Biomedical subjects

Y Miyazaki

Publications and source records attributed to Y Miyazaki.

At least 19 recordsLinked to original sources

PubMed1992

[Gianturco expandable metallic stents in the treatment of tumor thrombus in portal vein--preliminary clinical experience].

Two cases of hepatocellular carcinoma with protal vein invasion (Vp3) were successfully treated by Gianturco expandable metallic stents (GEMS). Each case was treated through the different approach, i.e. the percutaneous transhepatic or ileocolic venous route. GEMS was easily expanded within the protal vein and carcinoma thrombi were pushed against the walls, resulting in increase of portal blood flow. The GEMS might improve the impaired portal blood flow with hepatic failure and esophagogastric varices, in spite of the possibilities of dissemination and ingrowth of carcinoma thrombi.

Aged↗

PubMed1992

Destabilization of ornithine decarboxylase by transfected antizyme gene expression in hepatoma tissue culture cells.

The degradation of ornithine decarboxylase (ODC) is stimulated by polyamines in a protein synthesis-dependent manner. It has been suggested that antizyme, an ODC-inhibiting protein induced by polyamines, is involved in the process of polyamine-stimulated ODC decay. In this study, we investigated the direct effect of antizyme on ODC decay in hepatoma tissue culture (HTC) cells. A truncated rat antizyme cDNA, Z1, was inserted into an expression vector at a site under the control of a glucocorticoid-inducible promoter and transfected into HTC cells. In the transfected cells dexamethasone increased the amount of Z1 mRNA and induced active antizyme in the absence of exogenous polyamines. When dexamethasone was added to cells with a high level of ODC, rapid decays of ODC activity and protein were elicited after a lag time. Cycloheximide abolished the effect of dexamethasone. These effects of dexamethasone were not observed in control HTC cells transfected with the chloramphenicol acetyltransferase gene. This study indicated that, once induced, antizyme stimulated ODC degradation independently of polyamines and strongly supported our previous hypothesis that the ODC decay-accelerating action of polyamines is mediated by antizyme.

Animals↗

PubMed1992

Intranuclear topological distribution of HIV-1 trans-activators.

Subcellular localization of human immunodeficiency virus type I (HIV-1) Tat and Rev was examined using a confocal laser scanning microscope (CLSM). In transfected COS-7 cells, Tat resided exclusively in the perinocleolar region, while Rev infiltrated fully into the nucleoli. The chimeric Tat in which the nucleolar targeting signal was replaced by that of Rev, which retains trans-acting activity of Tat, remained still in the perinucleolar region as wild-type Tat. Perinucleolar distribution of Tat protein suggests the existence of a novel nucleolar architecture that affects transcription.

Amino Acid Sequence↗

PubMed1992

Antizyme, a protein induced by polyamines, accelerates the degradation of ornithine decarboxylase in Chinese-hamster ovary-cell extracts.

Ornithine decarboxylase (ODC), the key regulatory enzyme for polyamine biosynthesis, is known to have a short intracellular half-life, and antizyme, an ODC-binding protein induced by polyamines, has been suggested to be involved in the process of ODC degradation. In the present study we demonstrated that antizyme markedly accelerated ATP-dependent degradation of ODC in vitro in an extract from ODC-overproducing Chinese-hamster ovary cells.

Adenosine Triphosphate↗

PubMed1992

Cloning and characterization of a rat gene encoding ornithine decarboxylase antizyme.

We cloned an ornithine decarboxylase antizyme-encoding gene (Oaz) from a rat liver genomic library. The entire gene was located on a 4367-bp EcoRI fragment, which corresponded to one of two fragments hybridizable with the antizyme-encoding cDNA, Z1, on Southern blot analysis. Sequence analysis of the cloned gene showed that it consisted of five exons which were identical with the cDNA. The transcription start points of the Oaz mRNA were located 75 and 76 nucleotides upstream from the first ATG codon, as determined by S1 nuclease protection and primer extension analyses. The 5'-flanking region of the gene contained typical promoter motifs, such as a TATA box and Sp1-binding sites. Introduction of a chimeric gene consisting of the 5'-flanking region and the bacterial cat gene into Chinese hamster ovary cells revealed a promoter activity in the region, which was comparable in strength to that of the simian virus 40 promoter. In addition, we isolated a 12-kb EcoRI fragment, the other sequence hybridizable to the cDNA. Sequence analysis showed that it represented a processed Oaz pseudogene and was not able to encode any active protein.

Animals↗

PubMed1992

Complete excision and panpleuropneumonectomy resulting in long-term survival for a teenager with invasive thymoma: report of a case.

