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Biomedical subjects

M Inoue

Publications and source records attributed to M Inoue.

At least 145 records · Page 8Linked to original sources
PubMed1995

[Haemophilus aphrophilus isolated from the blood of a patient with infective endocarditis].

On July 1994, a 62-year-old female, having a history of mitral regurgitation, was admitted because of high fever, hematuria and conjunctival petechiae. She was diagnosed as having infective endocarditis with mitral valve vegetation proved by ultrasonic cardiography. The gram negative rods were isolated from blood cultures performed five times, performed prior to the administration of antibiotics. The isolates were identified as strains of H. aphrophilus. After two days of treatment with PCG (12 million units/day), the organism became undetectable from the blood. Since the minimal inhibitory concentrations (MICs) of PCG and ABPC were ranged between 0.06-2.0 micrograms/ml and 0.06-0.5 microgram/ml, respectively, ABPC was selected as a first choice antibiotic instead of PCG. ABPC was given 12 g/day for the first 3 days, then 6 g/day for 28 days, followed by 3 g/day for 7 days. The patient recovered and was discharged after the 55 hospital days. H. aphrophilus grew on BTB lactose agar, chocolate agar and sheep blood agar, but failed to grow on MacConkey agar. H. aphrophilus produced smooth transparent nonhaemolytic micro colonies after 48 hours on sheep blood agar and chocolate agar plates. Atmosphere with 5% CO2 failed to enhance their growth. All the five strains of H. aphrophilus isolated, required neither factors V nor X. Positive synthesis of porphyrin from delta-aminolevlinic acid confirmed their ability to grow without X factor. For the correct identification of H. aphrophilus strains, fermentation test of glucose, lactose, maltose and sucrose in either phenol red broth or CTA medium are necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Ampicillin↗
PubMed1995

Autolysis of methicillin-resistant Staphylococcus aureus is involved in synergism between imipenem and cefotiam.

Imipenem-induced autolysis and the activity of imipenem plus cefotiam were studied in 16 strains of methicillin-resistant Staphylococcus aureus (MRSA). The degree of imipenem-induced autolysis and the rate of synergistic action of imipenem plus cefotiam varied among strains and did not correlate with susceptibility to either imipenem or cefotiam. However, the degree of autolysis correlated well with susceptibility to the synergistic action of imipenem plus cefotiam. In methicillin-susceptible S. aureus strains, both imipenem-induced autolysis and the synergistic activity of the combined drugs were less than those observed in MRSA strains. Differences in the degree of autolysis were not due to differences in autolytic enzyme production. The autolysis of imipenem-pretreated MRSA was enhanced further by cefotiam, while treatment of cells in the reverse order did not enhance autolysis. These findings indicate that cell wall impairment in MRSA is caused by exposure to imipenem but not to cefotiam and that this difference in drug actions results in synergism between imipenem and cefotiam. The possible participation of penicillin-binding proteins PBP 2' and PBP4 in the observed effect is discussed.

Bacterial Proteins↗
PubMed1995

Changes in circulatory status and transport function of the liver induced by reactive oxygen species.

To elucidate the pathogenesis of microcirculatory disturbance of the liver after ischemia and reperfusion, the effect of reactive oxygen species on hepatic circulatory status and transport function for a cholephilic compound was studied in an isolated perfused rat liver. Perfusion of the liver with a medium containing hypoxanthine and xanthine oxidase significantly increased the portal pressure, with concomitant decrease in intrahepatic vascular volume and hepatic uptake of bromosulfophthalein (BSP). Similar changes were also elicited by infusion of serotonin, which induces contraction of sinusoidal endothelial cells. Either superoxide dismutase or catalase added in the perfusion medium partially inhibited the oxidase-induced changes in portal pressure, vascular volume of hepatic sinusoid, and BSP transport. In the presence of superoxide dismutase, either catalase or erythrocytes inhibited the oxidase-induced changes completely. These results indicated that superoxide anion and hydrogen peroxide might induce contraction of hepatic resistance vessels, capacitance vessels, and/or sinusoidal endothelial cells and that this contraction decreased the vascular bed in the liver and the time for interaction of circulation substrates with hepatocytes, thereby decreasing hepatic transport for cholephilic ligands such as BSP.

