Biomedical subjects

Y Kataoka

Publications and source records attributed to Y Kataoka.

At least 19 recordsLinked to original sources

PubMed1992

In vitro quantitative autoradiography of [125I]alpha-bungarotoxin binding at the motor end-plates of experimental autoimmune myasthenia gravis.

A quantitative evaluation was made of nicotinic acetylcholine receptors (AChR) at the motor end-plates in experimental autoimmune myasthenia gravis (EAMG). Female Lewis rats were immunized with AChR protein purified from electric organs of Narke japonica. The forelimb digit extensor muscle obtained in the chronic stage of the controls and EAMG were studied using [125I]alpha-bungarotoxin, in vitro and autoradiographically. The maximum binding capacity (Bmax) values of the controls and EAMG were calculated to be 237.7 +/- 13.0 fmol/mg (n = 4) and 42.0 +/- 4.1 fmol/mg (n = 4), respectively (P less than 0.001), and the dissociation constant (Kd) values were 11.7 +/- 1.6 nM and 7.6 +/- 0.9 nM, respectively. This in vitro autoradiographic method revealed a quantitative reduction of AChR at the motor end-plates in EAMG.

Animals↗

PubMed1992

C-type natriuretic peptide-22 differentiates between natriuretic peptide receptors in rat choroid plexus and subfornical organ.

Atrial natriuretic peptide (ANP) receptors in the rat choroid plexus and subfornical organ were characterized with C-type natriuretic peptide-22 (CNP-22) and 125I-Tyr0-CNP-22. The receptor autoradiographic method we used revealed that 125I-Tyr0-CNP-22 specifically bound to the choroid plexus, but only slightly to the subfornical organ, areas densely labeled with 125I-alpha-rat ANP (125I-rANP). CNP-22 significantly inhibited 125I-rANP binding to the choroid plexus; however, the peptide did not affect 125I-rANP binding to the subfornical organ. Thus, the characteristics of ANP receptors in the rat choroid plexus and subfornical organ are probably different.

Amino Acid Sequence↗

PubMed1992

Specific binding sites for 125I-endothelin-1 in the porcine and human spinal cord.

Specific binding sites for 125I-endothelin-1 (125I-ET-1) in the spinal cord were investigated using quantitative receptor autoradiographic and chemical cross-linking methods. The binding sites were highly concentrated in porcine and human spinal cord areas corresponding anatomically to the dorsal horn (Rexed's laminae I-III), an area around the central canal (lamina X) and the principal part of the intermediolateral nucleus (IMLp). The localization of the binding sites differed from those of 125I-omega-conotoxin GVIA (125I-CgTx) and 125I-Bolton-Hunter substance P (125I-BH-SP), with the exception that the IMLp shared 125I-ET-1 with 125I-CgTx and 125I-BH-SP binding sites. Specific 125I-ET-1 binding sites in the areas examined were characteristically single and of high affinity. There were no differences between the potencies of unlabeled ET family peptides, ET-1, ET-2, ET-3 and sarafotoxin S6b at inhibiting 125I-ET-1 binding to the areas. Chemical cross-linking studies showed that 125I-ET-1 and 125I-ET-3 mainly bound to a protein with molecular mass of 43 kDa in the porcine and human thoracic spinal cord membranes. The present finding shows the neuronal significance of this newly discovered peptide in the spinal cord.

Aged↗

PubMed1992

Endothelin-3 stimulates the release of catecholamine from cortical and striatal slices of the rat.

Endothelin-3 (ET-3) evoked the release of dopamine/noradrenaline from cortical slices and dopamine from striatal slices in a concentration-dependent manner. This action peaked slowly and was long-lasting in real-time monitoring, being different from the high K(+)-evoked response. The striatal response to 10 microM of ET-3 was reduced by extracellular Ca2+ depletion to 40% of control and by Ca2+ antagonists, especially nifedipine and flunarizine, to 40% of control. Our findings suggest that ET has a physiological significance in the brain as a neuromodulator for catecholaminergic transmission.

Animals↗

PubMed1992

Antimutagenic effects of radioprotector WR-2721 against fission-spectrum neurons and 60Co gamma-rays in mice.

