Search PubMed⌕ Search

Biomedical subjects

T Taira

Publications and source records attributed to T Taira.

At least 19 recordsLinked to original sources

52 mJ narrow-bandwidth degenerated optical parametric system with a large-aperture periodically poled MgO:LiNbO3 device.

We have demonstrated efficient, high-energy, narrow-spectral-bandwidth 2.128 microm pulse generation by use of periodically poled MgO:LiNbO3 devices with a 36 mm length and a 5 mm x 5 mm large aperture. A free-running degenerated optical parametric oscillator (OPO) pumped with a Q-switched 1.064 microm Nd:YAG laser exhibits a high slope efficiency of 75% and an optical-to-optical conversion efficiency of 70% with a broad spectral bandwidth (>100 nm). In a configuration with a spectrally narrowed master oscillator followed by a power amplifier, we have achieved an output pulse energy of 52 mJ with a spectral bandwidth of less than 2 nm at the degeneracy point. The total optical-to-optical conversion efficiency of the system reached 50%.

Journal Article↗

Enhanced hippocampal GABAergic inhibition in mice overexpressing heparin-binding growth-associated molecule.

Heparin-binding growth-associated molecule is a developmentally regulated extracellular matrix protein promoting neurite outgrowth, axonal guidance and synaptogenesis. In the hippocampus, heparin-binding growth-associated molecule is expressed in an activity-dependent manner, and has been shown to suppress long-term potentiation of glutamatergic synapses in the area CA1, but the mechanisms underlying this action are unknown. One of the mechanisms by which extracellular matrix proteins might modulate fast synaptic transmission is by altering GABAergic function. Therefore, we have studied the properties of GABAA receptor-mediated inhibition in hippocampus of mutant mice overexpressing heparin-binding growth-associated molecule (heparin-binding growth-associated molecule transgenics). Under control conditions the wild-type mice have much higher level of long-term potentiation than the transgenics. However, in the absence of the GABAA receptor-mediated-inhibition a similar level of long-term potentiation is seen in both strains. In field potential recordings blockade of GABAA receptors by picrotoxin resulted in more accentuated increase in the CA1 population spike in the transgenics than in the wild-type animals. Whole-cell patch-clamp recordings revealed that when compared with the wild-type animals the transgenic mice had higher frequency of spontaneous inhibitory postsynaptic currents in CA1 pyramidal neurons. However, the frequency of action potential-independent miniature inhibitory postsynaptic currents was similar in both strains. Further, the transgenics had reduced paired-pulse depression of inhibitory postsynaptic currents, which was insensitive to the blockade of GABAB receptors in contrast to wild-type mice. The results demonstrate that the mice overexpressing heparin-binding growth-associated molecule have accentuated hippocampal GABAA receptor-mediated inhibition, which in turn may explain the lowered predisposition of glutamatergic synapses to undergo plastic changes in these animals. Thus, our findings suggest a mechanism by which heparin-binding growth-associated molecule can regulate synaptic plasticity.

Animals↗

Proper SUMO-1 conjugation is essential to DJ-1 to exert its full activities.

DJ-1 is a multifunctional protein that plays roles in transcriptional regulation and antioxidative stress, and loss of its function is thought to result in the onset of Parkinson's disease (PD). Here, we report that DJ-1 was sumoylated on a lysine residue at amino-acid number 130 (K130) by PIASxalpha or PIASy. The K130 mutation abrogated all of the functions of DJ-1, including ras-dependent transformation, cell growth promotion and anti-UV-induced apoptosis activities. Sumoylation of DJ-1 was increased after UV irradiation concomitant with a pI shift to an acidic point of DJ-1. Furthermore, L166P, a mutant DJ-1 found in PD patients, and K130RX, an artificial mutant containing four mutations in DJ-1, were improperly sumoylated, and they became insoluble, partly localized in the mitochondria and degraded by the proteasome system. Both L166P-expressing cells and DJ-1-knockdown cells were found to be highly susceptible to UV-induced cell apoptosis.

Amino Acid Sequence↗

Room-temperature, continuous-wave 1-W green power by single-pass frequency doubling in a bulk periodically poled MgO:LiNbO3 crystal.

Continuous-wave high-power green light generation at room temperature is reported in a single-pass frequency-doubling configuration with bulk periodically poled MgO:LiNbO3 crystal placed outside a diode end-pumped Nd:GdVO4 laser. The MgO:LiNbO3 samples of 6.95-microm domain period, uniform periodicity, and 50% duty cycle along the entire crystal length are fabricated by use of a high-voltage multipulse poling method. A maximum power of 1.18 W at 531 nm with 16.8% conversion efficiency is obtained from a 2-mm-thick, 25-mm-long MgO:LiNbO3 crystal; the corresponding internal green power and conversion efficiency are 1.38 W and 19.6%, respectively, whereas the normalized conversion efficiency is 3.3%/W.

Journal Article↗

Highly efficient 1063-nm continuous-wave laser emission in Nd:GdVO4.

Highly efficient 1-microm continuous-wave laser emission in 3-mm-thick, 0.5- and 1.0-at. % Nd:GdVO4 crystals longitudinally pumped at 879 nm into the laser emitting level is reported. Under Ti:sapphire pumping, the slope efficiency in absorbed power is approximately 80% for both crystals, while the slope efficiency, the optical-to-optical efficiency (at 1700-mW pump power), and the laser threshold in incident power are 79%, 78%, and 31 mW for 0.5-at. % Nd and 80%, 77%, and 40 mW for 1.0-at. % Nd, respectively. The slope efficiency is close to the quantum defect limit, the difference being fully accounted for by the residual optical losses. Under 879-nm diode laser pumping, the slope efficiency and the optical-to-optical efficiency in absorbed power of the 0.5-at. % Nd:GdVO4 crystal are 60% and 53%, owing to poorer superposition of the pumped and the laser mode volumes.

