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Y Ishida

Publications and source records attributed to Y Ishida.

At least 379 records · Page 21Linked to original sources
PubMed1994

[Simultaneous assessment of exercise-induced abnormalities in myocardial perfusion and regional wall motion by using 99mTc-tetrofosmin].

To clarify the usefulness of the combined assessment of exercise (EX)-induced abnormalities in myocardial perfusion and regional wall motion for detecting coronary artery disease (CAD), we carried out first-pass radionuclide angiography and myocardial perfusion imaging during EX and at rest by 99mTc-tetrofosmin. Twenty-four patients with angiographically proven CAD, 9 (Gp A) with single and 15 (Gp B) with multivessel disease, were studied. The sensitivity for the detection of CAD was 78% of Gp A, 73% of Gp B in planar image and 78%, 87% in SPECT image, respectively. When left ventricular ejection fraction and regional ejection fraction (rEF) were combined with the result of myocardial perfusion, sensitivity increased up to 89% of Gp A, 100% of Gp B. Diagnostic accuracy of LAD, LCX and RCA was 79%, 88% and 83%, respectively. Regional EF in ischemic areas decreased during EX in both Gps, particularly in Gp B. Regional EF in relatively normal perfusion areas did not significantly change in Gp A, but decreased in Gp B. These results suggest that 99mTc-tetrofosmin contributes to the improvement of sensitivity for CAD by combined assessment of EX-induced wall motion and myocardial perfusion abnormalities.

Aged↗
PubMed1993

[Detectability of diagonal branch disease with other branch lesions by 201TlCl exercised myocardial scintigraphy].

The detectability of coronary diagonal (Dx) branch disease in 24 patients (16 with myocardial infarction, 8 with angina pectoris; mean age of 56) with other branch (left anterior descending branch [LAD], left circumferential branch [LCX], or right coronary artery [RCA]) diseases was reviewed with 201TlCl exercised myocardial planar and SPECT images. In Dx branch disease with LAD #7 lesion (n = 10), Dx perfusion abnormality was detected in planar and SPECT images in 3 (30%) and 8 patients (80%), respectively. In Dx branch disease with LCX lesion (n = 7), Dx perfusion abnormality was detected in planar and SPECT images in 3 (43%) and 4 patients (57%), respectively. In Dx branch disease with RCA lesion (n = 7), Dx perfusion abnormality was detected in only 1 (14%) and 2 patients (29%), respectively. In conclusion, SPECT is a useful modality for detecting Dx branch disease, but it is sometimes hard to detect Dx branch disease with LCX and RCA lesions.

Coronary Disease↗
PubMed1993

Two separate mechanisms of T cell clonal anergy to Mls-1.

T cell tolerance to superantigen can be mediated by clonal anergy in which Ag-specific mature T cells are physically present but are not able to mount an immune response. We induced T cell unresponsiveness to minor lymphocyte stimulations locus antigen (Mls)-1a in mice transgenic for TCR V beta 8.1 in three different systems: 1) injection of Mls-1a spleen cells, 2) mating with Mls-1a mice, and 3) bone marrow (BM) chimeras in which Mls-1a is present only on nonhematopoietic cells. CD4+8-V beta 8.1+ cells from all these groups did not proliferate in response to irradiated spleen cells from Mls-1a mice. We compared the response of these cells by T cell/stimulator cell conjugate formation, Ca2+ mobilization, and proliferation assays. The mechanisms underlying the unresponsiveness of these T cells appear to differ. CD4+8-V beta 8.1+ cells from Mls-1a spleen cell-injected mice mobilized cytoplasmic Ca2+ but proliferated at a reduced level in response to cross-linking with anti-TCR mAb. However, these cells formed conjugates, mobilized Ca2+, and proliferated in response to Mls-1a when activated B cells were used as stimulators, although they produced reduced levels of IL-2. In Mls-1a/b V beta 8.1 transgenic mice, a subset in CD4+8-V beta 8.1+ cells did not mobilize cytoplasmic Ca2+ after TCR cross-linking. Their conjugate formation, Ca2+ mobilization, or proliferation in response to Mls-1a on activated B cells was undetectable. Finally, CD4+8-V beta 8.1+ cells from the BM chimeras proliferated to TCR cross-linking at a partially reduced level and formed conjugates, mobilized Ca2+, and proliferated in response to Mls-1a on activated B cells. These features suggest that the mechanisms underlying the maintenance of anergy in Mls-1a spleen cell-injected mice are distinct from those in Mls-1a mice.

