Biomedical subjects

M Okada

Publications and source records attributed to M Okada.

At least 19 recordsLinked to original sources

PubMed1992

Reactive proliferation of astrocytes studied by immunohistochemistry for proliferating cell nuclear antigen.

Astrocyte proliferation in the stab-wounded cerebral cortex of mice was studied using double immunohistochemistry for proliferating cell nuclear antigen (PCNA) and glial fibrillary acidic protein (GFAP). The number of GFAP-positive astrocytes increased markedly from day 0.5 to day 3 after stab wounding. Some GFAP-positive astrocytes in the immediate vicinity of the wound were found to be positive for PCNA. However, the maximum number of these double positive astrocytes was only 5-6% of the number of GFAP-positive astrocytes. This maximum value was observed on days 2.5 and 3. The present study revealed that astrocytes are able to reactively express PCNA, an intrinsic marker of DNA replication. On the other hand, it is suggested that the proliferation of astrocytes in the wounded cerebral cortex is limited, in contrast with their marked reactive up-regulation of GFAP.

Animals↗

PubMed1992

Nerve growth factor suppresses apoptosis of murine neutrophils.

We investigated inhibitory activity of nerve growth factor (NGF) on apoptosis of murine peritoneal exudate neutrophils. During culture for 9 h, apoptotic cells were identified by morphological changes under a light microscope: nuclear pyknosis and chromatin condensation with or without cytoplasmic vacuolation. The apoptotic state was confirmed by DNA fragmentation indicating the endogenous endonuclease activation. When neutrophils were incubated in the presence of NGF, the proportion of cells with the morphological changes was decreased in a dose-dependent manner, and the development of the characteristic DNA fragmentation was restricted. The apoptosis-suppressing activity of NGF was abolished by the addition of anti-NGF monoclonal antibody. These results suggest that NGF may suppress neutrophil apoptosis by preventing the endogenous endonuclease activation.

Animals↗

PubMed1992

[Evaluation of aortic distensibility using cine MR imaging].

Regional aortic distensibility was measured noninvasively using cine MR imaging to determine whether it correlates with aging or risk of coronary artery disease (CAD). Twenty-two patients with CAD confirmed by angiography and 33 without CAD underwent cine MR imaging. Thirty-two sequential images were obtained in one cardiac cycle. The cross sectional area of the descending thoracic aorta was measured on both diastolic (A) and systolic (A') images. Aortic distensibility (A.D.) was calculated from the following equation: A.D. = (A'-A)/A/delta P. (delta P represents pulse pressure). Results of a simple regression analysis showed that decreased regional aortic distensibility was significantly correlated with the age of the patients (r = -0.762, p less than 0.005). In addition, the parameter was lower in patients with CAD than those without CAD (p less than 0.05). In conclusion, regional aortic distensibility derived from cine MR imaging is a useful parameter to evaluate not only aging but also pathological atherosclerosis of the aorta. In addition, this parameter might have some potential to evaluate the prediction of CAD in patients with normal serum cholesterol.

Adolescent↗

PubMed1992

Effects of the N-methyl-D-aspartate antagonists on the rise in [Ca2+]i following depolarization in aged rat brain synaptosomes.

The effects of non-competitive NMDA antagonists, MK-801 and dextrorphan in relation to the rise in intracellular Ca2+ concentrations ([Ca2+]i) after stimulation with 15 mM K+ in whole brain synaptosomes from young (3 months old) and aged (24 months old) Fisher344 rats were examined. A fluorescent chelating agent, Rhod-2, was employed to monitor any alterations of K(+)-evoked [Ca2+]i. In young rats, the rise in [Ca2+]i following depolarization was affected by neither dextrorphan (1, 10, 100 microM) nor MK-801 (0.1, 1, 10 microM), while in aged rats, 1 microM dextrorphan and 0.1 microM MK-801 brought about a significant increase in [Ca2+]i following depolarization. In low Mg2+ medium, 10 microM MK-801 and 100 microM dextrorphan significantly inhibited the rise in [Ca2+]i after stimulation with 15 mM K+ in young rats, while neither dextrorphan nor MK-801 could affect the rise in [Ca2+]i significantly in aged rats. When 100 microM NMDA was applied in a medium containing 1.2 mM Mg2+, the rise in [Ca2+]i following depolarization was slightly inhibited by 1 microM MK-801 in young rats, but it was not inhibited significantly by dextrorphan. In aged rats, both 100 microM dextrorphan and 10 microM MK-801 strongly inhibited the rise in [Ca2+]i following depolarization in the presence of 100 microM NMDA. Instead of NMDA, when 100 microM alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), a non-NMDA receptor agonist, was applied, dextrorphan did not inhibit the rise in [Ca2+]i. In low Mg2+ medium, 100 microM NMDA potentiated the inhibitory effect of 10 microM dextrorphan in young rats, while 100 microM dextrorphan or MK-801 did not show any further inhibition by adding 100 microM NMDA. The addition of 100 microM AMPA did not affect the effect of dextrorphan in a low Mg2+ medium in young rats. These results suggest that NMDA antagonist-mediated [Ca2+]i homeostatic system may alter through aging. In addition, the findings that NMDA potentiated the inhibitory effect of NMDA antagonist, which being further potentiated by aging or lowered extrasynaptosomal Mg2+, indicate the possibility that the Mg2+ block to NMDA receptors might be attenuated through aging.