Animals↗
PubMed1995

Superoxide dismutase derivative reduces oxidative damage in skeletal muscle of rats during exhaustive exercise.

A superoxide dismutase derivative (SM-SOD) that circulates and is bound to albumin with a half-life of 6 h was injected intraperitoneally into rats before exhaustive treadmill running to study its antioxidant scavenging capacity in the plasma and soleus and tibialis muscles. The exercise induced a marked increase in xanthine oxidase activity in plasma and an increase in thiobarbituric acid-reactive substances in the plasma as well as in the soleus and tibialis muscles of nonadministered rats immediately after the exercise. The immunoreactive content and activity of both SOD isoenzymes (Cu,Zn-SOD and Mn-SOD) of the nonadministered rats increased in the soleus and tibialis muscles immediately after running. SM-SOD treatment definitely attenuated the degree of the increase in thiobarbituric acid-reactive substances and xanthine oxidase in all samples examined immediately after exercise. Glutathione peroxidase activity significantly increased in the soleus muscle of nonadministered rats 1 day after running, whereas catalase activity remained unchanged throughout the experimental period. These results suggest that a single bout of exhaustive exercise induces oxidative stress in skeletal muscle of rats and that this oxidative stress can be attenuated by exogenous SM-SOD.

Animals↗
PubMed1995

Inhibition of puromycin-induced renal injury by a superoxide dismutase derivative with prolonged in vivo half-life.

To know the possible involvement of reactive oxygen species and the site(s) of their action in puromycin aminonucleoside (PAN)-induced renal injury, two types of superoxide dismutase (SOD) derivatives were synthesized: one (SM-SOD) circulates bound to albumin with a half-life of 6 h and the other (AH-SOD) linked with hexamethylenediamines rapidly undergoes glomerular filtration and accumulates in renal proximal tubule cells without being excreted in urine. When injected intravenously to the rat, PAN induced a marked proteinuria, increased plasma levels of cholesterol and triglyceride, and suppressed the growth of animals. Intravenously administered SM-SOD significantly inhibited such changes induced by PAN. However, native SOD which rapidly undergoes urinary excretion failed to inhibit the renal injury caused by PAN. Though AH-SOD markedly accumulated in renal proximal tubule cells, it also failed to inhibit the renal injury. These results suggested that superoxide and/or its hazardous metabolite(s) in and around the renal glomerulus, but not in tubule cells, may play critical roles in the pathogenesis of PAN-induced renal injury.

Animals↗
PubMed1995

Activation of protein kinase C increases adenosine production in the hypoxic canine coronary artery through the extracellular pathway.

Both ischemia and hypoxia increase adenosine production in the heart. This study tested whether hypoxia increases adenosine production in the coronary artery via ecto-5'-nucleotidase and the role of protein kinase C in this condition. Canine left circumflex coronary artery was rapidly removed and incubated in 10 mL Krebs-Henseleit solution for 30 minutes. The Krebs-Henseleit solution contained 5'-iodotubercidin and 2'-deoxycoformycin, which inhibit adenosine kinase and adenosine deaminase, respectively. Adenosine production was measured in intact coronary arteries under normoxic conditions (16.2 +/- 1.2 pmol/mg protein). Adenosine production was reduced by 27% after removal of endothelium. Ecto-5'-nucleotidase activity of coronary arteries with and without endothelium was 51 +/- 6 and 41 +/- 4 nmol/mg protein per minute under normoxic conditions. Hypoxia increased adenosine production to 27.0 +/- 2.3 and 20.0 +/- 0.8 pmol/mg protein with and without endothelium. Hypoxia also increased ecto-5'-nucleotidase activity of coronary arteries with and without endothelium (74 +/- 8 and 53 +/- 5 nmol/mg protein per minute; P < .05). Increases in adenosine production under hypoxic conditions were blunted by both an inhibitor of ecto-5'-nucleotidase and inhibitors of protein kinase C. Activation of ecto-5'-nucleotidase was blunted by an inhibitor of protein kinase C. These results indicate that hypoxia increased extracellular adenosine production and activated ecto-5'-nucleotidase via activation of protein kinase C in coronary arterial smooth muscle and endothelial cells. Increased adenosine production in coronary arteries during hypoxia may contribute to coronary vasodilation and cardioprotection against ischemic injury.

