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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 685 records · Page 38Linked to original sources
PubMed1994

Role of endogenous atrial natriuretic peptide on systemic and renal hemodynamics in heart failure rats.

To investigate the role of endogenous atrial natriuretic peptide (ANP) in rats with heart failure (HF), we administered HS-142-1 (HS; 3 mg/kg body wt iv), a novel nonpeptide ANP-receptor antagonist, to rats with surgically induced myocardial infarction and sham-operated rats. HF was characterized by a higher left ventricular end-diastolic pressure and higher plasma ANP concentration vs. controls. HS administration significantly reduced the plasma and urinary levels of guanosine 3',5'-cyclic monophosphate in rats with HF [plasma concentration 10.6 +/- 2.6 vs. 2.7 +/- 0.4 nM (P < 0.05); urinary excretion 48 +/- 8 vs. 12 +/- 2 pmol/min (P < 0.05)]. Systemic and renal hemodynamics were unaffected by HS administration. Urine flow (-35%) and urinary sodium excretion (-50%) were significantly decreased after HS only in those rats with HF that had no changes in systemic and renal hemodynamics. These results suggest that the elevated ANP levels in HF do not contribute directly to the maintenance of systemic hemodynamics but rather compensate for the HF mainly via diuresis and natriuresis, achieved by the inhibition of renal tubular reabsorption rather than by renal vasodilatation.

Animals↗
PubMed1994

IgA deposits might not influence the production of extracellular matrix in glomeruli of ddY mice, a spontaneous animal model for IgA nephropathy.

Immunofluorescence studies were carried out to determine whether the expression of extracellular matrix (ECM) in glomeruli of ddY mice, a model for IgA nephropathy (Berger's disease), is influenced by treatment with a rat monoclonal antibody to murine CD4 molecules (mAb CD4). This mAb CD4 showed a selective decrease in the number of CD4+ T cells in the peripheral blood of ddY mice as described previously. The ddY mice were initially treated with intravenous injections, followed by weekly intraperitoneal injections of mAb CD4. In immunofluorescence, the mean intensity of IgA deposits in the renal glomerular mesangial areas and capillary walls of the treated ddY mice was significantly lower than that in saline-treated control mice at comparable ages. There was no significant difference in the distribution or intensity of ECM components, i.e. type IV collagen, fibronectin and heparan sulfate proteoglycan, in glomeruli between the mAB CD4-treated and the control ddY mice. In light microscopy, mesangial expansion in the treated ddY mice was milder than that found in the saline control mice. No significant differences in the average number of intraglomerular cells, levels of serum IgA and urinary protein between the treated and control ddY mice were observed. Thus, it appears that although CD4+ T cells modulate the amounts of glomerular IgA deposits, other factors may be involved in the expression of ECM in glomeruli of IgA nephropathy in ddY mice.

Animals↗
PubMed1994

Interleukin-8 gene expression in middle ear effusions.

Interleukin-8 (IL-8), a monocyte- and macrophage-derived cytokine, displays potent chemotactic-activating properties toward neutrophils, and thus may contribute to the pathogenesis of otitis media with effusion (OME). The objective of this investigation was to demonstrate the expression of the IL-8 gene in middle ear effusion (MEEs) of children and adults with OME. Ribonucleic acids (RNAs) were extracted from MEEs from 16 ears of 13 pediatric patients and 12 ears of 12 adult patients with OME. The RNAs were reverse-transcribed and amplified by the polymerase chain reaction. Interleukin-8 transcripts were detected in 75% of both pediatric (12/16) and adult MEEs (9/12). The levels of expression of IL-8 and beta-actin messenger RNAs were quantitated. No significant difference was observed in IL-8/beta-actin ratios between pediatric MEEs and adult MEEs. These data suggest that IL-8 may contribute to neutrophil involvement in both pediatric and adult OME.

Actinin↗
PubMed1994

Structural diversity of band 4.1 superfamily members.

