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Biomedical subjects

M Miyamoto

Publications and source records attributed to M Miyamoto.

At least 397 records · Page 22Linked to original sources
PubMed1990

[Valvuloplasty for acute mitral insufficiency caused by torn chordae (Carpentier method): report of a case].

A 66-year-old female was admitted to our hospital with acute heart failure (NYHA III), and diagnosed as an MR + Tr. The cause of MR was torn chordae of the posterior leaflet of the mitral valve. A prolapse part of the posterior leaflet was resected and sutured by McGoon's method. Valvuloplasty was performed by using a Carpentier ring. Postoperative course was uneventful. She recovered well after the operation. Histological examination of the valve showed myxomatous degeneration.

Aged↗
PubMed1989

Convulsant peptides related to corticotropin-releasing factor (CRF).

Corticotropin-releasing factor (CRF) and its related peptides have some conserved primary regions. We have taken an interest in the characteristic conserved sequence, Pro-Pro-Ile-Ser, which is located in the proximal N-terminal region of the CRF family. This sequence is not included in any other biologically active peptide and protein. Biological function of this N-terminal region has not become known yet. We synthesized seventeen peptide fragments of human CRF and sauvagine which involved either this entire N-terminal sequence or part of it and determined their behavioural effect after intracerebroventricular injections to mice. Several peptides which included the Pro-Pro-Ile region as the N-terminal segment and their caused a transient convulsion dose-dependently. H-Pro-Pro-Ile-OH (human CRF(4-6)) exhibited the strongest effect among these active peptides. However, these convulsant peptides did not affect the secretion of immunoreactive corticotropin in rats.

Amino Acid Sequence↗
PubMed1989

Interleukin-6 as a neurotrophic factor for promoting the survival of cultured basal forebrain cholinergic neurons from postnatal rats.

Human recombinant interleukin-6 (IL-6, B-cell stimulating factor-2) was capable of supporting neuronal survival in cholinergic neuron culture, prepared from 10-day-old rat brain septal region. Cell survival of the cultured cholinergic neurons was estimated by measuring the remaining choline acetyltransferase (ChAT) activities after 6 days of culture. IL-6 at a concentration of 5 ng/ml maintained a more than 3-fold higher ChAT activity in the culture as compared with that in cultures without IL-6. The maximal dose of IL-6 was near 50 ng/ml. The concomitant addition of mouse nerve growth factor (NGF) and IL-6, both at maximal doses, had a synergistic effect on cholinergic cell survival. These results indicate that IL-6 can act as a neurotrophic agent, independent of the action of NGF, supporting neuronal survival of cultured postnatal rat septal cholinergic neurons. On the other hand, IL-6 did not affect the differentiation of the cultured embryonic rat septal cholinergic neurons, differently from the differentiation action by NGF.

Animals↗
PubMed1989

Structurally similar but functionally distinct factors, IRF-1 and IRF-2, bind to the same regulatory elements of IFN and IFN-inducible genes.

Viral infections commonly induce expression of type I interferon (IFN) genes. The induction is transient and involves transcriptional activation wherein a positive factor, IRF-1, binds to upstream regulatory cis elements. In the present study we report the isolation of a cDNA encoding a novel factor, termed IRF-2, that interacts with the same nucleotide sequence elements as IRF-1. Both genes are inducible not only by virus but also by IFN. Unlike IRF-1, IRF-2 does not function as an activator; rather, it suppresses the function of IRF-1 under certain circumstances. Our results suggest that transcription of the IFN and IFN-inducible genes is regulated by two similar trans-acting factors that apparently compete for the same cis-acting recognition sequences, but which have opposite effects.

Amino Acid Sequence↗
PubMed1989

A case of concomitant association of duodenal carcinoma and jejunal carcinoma with cerebral metastasis.

A case of concomitant association of primary suprapapillary and jejunal carcinomas with cerebral metastasis is reported. A 42-year-old woman was admitted to our hospital complaining of melena. Preoperative endoscopy and abdominal angiography showed primary suprapapillary carcinoma, and brain CT showed a high density mass in the right parietal lobe causing involuntary movement of the left upper extremity. During surgery another tumor was revealed in the jejunum about 80 cm from the Treitz' ligament. These were removed surgically and examined histologically.

