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Biomedical subjects

M Miyamoto

Publications and source records attributed to M Miyamoto.

At least 433 records · Page 24Linked to original sources
PubMed1989

[Congenital coronary artery fistula draining into the superior vena cava with giant saccular aneurysm--report of a case].

A 42-year-old woman who had a coronary artery fistula, associated with a giant coronary saccular aneurysm was reported. The coronary artery fistula originated from the proximal portion of the right coronary artery drained into the superior vena cava. The chief complaint was heart murmur which was detected at the 2nd intercostal space of the right sternal border. No other symptoms were present. The aneurysm was approximately 5 X 7 cm in size. In the operation using cardiopulmonary bypass, the proximal and distal portions of the coronary artery fistula were ligated successfully without aneurysmorrhaphy. The postoperative conditions was even without any complications. Congenital coronary artery fistulas with a giant saccular aneurysm should be surgically treated as soon as possible because of potential risk of aneurysmal rupture.

Adult↗
PubMed1989

[Early operation for postinfarction ventricular septal perforation; report of three cases].

Three patients underwent surgery for postmyocardial infarction ventricular septal perforation (VSP) within 3 to 21 days after onset of infarction. The hemodynamic stabilization was not obtained despite aggressive medical treatment including Intra-aortic Balloon Pumping (IABP) in one patient. The others had sudden hemodynamic deterioration during IABP support. In two of the three cases, the VSP were closed via transinfarct ventriculotomy with double Dacron patch, and ventricular wall reconstruction was performed to sandwich the double septal patch between ventricular free walls with Dacron felt strips. Two of the three patients survived. Our experience suggests that early surgical intervention is essential unless medical therapy results in clinical improvement and the double patch method may provide a successful operative repair and comeout.

Adult↗
PubMed1989

[Anesthetic management of caesarean section in a patient with idiopathic thrombocytopenic purpura and placenta praevia].

A 24-year-old female with idiopathic thrombocytopenic purpura (ITP) and total placenta praevia was scheduled for caesarean section. Anesthetic management during caesarean section with ITP and placenta praevia is critical because of possibility of massive intra- and postpartal bleeding. The patient received prednisolone 30 mg per day for 10 days before surgery. Bleeding time and value of platelet count returned to normal range on the operative day. Hydrocortisone 100 mg and atropine sulfate 0.3 mg were given intravenously just before the start of anesthesia. Anesthesia was induced with thiamylal 4 mg.kg-1 and SCC 1 mg.kg-1 and maintained with N2O-O2-enflurane. A baby girl was delivered after 7 min, and the Apgar score was 9 at 1 min after delivery. Intraoperative bleeding totaled 1,314 ml, but we could avoid total hysterectomy.

Adult↗
PubMed1989

Beige rat: a new animal model of Chediak-Higashi syndrome.

Although Chediak-Higashi syndrome (CHS) has been found in various mammalian species, it has not been described in rats. Since giant granules characterizing CHS are easily recognizable in mast cells of beige (CHS) mice, we screened mast-cell granules in the auricle of some mutant rats, of which coat color was diluted by mutation. Giant granules of mast cells were found in a mutant trait that occurred in the inbred colony of the DA strain rat maintained in Hamamatsu University School of Medicine. Giant granules were also observed in neutrophils and pigment cells of the eye. In this mutant, either spontaneous migration or chemotaxis of neutrophils was impaired, and the bleeding time was prolonged. Blood serotonin level of the mutant was about one tenth that of the normal congenic rat, and injection of serotonin normalized the bleeding time of the mutant. Moreover, the natural killer activity of the mutant was significantly impaired. These results indicated that this mutation was comparable to CHS of humans and mice, and we designated it as "beige." Since rats are more favorable than mice for some types of experiments, the beige rat is potentially useful as an animal model of CHS.

Animals↗
PubMed1989

Antioxidants protect against glutamate-induced cytotoxicity in a neuronal cell line.

The effects of reducing agents and antioxidants on L-Glutamate (Glu)-induced cytotoxicity were examined in the N18-RE-105 neuronal cell line. The cytotoxicity by Glu (1 and 10mM) was potentiated by exposure to growth medium containing a low concentration of cystine (5-100 microM), instead of the normal medium containing 200 microM cystine. In contrast, the toxicity was suppressed by increasing the cystine concentration to 500 to 1000 microM. Reducing agents, cysteine (30-1000 microM), dithiothreitol (10-250 microM) and glutathione (GSH, 10-1000 microM) also protected the cells against the cytotoxicity of 10 mM Glu in a concentration-dependent manner. The antioxidants vitamin E (10-100 microM), idebenone (0.1-3 microM) and vinpocetine (10-100 microM) also provided marked protection against the cytotoxicity of Glu (10 mM) or quisqualate (1 mM). Antioxidants also prevented the delayed cell death caused by lowering the concentration of cystine in the medium to 5 microM. Incubation of the cells with 10 mM Glu caused a marked decrease in cellular GSH levels. Although cysteine and dithiothreitol prevented the GSH reduction caused by Glu, antioxidants did not. The cellular levels of oxidants were assessed using 2,7-dichlorofluorescin, a probe that accumulates within cells and is converted to a fluorescent product by oxidation. Glu (10 mM) caused a marked increase in such fluorescence, whereas vitamin E and idebenone reduced markedly the number of fluorescent cells to control levels even added with 10 mM Glu. These results indicate that oxidative stress due to loss of cellular levels of GSH is one mechanism whereby Glu/quisqualate exert cytotoxicity and suggest that centrally active antioxidants may reduce neuronal damage in pathologic conditions associated with excessive Glu release.

