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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 379 records · Page 21Linked to original sources
PubMed1999

Prostaglandin E receptor subtypes involved in stimulation of gastroduodenal bicarbonate secretion in rats and mice.

We investigated prostaglandin E (EP) receptor subtypes responsible for the HCO3- stimulatory action of prostaglandin E2 (PGE2) in the gastroduodental mucosa, by examining the effects of various prostanoids with subtype specific EP receptor agonists in rats and those of PGE2 in knockout mice lacking EP1 or EP3 receptors. In rats, gastric HCO3- secretion was stimulated by i.v. administration of PGE2, 17-phenyl PGE2 the selective EP1 agonist as well as sulprostone the EP1 and EP3 agonist, but was not affected by other EP agonists such as butaprost the selective EP2 agonist, ONO-NT-012 the selective EP3 agonist or 11-deoxy PGE1 the EP3 and EP4 agonist. In contrast, the HCO3- secretion in rat duodenums was stimulated by PGE2, sulprostone, ONO-NT-012 as well as 11-deoxy PGE1 but not affected by either 17-phenyl PGE2 or butaprost. The HCO stimulatory effect of sulprostone in the stomach was significantly inhibited by ONO-AE-829, the selective EP1 antagonist. On the other hand, PGE2 applied topically to the mucosa for 10 min caused a dose-dependent increase of HCO3- secretion in both the stomach and duodenum of wild-type mice. The HCO3- stimulatory action of PGE2 in the stomach was also observed dose-dependently in knockout mice lacking EP3-receptors but was absent in EP1-receptor knockout mice, while the stimulatory effect in the duodenum was observed in EP1-receptor knockout mice, similar to wild-type animals, but not in knockout mice lacking EP3-receptors. These results indicate that PGE2 stimulates HCO3- secretion via different EP receptor subtypes in the stomach and duodenum; the former is mediated by EP1-receptors, while the latter mediated by EP3-receptors.

Animals↗
PubMed1999

Ulcerogenic and healing impairing actions of monochloramine in rat stomachs: effects of zinc L-carnosine, polaprezinc.

Effects of a novel zinc compound (polaprezinc), N-(3-aminopropionyl)-L-histidinato zinc, on the mucosal ulcerogenic and healing impairing responses induced by monochloramine (NH2Cl) were examined in rat stomach. Oral administration of NH2Cl (> 60 mM) produced severe hemorrhagic lesions in unanesthetized rat stomachs with a marked increase of thiobarbituric acid reactants (TBAR). Pretreatment of the animals with polaprezinc (3 approximately 30 mg/kg, p.o.) showed a dose-dependent inhibition against gastric ulcerogenic and TBAR responses induced by NH2Cl (120 mM). Likewise, mucosal exposure to NH4OH (60 mM) in urethane anesthetized stomachs made ischemic by bleeding from the carotid artery (1 ml per 100 g body w.t.) resulted in severe gastric lesions. This ulcerogenic response caused NH4OH plus ischemia was also attenuated by prior application of polaprezinc as well as taurine (25 mg/ml, 1 ml). On the other hand, the healing of gastric mucosal lesions induced by NH2Cl occurred more slowly than of ethanol-induced lesions, and the latter was significantly delayed by the repeated administration of NH2Cl. Polaprezinc (> 10 mg/kg, p.o.) given twice daily for 7 days not only accelerated the healing of NH2Cl-induced gastric lesions but also antagonized the delayed healing of ethanol-induced lesions in the presence of NH2Cl as well. Polaprezinc showed a scavenging action against NH2Cl in vitro. These results suggest that NH2Cl caused deleterious action on the healing of pre-existing acute lesions as well as irritating action to the mucosa in the rat stomach. Polaprezinc not only protects the stomach against injury caused by NH2Cl but also promotes healing of NH2Cl-induced gastric lesions as well as the delayed healing of ethanol-induced lesions caused by NH2Cl. Although the detailed mechanisms underlying these actions of polaprezinc remain unknown, they may be partly attributable to a scavenging action of this agent against NH2Cl.

