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Biomedical subjects

J Tanaka

Publications and source records attributed to J Tanaka.

At least 217 records · Page 12Linked to original sources
PubMed1999

Effect of carboxyl group in O-methacryloyl-N-acyl tyrosines on adhesiveness to unetched human dentin.

We have reported that the carboxylic group plays an important role in the adhesion of methacryloyl amino acid--2-hydroxyethyl methacrylate type restorative resin to dentin surfaces. However, our study so far has been limited to the methacryloyl amino acid that has only one carboxylic acid. In this investigation, three new O-methacryloyl-N-acyl tyrosines (MAATY) that have one or two carboxylic groups in the acyl group, and thus two or three carboxylic groups in MAATY, were prepared and evaluated for their bond strength to unetched dentine. Higher bond strength was observed when the MAATY contained larger number of carboxylic acid groups. Factor analysis of the bonding strength revealed that the hydrogen bond ability of the carboxylic acid and the hydrophile-lipophile balance (HLB) affected the bond strength.

Adhesiveness↗
PubMed1999

The role of accessory cells in allogeneic peripheral blood stem cell transplantation.

Granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood mononuclear cells (G-PBMC) have been used increasingly to reconstitute hematopoiesis after myeloablative therapy in allogeneic transplantation. Compared with conventional bone marrow, faster engraftment is consistently observed with G-PBMC, with differences more pronounced in platelet than in neutrophil recovery. G-PBMC contain not only severalfold more CD34+ cells than bone marrow but also, on average, 50-fold more monocytes, which may stimulate stromal cell function and facilitate engraftment. Although G-PBMC also contain 10-fold more T cells, the incidence and severity of acute graft-vs.-host disease (GVHD) is no higher than that observed in allogeneic bone marrow transplantation. Hypothetically, these clinical observations can be explained by the direct effect of G-CSF on T cell function as demonstrated by polarization of T cells expressing the T helper type 2 (Th 2) cytokine interleukin (IL)-4 in the murine model. Alternatively, G-PBMC may contain cells that actively suppress donor T cell responsiveness. Recent reports indicate that the large number of CD14+ monocytes in G-PBMC can suppress donor T cell proliferation in vitro. This effect may be attributable to both the increased ratio of CD14+:CD3+ cells in G-PBMC and the evidence that CD14+ cells in G-PBMC have decreased expression of both B7.2 and HLA-DR. There is some indication that natural killer (NK) cell number and function may be augmented in G-PBMC, which could have a favorable impact on the graft-vs.-leukemia (GVL) effect. Therefore, both the CD34+ and accessory cell content of G-PBMC may be important in early engraftment by controlling acute GVHD and facilitating GVL.

Antigen-Presenting Cells↗
PubMed1999

Factors influencing arteriovenous fistula dysfunction in Japanese patients on chronic hemodialysis.

Arteriovenous fistula dysfunction is a constant problem in chronic hemodialysis patients. We investigated the factors influencing fistula dysfunction in 184 patients on chronic hemodialysis. Stepwise regression analysis and Cox proportional hazards model were used to assess the relationship between fistula dysfunction and age, sex, duration of hemodialysis, diabetes mellitus, hematocrit, serum creatinine, blood urea nitrogen, Kt/V, prothrombin time, blood pressure, anticoagulant therapy, dose of erythropoietin, calcium channel blocker therapy, and angiotensin-converting enzyme inhibitor therapy. Fistula dysfunction showed a significant relationship with a low systolic blood pressure, a low hematocrit, the presence of diabetes mellitus, and angiotensin-converting enzyme inhibitor therapy. These results suggested that treatment with angiotensin-converting enzyme inhibitors may help to prevent fistula dysfunction.

Adult↗
PubMed1999

Effects of tap water on esophageal burns in dogs from button lithium batteries.

Incidences of swallowing lithium batteries have been increasing. A lithium battery is more dangerous than button alkali batteries because the tissue erosion and perforation of the esophagus is more rapid than with button alkali batteries. We hypothesized that a bolus fresh water wash out or dilution of the alkali produced by the direct current flow, and/or inhibition of the alkali production by interrupting the direct current flow, might lessen the severity of the necrotic injury at a contact esophageal site with a battery. Model CR2032 lithium batteries were fixed in the esophagus of 21 adult mongrel dogs for 15, 30, 60 or 90 min. In 9 of the dogs serial 20 mL boluses of tap water (adjusted pH at 7.0 by bicarbonate) were administered at 15-min intervals after placement of the battery. The esophageal injuries were graded microscopically according to the depth of the necrosis. The consumed electricity of the batteries was also evaluated. Serial bolus administration of water reduced the consumed electricity of the batteries significantly 30 and 60 min after fixation and delayed the corrosive change in a contact esophageal area during the first 30 min. Dosing with tap water as soon as possible within 30 min after ingestion seemed a useful first aid measure to prevent esophageal injury after accidental swallowing of a lithium battery.

