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Biomedical subjects

A Takada

Publications and source records attributed to A Takada.

At least 163 records · Page 9Linked to original sources
PubMed1995

Remnant-like lipoproteins stimulate whole blood platelet aggregation in vitro.

We have developed a simple, rapid assay method to measure remnant-like lipoproteins by using an immunoaffinity gel mixture of anti apo B-100 and apoA-1 antibodies to Sepharose 4B. Characterization of the unbound lipoproteins has shown that they represent chylomicron and VLDL remnant particles (RLP). Preincubation of whole blood with RLP resulted in the enhanced activation of aggregation with ADP and collagen. Such enhancement was not observed in the presence of lipoprotein deficient serum or albumin preparation. The extent of enhancement was 2.78 times by 7.5 microM of ADP and 44 times by 0.5 microgram/ml of collagen in the presence of RLP-preparation 1 (RLP-1), respectively. In the presence of RLP-2, the enhancement was 5.37 times by 7.5 microM of ADP and 102 times by 0.5 microgram/ml of collagen, respectively. On the other hand RLP slightly inhibited PRP aggregation by these agonists. Inhibitions were 19% by 7.5 microM of ADP and 18% by 1.0 microgram/of collagen in the presence of RLP-1, respectively. Incubation of whole blood with RLP did not result in the release of factors to stimulate platelets or ADP- or collagen-induced platelet aggregation in vitro. The extents of enhanced aggregation in whole blood or inhibition in PRP were not correlated with RLP-cholesterol nor RLP-protein concentrations of RLP preparations used. These results may indicate that RLP not only interact with platelets but with erythrocytes or leukocytes. Our findings support the hypothesis that the postprandial increase in remnant lipoproteins is an atherosclerotic risk factor and may be a part of the reasons of thrombotic complications by stimulating platelets in patients with remnant hyperlipoproteinemia.

Adenosine Diphosphate↗
PubMed1995

Increased procoagulant and antifibrinolytic activities in the lungs with idiopathic pulmonary fibrosis.

To elucidate the pathophysiology of idiopathic pulmonary fibrosis (IPF), we examined procoagulant (tissue factor:TF), fibrinolytic (tissue type plasminogen activator:t-PA and urokinase type plasminogen activator:u-PA) and antifibrinolytic (plasminogen activator inhibitor-1:PAI-1 and PAI-2) activities in bronchoalveolar lavage (BAL) supernatant fluids and BAL cell lysates obtained from IPF patients. The results indicated that TF levels in BAL supernatant fluids from IPF patients were higher than those of normal subjects, especially in patients with progressive disease, suggesting that TF levels in the lung correlate with disease activity. PAI-1 levels in BAL supernatant fluids were significantly higher in IPF patients than in normal subjects (1.7 +/- 4.1 vs 0 ng/mg protein). PAI-2 levels in BAL cell lysates were also significantly higher in IPF patients than those in normal subjects (14.4 +/- 12.2 vs 3.0 +/- 3.0 ng/mg protein). However, u-PA levels in both BAL supernatant fluids and BAL cell lysates did not differ between the two groups. These observations suggest that u-PA inhibition exceeded u-PA activity in alveolar lining fluid resulting in an antifibrinolytic condition. Immunohistochemical analysis showed that TF was intensely stained in cuboidal epithelial cells and PAIs were positively stained in alveolar macrophages (AMs) and cuboidal epithelial cells, suggesting that cuboidal epithelial cells as well as AMs contribute to the increased procoagulant and antifibrinolytic activities in the lungs of IPF patients.

Aged↗
PubMed1995

In vitro effect of endothelin-1 on collagen, and ADP-induced aggregation in human whole blood and platelet rich plasma.

The effect of ET-1 on ADP- and collagen-induced platelet aggregation in whole blood and platelet rich plasma (PRP) was studied in 39 healthy volunteers. Although ET-1 itself did not cause platelet aggregation, a marked enhancement of ADP-induced aggregation after the preincubation with ET-1 for 5 min was observed in whole blood, but not in PRP. This ET-1 concentration and preincubation time-dependent phenomenon could be demonstrated only at threshold concentrations (5 and 7.5 microM) of ADP and is probably due to an interaction of ET-1 with cells which are involved in the whole blood aggregation, such as polymorphonuclear neutrophils. In whole blood and PRP an inhibition of collagen-induced aggregation after the preincubation with ET-1 was detected. In contrast to ADP, a direct influence of ET-1 on platelet activation after the addition of collagen is therefore more likely. These results suggest that human platelets may possess ET-1 receptor(s) and that ET-1 may also interact with other blood cells.