Administration, Oral↗
PubMed1999

[A longitudinal study of hand-mouth contacts of pre-term infants].

The developmental change of spontaneous hand movements were investigated longitudinally in 5 low-risk pre-term infants. The observation period was divided into three: 33-40, 41-52 and 53-60 weeks in order of gestational age. Both hand-mouth contacts (H-M-C) and hand-face contacts (H-F-C) were frequent in the 33-40-week period, and decreased drastically in the 41-48 week period. In the 53-60-week period, the number of H-F-C remained at a low level, while H-M-C increased again to the level of the first period. Furthermore, the mouth was open as the hand came into contact with it as frequently in the 33-40-week period as in the 53-60-week period. These findings suggest that H-M-C are neurologically distinct from H-F-C, and that the H-M-C before 41 weeks and after 50 weeks share some common components of this neurological mechanism.

Child Development↗
PubMed1999

Increased myocardial calcium cycling and reduced myofilament calcium sensitivity in early endotoxemia.

BACKGROUND: Mechanisms of cardiac dysfunction during endotoxemia are multiple and their targets uncertain. This study tested the hypothesis that endotoxin (LPS) induces abnormal calcium-activated contractile force in the heart. METHODS: Adult rabbits were given LPS intravenously; 2 hours later hearts were studied in the Langendorff mode. Measurements included peak developed pressure (PDP), myocardial oxygen consumption (MVO2), high-energy phosphates by 31P-NMR, and beat-to-beat intracellular calcium (Cai) by fluorescence spectroscopy. Myofibrillar calcium sensitivity was assessed from the relationship of PDP to Cai and the rate of diastolic Cai removal (tau Ca) was quantified. RESULTS: Force-calcium relationships were markedly depressed in LPS hearts despite increased Cai. MVO2 was increased in parallel with increased Cai. Taken together, these data denote myofilament calcium insensitivity and mechanical inefficiency. tau Ca was markedly prolonged in LPS hearts, indicating impaired calcium reuptake and/or extrusion. High-energy phosphates and intracellular pH were unaffected by LPS; however, inorganic phosphate (Pi) was significantly increased. Dobutamine further increased Cai and MVO2 in LPS hearts without significantly improving calcium-activated force. Pyruvate, an inotrope that reduces Pi, significantly improved contractility in LPS hearts. CONCLUSIONS: Endotoxemia rapidly induced futile calcium cycling and reduced myofibrillar calcium sensitivity. This state was resistant to beta-agonist inotropic stimulation; inotropes that normalize the calcium-force relationship may be more effective.

Actin Cytoskeleton↗
PubMed1999

[Molecular mechanisms of the pathway formation in the fetal rat cerebral neocortex].

Neural cell adhesion molecules (NCAMs), L1 and TAG-1, which are prominently expressed in the developing nervous system, have been shown to promote axonal growth and bundle formation of central neurons in vitro. In the cerebral neocortex of fetal rats, immunoreactions of L1 and TAG-1 were specifically localized on thalamic afferent axons and cortical efferent axons, respectively. L1-bearing thalamocortical axons preferentially extended in the subplate of the cortical anlage where neurocan, a brain-specific chondroitin sulfate proteoglycan (CSPG), was prominently expressed. In contrast, cortical efferent axons immunoreactive for TAG-1 did not enter the subplate and run in the intermediate zone where neurocan expression was less abundant. In addition, TAG-1-bearing axons extensively invaded regions expressing another type of brain-specific CSPG, phosphacan. In the cell culture system, neurite outgrowth of TAG-1-transfected PC 12 D cells was remarkably inhibited on the neurocan substrate, while the outgrowth on phosphacan substrate was significantly promoted. Although both L1 and TAG-1 have been reported to bind both neurocan and phosphacan in vitro, interactions between NCAMs and CSPGs in vivo indicate more complicated patterns than previously thought. Thus, the present results suggest that various patterns of functional correlation between NCAMs and CSPGs play important roles in the pathway formation of the rat cerebral neocortex.

Animals↗
PubMed1999

Modulation by endogenous nitric oxide of acid secretion induced by gastric distention in rats: enhancement by nitric oxide synthase inhibitor.

