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Biomedical subjects

K Okada

Publications and source records attributed to K Okada.

At least 523 records · Page 29Linked to original sources
PubMed1997

Development of an intravascular pumping oxygenator using a new silicone membrane.

A new intravascular pumping oxygenator (IVPO) was developed for intravascular gas exchange and circulatory assistance in critically ill patients with respiratory and circulatory failure. The IVPO utilizes new silicone hollow fibers (diameter, 1 mm; membrane width, 50 microns) and consists of two driving tubes for the oxygenation and pumping of circulating blood. The performance characteristics of the IVPO were studied using an experiment ex vivo model. With a mean hemoglobin concentration of 10.5 +/- 2.3 g/dl, total oxygen transfer was 5.6 +/- 1.5 ml/min at a blood flow of 200 ml/min and 6.3 +/- 2.2 ml/min at a blood flow of 250 ml/min. Total CO2 transfer was 3.8 +/- 1.4 ml/min at a blood flow of 200 ml/min and 4.2 +/- 1.6 ml/min at a blood flow of 250 ml/min. Blood flow increased to a maximum of 250 ml/min during IVPO pumping. This preliminary experiment demonstrated that the IVPO has the capacity to function both as circulatory assist pump and as an intravascular hollow fiber oxygenator.

Animals↗
PubMed1997

Right atrial separation procedure for eliminating chronic atrial fibrillation associated with atrial septal defect.

Chronic atrial fibrillation (AF) had been documented in a patient with atrial septal defect for 7 years. A right atrial separation procedure was performed for ablation of chronic AF, concomitant with repair of the atrial septal defect, and followed by atrial electrophysiological mapping. A horizontal transectional incision extending to the borders of the atrial septum and the tricuspid annulus was made. Cryolesions of the atrial isthmus between the margin of the upper incision and the tricuspid valve annulus were created at -60 degrees C for 2 minutes at a time. After the operation, the patient had restored normal sinus rhythm during a subsequent follow-up period of 48 months.

Atrial Fibrillation↗
PubMed1997

Rapid and differential detection of two analogous enterotoxins of Vibrio cholerae and enterotoxigenic Escherichia coli by a modified enzyme-linked immunosorbent assay.

The principle of a novel ELISA (nylon-slip immuno-test, NSIT) was applied to the differential detection of two analogous enterotoxins, cholera toxin (CT) of Vibrio cholerae and heat-labile enterotoxin (LT) of enterotoxigenic Escherichia coli. The results obtained for CT and LT detection by a single test were sufficiently sensitive (87.9 and 100%) and specific (100 and 94.7%) in the differential detection test, when compared with the result of a colony hybridization test with DNA probes. The results suggest that the novel ELISA is applicable to the diagnosis of bacterial infections, by means of differential immunological detection of toxins in a single test.

Bacterial Toxins↗
PubMed1997

[Nasopharyngeal flora and carriage rates of Haemophilus influenzae type b of healthy infants].

The present study investigates the nasopharyngeal flora and defines the carriage rates of Haemophilus influenzae type b of 144 healthy infants who visited the well-baby clinic. 224 nasopharyngeal swabs were obtained (44 swabs from 1-month-old infants, 96 swabs from 4 to 5-month-old infants and 84 swabs from 7 to 8-month-old infants), and 440 organisms were isolated. The most frequently isolated organism was Staphylococcus aureus (45.5%) followed by Corynebacterium (38.6%) from 1-month-old infants, Corynebacterium (55.2%) followed by S. aureus (32.3%) and Streptococcus pneumoniae (25.0%) from 4 to 5-month-old infants, Corynebacterium (59.5%) followed by S. pneumoniae (26.2%) from 7 to 8-month-old infants. Twenty-four strains of H. influenzae were isolated from 21 infants, being 1 strain from 1-month-old infant, 9 strains from 4 to 5-month-old infants, 14 strains from 7 to 8-month-old infants. Four type b strains were isolated from 3 infants, being 1 strain from 1-month-old infant, none from 4 to 5-month-old infant, 3 strains from 7 to 8-month-old infants. One of the three 7 to 8-month old infants also carried Hib when he was at the age of 1 month old. The nasopharyngeal carriage rates of H. influenzae of infants were 2.3% in 1-month-old infants, 9.4% in 4 to 5-month-old infants, 16.7% in 7 to 8-month-old infants and 10.7% in total. The carriage rates of Hib were 2.3% in 1-month-old infants, 0% in 4 to 5-month-old infant, 3.6% in 7 to 8-month-old infants and 1.8% in total.