Adenosine Diphosphate↗
PubMed1995

In vivo-synthesized radioactively labelled alpha-methyl serotonin as a selective tracer for visualization of brain serotonin neurons.

To investigate the use of alpha-[3H]methyl tryptophan (alpha-[3H]MTrp) as a tracer for the in vivo study of brain serotonergic neurons, we examined whether alpha-[3H]MTrp and its metabolite alpha-[3H]methyl serotonin (alpha-[3H]M5-HT) selectively label serotonergic neurons and whether once accumulated in these neurons, the radioactive metabolite behaves like endogenous serotonin. Rats received a systemic injection of 1-5 mCi of alpha-[3H]MTrp and 24 h later their brains were immediately removed or fixed by perfusion before removal. Tissue sections in which serotonergic neurons had been immunostained for 5-HT or its synthesizing enzyme, tryptophan hydroxylase, were processed for radioautography at the light and electron microscopic level. In another group of rats, the release of radioactivity from different brain areas was studied both under basal and depolarizing conditions. In the dorsal raphe nucleus, the light microscopic examination revealed almost complete colocalization between serotonergic neurons and those that accumulated radioactivity, with a heterogeneity in the content of alpha-[3H]M5-HT among the various cells. At the ultrastructural level, immunoidentified serotonergic perikarya and dendritic processes in the dorsal raphe nucleus, as well as nerve terminals in the cerebral cortex were also found to contain alpha-[3H]M5-HT. Under basal conditions, radioactivity was released from the brainstem raphe region and from projection areas such as the striatum and hippocampus. The basal output of alpha-[3H]M5-HT increased approximately twofold after a depolarizing 50 mM KCl solution was added to the perfusion fluid. These findings suggest that newly synthesized alpha-[3H]M5-HT can be released both at somatodendritic and terminal sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of beraprost sodium, a new prostaglandin I2 analog, on parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina.

The purpose of this study was to investigate the effects of beraprost sodium, a stable prostacyclin analog, on the parameters of hemostasis, fibrinolysis, and myocardial ischemia in patients with exertional angina. Thirty-one patients with exertional angina who had significant organic coronary artery stenosis in at least one of the three major coronary arteries were selected. All patients underwent quantitative exercise thallium-201 emission computed tomography before and 1 month after 120 micrograms per day of beraprost sodium administration. Before exercise, blood samples were collected from 8:30 a.m. to 9:30 a.m. after the patients had been lying in bed undisturbed for at least 10 minutes. Plasma platelet factor 4 (PF4), fibrinopeptide A (FPA), tissue plasminogen activator antigen (t-PA), and plasminogen activator inhibitor-1 activity (PAI-1) were measured. There were no significant differences in exercise parameters on both exercise tests. However, both the extent and severity scores of ischemia were significantly aggravated (p < 0.05 for both) during beraprost sodium administration. Plasma FPA levels decreased significantly during beraprost sodium administration (p < 0.01). Likewise, plasma PF4 levels decreased significantly during beraprost sodium administration (p < 0.05). As for plasma t-PA antigen levels, there was no significant difference before versus during beraprost sodium administration. Plasma PAI-1 activity levels decreased significantly during beraprost sodium administration (p < 0.05). The results indicate that beraprost sodium has strong antithrombogenic properties. However, its aggravation of myocardial ischemia may limit clinical usage.

Angina Pectoris↗
PubMed1995

Induction of protective antibody responses against pseudorabies virus by intranasal vaccination with glycoprotein B in mice.