The mechanism underlying acid hypersecretion induced by gastric distention was investigated in rats, especially in relation to endogenous nitric oxide (NO). Under urethane anesthesia, rat stomach was distended by instillation of saline (1-10 ml) through the acute fistula that was provided through a pylorus. Gastric samples were collected every 1 h, and the acid secretion was measured by titration with 100 mM NaOH. Gastric acid secretion was increased by distention, and the degree of stimulation was dependent on the volume of saline instillation; a maximal response occurred with 6-ml instillation, which maintained the intraluminal pressure of about 20 cm H(2)O. The increased acid secretory response induced by distention was completely blocked by omeprazole and significantly mitigated by vagotomy, sensory deafferentation, atropine, or famotidine but markedly enhanced by the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). On the other hand, the enhanced acid response in the presence of L-NAME occurred in an L-arginine-sensitive manner and was almost totally abolished by vagotomy and sensory deafferentation as well as by atropine. Gastric distention increased the release of NO metabolites and histamine into the gastric lumen. The NO metabolite release in the distended stomach was significantly decreased by vagotomy or L-NAME, whereas the histamine output was decreased by vagotomy but increased by L-NAME in an L-arginine-sensitive manner, respectively. These results suggest that 1) gastric distention increases acid secretion, initially through the perception by sensory neurons of the mechanical stimulation and mainly through the efferent vagocholinergic pathway, with the process being modified by endogenous NO, and 2) this molecule, released in a vagal-dependent manner, exerts a negative influence on acid secretion, at least in part by suppressing histamine release from the histamine-containing cells.

Animals↗
PubMed1999

A reverse flow-metabolism mismatch pattern on PET is related to multivessel disease in patients with acute myocardial infarction.

UNLABELLED: Hypoperfused myocardium with increased uptake of 18F-fluorodeoxyglucose (FDG) is considered to be ischemic but viable myocardium. However, the significance of a more severe defect of FDG than of 13N ammonia (NH3) (i.e., reverse flow-metabolism mismatch) is not well understood. METHODS: To study a reverse flow-metabolism mismatch pattern, PET with NH3 and FDG under glucose loading was performed in 35 patients within 2 wk after onset of first acute myocardial infarction (AMI) and in 29 patients with old myocardial infarction (OMI). The left ventricle was divided into nine segments on a bull's eye polar map, and the mean counts of NH3 (%NH3) and FDG (%FDG) were compared for the segment with the least %NH3. RESULTS: Ten patients in the AMI group demonstrated a marked reverse flow-metabolism mismatch pattern (greater than 10% difference between %NH3 and %FDG), whereas only 2 patients in the OMI group demonstrated the mismatch pattern (P < 0.05). Sixteen patients with AMI demonstrated %FDG > %NH3 (group 1), and 19 patients with AMI demonstrated %FDG < %NH3 (group 2). There were no significant differences in age, sex, location of infarction, diameter of stenosis of infarct-related artery or left ventricular ejection fraction between groups 1 and 2. Eleven patients in group 2 and only 3 in group 1 had multivessel disease (P < 0.02). There was no significant relationship between the number of diseased vessels and the flow-metabolism pattern in patients with OMI. CONCLUSION: The finding of a reverse flow-metabolism mismatch on PET in the subacute phase of myocardial infarction was closely related to multivessel disease.

Adult↗
PubMed1999

[Relationship between regular exercise and life style, social network, education and subjective symptoms in Japanese middle aged and elderly residents].