The antimutagenic effects of the radiation protective agent, S-2-(3-aminopropylamino)ethylphosphorothioic acid (WR-2721), were studied against fission-spectrum-neutron- and 60Co-gamma-ray-induced mutagenesis in mice. Mutagenesis at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus was measured 56 days following whole-body irradiation with JANUS neutrons (single doses, 50-150 cGy) or 60Co photons (single doses, 250-750 cGy). Splenic T lymphocytes from B6CF1 mice were grown in round-bottomed 96-microwell culture plates with or without the selective agent 6-thioguanine (6-TG). The mutant frequency, as a result of exposure to neutrons or 60Co photons, increased 100-fold with dose. Doses of 150 cGy neutrons and 750 cGy 60Co photons were equally mutagenic. When animals were injected with WR-2721 at a dose of 400 mg/kg body weight, i.p., 30 min before whole-body irradiation with JANUS neutrons or 60Co photons, mutant frequencies were significantly reduced at all radiation doses (i.e. protection factors of 1.4 and 2.4, respectively). Thus, the aminothiols are effective antimutagens. A novel clinical application of these compounds could be in their use to protect against radiation- and/or chemotherapy-induced genotoxic damage to normal cells.

Amifostine↗

PubMed1992

The radioprotector WR-2721 reduces neutron-induced mutations at the hypoxanthine-guanine phosphoribosyl transferase locus in mouse splenocytes when administered prior to or following irradiation.

An in vitro T-lymphocyte cloning technique has been applied to study the effects of JANUS fission-spectrum neutron irradiation and the radioprotector S-2-(3-aminopropylamino) ethylphosphorothioic acid (WR-2721) on the subsequent development of somatic mutations at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus in hybrid B6CF1 male mice. In control studies performed to establish an in vitro cloning technique, the mutant frequencies of splenic T-lymphocytes, as a result of exposure to a 100 cGy dose of neutrons, increased with time from a control level of 9 x 10(-7) to a maximum value of 1.7 x 10(-5) at 56 days following irradiation. Between 56 and 150 days after irradiation, mutant frequencies were observed to plateau and remain stable. All subsequent determinations were performed at 56 days following the experimental treatment of animals. WR-2721 at a dose of 400 mg/kg was effective in protecting against the induction of hprt mutants (i.e. a mutant frequency reduction factor, MFRF) following the largest dose of neutrons used (i.e. 150 cGy), whether it was administered i.p. 30 min before, 5 min after, 3 h after, or three times at 3, 24, and 48 h after, as evidenced by MFRFs of 6.0, 6.6, 4.8 and 5.8 respectively. The antimutagenic effectiveness of WR-2721 administered 30 min prior to irradiation was unaffected, even when the dose was reduced to 200 mg/kg, MFRF = 7.0; 100 mg/kg, MFRF = 3.8; and 50 mg/kg, MFRF = 8.9. These findings confirm our earlier report using the radioprotector N-(2-mercaptoethyl)-1,3-diaminopropane (WR-1065) under in vitro conditions, and demonstrate that these agents can be used as effective antimutagens even when they are administered up to 3 h following radiation exposure.

Amifostine↗

PubMed1992

CD7 expression in malignant pleural mesothelioma.

CD7 antigen was found to be expressed on malignant mesothelioma arising from the right pleura in a 15-year-old girl not only by immunostaining using monoclonal antibodies, but also by Northern blot analysis. The level of expression in this tumor was comparable to those in T-cell lines, Jurkat and CCRF-CEM. Cytogenetic analysis of the tumor showed hypodiploidy (n = 43). CD7 has been regarded as one of the hematopoietic cell markers selectively expressed on the majority of T cells and multipotential stem cells. To our knowledge, this is the first report of a non-hematopoietic tumor expressing CD7.

Adolescent↗

PubMed1992

Activation of protein kinase C suppresses the gamma-aminobutyric acidB receptor-mediated inhibition of the vesicular release of noradrenaline and acetylcholine.

Modulation of the gamma-aminobutyric acidB (GABAB) receptor-mediated response by protein kinase C (PKC) was examined with regard to inhibition by stimulation of the GABAB receptor of stimulation-evoked release of noradrenaline (NA) from slices of cerebellar cortex and of acetylcholine (ACh) from strips of ileum. 12-O-Tetradecanoylphorbol 13-acetate (TPA) potentiated the high K(+)-evoked Ca2+-dependent release of NA and ACh, but not the ouabain-evoked release, even in the presence of external Ca2+. The potentiating effect was antagonized by sphingosine, thereby suggesting that PKC participates in the exocytotic-vesicular release of neurotransmitters, but does not do so in case of a nonvesicular release. GABA inhibited the high K(+)-evoked release of NA and ACh, but not the ouabain-evoked Ca(2+)-independent release. The effect of GABA was mimicked by baclofen and was antagonized by phaclofen, thereby suggesting that stimulation of the GABAB receptor inhibits the vesicular but not the nonvesicular release of neurotransmitters. TPA suppressed the GABAB receptor-mediated inhibition of high K(+)-evoked release of NA and ACh. The effect of TPA was antagonized by sphingosine. These results indicate that stimulation of the GABAB receptor inhibits the stimulation-evoked Ca(2+)-dependent release of neurotransmitters and that activation of PKC suppresses the GABAB receptor-mediated response.