Corynebacterium↗
PubMed1997

Purification and characterization of phenylacetaldehyde reductase from a styrene-assimilating Corynebacterium strain, ST-10.

A novel phenylacetaldehyde reductase was purified about 50-fold to homogeneity from Corynebacterium sp. strain ST-10, which can assimilate gaseous styrene as the sole carbon and energy source. The enzyme was inductively synthesized when grown on gaseous styrene and had an important role in styrene metabolism in vivo. The enzyme had a molecular weight of 155,000 and was composed of four identical subunits (molecular weight, 42,000). The enzyme catalyzed the reduction of not only phenylacetaldehyde but also various aldehydes and ketones; however, it did not catalyze the reverse reaction, the dehydrogenation of 2-phenylethanol. The enzyme required NADH as a cofactor and showed no activity with NADPH; therefore, it was defined as an NADH-dependent phenylacetaldehyde reductase. The enzyme stereospecifically produced (S)-(-)-1-phenylethanol from acetophenone; therefore, it would be useful as a biocatalyst.

Acetaldehyde↗
PubMed1997

Cloning of the sdsA gene encoding solanesyl diphosphate synthase from Rhodobacter capsulatus and its functional expression in Escherichia coli and Saccharomyces cerevisiae.

Different organisms produce different species of isoprenoid quinones, each with its own distinctive length. These differences in length are commonly exploited in microbial classification. The side chain length of quinone is determined by the nature of the polyprenyl diphosphate synthase that catalyzes the reaction. To determine if the side chain length of ubiquinone (UQ) has any distinct role to play in the metabolism of the cells in which it is found, we cloned the solanesyl diphosphate synthase gene (sdsA) from Rhodobacter capsulatus SB1003 and expressed it in Escherichia coli and Saccharomyces cerevisiae. Sequence analysis revealed that the sdsA gene encodes a 325-amino-acid protein which has similarity (27 to 40%) with other prenyl diphosphate synthases. Expression of the sdsA gene complemented a defect in the octaprenyl diphosphate synthase gene of E. coli and the nonrespiratory phenotype resulting from a defect in the hexaprenyl diphosphate synthase gene of S. cerevisiae. Both E. coli and S. cerevisiae expressing the sdsA gene mainly produced solanesyl diphosphate, which resulted in the synthesis of UQ-9 without any noticeable effect on the growth of the cells. Thus, it appears that UQ-9 can replace the function of UQ-8 in E. coli and UQ-6 in S. cerevisiae. Taken together with previous results, the results described here imply that the side chain length of UQ is not a critical factor for the survival of microorganisms.

Alkyl and Aryl Transferases↗
PubMed1997

The ispB gene encoding octaprenyl diphosphate synthase is essential for growth of Escherichia coli.

The Escherichia coli ispB gene encoding octaprenyl diphosphate synthase is responsible for the synthesis of the side chain of isoprenoid quinones. We tried to construct an E. coli ispB-disrupted mutant but could not isolate the chromosomal ispB disrupted mutant unless the ispB gene or its homolog was supplied on a plasmid. The chromosomal ispB disruptants that harbored plasmids carrying the ispB homologs from Haemophilus influenzae and Synechocystis sp. strain PCC6803 produced mainly ubiquinone 7 and ubiquinone 9, respectively. Our results indicate that the function of the ispB gene is essential for normal growth and that this function can be substituted for by homologs of the ispB gene from other organisms that produce distinct forms of ubiquinone.

Alkyl and Aryl Transferases↗
PubMed1997

Adenosine stimulates nitric oxide synthesis in rat cardiac myocytes.