OBJECT AND METHODS: A community-based survey of 12,630 residents of Gunma Prefecture aged 40 to 69 years was conducted to investigate the relationship between the habit of regular exercise and life style, social network, and subjective physical and mental symptoms in particular. The subjective physical and mental symptoms were measured using the Todai Health Index (THI). The response rate was 91.6%. A total of 6,736 responses were analyzed after excluding respondents with chronic diseases from the analysis. On the question about the habit of regular exercise ("Do you exercise regularly?"), the responses were divided into three categories: 1. Often, 2. Sometimes, 3. Hardly ever or Never. RESULTS AND CONCLUSION: The results are summarized as follows: 1. The proportions of residents who exercise "often" were 14.2% and 11.1% for males and females, respectively, while those of "hardly ever or never" were 52.3% and 59.4% for males and females, respectively. More males than females had the habit of regular exercise. Respondents were divided into three age categories: 40-49, 50-59 and 60-69 years. Among the female respondents, it was shown that the older the age category the greater the habit of regular exercise. 2. Both male and female respondents who had regular exercise habits scored significantly lower on the THI scales for vague complaints, depression, and irregularity of life, while they scored higher on the aggression and lie (social desirability) scales. 3. Both male and female respondents who had regular exercise habits also tended to have be better perceived health and social networking, i.e. having close friends, having a hobby and involvement in community social activities, as well as taking care of pets. This group also had a higher average education level and less of a smoking habit. This study suggests that regular exercise habit correlates not only with physical health and fitness levels but with mental health status as well.

Adult↗
PubMed1999

[Effect of adenosine on isolated afferent arterioles].

We investigated the direct effect of adenosine on afferent arterioles (Af-Arts) and the receptor subtype that mediates the constrictor or dilator action of adenosine. Af-Arts were isolated from the superficial cortex of rabbit kidney and perfused in vitro. Adenosine added to either the lumen or bath constricted the Af-Arts in a dose-dependent manner. This constriction was blocked by the A1 receptor antagonist, 6-oxo-3-(2-phenylpyrazole(1,5-a)pyridin-3-yl)-1 (6H)-pyridazinebutyric acid (FK838) or 8-cyclopentyl-1, 3-dipropylxanthine(DPCPX). We also examined the effect of adenosine on preconstricted Af-Arts with norepinephrine. Adenosine added to either the lumen or bath further constricted the preconstricted Af-Arts. In the presence of FK838, adenosine added to either the lumen or bath dilated the preconstricted Af-Arts, but in a different dose-dependent manner. Adenosine-induced dilation was inhibited by the A2 receptor antagonist, 3, 7-dimetyl-1-propargylxanthine(DMPX). These data indicate that adenosine constricts Af-Arts via A1 receptors and that adenosine dilates preconstricted Af-Arts via A2 receptors when A1 receptors are blocked.

Adenosine↗
PubMed1999

Dual action of nitric oxide in pathogenesis of indomethacin-induced small intestinal ulceration in rats.

We investigated the pathogenic role of nitric oxide (NO) in indomethacin-induced intestinal ulceration in rats. Nonfasting animals responded to a single administration of indomethacin (10 mg/kg, s.c.), resulting in multiple hemorrhagic lesions in the small intestine, mostly the jejunum and ileum. The damage was first observed 6 hr after indomethacin, the severity increasing progressively with time up to 24 hr later, accompanied with the gene expression of inducible NO synthase (iNOS) and the increase of nitrite and nitrate (NOx) contents in the mucosa. The ocurrence of damage was significantly prevented when iNOS induction was inhibited by dexamethasone given either once 0.5 hr before or twice 0.5 hr before and 6 hr after indomethacin. Likewise, aminoguanidine (a relatively selective iNOS inhibitor) reduced the severity of damage, irrespective whether given twice or as a single injection 6 hr after indomethacin. By contrast, the non-selective NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) exhibited a biphasic effect, depending on the time of administration; the pre-administration worsened the damage, while the later administration reduced the severity of these lesions, yet both responses occureed in a L-arginine-sensitive manner. Pre-administration of L-NAME, but not aminoguanidine, significantly decreased NOx production in the intestinal mucosa of normal rats, while the increase of NOx production following indomethacin was significantly suppressed by the later administration of aminoguanidine as well as L-NAME. These results suggest that NO exerts a dual action in the pathogenesis of indomethacin-induced intestinal ulceration; NO generated by cNOS is protective against indomethacin, by maintaining the integrity of intestinal mucosa, while NO derived by iNOS plays a key pathogenic role in the ulcerogenic process.

Animals↗
PubMed1999

[Mumps virus].

