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Biomedical subjects

F Tanabe

Publications and source records attributed to F Tanabe.

At least 37 records · Page 2Linked to original sources
PubMed1993

The properties and mec A gene of the methicillin-resistant Staphylococcus aureus isolated in Fukushima Medical College Hospital.

The 106 methicillin-resistant strains of Staphylococcus aureus (MRSA) isolated in Fukushima Medical College Hospital were examined for their properties and mecA gene. The strains produced four types of coagulase, of which type II was the most common, produced by 84 (79.2%). Beta-lactamase was produced by 58 (50%). Enterotoxins were produced by 45 (42.5%), most of which (39/106, 36.8%) were of type A. Thirty-four strains (32.1%) produced both enterotoxins and toxic shock syndrome toxin-1. All strains were susceptible to vancomycin and arbekacin, although they were mostly resistant to many other antibiotics. Using the polymerase chain reaction (PCR) technique, the mecA gene was detected in 57 (91.9%) of the 62 strains used. In addition, one of the 42 methicillin-susceptible strains isolated had the mecA gene. These results indicate that detection of the mecA gene by the PCR technique is a rapid and accurate way to identify methicillin resistance.

Bacterial Proteins↗
PubMed1992

The genotoxicity of UVA irradiation in Drosophila melanogaster and the synergistic action of 8-methoxypsoralen and UVA.

To study the genotoxicity of near-ultraviolet light (UVA) on a whole body, Drosophila melanogaster larvae were irradiated with UVA and the emerging flies were examined for the mutant wing spot formation. The genotoxicity of UVA was also assayed with the in vivo DNA-repair test using males with repair-deficiency at the mei-9 and mei-41 locus and the matching repair-proficient females. Third-instar larvae were placed in a plastic Petri dish, which was covered with soft glass, and irradiated with black light at 4-5 W/m2. This irradiation resulted in an increase in mutant wing-hair spots. After a 15 h irradiation (approximately 240 kJ/m2), the mutant clone frequencies found in the adult flies (spots/wing) were: 1.68 for the small single spots, 0.38 for the large single spots and 0.11 for the twin spots, while at zero time they were 0.68, 0.06 and 0.02 respectively. On the other hand, the UVA irradiation was negative in the in vivo DNA-repair test, indicating that the UVA-induced DNA lesion may not be subject to repair by the mei-9 and mei-41 functions. The presence of 8-methoxypsoralen (8-MOP) during the irradiation remarkably enhanced somatic mutations, and showed a strong DNA-damaging effect in the repair test. For example, a 15 h UVA irradiation with 26.7 microM 8-MOP resulted in a 14-fold increase in the number of twin spots per wing as compared with the frequency obtained on treatment with UVA alone. Treatment of the larvae with 8-MOP alone gave no mutant clones or DNA damage. A high frequency in twin spot formation was also observed in this UVA + 8-MOP treatment, indicating that extensive chromosomal recombinations took place in the somatic cells.

Animals↗
PubMed1990

Thiol proteinase inhibitors reverse the increased protein kinase C down-regulation and concanavalin A cap formation in polymorphonuclear leukocytes from Chediak-Higashi syndrome (beige) mouse.

Protein kinase C (PKC) plays an essential role in intracellular signal transduction for various cell functions, including concanavalin A (Con A)-induced cap formation. This enzyme is known to be proteolysed by calpain, which is a Ca2(+)-dependent thiol proteinase. As reported previously, in polymorphonuclear leukocytes (PMNs) from beige mouse, the model of Chediak-Higashi syndrome, Con A-induced cap formation significantly increased compared with that in normal mouse. However, after pretreatment of beige PMNs with the thiol proteinase inhibitors leupeptin or E-64, the capping decreased to normal levels. Meanwhile, Con A-induced the translocation of PKC from the cytosolic to membrane fraction within 5 min in both mice, which is essential to the activation of this enzyme. However, after the translocation, an abnormal rapid decline in membrane-bound PKC activity was noted in beige mouse PMNs. Both leupeptin and E-64 also corrected the rapid decline in PKC activity observed in the beige mouse. These findings suggest that the normalization of Con A cap formation in beige mouse PMNs by the thiol proteinase inhibitors is associated with the correction of abnormality in PKC activity.

Animals↗
PubMed1990

Protein kinase C inhibitors enhance concanavalin A cap formation in polymorphonuclear leukocytes.