We investigated the effects of adenosine on nitric oxide (NO) synthesis by measuring the production of nitrite, a stable metabolite of NO, in cultured neonatal rat cardiac myocytes. Incubation of cultures with interleukin-1 beta (10 ng/ml) for 24 h caused a significant increase in nitrite production. The interleukin-1 beta-induced nitrite production by cardiac myocytes was significantly increased by adenosine or its stable analog 2-chloroadenosine in a dose-dependent manner (10(-7)-10(-4) M). The adenosine A2-receptor antagonist KF-17837 (10(-6) M), but not the A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (10(-6) M), significantly inhibited 2-chloroadenosine-mediated nitrite production. The 2-chloroadenosine-induced nitrite production by interleukin-1 beta-stimulated cells was accompanied by inducible NO synthase mRNA and protein accumulation. In the presence of N6, 2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (cAMP) (10(-3) M) or isoproterenol (10(-5) M), interleukin-1 beta-induced nitrite accumulation was further increased, but the effect of 2-chloroadenosine was not additive or synergistic. The protein kinase C inhibitor calphostin C did not inhibit the effect of 2-chloroadenosine. These results indicate that adenosine acts on A2 receptors and augments NO synthesis in interleukin-1 beta-stimulated cardiac myocytes, at least partially through a cAMP-dependent pathway.

2-Chloroadenosine↗
PubMed1997

Alteration in water channel AQP-2 by removal of AVP stimulation in collecting duct cells of dehydrated rats.

Dehydration increased the expression of aquaporin of collecting duct (AQP-2) and translocated AQP-2 to the apical plasma membranes from cytoplasmic vesicles of collecting duct cells. We determined whether the abrupt decrease in circulating arginine vasopressin (AVP) by giving excess water affects the expression of AQP-2 mRNA and subcellular localization of AQP-2 in collecting duct cells of the dehydrated rats. The 72-h water deprivation increased plasma AVP levels to 3.1 pg/ml and the expression of AQP-2 mRNA by 336% in rats, which were concomitantly abolished by the 40 ml/kg oral water load. A 50% inhibition ofAQP-2 mRNA expression was obtained with 20 min after the forced water load. In immunohistochemistry and electron microscopy, the AQP-2 was manifestly present around the apical edge of collecting duct cells in the 72-h dehydrated rats. The AQP-2 was diffusely translocated into the cytoplasm 1 h after the forced water administration. These results indicate that AVP plays the on-off regulation of AQP-2 mRNA expression and that a majority of AQP-2 is regulated by the shuttle recycling in the collecting duct cells.

Animals↗
PubMed1997

A monoclonal antibody (1F3) to human glomerular epithelial cells: a new marker for renal epithelial cell injury.

In order to identify a new cell surface antigen as a potential marker of renal epithelial cell injury, we produced a monoclonal antibody (Mab), 1F3, by immunizing mice with cultured human glomerular cells. Immunofluorescence (IF) and immunoelectron microscopy (IEM) studies demonstrated that 1F3-recognizing antigen (1F3 antigen) was strongly expressed on the cell surface of glomerular podocytes and very weakly on parietal epithelial cells. 1F3 antigen was not expressed in any other cells in the normal kidney. Immunoprecipitation analysis using metabolically labeled glomeruli revealed that 1F3 recognized a 125-kD protein under reducing conditions. IF studies of biopsy specimens from patients with a variety of glomerular and tubulointerstitial diseases showed that 1F3 antigen was almost negative in cellular crescents but was strongly expressed in fibrocellular crescents. When glomerular sclerosis appeared, the expression of 1F3 antigen decreased in sclerotic areas of glomeruli. 1F3 antigen became positive in atrophic tubules that were seen in diseased kidneys. Severity of tubular atrophy correlated well with the extent of tubular expression of 1F3 antigen. These results indicate that Mab, 1F3 marks phenotypic changes of renal epithelial cells under disease conditions and may be a useful marker for progressive kidney diseases.

Animals↗
PubMed1997

Arginine vasopressin increases nitric oxide synthesis in cytokine-stimulated rat cardiac myocytes.

We investigated the effects of arginine vasopressin (AVP) on nitric oxide (NO) synthase activity in cardiac myocytes by measuring the production of nitrite, a stable metabolite of NO, and the expression of inducible NO synthase (iNOS) mRNA and protein. Incubation of cultured neonatal rat cardiac myocytes for 24 hours with interleukin-1beta (IL-1beta) caused a significant increase in NO production. Both AVP and V1a receptor agonist [Phe2,Ile3,Orn8]vasopressin augmented NO synthesis in IL-1beta-stimulated, but not in unstimulated myocytes, in a dose-dependent manner. The V1a receptor antagonist [d(CH2)[5]1,O-Me-Tyr2,Arg8]vasopressin completely inhibited the effect of AVP. The AVP-induced NO production by IL-1beta-stimulated cells was accompanied by increased iNOS mRNA and protein accumulation. AVP caused a significant increase in cytosolic free Ca2+ levels of cardiac myocytes, whereas it showed no effect on cytosolic cAMP levels. After protein kinase C activity was functionally depleted by treating cells with phorbol 12-myristate 13-acetate for 24 hours, AVP did not augment IL-1beta-induced NO production. The effect of AVP was also inhibited in the presence of the protein kinase C inhibitor calphostin C. The addition of AVP increased protein kinase C activity in cardiac myocytes, and its effect was significantly inhibited in the presence of calphostin C. These results support the hypothesis that the heart may be a target organ for AVP and that AVP modulates IL-1beta-induced iNOS expression in myocytes through the V1a receptor, which is mediated at least partially via activation of protein kinase C.