Animals↗
PubMed1999

[Iron].

Explore the source record for details and available documents.

Female↗
PubMed1999

[Leukocytapheresis for ulcerative colitis].

Leukocytapheresis(LCAP) and Granulocytapheresis(GCAP) are classified as extracorporeal circulation therapy(ECCT). These therapies are a novel, effective way to treat patients with ulcerative colitis(UC). During 7 weeks of intensive therapy(LCAP weekly, predonisolone(PSL) 30-80 mg/day), UC patients treated with LCAP revealed significant improvements on their subjective and objective symptoms compared to patients treated with PSL intravenous administration. Moreover, LCAP has been recognized as safer than other drugs for UC. In our previous study, only 9.9% out of 1,978 LCAP sessions showed some side effects, and most were mild and temporary. Therefore, LCAP could be the first choice to treat UC patients who resist and/or reveal severe complications against ordinary drug therapies.

Adolescent↗
PubMed1999

[Table-moving contrast-enhanced MR angiography of abdominal aortic aneurysm].

Table-moving contrast-enhanced MR angiography (MRA) was performed in 14 cases of abdominal aortic aneurysm to evaluate its clinical usefulness. In all cases, aneurysms were clearly demonstrated and image quality was clinically acceptable. Findings of reconstructed MRA were highly consistent with those of DSA, and thrombosed areas were confirmed on source images. Main aortic branches including renal arteries, common iliac arteries, and internal and external iliac arteries were readily identified on reconstructed MRA and/or source images. Additional findings such as thoracic aortic aneurysm (n = 1), common iliac aneurysm (n = 6), external iliac aneurysm (n = 1), internal iliac aneurysm (n = 1), femoral arterial obstruction (n = 2), and femoral arterial stenosis (n = 4) were also detected. Although table-moving MRA may have disadvantages like reduced blood signal and limited spatial resolution compared with the conventional contrast-enhanced technique, the images that were obtained provided sufficient contrast and resolution for preoperative evaluation. Because abdominal aortic aneurysm is accompanied by various arterial abnormalities in many of the large arteries, table-moving MRA was considered a suitable technique for comprehensive assessment.

Aged↗
PubMed1998

Self-protection of PC12 cells by 6R-tetrahydrobiopterin from nitric oxide toxicity.

Nitric oxide (NO) has cytotoxic effects but NO producing neurons are resistant to NO toxicity. These results suggest the presence of self-protecting factors for NO toxicity. Recently, 6R-tetrahydrobiopterin (6R-BH4), a cofactor for NO synthase (NOS), has been reported to degrade NO raising the possibility that 6R-BH4 acts as a self-protecting factor for NO toxicity. In PC12 cells which have NOS, three-day culture with sodium nitroprusside (SNP) or NOC-12, NO generators, at 10-100 microM increased nitrite and nitrate concentrations in the culture medium and induced death of PC12 cells. Coadministration of 6R-BH4 (10 or 30 microM) with SNP or NOC-12 prevented cell death with reduction of nitrite and nitrate in the medium. Inhibition of 6R-BH4 synthesis by 2,4-diamino-6-hydroxypyrimidine (DAHP), an inhibitor for GTP cyclohydrolase I, decreased cellular 6R-BH4 content and viable cell number. The inhibiting effects of DAHP were restored by exogenous 6R-BH4. NOS activity, as estimated by nitrite concentrations in the medium, was unchanged by DAHP. Hypoxanthine and xanthine oxidase, which produce superoxide, mimicked the cell-protecting effect of 6R-BH4 which is reported to generate superoxide during its autoxidation. These results suggest that 6R-BH4 acts as a self-protecting factor for NO toxicity with generation of superoxide in NO-producing neurons.

Animals↗
PubMed1998

Interaction of myosin phosphatase target subunit 1 with the catalytic subunit of type 1 protein phosphatase.