Several proteins contain the domain homologous to the N-terminal half of band 4.1 protein, indicating the existence of a superfamily. The members of this 'band 4.1' superfamily are thought to play crucial roles in the regulation of cytoskeleton-plasma membrane interaction just beneath plasma membranes. We examined the structural diversity of this superfamily by means of the polymerase chain reaction using synthesized mixed primers. We thus identified many members of the band 4.1 superfamily that were expressed in mouse teratocarcinoma F9 cells and mouse brain tissue. In total, 15 cDNA clones were obtained; 8 were identical to the corresponding parts of cDNAs for the known members, while 7 appeared to encode novel proteins (NBL1-7: novel band 4.1-like proteins). Sequence analyses of these clones revealed that the band 4.1 superfamily can be subdivided into 5 gene families; band 4.1 protein, ERM (ezrin/radixin/moesin/merlin/NBL6/NBL7+ ++), talin, PTPH1 (PTPH1/PTPMEG/NBL1-3), and NBL4 (NBL4/NBL5) families. The NBL4 family was first identified here, and the full-length cDNA encoding NBL4 was cloned. The deduced amino acid sequence revealed a myristoylation site, as well as phosphorylation sites for A-kinase and tyrosine kinases in its N-terminal half, suggesting its involvement in the phosphorylation-dependent regulation of cellular events just beneath the plasma membrane. In this study, we describe the initial characterization of these new members and discuss the evolution of the band 4.1 superfamily.

Amino Acid Sequence↗
PubMed1994

Studies on pharmacological activation of human immunoglobulin G by chemical modification and active subfragments. XIII. Effect of carboxamidemethylated Fc fragment (CM-Fc) on type II collagen-induced arthritis in DBA/1J mice.

The effect of carboxamidemethylated Fc fragment (CM-Fc) from human immunoglobulin G (IgG) on type II collagen (C II)-induced arthritis (CIA) in DBA/1J mice was studied. CM-Fc suppressed the development of CIA while Fc fragment did not. CM-Fc inhibited the increase in serum anti-C II IgG. CM-Fc suppressed C II-induced delayed type hypersensitivity (DTH) in DBA/1J mice. Moreover, the C II-induced proliferation of splenocytes from mice immunized with C II was suppressed by the administration of CM-Fc. Following an analysis of the lymphocyte population, a decreased percentage of B220+ cells and ratio of L3T4+/Ly-2+ cells was observed in lymph nodes of CM-Fc administered mice as compared with those of control group. These results suggest that CM-Fc inhibits CIA by regulating lymphocyte function.

Animals↗
PubMed1994

Comparison of the effects of dobutamine and isoproterenol in ischemic hearts by phosphorus-31 nuclear magnetic resonance spectroscopy.

We compared the effects of 2 inotropic agents, dobutamine and isoproterenol on regional coronary blood flow, contractile function, hemodynamics and levels of phosphate compounds in the acutely ischemic canine heart. Dogs were instrumented to determine regional coronary blood flow (non-radioactive microsphere method), contractile function (sonomicrometry), and hemodynamics. Myocardial phosphate compounds were measured simultaneously by the phosphate-31 (31P) magnetic resonance spectroscopic technique. Both drugs augmented the global performance of the heart, but produced no significant improvement in regional contractile function in the ischemic region. Isoproterenol significantly increased the ratio of inorganic phosphate to phosphocreatine in the ischemic region, as compared to dobutamine. However, no significant differences were seen in myocardial lactate consumption with inotropic stimulation between the 2 groups. 31P magnetic resonance spectroscopy could be used to differentiate between the effects of dobutamine and isoproterenol on energy metabolism in ischemic myocardium despite the lack of significant differences in regional function and myocardial lactate consumption. The significant tachycardia without an augmentation of systemic blood pressure induced by isoproterenol may account for this unfavorable effect on myocardial energy metabolism.

Animals↗
PubMed1994

The deleterious effects of exogenous angiotensin I and angiotensin II on myocardial ischemia-reperfusion injury.

Angiotensin II is well known to have a cardiotoxic effects. However, it is still unclear whether exogenous angiotensin I or angiotensin II has a deleterious effect on myocardial ischemia-reperfusion injury. To examine this deleterious effects, we administered angiotensin I and angiotensin II to perfused hearts before ischemia, and measured creatine kinase (CK) release and cardiac function during subsequent reperfusion. Wistar Kyoto rats were used and the hearts were perfused by the Langendorff technique at a constant flow (10 ml/min). Seven hearts were perfused for 20 min and then subjected to 15 min of global ischemia (Control). In the experimental groups, during the 5 min before ischemia, we administered 100 ng/ml angiotensin I (Ang I; n = 9), 1 microgram/ml enalaprilat (ACEI; n = 5), both agents (ACEI + Ang I) (n = 6), or 10 ng/ml angiotensin II (Ang II; n = 6). The perfusates were then sampled to measure angiotensin II. After 15 min of ischemia, the hearts were reperfused with control perfusate. Throughout the 20 min of reperfusion, the effluent was collected to measure cumulative CK release. Angiotensin I increased coronary perfusion pressure (CPP) by 32 +/- 4 mmHg, however, the angiotension converting enzyme inhibitor inhibited the increase of CPP by angiotension I (11 +/- 1 mmHg) (p < 0.01). The contents of angiotensin II in the effluent in Ang I and Ang I + ACEI were 11.5 +/- 1.9 ng/ml and 4.0 +/- 0.5 ng/ml (p < 0.01). After 20 min of reperfusion, the left ventricular developed pressure was unchanged in all of the groups. CPP was also unchanged by ischemia in all of the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1994

Time course of the recovery of adenosine triphosphate content with adenosine in post-ischemic hearts--a 31P magnetic resonance spectroscopy study.

