastable phase) and crystalline (stable phase). Pyrolysis initiation temperatures of these three types of CET-Na have been demonstrated to become higher in this order. A new parameter for the evaluation of non-crystallinity of CET-Na has been introduced, in which the ratio is calculated from the data of the total weight loss observed through the pyrolysis of both amorphous and quasi-crystalline CET-Na against the total weight loss of all components during the pyrolysis of sample specimen. The ratio thus calculated is defined as "non-crystallinity". This new parameter has successfully been introduced to establish a good correlation to the degree of increasing color intensity with aging of freeze-dried CET-Na.

Calorimetry, Differential Scanning↗
PubMed1989

[Crystallization and subsequent freeze-drying of cephalothin sodium by seeding method].

Cephalothin sodium (CET-Na) in crystals can be obtained by freezing the aqueous solution and subsequent warming at a fixed temperature for facilitating crystallization prior to vacuum application for drying. The product has, however, been found to unavoidably contain traces of the amorphous CET-Na, which causes a rapid color development during storage. By using thermal analysis, differential scanning calorimetry (DSC), electric conductometry, and polarized light cryomicrographic techniques, the solubilities in water, freezing point, eutectic point, and melting behavior of CET-Na in aqueous solution were investigated. The investigation demonstrated that CET-Na in supersaturated aqueous solution is very stable, and that seeding with microcrystalline CET-Na to the supersaturated solution and subsequent cooling of the mixture till its freezing point gives neither any evidence for crystallization nor for growth of the seed crystals. The freeze-drying of CET-Na in the supersaturated solution after seeding has been demonstrated to give crystalline CET-Na containing neither of amorphous nor of quasi-crystalline form.

Cephalothin↗
PubMed1989

The complement system in the acute phase of myocardial infarction.

Although some studies suggest that complement activation is involved in the development of acute myocardial infarction, there has been little convincing evidence of a change in the complement system in patients suffering from myocardial infarction. In this study circulating levels of C3a, C3, C4 and the total hemolytic complement titer (CH50) were serially measured in 12 patients with acute myocardial infarction up to 10 days after an attack. The plasma C3a level was greatly elevated throughout the post-attack observation period. The C3, C4 and CH50 levels were significantly increased above those controls on days 8, 9 and 10 after infarction. These findings indicate that there is complement activation in patients with acute myocardial infarction, and suggest a pathogenetic role for complement activation in the development of myocardial damage after infarction.

Acute-Phase Reaction↗
PubMed1989

Effect of nifedipine on left ventricular function during exercise in patients with stable effort angina. Relation of its efficacy to the severity of coronary artery disease.

To evaluate whether the effect of nifedipine on left ventricular function relates to the severity of coronary artery disease (CAD) or not, supine graded ergometer exercise testing was performed before and after sublingual administration of 10 mg nifedipine in 24 patients with stable effort angina. To minimize the effect of nifedipine on myocardial oxygen consumption, exercise before and after nifedipine was discontinued at the same target rate pressure product. Percent (%) left ventricular ejection fraction (EF) [EF during exercise/EF at rest.100] was measured before and after nifedipine by radionuclide angiocardiography. The angiographic degree of CAD was defined by Gensini's CAD scoring as follows: severe CAD: greater than or equal to 50, moderate: less than 50 greater than 20 and mild: less than or equal to 20. After nifedipine, left ventricular function (%EF) was improved in all 6 patients with mild CAD, but was worsened in all 9 patients with severe CAD. Maximal ST segment depression during exercise was improved in 5 of 6 patients with mild CAD, while improvement was induced in 5 of 9 patients with moderate CAD and in 3 of 9 patients with severe CAD. Jeopardy of coronary collateral vessels may have an influence on the effect of nifedipine. It is suggested that the effect of nifedipine on left ventricular function is influenced by the severity of CAD when most of its effect on myocardial oxygen consumption is eliminated.

Adult↗
PubMed1989

The significance of abnormal systolic blood pressure response during supine ergometer exercise and postexercise in ischemic heart disease, studied by exercise radionuclide ventriculography.

The prognostic value of abnormal postexercise systolic blood pressure (BP) response has not been investigated. Therefore, the significance of abnormal BP response during exercise and postexercise was examined in 169 patients with ischemic heart disease subjected to supine ergometer exercise gated equilibrium radionuclide ventriculography, coronary arteriography, and follow up averaging 3.6 years. Abnormal BP response during exercise (exertional "hypotension") was defined as 1) a failure of BP to rise by at least 11 mmHg or 2) an initial rise in BP but subsequent fall by more than 10 mmHg during exercise. Abnormal BP response during postexercise (postexercise "hypertension") was defined as an increase of more than 10 mmHg above the peak exercise BP. Of 169 patients, 51 (30%) had an abnormal BP response. Four types of BP response were identified: exertional "hypotension" (group 1a, n = 11), postexercise "hypertension" (group 1b, n = 30), exertional "hypotension" with postexercise "hypertension" (group 1c, n = 10) and normal BP response (group 2, n = 118). Both average exercise duration and peak heart rate were significantly lower in groups 1a, 1b and 1c than in group 2. The severity of exercise ST-segment depression was greater in groups 1b and 1c than in group 2. However, there was no significant difference in the severity of exercise ST-segment depression between group 1a and group 2. A decline in ejection fraction occurred more frequently in groups 1b and 1c than in group 2. Patients in groups 1a, 1b and 1c had more extensive coronary artery disease (CAD) than did patients in group 2. Medically treated patients with an abnormal BP response (groups 1a, 1b and 1c) had a poorer prognosis than did those with a normal BP response (group 2). These findings suggest that an abnormal BP response during supine exercise is infrequent, but is usually associated with impaired exercise tolerance and severe CAD. An abnormal postexercise BP response is also infrequent, but is more closely associated with evidence of myocardial ischemia and global left ventricular dysfunction than exertional "hypotension". In conclusion, postexercise "hypertension" has the same value as exertional "hypotension" as a predictor of poor prognosis.

Angina Pectoris↗