Aging↗

PubMed1992

The facilitating and suppressing effects of delta 9-tetrahydrocannabinol on the rise in intrasynaptosomal Ca2+ concentration in rats.

The effects of delta 9-tetrahydrocannabinol (delta 9-THC) on the rise in intracellular Ca2+ concentrations ([Ca2+]i) after stimulation with 15 mM or 29 mM K+ in rat whole brain synaptosomes were examined. A fluorescent chelating agent, Rhod-2, was employed to monitor any alterations of K(+)-evoked [Ca2+]i. Pretreatment with 10(-10) M delta 9-THC for 3 min enhanced K(+)-evoked [Ca2+]i significantly, while 10(-9), 10(-8) or 5 x 10(-8) M delta 9-THC significantly inhibited the K(+)-evoked [Ca2+]i. These results suggest that delta 9-THC had a biphasic effect on the K(+)-evoked Ca2+ response in rat brain synaptosomes.

Animals↗

PubMed1992

Experimental atrophic rhinitis in 2 and 4 month old pigs infected sequentially with Bordetella bronchiseptica and toxigenic type D Pasteurella multocida.

Experimental infections with Bordetella bronchiseptica and/or toxigenic type D Pasteurella multocida were studied in 2- and 4-month-old primary specific-pathogen-free pigs. None of the 2-month-old pigs inoculated with B. bronchiseptica or P. multocida alone developed turbinate atrophy. All the pigs inoculated with B. bronchiseptica (10(7) CFU/head) and P. multocida (10(9) CFU/head for 5 consecutive days) together, however, developed clinical and post-mortem signs of atrophic rhinitis (AR) similar to the naturally occurring disease. Slight to severe turbinate atrophy was observed in the 4-month-old pigs inoculated with B. bronchiseptica and P. multocida (at the same concentration as above) at necropsy.

Animals↗

PubMed1992

Molecular cloning and expression of chicken C-terminal Src kinase: lack of stable association with c-Src protein.

Cloning and sequencing of chicken C-terminal Src kinase (CSK), a tyrosine kinase that phosphorylates the regulatory C-terminal tyrosine residue present on cytoplasmic tyrosine kinases of the Src family, demonstrated a high degree of interspecies conservation as well as src homology 2 and 3 domains N-terminal to the kinase domain. The lack of autophosphorylation sites distinguishes CSK from other tyrosine kinases. CSK is unique and does not belong to a gene family, suggesting that it may phosphorylate other members of the Src family of tyrosine kinases in addition to c-Src. Since complex formation between c-Src and CSK seemed a likely regulatory step in the control of c-Src kinase activity, such an association was investigated by immunoprecipitation and Western blotting as well as intracellular localization studies. Although some portions of CSK were found in a membrane fraction, no complex formation between CSK and c-Src was observed, suggesting that the src homology 2 domain of CSK does not play a role in the direct interaction of c-Src.

Amino Acid Sequence↗

PubMed1992

Myelopathy due to large veins draining recurrent spontaneous caroticocavernous fistula.

A 45-year-old woman developed a myelopathy 9 years after a spontaneous left caroticocavernous fistula (CCF) was treated by a trapping procedure, with clipping distal to the fistula and ligation of the common carotid artery. Spinal MRI and vertebral angiography revealed recurrence of the CCF and gigantic tortuous veins draining through the brain stem down to the midcervical spinal cord. The abnormal veins and myelopathy disappeared after surgical closure of the CCF.