Adenocarcinoma↗
PubMed1989

Involvement of a cis-element that binds an H2TF-1/NF kappa B like factor(s) in the virus-induced interferon-beta gene expression.

Interferon-beta (IFN-beta) gene is transcriptionally activated following virus infection of various cell types such as fibroblasts. In the previous studies, regulatory DNA sequences that mediate the virus-induced transcriptional activation have been identified within the 5'-flanking region (up to around -117 respect to the CAP site) of the human IFN-beta gene. The sequences contain binding sites (-100 to -61) for a transcriptional activator, IRF-1, the gene of which is also virus-inducible. In the present study, we focused on an additional cis-element, located between the IRF-1 binding sites and TATA box. Interestingly, the element coincides with the previously identified elements for the transcription factors H2TF-1 and NF kappa B. The element, when tandemly repeated, functions in activating the distal gene expression in either constitutive or virus-inducible manner depending on the cell type. The results suggest the importance of cooperation between IRF-1 and H2TF-1/NF kappa B-like factor in the maximal IFN-beta gene induction.

Animals↗
PubMed1989

Colocalization of NGF receptor immunoreactivity and [3H]GABA uptake activity in developing rat septum/diagonal band neurons in vitro.

Neurons in the septum (SEP) and vertical limb of the diagonal band (vDB) of 6-day-old rats were dissociated and cultured for 3 days. Cells with high affinity uptake mechanism for gamma-aminobutyric acid (GABA) were identified autoradiographically using 16 nM [3H]GABA. Cells that expressed nerve growth factor (NGF) receptor immunoreactivity were identified immunocytochemically using MC192, a monoclonal antibody against NGF receptor. Double labeling experiments combining [3H]GABA uptake with immunostaining for NGF receptor showed that 46% of the NGF receptor-immunoreactive cells accumulated [3H]GABA. The result was discussed in relation to a possible involvement of the developing septal GABAergic neurons in NGF-induced neuronal survival.

Animals↗
PubMed1989

Nerve growth factor promotes survival of retrogradely labeled hippocampus-projecting neurons in the rat basal forebrain in vitro.

The effect of nerve growth factor (NGF) on the survival of neurons projecting to the hippocampus from developing medial septum and vertical limb of the diagonal band was studied in vitro. The neurons had previously been labeled retrogradely in vivo with fluorescent latex microspheres. The microspheres were injected bilaterally into the hippocampus of 5-day-old rats. Twenty to 24 h after the injection, cells from the basal forebrain were dissociated with papain and cultured for 3-5 days. The number of microsphere-labeled neurons in the culture with supplementation of NGF was much greater than that without NGF. The result clearly indicates a survival-promoting effect of NGF on these projection neurons.

Animals↗
PubMed1989

Induction of endogenous IFN-alpha and IFN-beta genes by a regulatory transcription factor, IRF-1.

Interferons (IFNs) have an important role in cell growth and differentiation. The most well-known function of IFNs is their antiviral activity; viral infections result in induction of the transcription of the IFN-alpha and IFN-beta genes. Recently we isolated the gene encoding a transcription factor, IRF-1, that may play a part in the induction of IFN genes. Interestingly, the IRF-1 gene itself is virus-inducible, suggesting the importance of de novo production of IRF-1 in IFN gene induction. Here we show that high-level expression of the cloned mouse IRF-1 gene in monkey COS cells results in the induction of endogenous IFN-alpha and IFN-beta genes without viral stimulation. Furthermore, we demonstrate the induction of these genes by an IRF-1/yeast GAL4 chimaeric transcription factor. This may be the first demonstration of the specific induction of silent chromosomal genes by transfection of a single transcription factor gene in mammalian cells.

Animals↗
PubMed1989

[Effects of glucagon and insulin on poly(ADP-ribose) polymerase activity and blood ketone body ratio after partial hepatectomy in rats].