The potent protein kinase C (PKC) inhibitors, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) and staurosporine, significantly enhanced concanavalin A (Con A)-induced cap formation in polymorphonuclear leukocytes (PMNs) from C57BL/6 mice after pretreatment for 30 min at concentrations of 10 microM and 1 nM, respectively. However, neither 10 microM of N-(2-aminoethyl)-5-isoquinolinesulfonamide dihydrochloride (H-9) nor N-(2-guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride (HA1004), which inhibit cyclic nucleotide-dependent protein kinases more effectively than other kinases, affected the capping. Meanwhile, treatment of PMNs with Con A induced the translocation of PKC from the cytosol to the membrane fraction within 5 min, which is considered to be important for the activation of this enzyme. When cells were pretreated with H-7 or staurosporine for 30 min at the concentrations that enhanced the capping, both the cytosolic and the membrane-bound PKC activity was inhibited during the further incubation with Con A. These results suggest that PKC may play an important role in the regulation of Con A-induced cap formation in PMNs.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Possible involvement of microfilaments in protein kinase C translocation.

We investigated the role of microfilaments in stimulus-induced translocation of protein kinase C (PKC) in polymorphonuclear leukocytes (PMNs) from C57BL/6 mice. Cytochalasin B and dihydrocytochalasin B almost completely inhibited PKC translocation induced by either TPA or Ca2+ ionophore after pretreatment of cells for 30 min. In addition, ML-9, a potent inhibitor of Ca2+/calmodulin-dependent myosin light chain kinase which regulate microfilament contraction, and a calmodulin antagonist W-7, also inhibited PKC translocation. These findings suggest the possibility that microfilaments are involved in the translocation of PKC.

Actin Cytoskeleton↗
PubMed1989

The thiol proteinase inhibitors improve the abnormal rapid down-regulation of protein kinase C and the impaired natural killer cell activity in (Chediak-Higashi syndrome) beige mouse.

Protein kinase C (PKC) is essential in intracellular signal transduction for various cell functions including natural killer (NK) cell activity. This enzyme is hydrolysed by calpain, which is Ca2+-dependent thiol proteinase. We showed here that in NK activity-deficient beige (bg/bg) mouse, the model of Chediak-Higashi syndrome, the translocated membrane-bound PKC activity declined rapidly in NK cell-enriched lymphocytes after TPA stimulation. However, the rapid decline was abolished by the pretreatment of cells with leupeptin (a thiol and serine proteinase inhibitor) or E64 (a thiol proteinase inhibitor). Furthermore, these reagents improved the impaired NK cell activity in beige mouse whereas they did not affect NK cell activity in C57BL/6 (+/+) and the heterozygous (+/bg) mice. Meanwhile, TPA stimulation induced only low levels in NK cytotoxic factors (NKCF) release from beige NK cells, but these reagents augmented the lowered NKCF release. These results suggest that the improvement of impaired NK cell activity in beige mouse by the thiol proteinase inhibitors may be due to the elimination of abnormal rapid down-regulation of PKC, resulting in the augmentation of the lowered PKC activity.

Animals↗
PubMed1989

Tumor necrosis factor enhances replication of human immunodeficiency virus (HIV) in vitro.

The effect of tumor necrosis factor (TNF) on the replication of human immunodeficiency virus type 1 (HIV-1) was investigated in several T4 lymphocyte cell lines. TNF markedly enhanced the cytopathogenicity of HIV-1, virion-associated reverse transcriptase (RT) activity in the cell culture supernatant, and viral antigen expression in MOLT-4 cells as early as 3 days after HIV-1 infection. A slight increase in RT activity was also observed in the supernatant of H9 cell cultures exposed to TNF. However, TNF did not increase either RT activity in MT-4 cell supernatants or viral antigen expression in HUT-78 cells. Thus, TNF is able to stimulate the replication of HIV-1 in de novo infected T4 cells although not all T4 cells seem to be sensitive to this stimulatory effect.

Antigens, Viral↗
PubMed1989

Inhibition of natural killer cell-mediated cytotoxicity by ML-9, a selective inhibitor of myosin light chain kinase.

To investigate the role of microfilaments in natural killer (NK) cell-mediated cytotoxicity, general microfilament inhibitors, cytochalasins B,D and dihydrocytochalasin B, and a selective inhibitor of myosin light chain kinase (MLCK) which regulates microfilament contraction, i.e. 1-(5-chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride (ML-9) were examined in an NK assay system. ML-9 inhibited NK cell activity in a dose-dependent manner without affecting target cell binding, whereas cytochalasins suppressed the binding. The dextran suspension method revealed that ML-9 inhibits the programming for the lysis stage of the lytic process. In the single cell assay, the addition of ML-9 after target cell binding had occurred inhibited the lysis of bound target cells, whereas the addition of cytochalasins in a similar manner did not affect it. Thus, these results suggest the possibility that microfilament contraction is involved in the lytic mechanism of NK cell-mediated cytolysis. However, the mechanism whereby cytochalasins inhibit target cell binding remains unclear.