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Humans↗
PubMed1999

[Renal sodium transport abnormality: Gitelman's syndrome and renal sodium transporter].

Recent studies using molecular biological methods have enabled us to identify the genetic abnormality in renal electrolyte metabolism. In renal tubules, diuretic sensitive Na transporter systems are present, and key molecules have been cloned. Thiazide-sensitive Na-Cl contransporter (TSC) is one of the molecules localized in the distal convoluted tubule, whose genetic abnormality causes Gitelman's syndrome (a variant of Bartter's syndrome characterized by dehydration, hypokalemic metabolic alkalosis, secondary aldosteronism lacking hypertension, hypomagnesemia, and hypocalciuria). We identified a mutation in TSC (Leu to Pro change at 623 amino acid position, L623P) in familial Gitelman's syndrome, and we confirmed the loss of TSC function by this mutation in a functional expression system using mammalian cells. This L623P mutation has been found in other patients with Gitelman's syndrome living in the northern part of Japan.

Bartter Syndrome↗
PubMed1999

Potential use of bioelectrical impedance analysis in the assessment of edema in pregnancy.

OBJECTIVE: To evaluate the validity of Bioelectrical Impedance Analysis (BIA) in the assessment of edema in pregnancy. METHODS: A prospective study of healthy women identified during the first trimester of pregnancy. From a pool of 200 eligible volunteers, BIA was conducted on 90 women during the rest of pregnancy and postpartum period. RESULTS: The values for bioelectrical impedance in normal pregnant women decreased gradually in the course of pregnancy, whereas a more remarkable decrease in the values was noted in eight patients who developed edema. The bioelectrical impedance (BI) changes correlated closely with body weight changes. There was a strong relation between bioelectrical impedance values and the degree of edema. The precedent decrease of the values before the onset of edema was noted in seven of the eight patients with edema. CONCLUSION: BIA can be a useful and practical method for the early detection and quantitative assessment of edema in pregnant women.

Adolescent↗
PubMed1999

Cytokine patterns and the effects of a preoperative steroid treatment in the patients with abdominal aortic aneurysms.

BACKGROUND: The aim of this study was to investigate the cytokine patterns of patients with abdominal aortic aneurysms and the effects of preoperative steroid administration on surgical stress. METHODS: From January 1996 to August 1996, 20 consecutive patients underwent an elective reconstruction of infrarenal abdominal aortic aneurysms. The patients were randomly divided into two groups consisting of a control group (n=10) and a steroid group (n=10), in whom 1 g of methylprednisolone was intravenously administered two hours before the operation. MEASURES: Interleukin-6 was serially measured and the perioperative parameters including C-reactive protein were compared between both the control and the steroid groups. RESULTS: The interleukin-6 values in the steroid group immediately after declamping, as well as at one and three postoperative days were significantly lower than those in the control group. C-reactive protein values at one postoperative day in the steroid group were also significantly lower than those in the control group. In one patient with a ruptured abdominal aortic aneurysm, the interleukin-6 values were higher than those in the patients undergoing elective surgery throughout the study. CONCLUSIONS: These results thus suggest that preoperative steroid administration using methylprednisolone in patients with abdominal aortic aneurysms appears to reduce surgical stress by decreasing cytokine release.

Aged↗
PubMed1998

Development of dual-acting agents for thromboxane receptor antagonism and thromboxane synthase inhibition. 3. Synthesis and biological activities of oxazolecarboxamide-substituted omega-phenyl-omega-(3-pyridyl)alkenoic acid derivatives and related compounds.

A novel series of oxazolecarboxamide-substituted omega-phenyl-omega-(3-pyridyl)alkenoic acid derivatives was discovered as potent dual-acting agents to block the TXA2 receptor and to inhibit the thromboxane synthase (TRA/TSI). Synthesis, structure-activity relationship (SAR), and in vitro and in vivo pharmacology of this series of compounds are described. Modification of the series revolved around the oxazole moiety to increase the hydrophilicity of the compounds and to correlate the biological activity with lipophilicity of the compounds. The most potent in the series was (E)-7-[4-[4-[[(4-cyclohexylbutyl)amino]carbonyl]-2-oxazolyl] phenyl]-7 -(3-pyridyl)hept-6-enoic acid (14) with Kd = 9.9 +/- 0.4 nM for the thromboxane receptor antagonism and IC50 = 55.0 +/- 17.9 nM for thromboxane synthase inhibition. The compound 14 was a selective TRA/TSI which exhibited desirable characteristics for oral activity, "shunt" effect to elevate PGI2 level, and absence of agonist activity.

