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Biomedical subjects

A Endo

Publications and source records attributed to A Endo.

At least 73 records · Page 4Linked to original sources
PubMed1999

The activation of the tissue plasminogen activator-plasmin system induced in the mouse hippocampus after injection of trimethyltin: possible proteolysis of highly polysialylated NCAM.

Trimethyltin (TMT) is a neurotoxicant that causes the death of granule cells and degrades highly polysialylated NCAM (PSA-NCAM) in the dentate gyrus. To investigate the role of the tPA-plasmin system in the degradation of PSA-NCAM, we injected trimethyltin (TMT) into mice. As a result, tPA activity was significantly increased in CA1-CA4 and the dentate gyrus after TMT injection. These results suggest that up-regulated tPA may contribute to the degradation of PSA-NCAM.

Animals↗
PubMed1999

Inhibition of plasminogen activator inhibitor-1 by 11-keto-9(E),12(E)-octadecadienoic acid, a novel fatty acid produced by Trichoderma sp.

We have recently found a novel fatty acid, 11-keto-9(E),12(E)-octadecadienoic acid (KOD), that enhances fibrinolytic activity of endothelial cells. The mechanism of action of KOD has been investigated. KOD increased 2-fold the plasmin activity of bovine aortic endothelial cells at 250 microM. The stimulation was dependent on plasminogen and was inhibited by anti-urokinase, whereas KOD did not enhance the urokinase-catalyzed plasminogen activation and the resulting plasmin activity in a cell-free system. Neither the production of urokinase nor the conversion of pro-urokinase to the active, two-chain form was elevated by KOD, but it decreased plasminogen activator inhibitor-1 (PAI-1) activity of cells and inactivated PAI-1 irreversibly in a purified system. These results demonstrated that the KOD enhancement of endothelial fibrinolytic activity was mediated, at least in part, by inactivation of PAI-1.

Animals↗
PubMed1999

QRST integral analysis of body surface electrocardiographic mapping for assessing exercise-induced changes in the spatial distribution of local repolarization properties in patients with coronary artery disease and in patients with previous anterior infarction.

We studied resting, postexercise, difference (postexercise - rest) QRST isointegral maps, and the correlation coefficient between resting and postexercise maps. Study I Fifteen controls and 48 patients without previous myocardial infarction were studied. In coronary syndrome X group (n = 14), no patients showed an abnormally negative area on the postexercise map. In coronary ST depression group (n = 26), 12 patients (46%) showed an abnormally negative area on the postexercise map, and the correlation coefficient was low. Although all control, syndrome X, and coronary ST depression patients showed the global-downward type of difference map, coronary ST elevation patients (n = 8) showed the right-downward and left-upward type, right-upward and left-downward type, or reversed saddle type. Coronary ST depression is related to a globally marked decrease in local repolarization forces. Coronary ST elevation is associated with multidirectional changes in local repolarization forces. Study II Fifty-one patients with previous anterior infarction (29 with residual ischemia and 22 without) were studied. The incidence of the global-positive type of maps was increased and that of the saddle-type map was decreased from rest to postexercise in both groups. The global-upward type or right-downward and left-upward type of difference map was observed in both groups, but the reversed saddle type, right-upward and left-downward type, or global-downward type was observed in the residual ischemia group (34%, 24%, and 14%, respectively). Residual ischemia causes multidirectional changes or a global decrease in local repolarization forces. In both studies, multidirectional changes in local repolarization forces may be related to the vulnerability to ventricular arrhythmias.

Adult↗
PubMed1998

Induction of low-density lipoprotein catabolism in Hep G2 cells by a fungal sesquiterpene ester, FR111142.

A search for agents that can enhance low density lipoprotein (LDL) catabolism in Hep G2 cells has led to the identification of a fungal sesquiterpene ester, FR111142, as an active compound. The treatment of Hep G2 cells with 40 microM FR111142 at 37 degrees C for 18 h caused a 1.9- to 2.2-fold elevation of binding, internalization and degradation of 125I-LDL in the cells. The Scatchard analysis of the specific 125I-LDL binding demonstrated that the agent caused an increase in the maximum LDL binding along with a slight decrease in the apparent dissociation constant value. The effect of FR111142 was not seen in cells treated by the agent for shorter periods or in cycloheximide-treated cells, suggesting that the effect involves an induction of LDL binding sites. Unlike 3-hydroxy-3-methyglutaryl CoA reductase inhibitors, FR111142 affected neither cholesterol synthesis nor the level of LDL receptor in Hep G2 cells. These results suggest that FR111142 enhances LDL catabolism in Hep G2 cells by a mechanism that involves a receptor other than LDL receptor.