Intranasal vaccination of mice with glycoprotein B (gB) of pseudorabies virus (PRV) induced specific IgA and IgG antibody responses in the secretion of the respiratory tract, resulting in protection of the animals against intranasal challenge with a lethal dose of virulent PRV. The immune response was enhanced by the use of cholera toxin B subunit as an adjuvant. The present results indicate that local vaccination with gB is a promising strategy to confer protective immunity on animals against PRV infection by inducing secretory antibodies on their mucosal surfaces where the primary replication of the virus occurs.

Administration, Intranasal↗
PubMed1995

Perpetuation of influenza A viruses in Alaskan waterfowl reservoirs.

To provide information on the mechanism of perpetuation of influenza viruses among waterfowl reservoirs in nature, virological surveillance was carried out in Alaska during their breeding season in summer from 1991 to 1994. Influenza viruses were isolated mainly from fecal samples of dabbling ducks in their nesting places in central Alaska. The numbers of subtypes of 108 influenza virus isolates were 1 H2N3, 37 H3N8, 55 H4N6, 1 H7N3, 1 H8N2, 1 H10N2, 11 H10N7, and H10N9. Influenza viruses were also isolated from water samples of the lakes where they nest. Even in September of 1994 when the most ducks had left for migration to south, viruses were still isolated from the lake water. Phylogenetic analysis of the NP genes of the representative isolates showed that they belong to the North American lineage of avian influenza viruses, suggesting that the majority of the waterfowls breeding in central Alaska migrate to North America and not to Asia. The present results support the notion that influenza viruses have been maintained in waterfowl population by water-borne transmission and revealed the mechanism of year-by-year perpetuation of the viruses in the lakes where they breed.

Alaska↗
PubMed1995

Spinocerebellar ataxia 1 (SCA1) in the Japanese: analysis of CAG trinucleitide repeat expansion and instability of the repeat for paternal transmission.

SCA1 is caused by expansion of an unstable CAG triplet repeat in a novel gene located on the short arm of chromosome 6. In 126 Japanese individuals from 12 pedigrees with SCA1, studies were done to determine if they carried this mutant gene. All the affected and pre-symptomatic individuals, determined by haplotype segregation analyses, carried an abnormally expanded allele with the range of 39-63 repeat units. This repeat size inversely correlated with the age at onset. However, contrary to reported results, size of the repeat did not correlate with gender of the transmitting parent. Therefore, the CAG triplet repeat instability on paternal transmission is not likely to be fundamental to SCA1.

Adolescent↗
PubMed1995

Efficacy of combination therapy with interferon and azidothymidine in chronic type C hepatitis: a pilot study.

The effects of interferon are seen in only a limited number of patients with hepatitis C virus (HCV) of the K1 type, indicating that a combination therapy with other antiviral drugs may be essential to obtain better results. In the present pilot study, the effects of combination therapy with interferon (IFN) and an antiviral drug azidothymidine (AZT) were analyzed. The combination therapy was conducted in 22 patients with chronic hepatitis C after obtaining their informed consent (combination group). Three or six million units of natural IFN alpha was administered daily for 3 weeks and then three times a week for 21 weeks. Combination therapy was initiated at the beginning of the 8th week of IFN treatment, 500 mg of AZT per day being given for 8 weeks. As a control, changes in HCV-RNA were also analyzed in patients treated with interferon alone (IFN-alone group). At the end of the treatment, blood was negative for HCV in 32.5% of the IFN-alone group and in 50.0% of the combination group, the difference not being significant. However, in patients with HCV-K1, HCV-negative rates were 14.2% in the IFN-alone group and 45.5% in the combination group, showing a significant difference. In patients with other HCV genotypes, HCV-negative rates did not different between the two groups. These results suggest that combination therapy with IFN and AZT may be an effective treatment for chronic type C hepatitis caused by the K1 type virus, although further studies on larger number of patients will be needed to obtain definite conclusions.

Adolescent↗
PubMed1995

Expression of renin and angiotensin-converting enzyme in human hearts.