Animals↗
PubMed1997

Subcortical silent brain infarction as a risk factor for clinical stroke.

BACKGROUND AND PURPOSE: No prospective studies have examined the rate of symptomatic ischemic or hemorrhagic stroke in patients with subcortical silent brain infarction (SSBI) who were otherwise neurologically normal at entry into the study. This report investigates SSBI, detected by MRI, as a clinical stroke risk factor. METHODS: MRI scans were performed in 933 neurologically normal adults (30 to 81 years; mean age, 57.5 +/- 9.2 years) without history of cerebrovascular diseases who received our health screening of the brain 1 to 7 years before investigation. We obtained information of their clinical stroke onset through sending out a questionnaire for subjects. We detected SSBI (focal T2 hyperintensities larger than 3 mm with correlative T1 hypointensity), FWT2HL (focal white matter T2 hypertensity lesions similar to SSBI but without correlative T2-hypointensity), and PVH (periventricular hyperintensity) by MRI. Age, sex, family history of stroke, history of hypertension, diabetes mellitus, lipids, hematocrit, blood pressure, fasting blood sugar, smoking, alcohol habits, ischemic changes on electrocardiogram, and sclerotic changes of retinal arteries were included in the analysis. RESULTS: Incidence of SSBI was 10.6% in all subjects. No cortical infarct was detected in this series. Multiple logistic regression analysis showed that hypertension (odds ratio [OR], 4.07; 95% CI, 2.57 to 6.45), diabetes (OR, 2.41; 95% CI, 1.20 to 4.85), alcohol habits > or = 58 g/day (OR, 2.58; 95% CI, 1.50 to 4.45), retinal artery sclerosis (OR, 2.14; 95% CI, 1.32 to 2.38), and age (OR, 1.77; 95% CI, 1.32 to 2.38) were significant and independent risk factors for SSBI. For FWT2HL, hypertension (OR, 4.49; 95% CI, 2.54 to 7.96) and age (OR, 2.08; 95% CI, 1.45 to 3.00) were also independent risk factors. Risk factors for PVH were age (OR, 3.46; 95% CI, 2.23 to 5.36), hypertension (OR, 3.06; 95% CI, 1.62 to 5.78), and retinal artery sclerosis (OR, 2.25; 95% CI, 1.02 to 4.96). We found 14 brain infarctions, 4 brain hemorrhages, and 1 subarachnoid hemorrhage during observation. Annual incidence of clinical stroke was higher in the subjects with SSBI than in those without focal lesions (10.1% versus 0.77%). ORs for clinical stroke onset were 10.48 for SSBI (95% CI, 3.63 to 30.21) and 4.81 for FWT2HL (95% CI, 1.13 to 20.58). The PVH did not relate to clinical stroke onset. CONCLUSIONS: The strong association of SSBI, FWT2HL, and PVH with hypertension suggests a common underlying mechanism (presumably small-vessel vasculopathy). The SSBI showed the most significant association for clinical subcortical stroke. The FWT2HL was also a risk factor for the stroke but was less significant than SSBI. The subjects with SSBI should be considered at high risk for clinical subcortical brain infarction or brain hemorrhage.

Adult↗
PubMed1997

Poststroke apathy and regional cerebral blood flow.