The effects of glucagon and insulin on liver nuclear poly(ADP-ribose) polymerase activity and blood ketone body ratio after rat partial (68%) hepatectomy were examined. Liver weight regeneration rate was enhanced by glucagon and insulin after 5th posthepatectomy day. The maximal value of poly(ADP-ribose) polymerase activity without glucagon and insulin was revealed as 368 +/- 64 pmole/mg/min on 5 days after the hepatectomy. In contrast, the enzyme activity with glucagon and insulin reached to the peak value as 253 +/- 42 pmole/mg/min on 2 days after the hepatectomy. The amounts of DNA per nuclear protein showed similar changes with the changes of poly (ADP-ribose) polymerase activity after the hepatectomy. Blood ketone body ratio showed almost similar changes in both groups, except transitional decrease in the group without glucagon and insulin on 5th postoperative day. It is suggested that, to promote remnant liver regeneration, the combined therapy of glucagon and insulin may act directly to nucleic acid metabolism through the changes of poly(ADP-ribose) polymerase activity and preserve energy charge level by the suppression of NAD consumption by massive poly(ADP-ribose) formation.

Animals↗
PubMed1989

Myocardial protection by a left ventricular assist device during reperfusion following acute coronary occlusion.

To evaluate the effects of a left ventricular assist device (LVAD) during the reperfusion period following acute coronary occlusion, sixteen mongrel dog hearts were subjected to 1 hour's occlusion of the circumflex coronary artery and then reperfused for 6 hours. In seven control dogs (control group), the hearts were reperfused without any support. In nine LVAD dogs (LVAD group), however, the left ventricles were supported by the application of a pneumatic driven diaphragm-type pump for 5 hours and then reperfused for another hour without any device. Triphenyltetrazolium chloride was used to determine the extent of infarction. The results showed a significant reduction in the area of infarct (AI) as a percentage of the area at risk (AR) in the LVAD group compared with the control group, the AI/AR being 22.3 per cent for the control group versus 4.8 per cent for the LVAD group (p less than 0.05). The cardiac output was also significantly higher in the LVAD group compared with the control group. The per cent systolic shortening in the ischemic region of the LVAD group showed a significantly better recovery, being 75.8 per cent for the LVAD group versus 24.4 per cent for the control group (p less than 0.01). It was concluded that the application of a LVAD during reperfusion after 1 hour's coronary occlusion results in a significant reduction of infarct size and provides improvement in both regional and global cardiac function.

Animals↗
PubMed1989

Analysis of epidermal growth factor (EGF) receptor and effect of EGF on the growth of cultured Graves' and non-neoplastic human thyroid cells.

We analyzed epidermal growth factor receptors (EGF-R) and the growth stimulatory effects of epidermal growth factor (EGF) in the presence or absence of TSH on cultured human non-neoplastic and Graves' thyroid cells. All cells studied possessed EGF-R composed of two components. There was no significant differences in the binding characters of EGF-R among non-neoplastic thyroid cells whether they were obtained from thyroid tissues adjacent to malignant carcinoma or benign adenoma. Ten nM of EGF stimulated (3H)-thymidine (dTR) incorporation of non-neoplastic thyroid cells by about 50%. However, TSH had no effect on the growth of these cells. Both EGF-R binding parameters and cell proliferation effects of EGF and TSH were simultaneously examined in non-neoplastic thyroid cells from 8 patients. A significant inverse correlation (r = -0.757) was observed between binding affinity (Ka1) and EGF-induced increase of dTR incorporation. Binding capacity (Cmax) did not correlate significantly with dTR incorporation. In Graves' thyroid cells, all parameters of EGF-R were significantly lower than those of non-neoplastic thyroid cells, higher basal dTR incorporation was observed, and their goiter size significantly correlated with EGF-induced increase of dTR incorporation (r = 0.879) and also appeared to correlate inversely with Ka1. These data indicate a close relationship between the binding affinity of EGF-R and thyroid cell growth.

Cell Division↗
PubMed1989

Characterization of Japanese encephalitis virus envelope protein expressed by recombinant baculoviruses.

Recombinant baculoviruses containing the coding sequences of the viral structural proteins, i.e., the capsid (C) protein, the precursor to premembrane (preM) protein, and the envelope (E) protein, as well as a nonstructural protein, NS1, of Japanese encephalitis virus (JEV) were constructed. Infection of Spodoptera frugiperda cells with these recombinant viruses produced PreM and E proteins. The E proteins synthesized by the recombinants were shown to be glycosylated and similar in size to the authentic E protein. The E protein was found on the surface of infected cells. The antigenic properties of recombinant E proteins were evaluated using a panel of monoclonal antibodies produced against JEV E protein. It was demonstrated that all of the epitopes detectable on the authentic JEV E protein were present on the recombinant E protein expressed by a recombinant baculovirus containing the coding sequence for a part of C, PreM, E, and a part of NS1 proteins. However, for E protein expressed by a recombinant baculovirus having the coding sequence of only a part of PreM, but all of E and a part of NS1, one of the flavivirus cross-reactive epitopes was not detected. Mice immunized with cells infected with the recombinant baculoviruses developed neutralization antibodies.