Animals↗
PubMed1993

Lack of voltage sensitive potassium channels and generation of membrane potential by sodium potassium ATPase in murine T lymphocytes.

Voltage sensitive K+ channels, which are responsible for generation of membrane potential in most cells, are functionally absent in about one-third of peripheral murine T cells and greatly reduced in the rest as shown by resistance of their membrane potential to changes in extracellular potassium concentration and failure of K+ channel dependent volume regulation. Despite the absence of voltage- sensitive K+ channels, the membrane potential of peripheral T cells is between -60 and -70 mV, the same as thymocytes. A total of 40 to 70 mV of the membrane potential of peripheral T cells is produced by the direct electrogenic action of the asymmetric Na+K+ ATPase pump because the cells are depolarized by ouabain, an inhibitor of the pump, removal of extracellular potassium or reduction of temperature. The residual, ouabain-resistant membrane potential, is sensitive to the K+ channel blocker, quinine, and thus due to electrodiffusion through K+ channels. Na+ and K+ turnover, and sensitivity to ouabain, are the same in peripheral T cells and thymocytes. The predominant mechanism of membrane potential generation changes during T lymphocyte differentiation from electrodiffusion in the thymus to electrogenic in peripheral T cells and back to electrodiffusion upon peripheral cell activation.

Animals↗
PubMed1993

Inhibitory action of 4-aminopyridine on Ca(2+)-ATPase of the mammalian sarcoplasmic reticulum.

In the isolated guinea pig diaphragm muscle, 4-aminopyridine (4-AP) elicited a marked potentiation of twitch contraction evoked by direct electrical stimuli. Although tetraethylammonium (TEA) and charybdotoxin only slightly potentiated twitch contraction, 4-AP, but not TEA, also augmented a contractile response to caffeine. These effects of 4-AP on muscle contraction could not be interpreted by a simple inhibition of potassium channels on the plasma membrane. In the fragmented sarcoplasmic reticulum (SR) prepared from the guinea pig psoas muscle, 4-AP inhibited the ATP-driven Ca2+ uptake from the extravesicular medium. Furthermore, 4-AP at concentrations less than 10 mM elicited a selective inhibition of Ca(2+)-activated SR ATPase in a competitive manner against the Ca2+ concentration of the medium and 10 mM 4-AP showed the unsurmountable inhibition. 4-AP at 30 mM apparently inhibited activities of other ATPases such as Na+,K+- and myosin ATPases. In contrast, other potassium channel blockers such as TEA, apamin, charybdotoxin, and glibenclamide did not inhibit the SR function. These results suggest that, although the specific concentration range is rather small, 4-AP elicits an inhibition of SR Ca(2+)-pumping activity, leading to the marked potentiation of muscle contractile responses to electrical stimuli and caffeine.

4-Aminopyridine↗
PubMed1993

Flow cytometric analysis of the expression of PCNA during the cell cycle in HeLa cells and effects of the inhibition of DNA synthesis on it.

Flow cytometric bivariate DNA/PCNA analysis was performed to investigate the expression of PCNA during the cell cycle and the implication in DNA replication in HeLa cells, using a monoclonal antibody (PC10) to PCNA. The expression of PCNA was evident in almost all cells growing exponentially, when cells were fixed in methanol. The total amount of PCNA altered a little during the cell cycle. However, the treatment with Triton X-100 extracted 80-89% of total PCNA from the cells, resulting in the dramatic change of bivariate DNA/PCNA distribution pattern. PCNA was completely removed from nuclei in both G1 and G2 phases by the detergent treatment, whereas a certain amount of PCNA remained in S phase nuclei. After the treatment of cells with Triton X-100, PCNA was detected exclusively in S phase cells. The bivariate DNA/PCNA distribution pattern in cells treated with Triton X-100 was strikingly so similar to the DNA/BrdUrd distribution pattern that it was unable to differentiate one from the other. It is concluded that the detergent treatment of cells allows the rapid analysis of the cell cycle. The inhibition of DNA synthesis with 10 mM hydroxyurea elevated cellular PCNA content mainly due to the increase in the fraction of the detergent extractable PCNA. It was apparent, however, that in cells incubated with Triton X-100, the pattern of the bivariate DNA/PCNA distribution was not basically different from that in cells without HU treatment. The level of PCNA bound to nuclear structures (PCNA not extracted with detergent) increased in cells arrested at the G1/S boundary with the time of hydroxyurea treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1993

Developmental and functional impairment of T cells in mice lacking CD3 zeta chains.