5'-Nucleotidase↗
PubMed1995

Inhibition of growth hormone-releasing factor production in mouse placenta by cytokines using gp130 as a signal transducer.

The aim of this study was to investigate whether mouse placenta produces mature mouse GHRF (mGHRF) and whether cytokines regulate placental mGHRF production. Using Sephadex G-50 gel filtration chromatography and reverse phase HPLC, we identified immunoreactive mGHRF in acid-ethanol extract of placental tissues, which had chromatographic characteristics identical to those of hypothalamic mature mGHRF peptide. The major peak of immunoreactive GHRF in the medium from cultured placental cells was resolved by HPLC at a fraction identical to hypothalamic mature mGHRF. Interleukin-6 (IL-6), IL-11, leukemia inhibitory factor (LIF), and oncostatin-M, which all use gp130 as a signal transducer, significantly inhibited mGHRF secretion by cultured placental cells. However, IL-1 alpha and tumor necrosis factor-alpha had no effect on mGHRF secretion. Antibodies to IL-6 or IL-6 receptor completely blocked the inhibitory effect of IL-6 on mGHRF secretion. Anti-LIF, and oncostatin-M inhibited the expression of mGHRF messenger RNA. These results suggest that mouse placenta produces and releases the mature mGHRF, which is indistinguishable by chromatographic criteria from that produced by the hypothalamus, and that signals through gp130 lead to the inhibition of mGHRF production and release in the mouse placenta.

Animals↗
PubMed1995

Familial hypocalciuric hypercalcemia associated with mutation in the human Ca(2+)-sensing receptor gene.

Familial hypocalciuric hypercalcemia (FHH) is generally characterized by lifelong hypercalcemia without hypercalciuria and is inherited in an autosomal dominant manner. Affected individuals show abnormal parathyroid and renal responses to changes in the extracellular calcium concentration. A Japanese FHH family was screened for mutations in the Ca(2+)-sensing receptor gene by the polymerase chain reaction and single strand conformation polymorphism. The proband with hypercalcemia showed an abnormal pattern in exon 1 of the gene, whereas her two sisters with normocalcemia showed a normal pattern. The consanguineous parents with borderline serum calcium concentrations showed both patterns. Nucleotide sequence analysis identified a G-->C point mutation at nucleotide 118 that resulted in the conversion of the normal codon for proline into a codon for alanine at amino acid 40 (numbered according to the bovine complementary DNA). The proband was homozygous for the mutation, and the parents were heterozygous. These results imply that this mutation in the human Ca(2+)-sensing receptor gene causes FHH and that the dosage of the gene defect determines disease phenotype.

Adult↗
PubMed1995

Studies on constituents with cytotoxic and cytostatic activity of two Turkish medicinal plants Phlomis armeniaca and Scutellaria salviifolia.

Ten known glycosidic compounds, betulalbuside A (1), 8-hydroxylinaloyl,3-O-beta-D-glucopyranoside (2) (monoterpen glycosides), ipolamide (3) (iridoid glycoside), acteoside (verbascoside) (4), leucosceptoside A (5), martynoside (6), forsythoside B (7), phlinoside B (8), phlinoside C (9), and teuerioside (10) (phenylpropanoid glycosides) were isolated from methanolic extracts of Phlomis armeniaca and Scutellaria salviifolia (Labiatae). Structure elucidations were carried out using 1H-, 13C-NMR and FAB-MS spectra, as well as chemical evidence. The cytotoxic and cytostatic activities of isolated compounds were investigated by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) method. Among the glycosides obtained here, caffeic acid-containing phenylpropanoid (or phenethyl alcohol, or phenylethanoid) glycosides were found to show activity against several kinds of cancer cells. However, they didn't affect the growth and viability of primary-cultured rat hepatocytes. Study of the structure-activity relationship indicated that ortho-dihydroxy aromatic systems of phenylpropanoid glycosides are necessary for their cytotoxic and cytostatic activities.

Animals↗
PubMed1995

Selective induction of cell death in cancer cells by gallic acid.

