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Biomedical subjects

H Okayama

Publications and source records attributed to H Okayama.

At least 55 records · Page 3Linked to original sources
PubMed1998

Increased circulating soluble form of Fas in patients with dilated cardiomyopathy.

To examine the prognostic role of the circulating soluble form of Fas (sFas), circulating sFas levels were measured in 33 patients with dilated cardiomyopathy (DCM) and 12 age-matched normal control subjects (NC) using an enzyme-linked immunosorbent assay (ELISA). Circulating sFas levels in DCM were significantly higher than those in NC (2.42+/-1.02 vs 1.66+/-0.20 ng/ml, p=0.015). Patients with DCM were stratified into 2 groups [group I (n=15): sFas > or =2.06 ng/ml; group II (n=18): sFas <2.06 ng/ml] on the basis of the mean value plus 2SD of circulating sFas level in NC. The circulating sFas level was significantly increased in relation to the severity of heart failure and correlated positively to left ventricular end-diastolic pressure in DCM. However, there were no significant differences in left ventricular dimension between the 2 groups. There were 5 deaths from worsening heart failure in group II, but there were no deaths in group I during the follow-up period. In conclusion, circulating sFas levels were increased in patients with DCM. Circulating sFas levels are increased in proportion to the severity of heart failure and may provide prognostic information independent of left ventricular geometry.

Cardiomyopathy, Dilated↗
PubMed1998

Suppression of gene expression and production of interleukin 13 by dexamethasone in human peripheral blood mononuclear cells.

We examined the effect of dexamethasone on the gene expression and production of interleukin (IL)-13 by human peripheral blood mononuclear cells from healthy controls. The gene expression was assessed semiquantitatively by sequential transcription polymerase chain reaction and Southern blot analysis, and the production of this cytokine was assessed by enzyme-linked immunosorbent assay (ELISA). Dexamethasone suppressed IL-13 gene expression induced by stimulation with phytohemagglutinin and phorbol 12-myristate 13-acetate in a dose-dependent manner, with 96% suppression at 10(-6) M, and also suppressed the increased production of IL-13. This is suggested to be one of the mechanisms by which glucocorticoids suppress allergic inflammation.

Anti-Inflammatory Agents↗
PubMed1997

Identification of open reading frames in Schizosaccharomyces pombe cDNAs.

A total of 214 non-overlapping cDNA clones from Schizosaccharomyces pombe were selected and completely sequenced. The clones not previously reported were divided into the following three groups: 1) homologous to Saccharomyces cerevisiae genes (139 clones); 2) homologous to genes from other organisms but not to those from Sac. cerevisiae (4 clones); and 3) no similar sequences (40 clones). Among the 31 sequences identical to those in the public databases, 4 genes have regions corresponding to introns. Protein sequences which had homologs both in budding yeast and mammals were compared with those from Sac. cerevisiae and mammals. The search revealed that the evolutionary distances among these species are similar at least with genes of this category.

Amino Acid Sequence↗
PubMed1997

Class Ia antiarrhythmic drug cibenzoline: a new approach to the medical treatment of hypertrophic obstructive cardiomyopathy.

BACKGROUND: The class Ia antiarrhythmic drug disopyramide relieves the outflow tract obstruction of hypertrophic obstructive cardiomyopathy (HOCM). Disopyramide, however, has several adverse effects, such as dysuria and thirst, resulting from its anticholinergic activity. A new class Ia antiarrhythmic drug, cibenzoline, has little anticholinergic activity. The aim of this study is to elucidate whether cibenzoline attenuates left ventricular pressure gradient (LVPG) in patients with HOCM. METHODS AND RESULTS: Ten patients with HOCM (mean age, 59+/-12 years) participated in this study. LVPG and left ventricular functions were measured before and 2 hours after administration of a single oral dose of 150 or 200 mg cibenzoline. LVPG decreased from 123+/-60 to 39+/-33 mm Hg (P=.0026). The E/A ratio in transmitral Doppler flow increased from 1.20+/-0.84 to 2.00+/-1.72 (P=.029). Isovolumic relaxation time increased from 73+/-16 to 101+/-23 ms (P=.0026). Left ventricular diastolic dimension remained unchanged, but left ventricular systolic dimension enlarged significantly, from 21.6+/-2.4 to 26.2+/-3.3 mm (P=.0004). Fractional shortening decreased from 47.6+/-6.1% to 34.6+/-8.8% (P=.0007). Left ventricular ejection time index decreased significantly, and preejection period index increased in all the patients. Decreased LVPG remained maintained even in the long-term treatment with cibenzoline. Conclusions These results indicate that cibenzoline can markedly attenuate LVPG in patients with HOCM. A decrease in myocardial contractility seems to be closely related to a marked decrease in LVPG.