CD3 zeta is a component of the T cell antigen receptor (TCR) complex and is important for signal transduction. We have established mice selectively lacking CD3 zeta but able to express CD3 eta, a polypeptide produced from the same locus through alternative splicing, using the method of gene targeting in embryonic stem cells. In homozygous mutant mice, the numbers of thymocytes and peripheral T cells were greatly reduced and the expression levels of TCR on these cells were 5-fold lower than those on wild-type cells. By contrast, TCR gamma delta+ intestinal intraepithelial lymphocytes were not obviously affected by the mutation. T cells from homozygous mutants exhibited an impaired proliferative response. These results imply that CD3 zeta has a critical role in the development and signal transduction of T cells in vivo.

Animals↗
PubMed1993

Effects of bone-seeking hormones on DNA synthesis, cyclic AMP level, and alkaline phosphatase activity in cultured cells from human posterior longitudinal ligament of the spine.

In a study of the osteogenesis capability of the human posterior longitudinal ligament of the spine, ligament cells were isolated and cultured. The effect of bone-seeking hormones, such as parathyroid hormone (PTH), calcitonin (CT), prostaglandin E2 (PGE2), and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], on the ligament cells was investigated with respect to DNA synthesis, adenosine-3',5'-cyclic monophosphate (cAMP) levels, alkaline phosphatase (ALP) activity, and acid phosphatase (ACP) activity. Cell lines obtained from nonossified sites in patients with ossification of the posterior longitudinal ligament of the spine (OPLL) were found to have several different phenotypic characteristics for osteoblasts: high ALP activity, PTH- and PGE2-stimulated increases in cAMP, and responses to both CT and 1,25-(OH)2D3. It is clear that proliferation and differentiation in such ligament cells are controlled by various types of bone-seeking hormones, and it was suggested that many cells with osteoblast-like characteristics are present. These results are considered important with respect to the etiology of OPLL, and an experimental system using cultured ligament cells appears to be useful in research on OPLL.

Acid Phosphatase↗
PubMed1993

Regulation of IgD-receptor expression on murine T cells. II. Upregulation of IgD receptors is obtained after activation of various intracellular second-messenger systems; tyrosine kinase activity is required for the effect of IgD.

The presence of IgD receptors (IgD-R) on T cells during a primary response to antigen causes augmented antibody production and facilitates priming for a secondary response. Cross-linked, but not monomeric IgD leads to a rapid upregulation of these receptors on T cells. As shown in the present study, the rapid upregulation of IgD-specific receptors is also induced by cross-linking of T cell surface molecules known to mediate triggering of T cell activation, such as CD3, CD2, and Thy 1. Furthermore, IgD-R are also upregulated by pharmacologically active compounds that increase intracellular cAMP and by PMA/DiOG plus ionomycin, but not by either PMA or ionomycin alone. The upregulation of IgD-R by anti-CD3 is inhibited by both calphostin C and herbimycin A, while that due to DiOG plus ionomycin is only inhibited by calphostin C. Upregulation of IgD-R by increased cAMP is blocked by HA1004, but not by low concentrations of staurosporine or herbimycin A. IgD itself does not cause an increase in intracellular cAMP, protein kinase C translocation, influx of extracellular Ca2+, or a change in membrane potential. Relatively specific inhibitors of these activation pathways, HA1004, calphostin C, and neomycin, also fail to interfere with IgD-receptor upregulation by IgD itself. However, tyrosine kinase inhibitors, including herbimycin A, tyrphostin C11, and genistein, completely prevent the effect of IgD on IgD-R expression. Although an influx of Ca2+ is apparently not involved, a role for intracellular Ca2+ in the upregulation of IgD-R by IgD on T cells is indicated by the susceptibility to inhibition by BAPTA, W7, and FK520. We conclude that activation of at least three different second-messenger systems can cause IgD-R upregulation, but that the effect of IgD itself requires tyrosine kinase activity, perhaps in an intracellular Ca(2+)-dependent manner.

Animals↗
PubMed1993

Suprasellar embryonal carcinoma which developed ten years after local radiation therapy for pineal germinoma.