Animals↗
PubMed1989

[Surgical considerations after patch closure of atrial septal defect with tricuspid annuloplasty].

Two patients with complications of embolism during the early postoperative period after patch closure of atrial septal defect with tricuspid annuloplasty were reported. Case 1: A 58-year-old woman underwent closure of an atrial septal defect and tricuspid annuloplasty by means of Kay's technique for tricuspid regurgitation. She had an episode of thromboembolism in the bilateral common femoral arteries 7 days after surgery. Thromboembolectomy was performed successfully using Fogarty's embolectomy catheter. Case 2: A 49-year-old woman underwent closure of an atrial septal defect and the tricuspid annuloplasty using Carpentier ring for tricuspid regurgitation. The patient had transient left hemiparesis on the 5th postoperative day. Both patients had atrial fibrillation and mild pulmonary hypertension before surgery. In relatively old patients (over 40 years old) with atrial septal defect, tricuspid regurgitation and atrial fibrillation, anticoagulant therapy should be started immediately after surgery to prevent thromboembolism.

Female↗
PubMed1989

Effects of continuous infusion of cholinergic drugs on memory impairment in rats with basal forebrain lesions.

The effects of continuous infusion of cholinergic drugs on behavior in normal rats and on impaired acquisition and retention of several behavioral tasks in rats with basal forebrain (BF) lesions were investigated. Physostigmine and oxotremorine were infused continuously with a miniosmotic pump for 3 weeks, and the performance on several different behavioral tasks was examined during the infusion. In normal rats high doses of physostigmine (4 and 8 mg/kg/day s.c.) produced significant changes in general behavior and impaired performance in the Morris water maze. Oxotremorine (0.25-2 mg/kg/day s.c.) had no significant effects on general behavior or cognitive performance in normal rats, although severe cataracts developed at the high dose (4 mg/kg/day). A deficit in motor habituation in rats with BF lesions produced by bilateral injections of ibotenic acid (30 nmol on each side) was improved markedly by the chronic administration of physostigmine (2 mg/kg/day) and oxotremorine (1 mg/kg/day). BF lesions produced severe impairments in acquisition and retention in a passive avoidance task, an active avoidance and the Morris water maze, which was characterized by a marked disruption of retention. The impairment was also ameliorated markedly by the cholinergic drugs, whereas other behavioral impairments were not affected by the drugs. These results indicate that the continuous administration of cholinergic drugs produces a marked improvement of acquisition and retention in rats with BF lesions, and suggest that the impairment in cognitive performance, especially with regard to retention, caused by BF lesions is due to the disruption of the BF-cortical cholinergic pathway.

Acetylcholinesterase↗
PubMed1988

Regulated expression of a gene encoding a nuclear factor, IRF-1, that specifically binds to IFN-beta gene regulatory elements.

Expression of the interferon-beta (IFN-beta) gene is induced by a variety of agents, including viruses. Evidence has been provided that a mouse nuclear factor, termed interferon regulatory factor-1 (IRF-1), specifically binds to the upstream regulatory region of the human IFN-beta gene and mediates virus-induced transcription of the gene. In this study, we describe the molecular cloning and characterization of the mouse and human cDNAs encoding IRF-1. Our results suggest that IRF-1 is also involved in the regulation of other genes such as IFN-alpha and MHC class I genes. Surprisingly, IRF-1 gene expression is dramatically induced by Newcastle disease virus in mouse L929 cells and by Concanavalin A in spleen cells. We show here that the IRF-1 gene possesses virus-inducible promoter.

Amino Acid Sequence↗
PubMed1988

Epidermal growth factor receptors on cultured neoplastic human thyroid cells and effects of epidermal growth factor and thyroid-stimulating hormone on their growth.