Actin Cytoskeleton↗
PubMed1988

Mechanism of inhibitory effect of glycyrrhizin on replication of human immunodeficiency virus (HIV).

Glycyrrhizin (GL) achieved a dose-dependent inhibition of the replication of human immunodeficiency virus type 1 (HIV-1) in MOLT-4 (clone No. 8) cells within the concentration range of 0.075 to 0.6 mM. Within this concentration range, GL also effected a dose-dependent reduction in the protein kinase C (PKC) activity of MOLT-4 (clone No. 8) cells. A well-known PKC inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), also proved inhibitory to HIV-1 replication in MOLT-4 (clone No. 8) cells. PKC inhibition may thus be considered as one of the mechanisms by which GL inhibits HIV-1 replication. In addition, GL may also owe its anti-HIV-1 activity, at least in part, to an interference with virus-cell binding, since the compound at 1.2 mM partially inhibited the adsorption of radiolabeled HIV-1 particles to MT-4 cells. At this concentration GL also suppressed giant cell formation induced by co-culturing MOLT-4 (clone No. 8) cells with MOLT-4/HTLV-IIIB cells, whereas the PKC inhibitor H-7 failed to do so.

Adsorption↗
PubMed1988

Rapid down-regulation of protein kinase C in (Chediak-Higashi syndrome) beige mouse by phorbol ester.

Protein kinase C(PKC) activity in macrophages and polymorphonuclear leukocytes was assayed in beige mouse, the model of Chediak-Higashi syndrome, control C57BL/6 and the heterozygous (+/bg) mice. Regarding enzyme activity in the cytosolic and membrane fractions of these cells, there was no difference between beige mouse and the control. After short-term activation by TPA, the translocated membrane-bound PKC activity in beige mouse decreased rapidly compared with that in control mouse. However, the cytosolic PKC activity decreased at just the same pace as the control. The change in [3H] PDBu binding paralleled the changes in PKC activity. An increase in Ca2+/phospholipid-independent protein kinase by TPA was notable in the membrane fraction of beige mouse. The increase in the kinase activity was abolished and the PKC activity recovered to normal level by the addition of calpain inhibitor, leupeptin, to the incubation of cells along with TPA. Therefore, these findings suggest that a rapid decrease in membrane-bound PKC activity in beige mouse by TPA stimulation is associated with calpain.

Animals↗
PubMed1988

Modulation of protein kinase C activity during inhibition of tumor cell growth by IFN-beta and -gamma.

We investigated the effects of human interferon(IFN)-beta and -gamma on protein kinase C activity in human HEp-2 and KHm-14 tumor cells during IFN-induced inhibition of cell growth. Cytosolic protein kinase C activity in both cell lines was strikingly decreased following treatment with either IFN-beta or -gamma. In the particulate fraction, IFN-gamma decreased protein kinase C activity within 1 hr but it reappeared after 24 hr, whereas IFN-beta decreased the activity during the inhibition of cell growth. Furthermore, phorbol-12,13-dibutyrate(PDBu)-binding activity was altered in parallel with the changes in protein kinase C activity induced by the IFNs. In summary, we showed that IFN-beta and -gamma cause long-term modulation of protein kinase C activity in these cultured tumor cells.

Cell Division↗
PubMed1988

Low-density lipoprotein oxidized by polymorphonuclear leukocytes inhibits natural killer cell activity.

We studied the effect of low-density lipoprotein (LDL) oxidized by opsonized zymosan-stimulated polymorphonuclear leukocytes (PMN) on natural killer (NK) cell activity. Oxidized LDL inhibited NK cell activity in a dose-dependent manner, whereas normal LDL left it unaffected. However, oxidized LDL did not inhibit antibody-dependent cell-mediated cytotoxicity (ADCC). Moreover, a positive correlation was observed between the amount of thiobarbituric acid-reacting substances (TBARS) on the sample of oxidized LDL and the degree of inhibition of NK cell activity. We also showed that oxidized LDL suppressed the binding capacity of purified large granular lymphocytes (LGL) to target cells without changing the lytic activity. These results therefore suggest that activated PMN can modulate NK cell activity by oxidizing LDL.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1988

A potent inhibitor of protein kinase C inhibits natural killer activity.