Animals↗
PubMed1989

Platelet aggregation induced by latex particles. I. Effects of size, surface potential and hydrophobicity of particles.

Latex particles induced platelet aggregation associated with the release of ATP from the platelets. The smaller the diameter of particles having the same surface structure, the greater numbers or greater total surface area of particles were required for both reactions. The higher hydrophobic and higher negatively charged particles, having a diameter of about 0.3 micron, induced platelet aggregation most easily. Hydrophilic particles without high negative surface potential activated platelets only a little. Particle-induced platelet aggregation is not only caused by colloidal electronic force and hydrophobic interaction between platelets and latex particles but also by factors concerning cell activation.

Adenosine Triphosphate↗
PubMed1989

Effects of idebenone on memory impairment induced in ischemic and embolization models of cerebrovascular disturbance in rats.

Two rat models of memory impairment in passive avoidance learning induced by cerebrovascular disturbance, were established to estimate the effects of a cerebral metabolic enhancer, idebenone. Transient and global cerebral ischemia in rats, produced by 4-vessel occlusion for 200 s immediately after the acquisition trial of passive avoidance learning, shortened the latencies in the retention test trial performed 24 h later. This retrograde amnesia was reversed significantly by idebenone administered orally or intraperitoneally at the doses of 10 and 30 mg/kg before the retention test trial. Idebenone at a dose of 10 mg/kg, given intraperitoneally before or immediately after the ischemia, also markedly inhibited the appearance of amnesia. In the second model, permanent and cerebral hemisphere embolization produced by injecting 2,000 microspheres into the internal carotid artery, significantly impaired passive avoidance learning performed 7 days later. The repeated administration of idebenone (30 mg/kg, i.p.). once a day after the embolization, significantly improved the impairment of passive avoidance learning in the embolized rats. Furthermore, physostigmine and arginine-vasopressin as reference compounds improved the impairment of passive avoidance learning in these models. These findings suggest that idebenone ameliorates memory impairment induced by cerebral vascular disturbance in rats.

Administration, Oral↗
PubMed1989

Protective effect of idebenone against hypoxia in mice.

The effects of idebenone on survival time of mice subjected to hypoxia induced by N2 and CO2 inhalation and KCN injection were studied. Idebenone (10, 20, 50 and 100 mg/kg, i.p.) prolonged the survival time of mice exposed to a hypoxic condition (98% N2, 2% O2) in a dose-dependent manner: significant prolongations were observed at doses higher than 20 mg/kg. The drug also exerted a similar elongation effect at the same doses under conditions of 100% CO2 gas inhalation and KCN injection (3 mg/kg, i.v.). The results suggest that idebenone protects against hypoxia by improving cerebral energy metabolism.

Animals↗
PubMed1989

Glutamate toxicity in a neuronal cell line involves inhibition of cystine transport leading to oxidative stress.

Glutamate binds to both excitatory neurotransmitter binding sites and a Cl(-)-dependent, quisqualate- and cystine-inhibited transport site on brain neurons. The neuroblastoma-primary retina hybrid cells (N18-RE-105) are susceptible to glutamate-induced cytotoxicity. The Cl(-)-dependent transport site to which glutamate and quisqualate (but not kainate or NMDA) bind has a higher affinity for cystine than for glutamate. Lowering cystine concentrations in the cell culture medium results in cytotoxicity similar to that induced by glutamate addition in its morphology, kinetics, and Ca2+ dependence. Glutamate-induced cytotoxicity is directly proportional to its ability to inhibit cystine uptake. Exposure to glutamate (or lowered cystine) causes a decrease in glutathione levels and an accumulation of intracellular peroxides. Like N18-RE-105 cells, primary rat hippocampal neurons (but not glia) in culture degenerate in medium with lowered cystine concentration. Thus, glutamate-induced cytotoxicity in N18-RE-105 cells is due to inhibition of cystine uptake, resulting in lowered glutathione levels leading to oxidative stress and cell death.

Animals↗