We recently encountered a case of suprasellar embryonal carcinoma which developed 10 years after local radiation therapy for pineal germinoma. This 29-year-old male was admitted because of abnormal behavior, disturbed consciousness, and increased intracranial pressure. Computed tomography and magnetic resonance imaging disclosed a tumor spreading from the suprasellar region to the third ventricle and the anterior horn of the left lateral ventricle, accompanied by fresh hemorrhage within the tumor. He underwent subtotal removal of the tumor, followed by chemotherapy with cisplatin and etoposide. The tumor was histologically rated as embryonal carcinoma with differentiation into yolk sac tumor and choriocarcinoma.

Adult↗
PubMed1993

Effect of vinconate against regional age-related changes in the gerbil brain.

We investigated age-related changes in the binding sites of muscarinic acetylcholine, forskolin, adenosine 3',5'-cyclic monophosphate (cAMP), and of a voltage-dependent L-type calcium channel blocker in the gerbil brain using receptor autoradiography. [3H]Quinuclidinyl benzilate (QNB), [3H]forskolin, [3H]cAMP, and [3H]PN200-110 were used to label muscarinic receptors, adenylate cyclase, cAMP-dependent protein kinase, and L-type calcium channels, respectively. In middle-aged animals (16-month-old gerbils), [3H]QNB, [3H]PN200-110, [3H]forskolin, and [3H]cAMP binding sites were elevated in the hippocampal region compared with that of young gerbils (4 weeks old). Further, a significant elevation in [3H]forskolin binding was seen in the nucleus accumbens. In contrast, [3H]QNB, [3H]PN200-110, and [3H]forskolin binding sites were reduced in the cerebellum, neocortex and thalamus, and hypothalamus in middle-aged animals, respectively. [3H]cAMP binding was not altered in other regions except for an elevation in the hippocampus. Thus, the age-related alterations in receptor binding may proceed by different mechanisms in various brain regions. Chronic vinconate treatment partly modulated the age-related alterations in [3H]QNB, [3H]forskolin, and [3H]cAMP binding in the hippocampus, but not that of [3H]PN200-110. Vinconate also regulated the age-related changes in [3H]forskolin binding in the nucleus accumbens. These results indicate that the age-related alterations in the binding sites of muscarinic acetylcholine, forskolin, cAMP, and L-type calcium channel blocker occur in particular in the hippocampus. Further, they suggest that a novel vinca alkaloid derivative, vinconate, can partly modulate age-related changes in these binding sites.

Acetylcholine↗
PubMed1993

Generation of high-density DNA markers from yeast artificial chromosome DNA by single unique primer-polymerase chain reaction.

We have developed a method for the whole sequence amplification of yeast artificial chromosome (YAC) DNA excised from preparative pulsed-field gel electrophoresis using single unique primer-polymerase chain reaction procedures. We used seven contiguous YAC clones, which span 2 Mbp of the Huntington disease gene region on 4p16.3, to amplify the YAC DNAs. The average size of the amplified DNA was approximately 300 bp long, and 12 DNA markers located on the YAC clones positively hybridized with these amplified products, implying that the sequences of the YAC clones were comprehensively amplified by our procedures. These amplified YAC DNAs greatly facilitate the characterization of YAC clones, leading to the detailed analysis of the defined chromosomal region.

Base Sequence↗
PubMed1993

Possible involvement of beta-PKC rather than that of alpha-PKC in differentiation of 3T3-L1 cells to adipocytes.

The change of subspecies of protein kinase C (PKC) was studied in 3T3-L1 cells in terms of their differentiation to adipocytes. 3T3-L1 cells feasible to differentiate to adipocytes by exposure to 3-isobutyl-1-methylxanthine (IBMX) and dexamethasone had both alpha- and beta-PKC. However, 3T3-L1 cells unfurnished with such feasibility had only alpha-PKC. alpha-PKC, therefore, seems to be more deeply involved in differentiation of 3T3-L1 cells to adipocytes than alpha-PKC.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Ca(2+)-dependent aggregation of rabbit platelets induced by maitotoxin, a potent marine toxin, isolated from a dinoflagellate.