Anticholesteremic Agents↗
PubMed1998

Proteolysis of highly polysialylated NCAM by the tissue plasminogen activator-plasmin system in rats.

Tissue-type plasminogen activator (tPA), a serine protease which converts the zymogen plasminogen to the active protease plasmin, is believed to regulate neurite extension and neural cell migration by modulating extracellular metabolism. The highly polysialylated form of the neural cell adhesion molecule (NCAM-H) is strongly expressed in the developing brain and is believed to play a role in organizing the neural network. In this report, we incubated neonatal rat brain homogenates with human tPA and rat plasminogen in order to determine whether NCAM-H would be degraded. NCAM-H was degraded by plasmin which was formed from rat plasminogen by human tPA. The degradation was inhibited by the addition of plasminogen activator inhibitor type 1 (PAI-1) or aprotinin. These results suggest a possible contribution of the tPA-plasmin system to NCAM-H turnover in the developing brain.

Aging↗
PubMed1998

Effects of a new angiotensin-converting enzyme inhibitor, alacepril, on changes in neurohormonal factors and arterial baroreflex sensitivity in patients with congestive heart failure.

OBJECTIVE: Patients with heart failure have abnormal neurohormonal regulation during orthostatic stress, and abnormal arterial baroreflex function. This study investigated the effects of alacepril, a new angiotensin-converting enzyme inhibitor with sulfhydryls, on changes in neurohormonal factors during tilt and on the arterial baroreflex control of heart rate. METHODS: Plasma concentrations of noradrenaline, adrenaline, renin activity, angiotensin II, and atrial natriuretic peptide were measured at supine rest and after 30 degrees head-up tilt with measurements of central venous pressure and cardiac dimensions in seven patients with congestive heart failure (65 years, ejection fraction = 34%). Arterial baroreflex control of heart rate was assessed by phenylephrine bolus. The arterial baroreflex test was re-examined 3 h after oral alacepril (37.5 mg). The tilt and arterial baroreflex tests were repeated 12 weeks after alacepril treatment (50 mg x day(-1)). RESULTS: Heart rate, blood pressure, and neurohormonal factors did not differ before and after chronic alacepril, except for a trend toward an increase in renin activity (2.0 vs 4.9 ng x ml(-1) x h(-1)). Head-up tilt decreased central venous pressure (-2.5 mmHg) with a decrease in cardiac dimensions in the pre-alacepril phase. These changes were accompanied by increases in noradrenaline, adrenaline, and angiotensin II and a decrease in atrial natriuretic peptide. After chronic alacepril, the increase in noradrenaline during head-up tilt tended to be smaller (84 vs 30 pg x ml(-1)), with similar changes in central venous pressure (-3.4 mmHg) and cardiac dimensions. Both acute (3.6 vs 4.8 ms mmHg(-1)) and chronic (3.6 vs 6.7 ms mmHg(-1)) alacepril treatment was associated with a trend towards an increase in the arterial baroreflex control of heart rate. CONCLUSION: These results suggest that treatment with alacepril may cause a reduction of sympathetic activation during orthostatic stress and may enhance arterial baroreflex function in patients with mild to moderate heart failure.

Aged↗
PubMed1998

Phylogenetic analyses of the matrix and non-structural genes of equine influenza viruses.

Matrix (M) and nonstructural (NS) genes of thirteen equine H3N8 and H7N7 influenza viruses were sequenced and analyzed from an evolutionary point of view. The M and NS genes of H3N8 viruses isolated between 1989 and 1993 evolved into two minor branch clusters, including isolates from Europe and the American continent, respectively. It was noteworthy to reveal that the nucleotide sequences of the M and NS genes of an earlier American strain showed highest homology to those of recent European viruses. "Frozen evolution" was observed in the M and NS genes of A/eq/LaPlata/1/88. It was also evident that the NS gene of an H7N7 virus from 1977 was very similar to that of a 1979-H3N8 virus, while the M gene was closest phylogenetically to that of the earliest H7N7 virus isolated in 1956. Furthermore, the M2 protein of A/eq/Newmarket/1/77 virus contained a carboxyl terminal deletion of three amino acids. The evolutionary rates of the M and NS genes of H3N8 equine influenza viruses were estimated to be 5.4 x 10(-4) and 5.1 x 10(-4) substitutions per site per year, respectively, which were slower than those of human viruses.

Amino Acid Sequence↗
PubMed1998

Enhancement of low density lipoprotein binding to both low density lipoprotein receptor-positive and -negative cells by tetracycline antibiotics.