Aged↗
PubMed1997

Signature current of SO2-induced bronchitis in rabbit.

To investigate abnormalities of airway epithelial ion transport underlying chronic inflammatory airway diseases, we performed electrophysiological, histological, and molecular biological experiments using rabbits exposed to SO2 as a model of bronchitis. By comparison with control, the SO2-exposed trachea exhibited decreased short circuit current (Isc) and conductance associated with increased potential difference. In normal trachea, apical ATP induced a transient Isc activation followed by a suppression, whereas the bronchitis model exhibited a prolonged activation without suppression. This pathological ATP response was abolished by diphenylamine 2-carboxylate or Cl--free bath solution. A significant increase in net Cl- flux toward the lumen was observed after ATP in our bronchitis model. Isoproterenol or adenosine evoked a sustained Isc increase in SO2-exposed, but not in normal, tracheas. The Northern blot analysis showed a strong expression of cystic fibrosis transmembrane conductance regulator (CFTR) mRNA in SO2-exposed epithelium. The immunohistochemical study revealed a positive label of CFTR on cells located luminally only in SO2-exposed rabbits. We concluded that the prolonged ATP response in our bronchitis model was of a superimposed normal and adenosine-activated current. The latter current was also activated by isoproterenol and appeared as a signature current for the bronchitis model airway. This was likely mediated by CFTR expressed in the course of chronic inflammation.

Adenosine↗
PubMed1997

FMLP actions and its binding sites in isolated human coronary arteries.

The chemoattractant f-Met-Leu-Phe (FMLP) can modulate human coronary arterial tone without the involvement of peripheral leukocytes. We investigated the actions of FMLP and its cellular mechanism in human coronary arteries isolated 2-3 h after death. A single dose of FMLP (0.01-10 microM) produced transient contraction (or, followed by relaxation) responses in most human coronary rings examined. These responses to FMLP were in large part mediated by the generation of cyclooxygenase products, mainly thromboxane A2 (TXA2) and prostaglandin I2 (PGI2). Radiolabeled N-formyl hexapeptide. 125I-f-Nle-Leu-Phe-Nle-Tyr-Lys bound densely to intimal and adventitial sites that accumulated macrophages (CD68-positive) with a Kd of 14-29 nM and, further, weakly to the media with a Kd of 2.4-3.6 microM. Several cell types including macrophages, endothelial cells and smooth muscle cells were positively immunostained for both TXA2 synthase and PGI2 synthase. However, there was no significant relation between the magnitude of the responses to FMLP and dense macrophage accumulation in the intimal plaques or the adventitia. A reverse transcription-polymerase chain reaction showed predominant expression of FMLP receptor homologues, FPRH1 and FPRH2 mRNA, in human coronary medial tissues relative to that in leukocytes. In conclusion. FMLP produced transient tension changes in human coronary arteries, mainly via the generation of TXA2 and PGI2. This effect of FMLP did not appear to be mediated by the activation of densely accumulated intimal and/or adventitial macrophages, but by the activation of unidentified medial tissue cells which might have functional FMLP receptor homologues.

Adolescent↗
PubMed1997

Detection of surfactant protein-A gene transcript in the cells from pleural effusion for the diagnosis of lung adenocarcinoma.

PURPOSE: To determine whether detecting surfactant protein-A (SP-A) gene transcript in the cells from pleural effusion is useful for the diagnosis of lung adenocarcinoma. PATIENTS AND METHODS: We performed reverse transcription polymerase chain reaction (RT-PCR) analysis of SP-A gene transcript in the cells of pleural effusion from 42 consecutive patients with pleural effusion, including 7 patients with primary lung adenocarcinoma before their treatments. RESULTS: A cDNA segment of SP-A was amplified from the pleural fluid cells of all patients with primary lung adenocarcinoma, indicating the presence of the SP-A gene transcript. None of the remaining patients, including those with metastatic lung adenocarcinoma, showed positive for the SP-A gene transcript. CONCLUSION: These findings indicate that RT-PCR analysis of the SP-A gene transcript in pleural effusion is useful for the diagnosis of primary lung adenocarcinoma.

Adenocarcinoma↗
PubMed1997

A WD repeat protein controls the cell cycle and differentiation by negatively regulating Cdc2/B-type cyclin complexes.