Epidermal growth factor (EGF) receptors on primary-cultured human thyroid cells from 27 neoplasias (nine adenomas and 18 differentiated carcinomas) were analyzed and compared with those on the cultured nonneoplastic part of human thyroid cells. Total binding of 125I-EGF to the nonneoplastic part, adenoma, and carcinoma cells did not differ significantly. Scatchard analysis showed that the neoplastic human thyroid cells, like their adjacent nonneoplastic counterparts, consistently possessed EGF receptors with two components. In a paired study of five patients, the association constant of the carcinoma cells' high-affinity component (Ka1) was found to be significantly lower than that of adjacent nonneoplastic thyroid cells (P less than 0.05). Furthermore, a study of the cells from 18 carcinomas revealed that overall their Ka1s (4.15 +/- 0.82 x 10(9) M-1, mean +/- SEM) were significantly lower than those of adenoma cells (10.34 +/- 1.51 x 10(9) M-1, n = 9) and of nonneoplastic cells adjacent to them (8.32 +/- 0.84 x 10(9) M-1, n = 23). The difference in Ka1s for adenoma and nonneoplastic thyroid cells was not statistically significant. The number of receptor sites (Cmax) per cell was not significantly different in any of the three. Incorporation of [3H]thymidine (dThd) increased significantly in all kinds of thyroid cells examined following the addition of 10 nM EGF, and the paired study showed that the size of this increase was not significantly different in neoplastic and adjacent nonneoplastic cells. The addition of 300 microunits/ml of thyroid-stimulating hormone caused a significant increase in dThd incorporation by adenoma cells but not by carcinoma or nonneoplastic cells. Furthermore, combined treatment with EGF and thyroid-stimulating hormone additively promoted adenoma cell growth only. A close inverse relationship was observed between Ka1 and the stimulatory effect of EGF on the dThd uptake in both nonneoplastic thyroid cells and adenoma cells. Carcinoma cells also showed similar profiles, but Ka1 relative to dThd increases were much smaller than the other two.

Adenoma↗
PubMed1988

[A case of chemical hyperthyroidism induced by antiarrhythmic agent amiodarone].

Amiodarone, an antiarrhythmic agent, is known to occasionally induce alterations in thyroid function because of its iodine content and ability to inhibit T4 5'-monodeiodination. We herein describe the drug-induced chemical hyperthyroidism in a diabetic patient with ventricular premature beats. A 46-year-old man with well controlled diabetes mellitus revealed neck swelling during a 4 months' treatment with amiodarone for his frequent occurrence of ventricular premature beats. Physical findings were unremarkable other than grade III diffuse struma. Routine laboratory studies were almost normal. The results of thyroid function studies showed hyperthyroidism, including increases in T4 and free T4, slight increases in T3 and free T3, a marked increase in reverse T3 and a decrease in 123I 24-h uptake. TSH was low and did not respond to TRH. Antithyroid antibodies and TSH receptor antibodies were negative. The findings of the thyroid biopsy were unremarkable except for a mild follicular hyperplasia. After cessation of the drug, T3 and free T3 were returned to normal within 2 weeks, T4 and free T4 within 2 months and reverse T3 after 6 months. These data suggest that the struma and chemical hyperthyroidism observed in our patient were induced by amiodarone treatment.

Amiodarone↗
PubMed1988

Evidence for a nuclear factor(s), IRF-1, mediating induction and silencing properties to human IFN-beta gene regulatory elements.

Transcription of the human interferon-beta (IFN-beta) gene is induced by a variety of agents such as viruses, dsRNA and some cytokines. In this study, we describe a nuclear factor, termed interferon regulatory factor-1 (IRF-1), that is involved in the transcription of IFN-beta and possibly other genes. We demonstrate that IRF-1 functions in virus-induced transcription by interacting with previously identified, IFN-beta regulatory DNA elements. Our data suggest that IRF-1 participates in the transient formation of an induction-specific complex(es) with the regulatory elements. IRF-1 may also be involved in silencing the function of the SV40 enhancer juxtaposed to the regulatory elements in uninduced cells.

Animals↗
PubMed1988

Neuronal death in vitro: parallelism between survivability of hippocampal neurones and sustained elevation of cytosolic Ca2+ after exposure to glutamate receptor agonist.

Hippocampal neurones isolated from rat embryos were maintained on glial monolayers in a medium containing no L-glutamate (Glu). The administration of Glu for a limited period induced a massive death (loss) of neurones. The degree of neuronal loss increased with time after exposure to Glu. The extent of neuronal loss assessed 24 h after exposure to Glu was dependent upon the concentration Glu and on the duration of the exposure. An increase in concentration of external Ca2+ during the exposure to Glu enhanced the extent of loss. By contrast, an increment in concentration of environmental Mg2+ reduced the loss. The inhibitor of spike firing, tetrodotoxin (TTX) and the suppressor of Ca2+ entry, nitrendipine, both decreased the extent of loss, when delivered prior to Glu. The toxicity of Glu became progressively more apparent with further days of culture. The cytosolic concentration of Ca2+ ([Ca2+]i) in single hippocampal neurones was monitored by microscopic fluorometry under conditions equivalent to those in the death assay. The time required for the recovery of [Ca2+]i from the level elevated by exposure to Glu to pre-stimulus levels closely paralleled the degree of neuronal loss; i.e. high doses of Glu, long periods of exposure, high concentrations of external Ca2+, low concentrations of external Mg2+, and extended days of culture all retarded [Ca2+]i recovery, while TTX and nitrendipine accelerated it. These findings show that neuronal death resulting from an extraneous excitation (excitotoxicity) can be analyzed in vitro. Furthermore, substantial support has been provided to the hypothesis that excitotoxicity has an underlying mechanism, an excess loading of Ca2+ in neuronal cytoplasm.

Animals↗