Acetylcholine↗

PubMed1992

Inhibitory effect of NMDA on dopaminergic transmission in a slice preparation of rat globus pallidus.

The effect of N-methyl-D-aspartate (NMDA) on KCl-evoked endogenous dopamine (DA) release from slices of rat globus pallidus (GP) was examined. NMDA inhibited the KCl-evoked DA release in a dose-dependent manner. This inhibition was blocked by CPP, an NMDA antagonist. Tetrodotoxin partially antagonized the effect of NMDA. The NMDA-induced inhibition was also partially antagonized by bicuculline methiodide and was mimicked by muscimol. These results strongly suggest that 1) an activation of NMDA receptors exerts an inhibitory effect on dopaminergic transmission in GP and 2) GABAergic transmission is involved in the effect of NMDA.

Animals↗

PubMed1992

Nebracetam (WEB 1881FU) prevents N-methyl-D-aspartate receptor-mediated neurotoxicity in rat striatal slices.

The effects of nebracetam were investigated on N-methyl-D-aspartate (NMDA) receptor- and voltage-operated Ca2+ channels (VOCC)-mediated neural dysfunction by directly monitoring the real-time dynamics of dopamine released from rat striatal slices. Nebracetam (10(-5) and 10(-4) M) completely protected against striatal dopaminergic impairment induced by L-glutamate and NMDA, respectively. BAY K-8644-evoked striatal dysfunction was not blocked by nebracetam (10(-4) M). Therefore, nebracetam seems to produce a neuroprotective action by interacting, at least in part, with NMDA receptor-operated Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1992

Effect of hyperbaric oxygenation on femoral head osteonecrosis in spontaneously hypertensive rats.

We investigated the effects of hyperbaric oxygenation (HBO) on ischemic osteonecrosis and on ossification disturbance of the femoral heads in growing, spontaneously hypertensive rats (SHR). 10 male SHRs aged 5 weeks (Group A) and another 10 male SHRs aged 8 weeks (Group B) were treated with HBO at 2.8 atmosphere absolute (ATA) for 6 weeks in a total of 30 hours. The control animals, 10 male SHRs (Group C) and 10 male wistar Kyoto rats (WKY, Group D), were kept under normal laboratory conditions. All the rats were killed at the age of 17 weeks for microscopic examination. In Group A, there was no evidence of osteonecrosis, and only 2 femoral heads with ossification disturbance were observed. In Group B, there were 2 femoral heads with osteonecrosis and 1 with ossification disturbance. In contrast, there were 6 femoral heads with osteonecrosis and 4 with ossification disturbance in Group C. It was concluded that HBO prevented osteonecrosis and ossification disturbance of the femoral heads in SHR.

Age Factors↗

PubMed1992

Progression of avascular necrosis of femoral head and choice of treatment.

Observations of the disease course mainly by X-ray were made in 52 patients (85 joints) with avascular necrosis of the femoral head to determine the prognosis and to decide on treatment. The progression of the necrotic area is related to the activity of the original disease, to the size of the necrotic area in the early stages of the disease, and to whether or not the patient received steroid treatment. On the basis of the size and location of the necrotic area, the disease process is divided into four stages, I to IV. The affected heads are also classified into six types according to their site and extent, the degree of flatness of their weightbearing surface, and the presence of cystic lesion. Preventive treatment and conservative observation or transtrochanteric anterior rotational osteotomy and vascularized pedicle bone graft are applicable to cases in Stages I and II. Total hip joint arthroplasties and salvage procedures are performed in Stages III and IV. The usefulness of 99mTc bone scintigraphy was unexpectedly disappointing for diagnosis of the stages of the disease. However, MRI was sensitive for the diagnosis in the early stages of the disease.

Adult↗

PubMed1992

[Anesthesia for a patient with Bloom's syndrome].

Bloom's syndrome (BS) is a rare autosomal recessive disorder. The disease is due to chromosome breakage and recombination. The principal features of the syndrome are short stature of prenatal onset, a photosensitive telangiectasic erythema of the face and a marked predisposition to the development of malignant diseases. We are unaware of any previous report of the anesthetic management of a BS patient. In this paper, we reported the anesthetic experience of a male patient (37-yr-old, 26 kg, 136 cm) with Bloom's syndrome who underwent emergency laparotomy. The awake laryngoscopy was carried out, but we could not see the vocal cord directly. The trachea was blindly intubated and anesthesia was induced and maintained with fentanyl, vecuronium and enflurane in 100% oxygen. In a BS patient we should pay attention to potential difficulties with mask fit and laryngoscopy.

Adult↗

PubMed1991

Detection of Streptococcus suis type 2 in tonsils of slaughtered pigs using improved selective and differential media.