To understand the significance of the tissue renin-angiotensin system in the heart, we examined the expression of renin and angiotensin-converting enzyme (ACE) in autopsied human hearts. Samples were taken from organs obtained at autopsy from 15 patients without heart disease and 3 patients with heart disease (old myocardial infarctions, acute myocardial infarctions, and hypertrophic cardiomyopathy). We examined the expression of renin and ACE mRNA by using the reverse transcription-polymerase chain reaction (RT-PCR). RT-PCR showed the expression of renin in the right atria in all patients. However, expression of renin mRNA in the left ventricles was not found in any of the 15 hearts without heart disease. In contrast, renin mRNA was detected in the left ventricles in hearts with heart disease. ACE mRNA was detected in both the atria and the ventricles in normal hearts, and its expression did not alter in diseased hearts. These findings suggest that renin mRNA is expressed mainly in the right atria in normal hearts, but that its expression in the left ventricle can be activated in some pathological conditions.

Adult↗
PubMed1995

CAG repeat expansion of Machado-Joseph disease in the Japanese: analysis of the repeat instability for parental transmission, and correlation with disease phenotype.

Machado-Joseph disease (MJD) is caused by abnormal expansion of an unstable CAG repeat in a novel gene locating on chromosome 14q32.1. We analysed this CAG repeat polymorphism with 66 Japanese MJD patients. All the patients were selectively associated with abnormal expansion of the CAG repeat. Repeat length of the mutant allele did not overlap that of normal allele and closely correlated with not only age at onset but also with clinical phenotypes. CAG repeat size is apparently related to a wide variety of phenotypic presentations in MJD.

Adult↗
PubMed1995

Effects of nicotine and electric footshock on peripheral serotonergic measures and on platelet aggregation in whole blood of rats.

The effects of nicotine and electric foot shock as well as of their combination on blood serotonergic measures and on whole blood aggregation have been analyzed. In rats subjected to electric footshock a rise (p < 0.05) in plasma but not in whole blood serotonin was observed, whereas this parameter was not influenced in nicotine-treated rats when compared to the control group. The combination of nicotine with electric footshock only slightly increased plasma serotonin and showed no effect on whole blood serotonin, but 5-hydroxyindole acetic acid (5-HIAA), the major metabolite of serotonin (5-HT), as well as the 5-HIAA/5-HT ratio were markedly increased (p < 0.01) suggesting an enhanced turnover of 5-HT under these conditions. The collagen-induced aggregation in whole blood was not influenced in nicotine-, in footshock- nor in combined-treated rats when compared to the controls. Our data indicate that stress as well as the combination of stress with nicotine may affect the serotonergic system which is in contrast to the exposure to nicotine alone.

Animals↗
PubMed1995

Changes in the central and peripheral serotonergic system in rats exposed to water-immersion restrained stress and nicotine administration.

The effects of water-immersion restraint stress (WS) on chronically nicotine-administered rats were studied in the blood and various regions of the brain. Serotonin (5-HT) levels increased in the hypothalamus, hippocampus, cortex and cerebellum following the administration of nicotine. 5-HT levels increased in all the brain regions following stress. Nicotine decreased stress-induced increased levels of 5-HT in the hippocampus and cerebellum. Nicotine administration alone increased 5-hydroxyindole acetic acid (5-HIAA) levels in the hippocampus and cerebellum. Stress alone also increased 5-HIAA levels in all the brain regions. In the cortex, 5-HT and 5-HIAA levels further increased following the administration of a combination of stress and nicotine compared to rats given stress alone. In the blood as well as in all the brain regions, except the cerebellum, stress or nicotine administration did not affect tryptophan levels. Stress given to nicotine-administered rats resulted in a decrease in tryptophan levels in the blood and plasma. Although 5-HT and 5-HIAA levels were not influenced by stress and/or nicotine administration, the 5-HIAA/5-HT ratio increased in the blood and plasma of rats administered with nicotine and exposed to stress. The effects of nicotine on the serotonergic system depend upon the kind of stress given together with the organs and brain regions involved.

Analysis of Variance↗
PubMed1995

Amino acids, serotonin, and 5-hydroxyindoleacetic acid following foot shock in rats.