In the investigation of the sequences of myosin phosphatase target subunit 1 (MYPT1) involved in binding the substrate and catalytic subunit of protein phosphatase type 1 (PP1c), fragments of MYPT1 were prepared and characterized. The shortest fragment capable of full activation of PP1c contained the sequence of residues 1-295. Within this fragment, the N-terminal sequence of residues 1-38 is involved in activation of PP1c (kcat) and the ankyrin repeats (residues 39-295) were involved in substrate binding (Km). The ankyrin repeats alone (residues 39-295) and the C-terminal fragment of residues 667-1004 did not activate PP1c. Using gel filtration, an interaction with PP1c was detected for the sequences of residues 1-295, 17-295, and 1-170. Affinity columns were prepared with various fragments to assess binding of PP1c. Binding to the column with residues 1-295 was strongest, followed by the binding to the column with residues 1-170. A weak interaction was observed with the column with residues 1-38. The column with residues 1-295 was used to isolate PP1c from gizzard. The purified PP1c was activated by MYPT1 and fragments to a greater extent than previous preparations. These results suggest that the N-terminal sequence (residues 1-38) and the ankyrin repeats are involved in binding PP1c. The C-terminal ankyrin repeats appear to be dominant, but there is an interaction of PP1c with the N-terminal ankyrin repeats. The N-terminal peptide has two apparent functions, the binding of PP1c via the consensus binding sequence and activation of PP1c by the sequence of residues 1-16.

Animals↗
PubMed1998

Direct evidence of NO production in rat hippocampus and cortex using a new fluorescent indicator: DAF-2 DA.

The biological functions of nitric oxide in the neuronal system remain controversial. Using a novel fluorescence indicator, DAF-2 DA, for direct detection of NO, we examined both acute rat brain slices and organotypic culture of brain slices to ascertain NO production sites. The fluorescence intensity in the CA1 region of the hippocampus was augmented, especially after stimulation with NMDA, in acute brain slices. This NO production in the CA1 region was also confirmed in cultured hippocampus. This is the first direct evidence of NO production in the CA1 region. There were also fluorescent cells in the cerebral cortex after stimulation with NMDA. Imaging techniques using DAF-2 DA should be very useful for the clarification of neuronal NO functions.

Animals↗
PubMed1998

Atypical protein kinase Clambda binds and regulates p70 S6 kinase.

p70 S6 kinase (p70 S6K) has been implicated in the regulation of cell cycle progression. However, the mechanism of its activation is not fully understood. In the present work, evidence is provided that an atypical protein kinase C (PKC) isotype, PKClambda, is indispensable, but not sufficient, for the activation of p70 S6K. Both the regulatory and kinase domains of PKClambda associate directly with p70 S6K. Overexpression of the kinase domain without kinase activity or the regulatory domain of PKClambda results in the suppression of the serum-induced activation of p70 S6K. In addition, two types of dominant-negative mutants of PKClambda, as well as a kinase-deficient mutant of p70 S6K, suppress serum-induced DNA synthesis and E2F activation. The overexpresion of the active form of PKClambda, however, fails to activate p70 S6K. These results suggest that PKClambda is a mediator in the regulation of p70 S6K activity and plays an important role in cell cycle progression.

Amino Acid Sequence↗
PubMed1998

Astrocytes modulate nitric oxide production by microglial cells through secretion of serine and glycine.

We investigated lipopolysaccharide (LPS)-induced nitric oxide (NO) production by rat microglia in neuron-microglia and astrocyte-microglia cocultures to evaluate the influence of neurons and astrocytes on microglial activity. Microglial cells solely cultured in medium devoid of serine (Ser), glycine (Gly) hardly expressed inducible NO synthase (iNOS), while those cocultured with neurons and astrocytes expressed iNOS. When microglial cells and astrocytes were separately cultured by using tissue culture inserts, which allowed the microglial cells to be exposed to only diffusible factors arising from astrocytes, NO production was significantly enhanced. On the other hand, neurons, when separated from microglial cells by the inserts, could not activate microglial cells possibly due to lacking of direct contact between neurons and microglial cells. NO production in pure microglial cultures was significantly enhanced in the presence of Ser/Gly at concentrations higher than 25 microM. Conditioned media obtained from microglia culture and neuron-microglia coculture contained less than 10 microM of Ser and Gly, while media from astrocyte culture and astrocyte-microglia coculture contained 33-41 microM Ser and 20-26 microM Gly. Accordingly, astrocytes modulate the activity of microglial cells by secreting Ser and Gly. The present study proposes a novel metabolic coupling between astrocytes and microglial cells via amino acids.

Animals↗
PubMed1998

Interleukin 3 prevents delayed neuronal death in the hippocampal CA1 field.