New selective and differential media were devised for the isolation and identification of Streptococcus suis type 2. The selective medium (NNCC) agar) was Todd-Hewitt broth containing 1.5% Bactoagar and 5% defibrinated sheep blood with addition of sodium azide (50 micrograms/ml), nalidixic acid (25 micrograms/ml), colistin (12.5 micrograms/ml) and crystal violet (2 micrograms/ml). The differential medium consisted of heart infusion agar and antiserum specific only for S. suis type 2. In a total of 291 pigs tested by a combination of these media, S. suis type 2 was isolated and confirmed from 40 of them (13.7%).

Agar↗

PubMed1991

Involvement of the dorsal hippocampus in mediation of the antianxiety action of tandospirone, a 5-hydroxytryptamine1A agonistic anxiolytic.

The effect of tandospirone, a 5-hydroxytryptamine (5-HT)1A agonist/anxiolytic, injected directly into dorsal hippocampus, on Vogel-type conflict behavior in rats was investigated and the findings were compared with the effects of diazepam and zopiclone. Tandospirone (30 micrograms/2 microliters and 60 micrograms/2 microliters) and diazepam (40 micrograms/2 microliters) but not zopiclone (20 micrograms/2 microliters), produced a potent anticonflict action in rats. The anticonflict action of tandospirone (30 micrograms/2 microliters), injected into the dorsal hippocampus, was significantly blocked by (-)-propranolol (5 mg/kg i.p.). The present findings provide evidence that suggests that tandospirone has an antianxiety action, presumably by stimulating 5-HT1A receptors in the dorsal hippocampus.

Animals↗

PubMed1991

Receptors for endothelin in the central nervous system.

The quantitative receptor autoradiographic method we used revealed that specific [125I]endothelin-1 ([125I]ET-1) binding sites are highly concentrated in the choroid plexus (ChP), subfornical organ (SFO), lacunosum molecular layer of the hippocampus (LMol), and granular layer of the cerebellum (GC) of the rat brain. [125I]ET-1 bound to the rat ChP and LMol with a high affinity and to the SFO and GC with a low affinity. The possibility that ET-1 acts as a neuropeptide within the central nervous system by interacting with specific receptors would have to be considered.

Animals↗

PubMed1991

Urinary excretion of terminal complement complexes in glomerular disease.

To evaluate renal terminal complement activation in patients with glomerular diseases, we measured terminal complement complexes (TCCs) in plasma and urine with sandwich enzyme-linked immunosorbent assay (ELISA) using a monoclonal antibody against a C9 neoepitope expressed on TCC and a polyclonal antihuman C7 antibody. TCCs were detectable in plasma but not in urine in most of normal controls. In plasma, TCC levels were elevated in 4 of 22 patients with lupus nephritis and in 6 of 12 with membranoproliferative glomerulonephritis. However all patients with IgA nephritis, focal glomerulosclerosis, idiopathic membranous nephritis and idiopathic minimal change nephrotic syndrome (MC) showed normal values. In urine, TCCs were detectable in almost all patients with heavy proteinuria (greater than or equal to 100 mg/ml) except MC. The TCCs present in urine were partially purified by gel filtration using Sepharose 6B and were found to contain C5, C6, C7, C8, C9 and S protein by ELISA. Although the molecular weight of TCC is similar to that of IgM, the fractional excretion rate of TCC was about 100 times higher than that of IgM. These results suggest that TCCs detectable in urine contain SC5b-9 complexes and are mostly of renal origin.

Adolescent↗

PubMed1991

Experimental infections of mice and pigs with Streptococcus suis type 2.

Five inbred strains of mice were tested for their susceptibility to Streptococcus suis type 2 including the type strain, two isolates from meningitis in pigs and two isolates from tonsils of clinically healthy pigs. C57BL/6, ICR and ddY strain mice showed lower susceptibility to all strains of S. suis type 2 than BALB/c and SS strain mice. The type strain and the isolates from diseased pigs produced septicaemia and meningitis in BALB/c and SS mice inoculated with 10(8) colony forming unit of the bacteria and 60 to 100% of these infected mice died. On the other hand, mice inoculated with the isolates from healthy pigs showed mild clinical signs but none of them died. In BALB/c mice which died or developed nervous signs, the purulent meningo-encephalitis, myocarditis, ophthalmitis, labyrinthitis and otitis media were observed. S. suis type 2 antigen was demonstrated in these lesions by immunoperoxidase staining using rabbit S. suis type 2 antiserum. These results were similar to those in the experimentally infected pigs with these virulent and avirulent strains against mice. These results indicate that BALB/c and SS strains of mice are useful as an experimental model of S. suis type 2 infections in pigs, and that there are virulent and avirulent strains against mice and pigs among the strains of S. suis type 2.

Animals↗