Concentrations of tryptophan, serotonin (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) in brain and plasma, as well as plasma amino acid composition, were measured after 1-h foot shock. Stress induced a rise in both plasma and brain 5-HIAA, whereas 5-HT concentration was found to be increased only in plasma. A prominent rise in brain tryptophan was observed, whereas in plasma, foot shock caused a significant increase only in tryptophan level. Concentrations of other amino acids were found to be either decreased or unchanged. Ratio of tryptophan to the other long-chain neutral amino acids increased significantly following foot shock. It is possible that stress-related changes in 5-HT turnover are due to increased plasma tryptophan, in turn causing a rise in brain tryprophan, necessary to cope with enhanced 5-HT metabolism, reflected as a rise in 5-HIAA levels.

Amino Acids↗
PubMed1995

Scavenging effects of Mallotus repandus on active oxygen species.

The active oxygen species scavenging potencies of Mallotus repandus (Willd.) Muell.-Arg. extracts were evaluated by the electron spin resonance (ESR) spin-trapping technique. Superoxide radical (O2.-) and hydroxyl radical (OH.) were supplied enzymatically from hypoxanthine-xanthine oxidase (HPX-XOD) reaction and hydrogen peroxide-ferrous sulfate (Fenton reaction), respectively, to the assay system. The ethyl acetate fraction of Mallotus repandus (stem) showed the greatest superoxide radical scavenger activity and the n-hexane fraction of Mallotus repandus (stem as well as root) the greatest hydroxyl radical scavenger activity.

Antioxidants↗
PubMed1995

Synthesis of serotonin in traumatized rat brain.

Previous studies have demonstrated that focal freezing lesions in rats cause a widespread decrease of cortical glucose use in the lesioned hemisphere and this was interpreted as a reflection of depression of cortical activity. The serotonergic neurotransmitter system was implicated in these alterations when it was shown that (1) cortical serotonin metabolism was increased widely in focally injured brain and (2) inhibition of serotonin synthesis prevented the development of cortical hypometabolism. In the present studies we applied an autoradiographic method that uses the accumulation of the 14C-labeled analogue of serotonin alpha-methylserotonin to assess changes in the rate of serotonin synthesis in injured brain. The results confirmed that 3 days after the lesion was made, at the time of greatest depression of glucose use, serotonin synthesis was significantly increased in cortical areas throughout the injured hemisphere. The increase was also seen in the dorsal hippocampus and area CA3, as well as in the medial geniculate and dorsal raphe, but not in any other subcortical structures including median raphe. Present results suggest that the functional changes in the cortex of the lesioned hemisphere are associated with an increased rate of serotonin synthesis mediated by activation of the dorsal raphe. We also documented by alpha-[14C]aminoisobutyric acid autoradiography that there was increased permeability of the blood-brain barrier, but this was restricted to the rim of the lesion.

Animals↗
PubMed1995

Changes in laminin content in livers of patients with alcoholic liver disease.

An increase in serum laminin levels has been reported in patients with liver disease; however, the mechanisms for this increase have not yet been clarified. In the present study, the laminin content of liver biopsy specimens obtained from patients with alcoholic liver disease and non-alcoholic liver disease was determined with a one-step sandwich enzyme-immunoassay system, using monoclonal antibodies for human placental laminin. Hepatic laminin content was significantly higher in patients with liver disease than in normal controls. In alcoholic liver disease, the content in patients with mild fibrosis was lower than in patients with advanced types of alcoholic liver disease. In non-alcoholic liver disease, the hepatic laminin content tended to increase in parallel with the progression of fibrosis. The laminin content in alcoholic liver disease was significantly higher than in the corresponding type of non-alcoholic liver disease. The ratio of laminin to total collagen content was highest in alcoholic liver disease showing mild fibrosis and decreased in parallel with the progression of fibrosis. In contrast, the ratio was low in all types of nonalcoholic liver disease. The ratio in patients with alcoholic liver disease was significantly higher than these with the corresponding non-alcoholic liver disease. Hepatic laminin content increased in parallel with the increase in hepatic type IV collagen in alcoholic liver disease, and the correlation was statistically significant. However, similar correlation was not found in non-alcoholic liver disease. These results indicate that the response to laminin synthesis to alcoholic liver disease is strong in mild fibrosis and reached a plateau at a relatively early stage of fibrosis. The stimulation for laminin synthesis in non-alcoholic liver disease is different from that in alcoholic liver disease.

Adult↗