An 18-year-old girl with invasive thymoma and pleural dissemination underwent a complete removal of the tumor with combined resection of the pericardium and a panpleuropneumonectomy of the left lung. At the time of writing, 70 months later, she was doing well under the classification of grade I performance status with no signs of recurrence. Thus, complete surgical removal of this tumor can prolong the survival time of patients with invasive thymoma and pleural dissemination.

Adolescent↗

PubMed1992

Detection of mutations in the insulin receptor gene in patients with insulin resistance by analysis of single-stranded conformational polymorphisms.

We analyzed single-stranded conformational polymorphisms to screen for mutations and polymorphisms in the insulin receptor gene in subjects with or without insulin resistance. Using this new technique, we demonstrated the existence of mutations in the insulin receptor gene which we had identified previously. In addition, a new mutation was found in exon 20 of the insulin receptor gene in a patient with moderate insulin resistance associated with morbid obesity, acanthosis nigricans, and polycystic ovary syndrome. The patient was heterozygous for a mutation substituting Leu (CTG) for Pro (CCG) at codon 1178. Pro1178 is a part of a characteristic sequence motif (D1150 F1151 G1152---A1177 P1178 E1179) common to many protein kinases. Analysis of single-stranded conformational polymorphisms was also used to estimate the frequency of a polymorphism at codon 1058. The two codons CAC (1058 His) and CAT (1058 His) both had a prevalence of 50% in 30 Japanese subjects. These data demonstrate that analysis of single-stranded conformational polymorphisms is a simple and sensitive screening method for mutations and polymorphisms in the insulin receptor gene in subjects with or without insulin resistance. Identification of a mutation in the insulin receptor gene in a patient with a moderate degree of insulin resistance associated with morbid obesity suggests that insulin receptor mutations may exist in patients with Type 2 (non-insulin-dependent) diabetes mellitus associated with a moderate degree of insulin resistance.

Amino Acid Sequence↗

PubMed1992

Hemolysis of phosphatidylcholine-containing erythrocytes by serratamic acid from Serratia marcescens.

1. The hemolysis by serratamic acid, "N-(D-3-hydroxydecanoyl)-L-serine and N-(D-3-hydroxydodecanoyl)-L-serine", was investigated with human and animal erythrocytes using serratamic acid-containing liposomes. 2. The hemolytic activity was found to depend on the incubation temperature and the concentration of the liposomes. 3. The concentration of serratamic acid for 50% hemolysis was 0.17 mM at 37 degrees C for 0.2% human erythrocyte suspension in the liposomes which composed of phosphatidylserine, cholesteryl nervonate and serratamic acid (1:0.50:0.37 by mol). 4. The hemolysis was shown specifically in human, horse and rabbit erythrocytes containing phosphatidylcholine, but not in sheep or bovine erythrocytes lacking phosphatidylcholine. 5. The hemolytic activity was strongly inhibited by the exogenous addition of phosphatidylcholine. It was suggested that the hemolysis by serratamic acid-containing liposomes was specific for phosphatidylcholine-containing erythrocyte membranes.

Animals↗

PubMed1992

Effect of L-cystine on toxicity of paraquat in mice.

The protective effect of L-cystine on the toxicity of paraquat (PQ) in mice was studied. Lipid peroxidation in the lung significantly increased after oral administration of PQ (200 mg/kg) and the increase in lipid peroxidation was prevented by L-cystine treatment (300 mg/kg). PQ administration produced an increase in superoxide dismutase (SOD) activity and a decrease in glutathione peroxidase (GSH-Px) activity in the lung at 24 h after PQ. L-Cystine treatment significantly prevented the changes in SOD and GSH-Px activity in the lung after PQ. L-Cystine treatment prevented the decrease in non-protein sulfhydryl (NP-SH) content in the lung after PQ administration. The tissue distribution and excretion of PQ after PQ administration were not changed by L-cystine treatment. Plasma aspartate aminotransferase activity did not change after PQ administration. These results suggest that L-cystine protects against the toxicity of PQ by maintaining reduced glutathione levels in the cells.

Animals↗

PubMed1992

Flow cytometric analysis on perforin induction in peripheral blood mononuclear cells with interleukin-2 or OK-432.