Some tetracycline (TC) antibiotics, including TC and anhydrotetracycline, have been found to enhance specific binding of low density lipoprotein (LDL) to both LDL receptor-positive and -negative cells at relatively higher concentrations. When incubated at 37 degrees C, the ability of LDL receptor-negative human fibroblasts to bind 125I-LDL was increased from < 2 to 45 ng/mg by 170 microM TC. In normal human fibroblasts and Hep G2 cells, 125I-LDL binding was elevated 1.4- to 2-fold by 113 microM TC. The 125I-LDL binding in the presence of TC was diminished by both heparin and EDTA. The enhancement by TC was not observed when 125I-LDL binding was assayed at 4 degrees C. TC enhanced LDL binding to paraformaldehyde-fixed Hep G2 cells, excluding LDL receptor induction in the mechanism. These results demonstrated that TC enhanced cellular LDL binding through a process not involving functional LDL receptors.

Anti-Bacterial Agents↗
PubMed1998

Effects of spironolactone on exercise capacity and neurohormonal factors in patients with heart failure treated with loop diuretics and angiotensin-converting enzyme inhibitor.

1. Treatment with spironolactone is reported to be useful when combined with loop diuretics and an angiotensin-converting enzyme (ACE) inhibitor in severe congestive heart failure (CHF). However, the effects of the addition of spironolactone on exercise capacity and neurohormonal variables have not been demonstrated. This study determined the effects of additive spironolactone on exercise capacity and neurohormonal factors in patients with mild CHF. 2. Oxygen uptake (VO2), plasma norepinephrine (NE), renin activity (PRA), angiotensin II (AII), aldosterone (ALD), and atrial natriuretic peptide (ANP) were measured at rest and after peak exercise in nine patients with CHF (six idiopathic and three ischemic cardiomyopathy; New York Heart Association (NYHA) classes II and III) who were already taking furosemide (mean 29 +/- 5 mg/day) and enalapril (mean 4.7 +/- 0.8 mg/day). Studies were repeated after 16 weeks of treatment with additive single daily dose of 25 mg of spironolactone. In four of nine patients, the exercise test was repeated after a 4-weeks washout of spironolactone. 3. Treatment with spironolactone caused natriuresis, decreased cardiothoracic ratio in chest X-ray (before vs. after treatment: 53.7 +/- 1.2 vs. 50.7 +/- 1.4%, P < 0.01), and improved NYHA functional class. Peak VO2 (17.1 +/- 1.6 vs. 17.5 +/- 2.2 ml/min/kg, NS) and heart rate and blood pressure responses to exercise were not altered. Resting NE (215 +/- 41 vs. 492 +/- 85 pg/ml, P < 0.01) and resting PRA (8.2 +/- 2.3 vs. 16.2 +/- 4.1 ng/ml/hr, P < 0.01) as well as peak NE (1618 +/- 313 vs. 2712 +/- 374 pg/ml, P < 0.01) and peak PRA (12.8 +/- 3.2 vs. 28.1 +/- 11.8 ng/ml/hr, P = 0.17) were augmented after additive spironolactone. ALD and AII were insignificantly increased, and ANP was insignificantly decreased at peak exercise after spironolactone treatment. Spironolactone washout was associated with a trend of the neurohormones to return toward pretreatment values. 4. In conclusion, chronic additive treatment with spironolactone was associated with neurohormonal activation both at rest and during exercise without changing the exercise capacity of patients with mild CHF who were already on loop diuretics and ACE inhibitor therapy.

Adult↗
PubMed1998

Time-dependent chemical compositions of 13N and 15O induced in air by the operation of a high energy electron accelerator.

Time-dependent chemical compositions for 13N and 15O induced in the air atmosphere of a high energy electron accelerator room have been studied using a computer simulation method. A radiation chemistry model was developed to describe the chemical reactions of 13N and 15O species with the air molecules and their radiolytic products. By assuming several chemical forms of 13N and 15O generated by the (gamma, n) reaction, the variations of the concentrations of 13N and 15O species were simulated under a radiation field. From the comparison between the simulations and experiment in a 100 MeV electron linear accelerator (linac) facility, the following conclusions were obtained: (1) Just after the (gamma, n) reaction, 25-50% of 13N and 15O are present as atoms (13N, 15O) and/or their ions (13N+, 15O+) and the remainder as nitrogen and oxygen molecules (13NN, 15OO) and/or their ions (13NN+, 15OO+); (2) Neutralization of 13N+ and 15O+ ions into 13N and 15O atoms occurs instantaneously and the same is the case with the neutralization of 13NN+ and 15OO+ ions to 13NN and 15OO molecules; (3) The neutralized 13N and 15O atoms react with the air molecules and the radiolytic products to form nitrogen oxide compounds and ozone, while 13NN and 15OO remain as these molecules. Factors that control the chemical reactions of 13N and 15O are discussed.

Computer Simulation↗