In the central nervous system, interleukin (IL)-3 has been shown to exert a trophic action only on septal cholinergic neurons in vitro and in vivo, but a widespread distribution of IL-3 receptor (IL-3R) in the brain does not conform to such a selective central action of the ligand. Moreover, the mechanism(s) underlying the neurotrophic action of IL-3 has not been elucidated, although an erythroleukemic cell line is known to enter apoptosis after IL-3 starvation possibly due to a rapid decrease in Bcl-2 expression. This in vivo study focused on whether IL-3 rescued noncholinergic hippocampal neurons from lethal ischemic damage by modulating the expression of Bcl-xL, a Bcl-2 family protein produced in the mature brain. 7-d IL-3 infusion into the lateral ventricle of gerbils with transient forebrain ischemia prevented significantly hippocampal CA1 neuron death and ischemia-induced learning disability. TUNEL (terminal deoxynucleotidyltransferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling) staining revealed that IL-3 infusion caused a significant reduction in the number of CA1 neurons exhibiting DNA fragmentation 7 d after ischemia. The neuroprotective action of IL-3 appeared to be mediated by a postischemic transient upregulation of the IL-3R alpha subunit in the hippocampal CA1 field where IL-3Ralpha was barely detectable under normal conditions. In situ hybridization histochemistry and immunoblot analysis demonstrated that Bcl-xL mRNA expression, even though upregulated transiently in CA1 pyramidal neurons after ischemia, did not lead to the production of Bcl-xL protein in ischemic gerbils infused with vehicle. However, IL-3 infusion prevented the decrease in Bcl-xL protein expression in the CA1 field of ischemic gerbils. Subsequent in vitro experiments showed that IL-3 induced the expression of Bcl-xL mRNA and protein in cultured neurons with IL-3Ralpha and attenuated neuronal damage caused by a free radical-producing agent FeSO4. These findings suggest that IL-3 prevents delayed neuronal death in the hippocampal CA1 field through a receptor-mediated expression of Bcl-xL protein, which is known to facilitate neuron survival. Since IL-3Ralpha in the hippocampal CA1 region, even though upregulated in response to ischemic insult, is much less intensely expressed than that in the CA3 region tolerant to ischemia, the paucity of IL-3R interacting with the ligand may account for the vulnerability of CA1 neurons to ischemia.

Animals↗
PubMed1998

Microglial cells prevent nitric oxide-induced neuronal apoptosis in vitro.

Apoptotic neuronal death is known to occur in the developing brain and in the mature brain of patients with ischemic and degenerative disorders. Although microglial cells are known to become activated in specific conditions, it has not been elucidated whether they enhance or prevent neuronal apoptosis. The present study was intended to observe how microglial cells are involved in neuronal death. When rat primary cortical neurons were incubated with a nitric oxide (NO) donor sodium nitroprusside (SNP; 300 microM) for 10 min, neuronal death occurred 12-16 hr later. The NO-induced neuronal death was inhibited by cycloheximide, and the SNP-treated neurons were characterized by nuclear fragmentation and intact cell membrane under electron microscopy. Agarose gel electrophoresis demonstrated DNA fragmentation of the SNP-treated neurons. Thus, the NO-induced neuronal death appeared to be apoptosis. When neurons were cocultured with rat primary microglial cells, the SNP treatment failed to induce the neuronal death. Because microglia-conditioned medium also prevented apoptotic neuronal death, microglial cells were considered to secrete antiapoptotic factors. The microglia-conditioned medium rescued neurons even when they were added to neuronal cultures after the SNP treatment, implying that the factors acted on neurons in a manner other than scavenging NO. Interleukin-3, interleukin-6, macrophage colony-stimulating factor, and basic fibroblast growth factor, which are known to be secreted by microglial cells, were not effective in preventing NO-induced neuronal death. Among microglia-derived substances, tumor necrosis factor alpha and plasminogen, which are heat-labile proteins, inhibited neuronal apoptosis. The neuroprotective action of the microglia-conditioned medium, however, still remained, even after it was heated. These findings suggest that microglial cells protect neurons against NO-induced lethal damage by secreting heat-labile and heat-stable neuroprotective factors in vitro.

Animals↗
PubMed1998

Adrenergic agonists suppress the proliferation of microglia through beta 2-adrenergic receptor.

The effects of several cyclic adenosine monophosphate (cAMP)-elevating agents on the proliferation of cultured rat microglia were investigated by immunocytochemical staining with an antibody against proliferating cell nuclear antigen (PCNA). Epinephrine, isoproterenol, forskolin and 8Br-cAMP suppressed the microglial proliferation. A beta2-selective agonist terbutaline but not a beta1-selective agonist dobutamine mimicked the effect of the above cAMP-elevating agents. Furthermore, a non-selective beta-receptor antagonist oxprenolol and a beta2-selective antagonist acebutalol, but not a beta1-selective antagonist butoxamine, counteracted the suppressive effects of the beta-agonists on microglial proliferation. These findings suggest that the beta-agonists suppress the proliferation of microglia by elevating intracellular cAMP level through an action on beta2-adrenergic receptor.

8-Bromo Cyclic Adenosine Monophosphate↗