In the fission yeast Schizosaccharomyces pombe, p34(cdc2) plays a central role controlling the cell cycle. We recently isolated a new gene named srw1(+), capable of encoding a WD repeat protein, as a multicopy suppressor of hyperactivated p34(cdc2). Cells lacking srw1(+) are sterile and defective in cell cycle controls. When starved for nitrogen source, they fail to effectively arrest in G1 and die of accelerated mitotic catastrophe if regulation of p34(cdc2)/Cdc13 by inhibitory tyrosine phosphorylation is compromised by partial inactivation of Wee1 kinase. Fertility is restored to the disruptant by deletion of Cig2 B-type cyclin or slight inactivation of p34(cdc2). srw1(+) shares functional similarity with rum1(+), having abilities to induce endoreplication and restore fertility to rum1 disruptants. In the srw1 disruptant, Cdc13 fails to be degraded when cells are starved for nitrogen. We conclude that Srw1 controls differentiation and cell cycling at least by negatively regulating Cig2- and Cdc13-associated p34(cdc2) and that one of its roles is to down-regulate the level of the mitotic cyclin particularly in nitrogen-poor environments.

Amino Acid Sequence↗
PubMed1997

Alterations in expression of sarcoplasmic reticulum gene in Dahl rats during the transition from compensatory myocardial hypertrophy to heart failure.

OBJECTIVES: To clarify whether the functional changes during the transition from compensatory myocardial hypertrophy to failure are associated with changes in sarcoplasmic reticulum gene expression. METHODS: We examined the gene expression of sarcoplasmic reticulum proteins [sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, calsequestrin and ryanodine receptor] in Dahl salt-sensitive (Dahl-S) rats fed a high-salt (8%) diet from the age of 6 weeks. In-vivo contractile functioning was evaluated using echocardiography, and gene expression of sarcoplasmic reticulum proteins in the left ventricle was analyzed by Northern blotting for each stage of left ventricular hypertrophy. RESULTS: SERCA messenger RNA (mRNA) levels in Dahl-S rats with compensatory hypertrophy did not change significantly, whereas phospholamban mRNA levels were increased by 61% (P < 0.01), and calsequestrin mRNA levels were increased by 130% (P < 0.01) compared with those in Dahl salt-resistant (Dahl-R) rats. SERCA mRNA levels in Dahl-S rats with decompensated dilatation were decreased by 32% (P< 0.05), whereas levels of phospholamban and calsequestrin mRNA remained unchanged. Ryanodine receptor mRNA levels did not change either with compensatory hypertrophy or with decompensated dilatation. CONCLUSIONS: Alterations in expression of sarcoplasmic reticulum gene may be related to changes in systolic and diastolic properties in compensatory hypertrophy and heart failure.

Animals↗
PubMed1997

Dexamethasone suppressed gene expression and production of interleukin-10 by human peripheral blood mononuclear cells and monocytes.

Interleukin-10 (IL-10) is known to inhibit T cell-mediated responses. IL-10 has also been shown to play an important pathogenetic role in allergic diseases. Glucocorticoid is known to inhibit the production and gene expression of many cytokines which induce inflammatory reactions. We examined the effect of dexamethasone on the gene expression and production of IL-10 by human peripheral blood mononuclear cells (PBMCs) and monocytes. PBMCs and monocytes from 5 healthy volunteers were incubated with or without dexamethasone for 1 h, then stimulated with 5 micrograms/ml lipopolysaccharide (LPS). Gene expression and production of IL-10 by human PBMCs were detected without stimulation and increased by LPS stimulation. Dexamethasone suppressed the gene expression and production of IL-10 by LPS-stimulated PBMCs in a dose-dependent manner by 41.6 and 61.1% at 10(-6) M, respectively. Also in monocytes, the gene expression and production of IL-10 were detected without stimulation, increased by LPS stimulation, and significantly suppressed by dexamethasone by 53.1 and 61.2% at 10(-6) M, respectively. This suppressive effect on IL-10 gene expression was not so potent compared with its effect on cytokines such as IL-5. The suppression of IL-10 production by glucocorticoid is suggested to be one of the important mechanisms by which glucocorticoids suppress allergic inflammation in the treatment of allergic diseases.

Blotting, Northern↗
PubMed1997

Patch-clamp characterization of secretory process in human basophils.

The effects of the intracellular Ca2+ concentration ([Ca2+]i) and a nonhydrolyzable guanosine triphosphate, guanosine 5'-o-(3-thiotriphosphate) (GTP-gamma-S), on secretion were studied by a patch-clamp technique in human basophils. When 10 microM Ca2+ were applied intracellularly, the granules dispersed rapidly, moved vigorously and fused to the cell membrane in 5 min. When the cells were exposed to 2 microM [Ca2+]i and 100 microM GTP-gamma-S, the granules dispersed gradually and granule fusion continued for 7-10 min. The plasma membrane conductance did not appreciably change with either 10 microM [Ca2+]i alone or 2 microM [Ca2+]i + 100 microM GTP-gamma-S. Intracellular application of Ca2+, 1-10 microM, caused a dose-dependent increase in cell membrane capacitance, which reflects granule membrane fusion, indicating exocytosis in a Ca2+ concentration-dependent manner. The addition of 100 microM GTP-gamma-S promoted an increase in the plasma membrane capacitance at concentrations from 0.1 to 2 microM [Ca2+]i and at 2 microM [Ca2+]i the increase was 4.4 times greater than that with 2 microM [Ca2+]i alone. These results indicate that certain G protein(s) promote Ca2+-dependent exocytosis in human basophils.