Gallic acid (3,4,5-trihydroxybenzoic acid) is a naturally occurring plant phenol obtained by the hydrolysis of tannins and is know to show some pharmacological activities. In screening anti-cancer agents in traditional Chinese medicines, gallic acid was found to show cytotoxicity against all cancer cells that we examined in this study (IC50s: 4.8-13.2 micrograms/ml). Gallic acid was found to show cytotoxicity against primary cultured rat hepatocytes and macrophages, and lesser cytotoxicity against fibroblasts and endothelial cells. Cell death in dRLh-84 cells occurred within 6h after gallic acid treatment at a concentration of more than 20 micrograms/ml. A study of structurally related compounds suggested that the cytotoxicity shown by gallic acid was not a common feature in phenolic compounds, but was a fairly specific characteristic of gallic acid. That is, three adjacent phenolic hydroxyl groups of gallic acid were responsible for the cytotoxicity, and the carboxyl group was not responsible, but seemed to be implicated in distinguishing between normal cells and cancer cells.

Animals↗
PubMed1995

Cytotoxic activity of bryonolic acid isolated from transformed hairy roots of Trichosanthes kirilowii var. japonica.

Bryonolic acid was isolated in high yield from transformed hairy root cultures of Trichosanthes kirilowii var. Japonica. Bryonolic acid exhibited cytotoxic activity to various tumor cells in vitro, independent of cell type. Normal cells such as rat hepatocytes are less sensitive to bryonolic acid. The appearance of a DNA ladder was detected in the bryonolic acid-treated HL-60RG cells, indicating that cell death triggered by bryonolic acid is due to apoptosis.

Animals↗
PubMed1995

Quantitative assessment of daily physical activity levels in patients with chronic heart failure by measuring energy expenditure--effects of converting enzyme inhibitor therapy.

Although a major goal in the treatment of chronic heart failure is to improve daily physical activity levels, this has not been assessed quantitatively. An increased daily activity level may be reflected by an increase in daily energy expenditure. In the present study, measurements of energy expenditure with a commercially available ambulatory calorimeter were first validated using cardio-pulmonary exercise tests in 5 normal volunteers. The energy expenditure measured by the calorimeter correlated well with that estimated from oxygen uptake (r = 0.89). Subsequently, the daily energy expenditure was serially measured with the calorimeter during long-term administration of the converting enzyme inhibitor ramipril for 24 weeks in 8 patients with chronic heart failure. Changes in echocardiographic parameters and exercise capacity were also studied. Peak oxygen uptake and anaerobic threshold assessed with symptom-limited maximal bicycle exercise were significantly increased 12 weeks or more after the initiation of treatment (P < 0.01 and P < 0.01, respectively). Left ventricular fractional shortening substantially, but not significantly, increased during this period (P < 0.1). These results strongly suggest that an overall improvement in heart failure was achieved after long-term ramipril therapy. The energy expenditure during daily activities was also significantly increased after ramipril therapy for 24 weeks (P < 0.01). Thus, the daily energy expenditure increased with improvement of heart failure, probably reflecting an increase in daily activity levels. We conclude that calorimetric measurement of daily energy expenditure is a novel and simple technique for quantitative evaluation of the effect of therapy on daily physical activity levels in patients with chronic heart failure.

Activities of Daily Living↗
PubMed1995

Adrenergic receptor-mediated Cl- transport in rabbit corneal endothelial cells.

Adrenoceptor-mediated Cl- transport in cultured rabbit corneal endothelium was examined using a Cl(-)-sensitive fluorescent dye. The intracellular Cl- concentration ([Cl-]i) in the endothelial cells was estimated to be about 30 mM. Noradrenaline (0.001-0.1 mM) transiently decreased the [Cl-]i in a dose-dependent manner. Such a decrease in [Cl-]i was completely antagonized by pretreatment with the alpha-adrenoceptor antagonist phentolamine (0.1 mM). The selective alpha 2-adrenoceptor agonist UK 14304-18 (5-bromo-6-[(4H,5H-imidazol-2-yl)amino]quinoxaline, 0.1 mM) persistently decreased the [Cl-]i, but neither the alpha 1-adrenoceptor agonist phenylephrine (0.1 mM) nor the beta-adrenoceptor agonist isoproterenol (0.1 mM) had any effect. The alpha 2-adrenoceptor agonist/antagonist yohimbine (0.1 mM) persistently and more strongly decreased the [Cl-]i than UK 14304-18 did. The yohimbine-induced decrease in the [Cl-]i was not further altered by UK 14304-18 or phenylephrine, but partly reversed by noradrenaline, isoproterenol and an adenylate cyclase activator, forskolin (0.1 mM). The yohimbine-induced decrease in [Cl-]i was inhibited by the carbonic anhydrase inhibitor acetazolamide (1 mM), and Cl-/HCO3- exchange inhibitors, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, but not by the H(+)-ATPase inhibitor N,N'-dicylohexylcarbodiimide. The forskolin-induced recovery in [Cl-]i was inhibited by the Na+/K+/Cl- cotransport inhibitor bumetanide (0.1 mM), but not by the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1995

Detection of Hepatozoon canis oocyst from ticks collected from the infected dogs.