Arteriovenous Fistula↗

PubMed1992

Retrograde cerebral perfusion with circulatory arrest in aortic arch aneurysms.

Two surgical cases of aortic arch aneurysms are presented. Retrograde (venoarterial) cerebral perfusion during circulatory arrest under deep hypothermia was performed to evacuate air and debris in cerebral vessels and preserve cerebral tissue. On postoperative day 1, the patients were conscious and alert with no neurological deficit. This technique is simple and can be applied during standard cardiopulmonary bypass. The technique is useful to avoid cerebral air and thromboembolisms.

Aged↗

PubMed1992

Effect of prostaglandin I2 and superoxide dismutase on reperfusion injury of warm ischemic lung.

A prostaglandin I2 (PGI2) analogue and superoxide dismutase (SOD) were administered to dogs with pulmonary denervation, and their effects on warm ischemic damage to the lung were studied. Twenty-seven adult mongrel dogs were divided into a control group (6 dogs), a PGI2 group (7 dogs), an SOD group (6 dogs), and a heparin group (8 dogs). The left pulmonary hilum was dissected, with PGI2 (1 microgram/kg) being administered to the PGI2 group and heparin (100 U/kg) to the heparin group. Then the left lung was placed in a warm ischemic state for 1 hour. The SOD group also received 20 mg/kg of SOD intravenously 1 minute before reperfusion. Before warm ischemia, immediately after reperfusion, and 1 hour and 2 hours afterward, the blood gases, left pulmonary vascular resistance, and other data were measured under right pulmonary artery clamping. Arterial oxygen tension showed significantly better values in the SOD and PGI2 groups than in the control and heparin groups. The left pulmonary vascular resistance increased with time in the control group but did not increase in the PGI2 group. Pulmonary microangiography showed that dilatation of the pulmonary arterioles was prominent in the PGI2 group. The quantity of pulmonary extravascular fluid was significantly less in the PGI2 and SOD groups than in the control and heparin groups. Histological examination showed marked collapse of capillaries, intraalveolar hemorrhage, and edema in the control and heparin groups, whereas these changes were only slight in the PGI2 and SOD groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

An approach to the generalized nurse scheduling problem--generation of a declarative program to represent institution-specific knowledge.

An approach to the nurse scheduling problem is presented. The critical problem in nurse scheduling in a hospital is how to determine the day-to-day shift assignments of each nurse for a specified period in a way that satisfies the given requirements as much as possible, where the requirements differ greatly depending on the hospital. We present a method for constructing an agency-independent core procedure which can be tailored to the peculiar requirements of an individual hospital. As a basis, a formal analysis of the problem was performed, and a general scheduling procedure was established. Based on the method, a software system which produces a scheduling program for a given institution was developed. A declarative program that represents institution-specific information is generated through an interview with the user and incorporated into the general procedure. Some of the programming technicalities and an application of the system are also presented.

Hospital Units↗

PubMed1992

Possible involvement of Na(+)-H+ exchange in the early phase of reperfusion in myocardial stunning.

Calcium overload during reperfusion after prolonged ischemia has been associated with the Na(+)-Ca2+ exchange system. It has been proposed that the promotion of Na(+)-Ca2+ exchange at reperfusion may be mediated by Na(+)-H+ exchange. To evaluate whether this hypothesis is applicable for stunned myocardium, we examined the influence of temporary suppression of Na(+)-H+ and/or Na(+)-Ca2+ exchange during early reperfusion in isolated rat hearts. Myocardial stunning was produced by global ischemia for 15 min at 37 degrees C. The initial reperfusate was given during the subsequent 10 min after ischemia, and followed by reperfusion with normal Krebs-Henseleit buffer solution for 40 min. Hemodynamic indices, creatine kinase in coronary effluent, and myocardial water content were measured during reperfusion. The functional recovery of stunned myocardium was improved with higher extracellular Na+ concentration and/or lower Ca2+ concentration of the initial reperfusate. Aortic flow recovery of group II (135 mM Na(+)-0.5 mM Ca2+) was 77.0 +/- 3.4%, which was substantially greater (P < 0.05) than that of other groups: group I (control, 135 mM Na(+)-1.5 mM Ca2+), 68.2 +/- 2.4%; group III (25 mM Na(+)-0.5 mM Ca2+), 48.7 +/- 2.9%; group IV (25 mM Na(+)-1.5 mM Ca2+), 21.6 +/- 1.5%. Administration of amiloride, an inhibitor of Na(+)-H+ exchange, in the initial reperfusate ameliorates cardiac damage and improved aortic flow recovery in a dose-dependent manner (10(-6) M, 70.1 +/- 3.7%; 10(-5) M, 77.3 +/- 1.7%; 10(-4) M, 82.0 +/- 2.1% vs control 68.2 +/- 2.4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗

PubMed1992

Detection of feline immunodeficiency proviral DNA in peripheral blood lymphocytes by the polymerase chain reaction.