A potent inhibitor of protein kinase C(PKC), 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), dose-dependently inhibited natural killer (NK) activity in large granular lymphocytes (LGL) pretreated at 37 degrees C for 30 min. However, neither N-(2-aminoethyl)-5-isoquinolinesulfonamide dihydrochloride (H-9), which inhibits more effectively cyclic nucleotide-dependent protein kinases than other kinases, nor N-(2-guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride (HA1004), which was used as a control for H-7, reduced NK activity. The inhibitor effect of H-7 was not due to changes in effector cell viability or target cell binding. We also found that H-7 suppresses PKC activity in both the cytosol and membrane fractions of LGL. From these findings, PKC is considered to play an essential role in the lytic mechanism of NK cell-mediated cytolysis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Natural killer activity enhancing substance in normal human serum.

We studied the effect of normal human serum on natural killer (NK) activity of normal peripheral lymphocytes. Both fresh serum and heat-inactivated (56 degrees C, 30 min) serum significantly enhanced NK activity, in a dose dependent manner, the limit being reached with a final concentration of 5%. However, antibody dependent cell-mediated cytotoxicity (ADCC) was not affected by heat-inactivated serum, although it did show the effects of fresh serum as complement. The serum absorbed with target cells also enhanced NK activity, so it indicated that the enhancing effect of normal serum was not due to the natural antibody against target cells in the serum. The serum was fractionated by Sephadex G-200 into fractions I, II and III in the order of elution. The enhancing factor existed in fraction III. When fraction III was further separated by Cibacron Blue-Sepharose, which selectively adsorbs albumin from serum, the enhancing activity existed in the albumin-rich subfraction. In addition, commercial human albumins had the NK enhancing activity, whereas native transferrin, platelet-derived growth factor (PDGF) or plasminogen did not. These results therefore suggest that the substance enhancing NK activity in normal serum is serum albumin, which is considered to have no significant effect on immune reaction.

Adjuvants, Immunologic↗
PubMed1987

Synergistic antiproliferative effect of interferon-beta in combination with bleomycin or neocarzinostatin on HeLa cells in culture: additive effect when combined with adriamycin or mitomycin C.

Human fibroblast interferon (IFN)-beta was administered in combination with the free radical-generating antiproliferative agents bleomycin (BLM), neocarzinostatin (NCS), adriamycin (ADM), and mitomycin C (MMC) to HeLa cells in culture. IFN showed a true synergistic antiproliferative activity in the presence of BLM or NCS. These effects were observed regardless of the ratio of IFN to BLM or NCS concentrations. However, the effect of IFN in the presence of ADM or MMC was additive. The possibility that IFN-beta potentiates the antiproliferative effects of these free radical-generating agents in a different manner is also discussed.

Antineoplastic Agents↗
PubMed1987

Interferon-alpha enhances the production of leukotriene B4 in murine peritoneal macrophages stimulated by opsonized zymosan.

Murine peritoneal macrophages pretreated with interferon (IFN)-alpha and then stimulated by opsonized zymosan produced two to three times more LTB4 than untreated macrophages. However, PGE2 production was not changed by IFN-alpha. Meanwhile, IFN-gamma did not affect the production of LTB4 and PGE2. From the results it is considered that IFN-alpha can modulate inflammation or host defence through the production of LTB4.

Animals↗
PubMed1983

Experimental biliary obstruction of rat. Initial changes in the structure and lipid content of erythrocytes.

The bile duct was ligated and the resulting changes in the plasma and erythrocyte lipid composition and in the shape of erythrocytes were observed. Electron microscopy at 8th hour after ligation revealed the appearance of spur cells, and on the 7th day target cells began to be observed. The appearance of spur cells was considered to be a reflection of abrupt increases in bile acid and bilirubin levels in the plasma. The conversion of spur cells to target cells which was observed was accompanied by increased levels of cholesterol and phosphatidylcholine in the erythrocytes. Plasma phosphatidylcholine and cholesterol levels were increased immediately after the commencement of ligation. On the other hand, erythrocyte phosphatidylcholine and cholesterol levels only gradually increased when compared to those in plasma, and the maximum value was observed from the 5th to the 7th day. The fatty acid composition of the increased plasma phosphatidylcholine after ligation resembled that of phosphatidylcholine in bile. On the other hand, the fatty acid composition of erythrocyte phosphatidylcholine changed remarkably between the 1st and 3rd days after bile duct ligation. These changes were also reflected by those of phosphatidylcholine in bile. These results led to the conclusion that the appearance of target cells observed in the present study was due to the accumulation of erythrocyte lipids which derived from bile. This is the first report on experimentally induced target cells and the mechanism for their appearance that seems applicable for humans.

Animals↗