Basophils↗
PubMed1997

Left ventricular hypertrophy precedes other target-organ damage in primary aldosteronism.

To elucidate whether there is a difference in the progression of target-organ damage between primary aldosteronism and essential hypertension, we compared left ventricular hypertrophy and extracardiac target-organ damage in 23 patients with primary aldosteronism and 116 patients with essential hypertension. The severity of hypertensive retinopathy and the renal involvement in primary aldosteronism were subclinical and similar to those in essential hypertension without left ventricular hypertrophy but significantly milder than those in essential hypertension with left ventricular hypertrophy. There was a strongly significant correlation between the degree of left ventricular mass index and the severity of hypertensive retinopathy and renal involvement independent of office blood pressure in essential hypertension. In contrast, left ventricular hypertrophy markedly progressed despite the mild extracardiac target-organ damage in primary aldosteronism. Left ventricular end-diastolic dimension index in primary aldosteronism (3.16+/-0.50 cm/m2) was significantly larger than in essential hypertension without (2.87+/-0.23) and with (2.88+/-0.22) left ventricular hypertrophy. On the other hand, there was no difference in extracardiac target-organ damage between 13 primary aldosteronism patients with eccentric left ventricular hypertrophy and the 26 essential hypertensive patients with eccentric left ventricular hypertrophy. The results suggest that predominantly volume load, be it due to aldosteronism or other mechanisms, resulting in eccentric left ventricular hypertrophy is less likely to cause extracardiac target-organ damage than hemodynamic or nonhemodynamic mechanisms resulting in concentric left ventricular hypertrophy.

Adult↗
PubMed1997

A zinc finger protein required for stationary phase viability in fission yeast.

Yeast cells exit the cell cycle and enter a metabolically inert stationary phase when starved for nutrients essential for normal proliferation. We have cloned a novel gene named rsv1+ (required for stationary phase viability) that is essential for fission yeast cell viability in a stationary phase induced by glucose starvation. rsv1+ encodes a 47 kDa protein with two zinc finger motifs that are partially homologous with Aspergillus nidulans CreA, Saccharomyces cerevisiae Mig1 and mammalian EGR-1/NGFI-A. Cells deleted for rsv1+ are unable to survive glucose starvation. Transcription of rsv1+ is negatively regulated by the cAMP pathway and induced by glucose starvation. Cells with the constitutively activated cAMP pathway are known to lose viability when grown to confluence or when starved for glucose. These cells are poor in rsv1+ induction and their viability loss is largely suppressed by ectopic expression of rsv1+. Thus, poor induction of rsv1+ is at least partially responsible for the viability loss. Analysis also showed that cells need to receive starvation signals before entry into the stationary phase in order to maintain viability in a glucose-poor environment.

Amino Acid Sequence↗
PubMed1997

[Mitral prosthetic valve replaced twice due to repeated prosthetic valve endocarditis: a case report].

A 38-year-old man was admitted to our hospital for detailed examination of fever, cough and yellow sputum. At the age of 32, be had mitral prosthesis for the first time, because of mitral regurgitation due to mitral valve prolapse. Four years previously, he had again undergone mitral prosthetic valve replacement due to prosthetic valve endocarditis due to staphylococcus epidemidis. This occasion, staphylococcus aureus was isolated by arterial blood culture. Transesophageal echocardiography detected vegetation attached to the mitral prosthetic valve and paravalvular leakage. The diagnosis was prosthetic valve endocarditis. He underwent a third mitral prosthetic valve replacement. Detection of the source of infection was difficult only by transthoracic echocardiography, and immediate transesophageal echocardiography seemed mandatory to diagnose bacterial endocarditis.

Adult↗
PubMed1996

CrkII signals from epidermal growth factor receptor to Ras.

A rat fibroblast mutant defective in oncogenic transformation and signaling from epidermal growth factor receptor to Ras has been isolated. The mutant contains dominant negative-type point mutations in the C-terminal SH3 domain of one crkII gene. Among the adapters tested, the mutant is complemented only by crkII cDNA. Expression of the mutated crkII in parent cells generates the phenotype indistinguishable from the mutant cell. Yet overexpression or reduced expression of Grb2 in the mutant before and after complementation with crkII have little effect on its phenotype. We conclude that adapter molecules are highly specific and that the oncogenic growth signal from epidermal growth factor receptor to Ras is predominantly mediated by CrkII in rat fibroblast.

Alleles↗