Restoration of the ATP level after brief ischemia is limited by slow de novo ATP synthesis and substrate loss in a salvage pathways for ATP synthesis, and complete recovery requires several days in the stunned heart. Adenosine is a substrate for myocardial ATP synthesis. We measured myocardial ATP in both ex vivo and in vivo experiments by 31P magnetic resonance spectroscopy (31P-MRS) and investigated the time course of ATP content recovery after application of adenosine. Guinea-pig perfused hearts were subjected to 30 min of global ischemia and reperfused for 3 h with 50 microM adenosine. The ATP level increased from 54 +/- 5% to 117 +/- 4% of the pre-ischemic value (p < 0.01). In dogs, we occluded the left anterior descending coronary artery for 40 min to produce regional ischemia. Afterwards, we administered 100 mumol/h adenosine into the left ventricle for 2 h. ATP levels increased from 63 +/- 4% to 77 +/- 5% of the pre-ischemic value with adenosine (p < 0.05). However, ATP levels did not increase for a few hours after reperfusion both ex vivo and in vivo. Our 31P-MRS studies demonstrated that brief ischemia depressed ATP levels and that administration of adenosine accelerated ATP formation in post-ischemic hearts.

Adenosine↗
PubMed1994

Mechanisms underlying stimulation of gastroduodenal HCO3- secretion by NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, in rats.

We investigated the mechanism underlying stimulation of HCO3- secretion by the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in the gastroduodenal mucosa of anesthetized rats. A chambered stomach (in the presence of omeprazole) or a duodenal loop was perfused with saline, and HCO3- secretion was measured at pH 7.0 by a pH-stat method. Intravenous administration of L-NAME increased gastroduodenal HCO3- secretion with a concomitant rise in arterial blood pressure and a decrease in heart rate, and the changes were all antagonized by simultaneous administration of L-arginine. Vagotomy had no effect on the increased blood pressure response, but significantly inhibited the decrease of heart rate and increase of HCO3- secretion caused by L-NAME. The HCO3- stimulatory action of L-NAME was also inhibited by prior administration of yohimbine or prazosin. These agents alone lowered blood pressure and reduced the magnitude of the blood pressure response caused by L-NAME, leading to inhibition of heart rate changes. When delta HCO3- output induced by L-NAME was plotted against delta blood pressure change (from basal values) under various conditions, a significant relationship was found between these two factors. These results suggest that L-NAME stimulates gastroduodenal HCO3- secretion in association with the inhibition of endogenous NO production, and this mechanism may be in part mediated by a neural reflex through the vagal efferent nerve, resulting from the pressor response to L-NAME.

Animals↗
PubMed1994

Sequencing and expression of sheep angiotensinogen cDNA.

A sheep liver cDNA library was screened with a BstEII fragment of human angiotensinogen cDNA to obtain sheep angiotensinogen cDNA. The cDNA sequence showed that preangiotensinogen consisted of 452 amino acid residues (49 kDa) of angiotensinogen and 24 residues of a signal peptide. Recombinant sheep angiotensinogen (56 kDa) was expressed in COS-7 cells.

Amino Acid Sequence↗
PubMed1994

Molecular cloning of the gene for microbial transglutaminase from Streptoverticillium and its expression in Streptomyces lividans.

The microbial transglutaminase (TGase)-producing strains S-8112 [Agric. Biol. Chem., 53, 2613-2617 (1989)] was identified as a variant of Streptoverticillium mobaraense. We amplified a partial gene fragment by polymerase chain reaction (PCR) using oligonucleotides synthesized from the amino acid sequence of TGase, and cloned the gene for TGase using the PCR amplified fragment as a probe. The gene encoded a precursor of TGase consisting of 406 amino acid residues, which comprised the prepro region of 75 amino acid residues and the mature region of 331 amino acid residues. We expressed the TGase gene in Streptomyces lividans under a tyrosinase promoter, and found an active and mature recombinant enzyme, indicating the processing of the gene product.

Amino Acid Sequence↗
PubMed1994

Chemical synthesis of the gene for microbial transglutaminase from Streptoverticillium and its expression in Escherichia coli.