Animals↗
PubMed1998

Glucose transporter upregulation improves ischemic tolerance in hypertrophied failing heart.

BACKGROUND: Achieving successful myocardial preservation of hypertrophied hearts remains a difficult problem. Despite reportedly higher glycolytic potential, we have achieved limited benefit in hypertrophied hearts with strategies that successfully promote anaerobic glycolysis and long-term ischemic preservation in nonhypertrophied models. We therefore tested the hypotheses that (l) glucose transport into myocytes is a critical limiting factor in hypertrophied heart and (2) stimulation of glucose transport with vanadyl sulfate would improve postischemic recovery. METHODS AND RESULTS: Left ventricular hypertrophy in rabbits was created by aortic banding of 7- to 10-day-old rabbits. At 4 weeks of age, 1 group of animals received oral vanadyl sulfate for 3 to 4 weeks. Glucose transport (measured by the conversion of 2-deoxyglucose to 2-deoxyglucose-6-phosphate; 31P-nuclear magnetic resonance), myocardial glucose transporter content (GLUT-1 and GLUT-4 by immunoblotting), and functional recovery from ischemia-reperfusion (isolated perfused Langendorff model) were measured. Myocardial glucose transport rate was significantly reduced in hypertrophied hearts without significant reductions in glucose transporter content; these hearts were significantly less tolerant of ischemia-reperfusion than age-matched controls. Vanadyl sulfate normalized glucose transport rate and improved tolerance to ischemia-reperfusion so that postischemic function equaled that seen in controls. Lactate production during ischemia, an indication of anaerobic glycolysis, was significantly higher in hearts from vanadate-treated animals. CONCLUSIONS: Despite reportedly higher glycolytic enzyme activities, maximal glucose transport appears to be reduced and is rate limiting in hypertrophied heart. Stimulation of membrane glucose transport with vanadyl sulfate significantly improved glycolytic flux and ischemic preservation in hypertrophied hearts.

Adaptation, Physiological↗
PubMed1998

Characterization of alg2 encoding a mannosyltransferase in the zygomycete fungus Rhizomucor pusillus.

ALG2 of Saccharomyces cerevisiae encodes the glycosyltransferase that mannosylates Man2GlcNAc2-dolichol diphosphate (PP-Dol) and Man1GlcNAc2-PP-Dol to form Man3GlcNAc2-PP-Dol. The genomic DNA and cDNA encoding an ALG2 homologue were cloned from the zygomycete fungus, Rhizomucor pusillus, and their nucleotide sequences were determined. The cloned cDNA under the control of the yeast GAL1 promoter complemented the temperature-sensitive (ts) growth of the alg2-1 mutant of S. cerevisiae, indicating that it represented a functional ALG2 homologue of R. pusillus. Five introns intervened the R. pusillus alg2 encoding a 455-amino-acid (aa) protein that showed end-to-end similarity in aa sequence to yeast Alg2 and contained a dolichol-binding consensus sequence (Val/Ile-x-Phe-x-x-Ile, where x is any aa) very near its C-terminus. The yeast alg2-1 gene had two mutation points at 377Gly to Arg and 386Gln to Lys. alg2-2 also contained two mutations at 54Glu to Lys and 377Gly to Arg. Site-directed mutagenesis of the fungal Alg2 and determination of their phenotypes in the yeast alg2-1 mutant showed that a mutation at 368Gly (equivalent to 377Gly of yeast Alg2) to Arg resulted in generation of a ts enzyme. The fungal Alg2 containing a mutation at the position corresponding to 54Glu or 386Gln of yeast Alg2 still complemented the ts growth of yeast alg2-1.

Amino Acid Sequence↗