Feline immunodeficiency virus (FIV) proviral DNA was detected by the polymerase chain reaction method (PCR). PCR products were detected by gel electrophoresis and ethidium bromide staining. The P-10, P-15 and P-24 regions of the gag gene of FIV were chosen as the target sequences for amplification, and three primer pairs were prepared. The PCR products subjected to amplification with each primer pair were found to possess sites of digestion by a restriction enzyme, as hypothesized. They did not react with feline leukemia virus (FeLV)-infected or feline syncytium-forming virus (FeSFV)-infected cell-derived DNA, and specifically amplified FIV-infected cell-derived DNA. FIV proviral DNA was detected by the PCR method with either primer pair (one-step amplification: single PCR) in DNA derived from peripheral blood lymphocytes (PBL) from 7 of 12 FIV antibody-positive cats. When PCR products in each of the 12 cats were subjected to a second amplification using the same primer pair (two-step amplification: double PCR), FIV proviral DNA was detected in all of the cats. When PBL samples collected from three cats that were negative and three that were positive in the single PCR were cultured for a few weeks in the presence of interleukin 2, FIV proviral DNA was detected in all six cats by the single PCR method. The results suggest that either the use of cultured PBL as the sample or the performance of the double PCR method enables simple and specific detection of FIV proviral DNA in PBL.

Animals↗

PubMed1992

Effects of zonisamide on extracellular levels of monoamine and its metabolite, and on Ca2+ dependent dopamine release.

The effects of zonisamide (3-sulfamoylmethyl-1,2-benzisoxazole), a novel anticonvulsant, on extracellular levels of monoamine and its metabolite in the striatum and hippocampus, and Ca2+ dependent monoamine release in the striatum of freely moving rats were studied by microdialysis. Zonisamide increased dopamine, homovanillic acid and 5-hydroxyindoleacetic acid, and decreased 3,4-dihydroxyphenylacetic acid in the rat striatum. However, zonisamide showed no effect on Ca2+ dependent dopamine release in the rat striatum. In the hippocampus, zonisamide increased dopamine, homovanillic acid, serotonin and 5-hydroxyindoleacetic acid and decreased 3,4-dihydroxyphenylacetic acid. The present results suggest that zonisamide facilitates dopaminergic and serotoninergic neurotransmission but does not affect Ca2+ dependent dopamine release within therapeutic plasma concentrations.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

IgA nephropathy in patients with congenital C9 deficiency.

The clinical, histologic, and immunopathological findings of three young Japanese males with congenital C9 deficiency and primary IgA nephropathy are reported. The C9 deficiency was discovered either through mass complement screening, or when low hemolytic activity for CH50 and normal C3 levels were detected in plasma. Hematuria and proteinuria were detected at the age of 8 or 9 years as a result of annual urinary screening tests for school children. Renal biopsy showed focal and segmental mesangial proliferation with small epithelial crescents in one patient, and mild, diffuse mesangial proliferation in two. IgA and C3 were deposited predominantly in the mesangial area, and staining for C9 was negative in these patients. Electron microscopy revealed electron dense deposits predominantly in mesangial and paramesangial zones. Immunohistochemical staining in renal biopsy tissues from two patients showed mesangial staining for C5, C8, and S-protein, but staining for C5b-9 neoantigen was completely negative. These results show that the formation of C5b-9 complex is not essential for the induction of human IgA nephropathy, and also for the proliferation of mesangial and even parietal epithelial cells.

Child↗

PubMed1992

Two modes of homologous C3 deposition on Ramos Burkitt's lymphoma cell substrains co-expressing DAF (CD55), CD59, and CR2 (CD21), and on cells lacking them.