1. Administration of maitotoxin (MTX), a dinoflagellate toxin, caused aggregation of rabbit washed platelets. The cytosolic Ca2+ concentration ([Ca2+]i), measured by fura-2 fluorescence technique, was also increased by the presence of MTX. Rates of aggregation response and [Ca2+]i-increase were dependent on tested concentrations (3-100 ng ml-1) of the toxin. 2. The MTX-induced platelet aggregation and [Ca2+]i-increase were totally abolished in a Ca(2+)-free solution. The successive administration of Ca2+ in the presence of MTX elicited the aggregation and increase in [Ca2+]i. 3. Ba2+ was capable of substituting for Ca2+ in the MTX-induced platelet aggregation. In the presence of external Ca2+, transition metals, Co2+, Cd2+ and Ni2+, inhibited the aggregation response to MTX. 4. Organic calcium antagonists (verapamil and nifedipine) as well as a cyclo-oxygenase-inhibitor (aspirin) did not apparently inhibit the aggregation response to MTX, except for a high concentration (10(-5) M) of verapamil, while procaine (10 mM) reduced the rate of platelet aggregation. 5. MTX also elicited a release of ATP from platelets, which was abolished in the absence of external Ca2+. 6. In contrast, thrombin 0.5 unit ml-1 could elicit platelet shape change, [Ca2+]i-increase and ATP-release in the absence of external Ca2+. 7. These results suggest that the MTX-induced platelet activation is caused by an enhanced Ca(2+)-influx presumably through voltage-independent Ca2+ channels on the plasma membrane.

Adenosine Triphosphate↗
PubMed1993

[Influence of cytotoxic chemotherapy on superoxide production by neutrophils in cancer patients].

The influence of cytotoxic chemotherapy on the number and function of peripheral neutrophils was studied in time sequence in 9 cancer patients; 6 patients with transitional cell carcinoma of urothelium treated with CAP, the combination of cyclophosphamide, adriamycin and cisplatin, and the other 3 with testicular tumor treated with PEB, the combination of cisplatin, etoposide and bleomycin. The neutrophil function was evaluated by the superoxide production, measuring chemiluminescence of the neutrophil suspension by a photometer. The peripheral neutrophil count (PNC) significantly (p < 0.01) decreased with the nadir count of 280 +/- 100/mm2 16.4 days after cytotoxic chemotherapy and recovered to the normal level by the next course. The neutrophil function declined significantly (p < 0.01) as PNC decreased, reached the minimum almost at the same time as PNC, and returned to the normal level by the next course. Of the 9 cases, the neutrophil function in 6 cases reached the minimum on the same day as that of PNC. The study shows that cytotoxic chemotherapy appears to impair the host defense mechanism in cancer patients not only in inducing neutropenia but also in deteriorating neutrophil function at the same time.

Adult↗
PubMed1993

Dependence of endothelium-mediated relaxation on oxygen and metabolism in porcine coronary arteries.

Hypoxia has major effects on endothelium-dependent relaxation. To further understand the underlying mechanism(s), we investigated the O2 dependence of the endothelium-dependent relaxations elicited by ionophore A-23187 or agonists substance P (SP) or thrombin (TB) in porcine coronary arteries. A-23187 elicits an endothelium-dependent relaxation of KCl- or U-46619-induced contractures that can be described in terms of a rapid and slow phase. The duration of the relaxation was dose dependent. SP (10 nM) and TB (0.1 U/ml) also elicited endothelium-dependent relaxations that were rapid but transient. Hypoxic conditions (95% N2-5% CO2 instead of 95% O2-5% CO2; PO2 < 1%) abolished the A-23187 rapid phase and the SP and TB transient relaxation but not the A-23187 slow phase. Threshold PO2 for the rapid phase was approximately 35 mmHg. Pretreatment with cyanide (5 mM), to inhibit respiration, or 2-deoxy-D-glucose, to inhibit glycolysis, had little effect. Similarly, propranolol (10 microM) or indomethacin (10 microM) had no effect on the relaxation to A-23187, TB, or SP. In contrast, both NO synthesis inhibitors and ouabain blunted all endothelium-dependent relaxations studied. Our results suggest that the rapid relaxations to A-23187, SP, and TB are sensitive to O2 but not mitochondrial respiration. The slow sustained relaxation induced by A-23187, however, is characterized by a sensitivity to O2 that is distinct from that of the rapid phase, yet is dependent on an intact endothelium and is affected by NO synthesis inhibitors. Thus the endothelium-dependent relaxation to A-23187 is probably mediated by NO, but its sensitivity to O2 suggests that two distinct mechanisms may be involved.

Animals↗