BACKGROUND AND PURPOSE: Although apathy has been reported as one of the neuropsychiatric symptoms following stroke, there have been no studies on regional cerebral blood flow (rCBF) in patients with apathy. In this study we estimated the severity of apathy using the Apathy Scale and examined its relationship to rCBF in 40 stroke patients (mean age, 71.4 years). METHODS: Neuropsychiatric batteries were performed including the Apathy Scale, verbal intelligence and frontal function tests, a depression scale, and an assessment of activities of daily living. The cortical rCBFs were measured by the 133Xe inhalation method. RESULTS: Twenty patients (50%) showed apathy. These patients showed significantly lower scores on verbal intelligence and frontal function tests and a significantly higher depression score than the nonapathetic group. On MRI images there was no relationship between the apathy score and specific regional distribution of lesions. The rCBFs of the bilateral hemisphere were significantly lower in the apathetic group than in the nonapathetic group. The apathetic group showed a significantly reduced rCBF in the right dorsolateral frontal and left fronto-temporal regions. Furthermore, the apathy score for all patients was significantly negatively correlated with rCBF in the same regions. CONCLUSIONS: These findings demonstrate that apathy is a frequent symptom among elderly stroke patients and may be accompanied by cognitive impairments, depressive state, and frontal dysfunction. The hypoactivity in the frontal lobe and anterior temporal regions may contribute to symptoms of apathy after stroke.

Activities of Daily Living↗
PubMed1997

Low molecular-weight G-actin binding proteins involved in the regulation of actin assembly during myofibrillogenesis.

We previously demonstrated that small G-actin binding proteins, cofilin, ADF and profilin, are involved in the actin dynamics during myofibrillogenesis (OBINATA, T. (1993). Int. Rev. Cytol., 143: 153-189.). To better understand how they are responsible for the regulation of actin assembly, the amounts of the actin-binding proteins were quantified by means of quantitative immunoblotting and compared with that of G-actin pool. The sum of the amounts of cofilin, ADF and profilin was insufficient at early developmental stages but sufficient at later stages to account for the pool of G-actin in muscle cells. We detected expression of thymosin beta 4 at a considerable level in young embryonic but not in adult skeletal muscles. We, therefore, conclude that the G-actin pool in young embryonic skeletal muscle is mainly due to cofilin, ADF, profilin and thymosin beta 4. Switching from a non-muscle-type (NM-) cofilin to a muscle-type (M-) cofilin was observed during muscle development of mammals. In order to clarify cofilin-dependent regulation of actin assembly in muscle cells, cofilin tagged with fluorescence dyes was introduced into C2 myoblasts by a micro injection method. The exogeneous cofilin, but not ADF, caused quick disassembly of actin filaments and accumulated in furrow region of dividing cells. The analogs of the unphosphorylated form (A3-cofilin) and the phosphorylated form (D3-cofilin) were prepared by converting Ser3, a regulatory phosphorylation site, to Ala or Asp. When A3-cofilin and D3-cofilin were injected into living cells, the former was concentrated at the membrane ruffles and cleavage furrow, while the latter showed only diffuse distribution in the cytoplasm. These results suggest that the subcellular distribution of cofilin as well as its interaction with actin in vivo is regulated by its phosphorylation and dephosphorylation.

Actin Depolymerizing Factors↗
PubMed1997

Arginine vasopressin inhibits nitric oxide synthesis in cytokine-stimulated vascular smooth muscle cells.

The purpose of this study was to investigate the effects of arginine vasopressin (AVP) on nitric oxide (NO) synthesis in vascular smooth muscle cells (VSMCs). We measured the production of nitrite, a stable metabolite of NO, and the expression of inducible NO synthase (iNOS) mRNA in cultured rat VSMCs. Incubation of VSMCs for 24 h with interleukin-1 beta (IL-1 beta) caused a significant increase in NO production. Both AVP and the V1a receptor agonist [Phe2, Ile3, Orn8]vasopressin inhibited NO synthesis in IL-1 beta-stimulated cells, but not in unstimulated cells, in a dose-dependent manner. The V1a receptor antagonist [d(CH2)5(1), O-Me-Tyr2, Arg8]vasopressin completely inhibited the effect of AVP. Incubation with IL-1 beta for 24 h induced the expression of iNOS mRNA in VSMCs, while AVP suppressed its expression. After functional depletion of protein kinase C activity by treating cells with phorbol 12-myristate 13-acetate for 24 h, AVP did not inhibit IL-1 beta-induced NO production. The effect of AVP was also inhibited in the presence of the protein kinase C inhibitor calphostin C in a dose-dependent manner. These results indicate that AVP inhibits IL-1 beta-induced iNOS expression in VSMCs through the V1a receptor, which is mediated at least partially via activation of protein kinase C.

Animals↗