We collected 220 ticks from 58 dogs infected with Hepatozoon canis from 1990 to 1992 in Yamaguchi and Fukuoka prefectures, the western provinces of Japan. These ticks were identified as Haemaphysalis campanulata, H. longicornis, H. flava, Ixodes ovata, and I. nipponensis. By histopathological examination of these ticks, two oocysts which seemed to be those of H. canis were observed in the haemocoele of an adult female H. longicornis and a nymph H. flava tick. The oocyst, about 300 x 150 microns in size, was composed of 50 to 70 sporocysts with 10 to 16 banana-shaped sporozoites each.

Animals↗
PubMed1995

Effects of V1- and V2-vasopressin (AVP) antagonists on the pressor, AVP and atrial natriuretic peptide responses to a hypertonic saline infusion in conscious anephric rats.

To examine the role of vasopressin (AVP) receptors in the regulation of the hemodynamics and release of atrial natriuretic peptide (ANP), and the participation of renal nerve inputs in the osmotic AVP release, hypertonic saline (HS) was infused into conscious, bilaterally nephrectomized rats with non-peptide, selective antagonists for the V1-receptor or V2-receptor of AVP. In the control group, HS alone increased mean arterial pressure, plasma ANP and AVP, plasma volume and plasma osmolality, and decreased the heart rate. In the V1-receptor antagonist group, an increase in the mean arterial pressure and a decrease in heart rate were completely abolished and an increase in plasma ANP was attenuated. In the V2-receptor antagonist group, increases in mean arterial pressure and plasma ANP and a decrease in heart rate were attenuated. However, the ratio of the changes in heart rate to the changes in mean arterial pressure in the V2-receptor antagonist group is significantly higher than that in the control group. In both experimental groups, increases in plasma AVP, plasma volume and plasma osmolality were not different from those in the control group. These results suggest that a HS-induced increase in mean arterial pressure is mediated by the pressor effect of AVP, mainly through V1-receptors, and that the depressor effect of AVP through V2-receptors may not influence tonically HS-induced hypertension. Moreover, HS-induced increase in plasma ANP is mediated mainly by increases in plasma volume and blood pressure, but may not be affected by a direct action of AVP to the heart. Renal afferent nerve inputs may not have effects on the regulation of osmotic AVP release.

Animals↗
PubMed1995

Analysis of an epitope sequence recognized by a monoclonal antibody MAb-5H4 against a porcine zona pellucida glycoprotein (pZP4) that blocks fertilization.

The zona pellucida glycoprotein that surrounds the mammalian oocyte has several target antigens that have potential use in the development of a contraceptive vaccine. In the present study, an epitope sequence recognized by a monoclonal antibody to the porcine zona pellucida glycoprotein ZP4 was determined. Three candidate peptides were synthesized, based on an epitope mapping by cDNA and an analysis of chain flexibility of porcine ZP4. Only one synthetic peptide, corresponding to amino acid positions 50-67, reacted with the monoclonal antibody; the other synthetic peptides, corresponding to positions 60-79 and 70-100, did not react. The reactive epitope was identified as CTYVLDPENL, corresponding to positions 50-59 of porcine ZP4. The peptide inhibited the reaction of the monoclonal antibody binding to native ZP4 in a dose-dependent manner. When the synthetic peptide 50-67 was used to immunize mice, the resultant antisera reacted not only with the synthetic peptide but also with native pig zona pellucida. In addition, anti-peptide 50-67 antibody inhibited porcine fertilization in vitro. It is thus concluded that the peptide identified as an epitope for the monoclonal antibody would be a promising candidate for the development of a contraceptive vaccine.

Amino Acid Sequence↗