Perforin is a protein present in the cytoplasmic granules of killer cells and is considered to be an important effector molecule. We assessed the perforin appearance via flow cytometry in human peripheral blood mononuclear cells stimulated in vitro for 3 days by recombinant interleukin-2 (rIL-2) or OK-432, a biological response modifier. The relationship between the lymphocyte subsets and perforin was investigated via two-color assay. CD4-positive cells had almost no perforin, and most of the CD16-positive cells did. Regarding the relationship with CD8, some of the bright positive cells (which were likely T cells) and most of the dull positive cells (likely NK cells) had perforin. Mean fluorescence was greatest in perforin-positive cells incubated with rIL-2, less in cells incubated with OK-432, and minimal in cells incubated in a medium without additives. Immunohistochemical staining with antiperforin antibody revealed that blast-transformed and enlarge cells were stained positively and that the intensity of staining of each cell alone was enhanced in cells incubated with OK-432 or rIL-2. If the fluorescence intensity of perforin-positive cells correlates with the amount of perforin in those cells, then the appearance of perforin was enhanced with OK-432, more enhanced with rIL-2, and consistent for cytotoxicity against K562 and Daudi cells. IL-2 was induced by OK-432, suggesting that the indirect effect of this IL-2 may play a role in OK-432-perforin induction. The results suggest that perforin may be an effector molecule in killer cells induced by rIL-2 or OK-432.

Cytotoxicity, Immunologic↗

PubMed1992

Pulsatile umbilical venous flow and its clinical significance.

OBJECTIVE: To determine the prevalence and significance of pulsatile waveforms from the umbilical vein. SETTING: A tertiary referral clinic for high risk pregnancies. SUBJECTS: 209 fetuses from 24-41 weeks gestation. MAIN OUTCOME MEASURES: The presence of pulsatile waveforms in the umbilical vein and the pregnancy outcome. RESULTS: 9/209 fetuses demonstrated pulsatile waveforms and seven had severe growth retardation or congenital anomalies of the heart. Pulsatile flow and abnormalities of the inferior vena cava waveforms were observed in these seven but not in the two infants who were born at term. Double pulsations are described for the first time. CONCLUSION: Examination of the umbilical venous waveform for pulsatile flow is a useful test as it indicates the presence of asphyxial cardiomyopathy or congenital heart lesions.

Blood Flow Velocity↗

PubMed1992

Tenascin expression in human chronic liver disease and in hepatocellular carcinoma.

Tenascin is an oligomeric glycoprotein of the extracellular matrix synthesized during embryonic development. It is prominently expressed in a variety of tumors. The role of tenascin in liver tissue is, however, unknown. We used immunocytochemistry to define the localization of tenascin and compare this with the localization of non-collagenous proteins, such as laminin and fibronectin, in normal human liver and pathological liver from patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. In normal liver, tenascin expression was localized along the sinusoidal and vascular wall. In fibrotic liver, tenascin was also observed in the region between the hepatic parenchyma and the fibrosing portal tracts, especially in areas of piecemeal necrosis in chronic hepatitis. Immuno-EM study of liver tissue in chronic hepatitis strongly suggested the synthesis and secretion of tenascin by fat-storing cells into the space of Disse. In hepatocellular carcinoma, tenascin was expressed in both the capsule and lobular septa, but not in the sinusoidal walls of the tumors. These results led us to postulate a close relationship between the occurrence of this protein and disease processes such as fibrosis and cancer invasion.

Carcinoma, Hepatocellular↗

PubMed1992

[Antigen detection in the murine models of systemic candidiasis].

We compared two latex agglutination tests for serum candidal antigen in murine models of systemic infection and gastrointestinal colonization. In the intravascular-infection model, mannan detection test was positive at 2 hours after inoculation, but Cand-Tec was less sensitive than mannan detection test in this model. In the gastrointestinal colonization model followed by systemic infection in neutropenic mice, the mannan antigen test became positive after 3 weeks of colonization with increased number of Candida of the stool, and Cand-Tec became positive after 5 weeks in neutropenic mice.

Animals↗

PubMed1992

[Four cases of respiratory tract infections caused by Corynebacterium pseudodiphtheriticum].

Four cases of respiratory tract infections caused by Corynebacterium pseudodiphtheriticum were reported. The first two patients developed pneumonia with Corynebacterium pseudodiphtheriticum during steroid therapy used against their underlying diseases. The other two patients had acute exacerbation of chronic pulmonary diseases caused by C. pseudodiphtheriticum. These four patients improved by antibiotic therapy. Though nondiphtheria corynebacteria are regarded as "normal flora" when they are isolated from sputum, they should be recognized as potential pathogens.

Aged↗

PubMed1992

Hypoxia-elicited contraction of aorta and coronary artery via removal of endothelium-derived nitric oxide.