We established decay-accelerating factor (DAF)/CD59-positive and -negative substrains of a human B cell line, Ramos, R(DAF+/CD59+) and R(DAF-/CD59-) respectively. Unexpectedly, treatment of R(DAF+/CD59+) cells with Mg2(+)-EGTA-serum resulted in efficient C3 deposition, while treatment of R(DAF-/CD59-) cells did not. All six substrains of R(DAF-/CD59-) cells were CR2-negative, and treatment of the cells with M177 [a membrane cofactor protein (MCP) cofactor-blocking antibody] and/or acidic buffer only minimally affected the extent of C3 deposition. However, when R(DAF-/CD59-) cells were pretreated with M177 followed by incubation with low conductivity (3 mS) Mg(2+)-EGTA-serum, C3 deposition leading to effective cytolysis was provoked. On the other hand, all seven R(DAF+/CD59+) substrains were CR2-positive and could potentially induce C3 autoactivation without cytolysis under physiological conditions. Both M177 and pH again minimally affected the extent of C3 deposition. However, conductivity altered the sensitivity to C3: at under 3.0 mS, R(DAF+/CD59+) cells became almost insensitive to alternative pathway-mediated C3 deposition. Anti-CR2 partially inhibited C3 deposition on R(DAF+/CD59+) cells and C3 deposition was abrogated on the CR2-lacking R(DAF-/CD59-) cells, suggesting that CR2 was associated with the deposition of C3. These results, together with the finding that fluid phase activation of complement did not enhance C3 deposition, suggest that there are two distinct modes of spontaneous homologous C3 deposition on human lymphoma cells. In one case, CR2 or its related molecules participates in C3 deposition overcoming the protective function of DAF/MCP and this type of C3 deposition is maximized under physiological conditions. In the other case, C3 deposition is induced by another homologous C3 activator that becomes functional under low conductivity conditions and the absence of DAF/MCP. These two modes of homologous alternative pathway activation would explain the reported instances of spontaneous C3 deposition on human B lymphoid cell lines (under physiological conditions in the presence of DAF/MCP) and on paroxysmal nocturnal hemoglobinuria erythrocytes (under low conductivity conditions in the absence of DAF/MCP).

Antigens, CD↗

PubMed1992

Intraoperative monitoring for thoracolumbar or lumbar surgery with somatosensory evoked potentials after double stimuli.

Somatosensory evoked potentials were after double stimuli on the posterior tibial nerve for the intraoperative monitoring in 58 thoracolumbar or lumbar surgeries. The first cortical positive potential P38 and P'38 after the second stimulus was recorded after double stimuli. Transient decreased amplitude more than 50% or missing potential of P'38 was found in 11 cases. These P'38 changes occurred in five procedures of retracting the nerve roots or dural sacs, three cases of reducing of thoracolumbar fractures, and two procedures of transpedicular screwing. No causative procedure was found in one case. In those 11 cases, 5 showed no abnormality in P38 potentials and 6 cases showed less decreased amplitude in P38 than in P'38. Consequently, P'38, which was evoked by the second stimulus, can be used for the intraoperative monitoring in the thoracolumbar and lower lumbar surgery.

Adolescent↗

PubMed1992

Cytotoxicity of activated platelets to autologous red blood cells.

Gel-filtered human platelets exerted lytic activity on autologous red blood cells (RBC) when they were coincubated at 37 degrees C with platelet-activating agents, such as thrombin, collagen, ADP, LPS or PMA in the absence of plasma. Lysis of activated platelets themselves did not occur during the incubation period examined. Morphological observations showed that RBC exposed to thrombin-activated platelets were fragmented and/or transformed into spherocytes. This haemolytic reaction by thrombin-activated platelets did not occur at 4 degrees C, or in the presence of agents which inhibited glycolysis or elevated intracellular levels of cAMP, indicating that energy-dependent and cAMP-regulated platelet metabolism was required for this reaction. When platelets and RBC were incubated in the same vessel, but were prevented from coming into direct cell to cell contact by means of a membrane barrier, their cytotoxicity was reduced but not eliminated completely. No cytotoxic activity against RBC was detected in platelet-free supernatants obtained by centrifugation after activation of platelets with thrombin. On the contrary, activated and washed platelets retained the activity. These observations suggested that the cytotoxic activity was carried by some diffusible and easily inactivated factors, which were continuously produced and liberated from activated platelets. Cyclo-oxygenase inhibitors inhibited the haemolytic activity of thrombin-activated platelets, suggesting a role for some products of platelet-cyclo-oxygenase pathway in platelet-mediated haemolysis. These results provide the first evidence for a direct role of activated platelets in mediation of RBC-damage in the absence of any plasma factors.

Blood Platelets↗