The gene coding for microbial transglutaminase (TGase) from Streptoverticillium, which consists of 331 amino acids, was chemically synthesized. The codons have been substituted for those mainly favored in yeast. Our strategy involved the construction of the TGase gene in five sections (54 oligomers) that contained unique restriction enzyme sites at both ends, which could readily be ligated to form the full-length product. The chemically synthesized gene was inserted downstream from the ompA signal peptide of the E. coli expression vector, pIN-III-ompA, which carries lpp and lac promotors. The resultant plasmid directed the expression of TGase, with the activity being secreted mainly into the periplasmic space of E. coli. The induced gene product was identical with native TGase in size and in immunological properties, though the enzyme activity was low.

Amino Acid Sequence↗
PubMed1994

Detection of lymphomatous involvement of the lung by bronchoalveolar lavage. Application of immunophenotypic and gene rearrangement analysis.

We report three cases of pulmonary involvement of non-Hodgkin's lymphoma in which immunophenotypic or gene rearrangement analysis of bronchoalveolar lavage (BAL) cells demonstrated monoclonality of T- or B-cell lineage. The first patient had T-cell lymphoma and developed pulmonary lesions. Surface marker analysis of the BAL cells revealed that CD8-positive lymphoid cells were dominant and Southern blot analysis of T-cell receptor gene detected gene rearrangement demonstrating monoclonality of T-cell lineage. The second patient presented with diffuse micronodular shadows on chest radiograph. Marked B-lymphocytosis in BAL fluid prompted us to analyze their clonality. The third was a case in which recurrence of primary pulmonary lymphoma was suspected. In the second and third case, the finding of marked increase in the number of CD 19-positive B lymphocytes with a single class of light chains proved a monoclonal population in BAL cells. With the review of other cases in our study and the relevant literature, we conclude that the clonal analysis of BAL cells is helpful in establishing the diagnosis of pulmonary involvement of T- or B-cell lymphoma.

Adult↗
PubMed1994

The effect of root conditioning with minocycline HCl in removing endotoxin from the roots of periodontally-involved teeth.

Noting the acid-conditioning effect of minocycline on the root surface, we investigated the ability of minocycline to remove endotoxin on untreated, diseased cementum in vitro. Root surface specimens affected by periodontal disease were immersed in minocycline solution (10 mg/ml, 50 micrograms/ml, and 5 micrograms/ml) for 10 minutes, 1 day, 3 days, and 7 days, and endotoxin eluted was determined by the limulus amoebocyte lysate (LAL) assay. Specimens serving as controls were treated by immersion in pyrogen-free water, agitation, polishing, or exposure to citric acid (pH 1.0) for 3 minutes. When the period of immersion was the same, the root treatment with minocycline (10 mg/ml) yielded a significantly higher rate of neutralization of endotoxin than that with a 5 micrograms/ml or 50 micrograms/ml solution. However, the detoxifying effect of this method was less adequate than that of polishing or treatment with citric acid solution. There was variability in the effects of polishing among the teeth tested. To obtain the expected effect of the root treatment with minocycline solution; i.e., removal of the endotoxin, the combining of minocycline with a mechanical root preparation, such as polishing or root planing, seems to be effective.

Analysis of Variance↗
PubMed1994

Tyrosine phosphorylation of beta-catenin and plakoglobin enhanced by hepatocyte growth factor and epidermal growth factor in human carcinoma cells.

The effect of hepatocyte growth factor/scatter factor (HGF/SF) and epidermal growth factor (EGF) on cadherin-mediated adhesion of human carcinoma cells was studied. HGF/SF induced scattering of colonic adenocarcinoma HT29 and gastric adenocarcinomas MKN7 and MKN74 cells. Likewise, EGF induced scattering of HT29 and MKN7 cells. These cells expressed E-cadherin, which was concentrated at cell-cell contact sites. When the scattering of these cells was induced by HGF/SF or EGF, the E-cadherin concentration at cell-cell boundaries tended to decrease. Immunoblotting analyses, however, demonstrated that these growth factor treatments did not alter the expression of E-cadherin and E-cadherin-associated proteins, alpha- and beta-catenin and plakoglobin. beta-Catenin, plakoglobin and an unidentified 115-kDa molecule associated with E-cadherin were found to be phosphorylated at tyrosine residues, and these phosphorylations were enhanced by the growth factor treatments. These results suggest that HGF/SF and EGF may modulate the function of the cadherin-catenin system via tyrosine phosphorylation of cadherin-associated proteins.

Cadherins↗