To characterize endothelium-derived contracting factor 1 (EDCF1) released under hypoxia, vascular rings isolated from spontaneously hypertensive rat (SHR) aorta and canine coronary artery were suspended for isometric tension recording in an organ chamber filled with a Krebs-Henseleit buffer. In SHR aorta precontracted with norepinephrine (10(-7) M), severe hypoxia induced an initial increase in tension by 36.7 +/- 7.5% followed by a 56.9 +/- 5.7% relaxation; moderate hypoxia induced only a sustained increase in tension by 20.6 +/- 2.5%. Inhibition of nitric oxide (NO) production with N omega-nitro-L-arginine methyl ester (L-NAME) (10(-3) M) augmented norepinephrine-induced precontraction by 76.1 +/- 12.3% and totally eliminated the hypoxic contraction. In canine coronary arteries precontracted with KCl (30 mM) in the presence of indomethacin (10(-5) M), severe hypoxia caused a sustained increase in tension by 68.9 +/- 7.3%, which was also abolished with L-NAME. When L-NAME (10(-3) M) was given after the precontraction, both of these vessels developed sustained contractions under normoxia and moderate hypoxia. These results suggest that the vasocontraction currently considered to be induced by EDCF1 is not caused by a contracting factor but rather is a contracting phenomenon derived from continuous inhibition of basal NO synthesis during hypoxia.

2,4-Dinitrophenol↗

PubMed1992

Correlation with blood pressure of the acetylcholine-induced endothelium-derived contracting factor in the rat aorta.

To examine a relation between the production of acetylcholine-induced endothelium-derived contracting factor and an increase in blood pressure, endothelium-dependent contraction and relaxation were evaluated by measuring the isometric tension of aortic rings from spontaneously hypertensive rats and Wistar-Kyoto rats at 5, 10, 20, and 30 weeks of age. In norepinephrine-precontracted rings, acetylcholine (10(-8) to 10(-5) M)-induced relaxations diminished at the doses of 10(-6) to 10(-5) M in both strains except at 5 weeks of age. Treatment with a thromboxane A2/prostaglandin H2 antagonist (ONO-3708) prevented this reduction in acetylcholine-induced relaxations in both strains and induced dose-dependent relaxations, which were completely inhibited by treatment with a nitric oxide inhibitor, NG-nitro-L-arginine methyl ester. In aorta treated with NG-nitro-L-arginine methyl ester without precontraction, acetylcholine induced dose-dependent contractions, which were greater in spontaneously hypertensive rats than in Wistar-Kyoto rats. These acetylcholine-induced contractions, which were observed only in rings with endothelium, were completely inhibited by treatment with ONO-3708 but not with a thromboxane A2 synthetase inhibitor (OKY-046). There was a statistically significant correlation between the acetylcholine-induced contractions and blood pressure. Release of 6-ketoprostaglandin F1 alpha by acetylcholine from the aorta was greater in spontaneously hypertensive rats. In vivo administration of another thromboxane A2/prostaglandin H2 antagonist (ONO-8809) (10 or 30 micrograms per body per day) for 3 weeks (5-8 weeks of age) did not affect blood pressure in either rat strain.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1992

Hypocalcemic cardiomyopathy in a patient with idiopathic hypoparathyroidism.

An idiopathic hypoparathyroidism-induced cardiomyopathy patient had severe long-lasting hypocalcemia. The dramatic improvement of cardiac function with correction of only the serum calcium concentration could be quantitatively demonstrated on both echocardiogram and ventriculogram. The concentration of the extracellular calcium ion was considered to have a direct effect on the strength of the myocardial contraction through excitation-contraction coupling. Furthermore, elevated serum creatine phosphokinase and lactate dehydrogenase levels which were thought to be delivered from skeletal muscle returned to the normal range concomitant with the correction of hypocalcemia. The serum calcium concentration and these enzyme level showed significant inverse correlations.

Cardiomyopathies↗

PubMed1992

Fatal pneumonia caused by Corynebacterium group JK after treatment of Staphylococcus aureus pneumonia.

A 76-year-old man who was admitted to the hospital because of chronic renal insufficiency and chronic hepatitis died of Corynebacterium group JK pneumonia, after showing a slight improvement by treatment of Staphylococcus aureus with sulbactam/cefoperazone and minocycline. Transtracheal aspiration (TTA) just before his death revealed numerous gram-positive bacilli phagocytized by many neutrophils and more than 10(8) colony forming units (CFU)/ml of Corynebacterium group JK. A drug susceptibility test showed Corynebacterium group JK was resistant to many antibiotics, with the exception of vancomycin and amikacin.

Aged↗