Journal Article↗

Diaphragm pacing with the spinal cord stimulator.

BACKGROUND: Diaphragm pacing with electrical stimulation of the phrenic nerve is an established treatment for central hypoventilation syndrome. The device, however, is not readily available, at least, in Japan. We applied the spinal cord stimulator for pain control to phrenic nerve stimulation. The purpose of this study is to evaluate the efficacy and feasibility of phrenic pacing with the compromise method. METHOD AND PATIENTS: We implanted a spinal cord stimulator in five patients with chronic central hypoventilation. The stimulation electrode was placed along the phrenic nerve in the neck, and the device was implanted in the anterior chest. We used the cyclic mode, and set the parameters at 1 second ramp up, 2 seconds on, 3 seconds off. The pulse width and the frequency were set at 150 microsec and 21 Hz respectively. The amplitude was adjusted to obtain sufficient tidal volume and to maintain PaCO2 at around 40 mmHg. FINDINGS: During the follow-up period from 3 to 34 months (mean 23), stable and sufficient ventilation were observed in all patients without complications. INTERPRETATION: Although longer follow-up is necessary, diaphragm pacing with the spinal cord stimulator is feasible for treatment of central hypoventilation syndrome.

Adult↗

The role of neurosurgical interventions for control of spasticity in neurorehabilitation: new findings on functional microanatomy of the tibial nerve.

Harmful spasticity after cerebral or spinal damage disturbs functional recovery in neurorehabilitation, but neurosurgical interventions for relief of spasticity are not widely performed, at least in Asian countries including Japan. We have been performing various types of neurosurgical treatment for spasticity such as selective peripheral neurotomy, selective dorsal rhizotomy, microsurgical DREZotomy, and intrathecal baclofen administration. We deal with both children and adults. From our experience of tibial neurotomy, in particular, we describe functional microsurgical anatomy of the tibial nerve in the popliteal fossa. This is the first report on this regional functional anatomy.

Electric Stimulation↗

Neurosurgical treatment for writer's cramp.

BACKGROUND: Writer's cramp is a type of focal dystonia due to dysfunction of the pallido-thalamo-cortical circuit. The symptom is refractory to most conservative treatment, though botulinum toxin injection is generally used for symptomatic relief. As a surgical treatment of dystonia we performed stereotactic nucleus ventrooralis (Vo) thalamotomy for dystonic cramp of the hand. METHOD: Eight patients (5 men, 3 women, age 26-40 yrs, mean 32.1 yrs) with medically intractable task-specific focal dystonia of the hand underwent Vo thalamotomy. Stereotactic target was chosen at the junction of the anterior and posterior Vo nuclei. FINDINGS: The mean duration of the symptom ranged from 3 to 6 years (mean, 4.0 yrs). All patients had complained of difficulty in writing. Six patients were professional workers, such as comic artist, guitarist, and barber, and, because of the dystonic symptoms at their professional work, they had stopped pursuing their profession. All patients showed immediate postoperative disappearance of dystonic symptoms, and the effect was sustained during the follow up period (3-29 months, mean 13.1 mo) except in one case. One patient showed partial recurrence of the symptom and underwent second thalamotomy 5 months after the initial surgery with satisfactory results. The score of the writer's cramp rating scale significantly (p < 0.001) decreased after Vo thalamotomy. There was no permanent operative complication. There was no mortality or permanent morbidity. INTERPRETATION: Although a longer follow-up is needed, stereotactic Vo thalamotomy is a useful and safe therapeutic option for writer's cramp.

Adult↗

Clinical application of drug pump for spasticity, pain, and restorative neurosurgery: other clinical applications of intrathecal baclofen.

Intrathecal baclofen has been successfully used for control of severe spasticity. Baclofen, an agonist of GABA-B receptor, has other potential effects on pain and recovery from coma. Sporadic episodes of dramatic recovery from persistent vegetative state are reported after intrathecal administration of baclofen. There are also reports on the use of baclofen for neuropathic pain including post-stroke central pain syndrome. Baclofen is also used for control of dystonia due to cerebral palsy or reflex sympathetic dystrophy. On the other hand, epidural spinal cord stimulation has been used for pain, spasticity, dystonia, or attempt to improve deteriorated consciousness, though the effects seem variable and modest. Similarity between baclofen and spinal cord stimulation is interesting in that both involves in spinal GABAergic system. The GABAergic system in the spinal cord plays a pivotal role in various clinical effects of these procedures.

Baclofen↗

Development of an artificial dermis preparation capable of silver sulfadiazine release.

This article describes the antibacterial effects of an artificial dermis impregnated with silver sulfadiazine (Ag-SD) in vitro as well as in vivo. In the in vitro test, silver release from the artificial dermis impregnated with Ag-SD, by immersion in collagenase solution was controlled by the degradation of the collagen sponge. The artificial dermis impregnated with 3% or higher doses of Ag-SD completely suppressed the growth of Pseudomonas aeruginosa (Ps.) or Staphylococcus aureus (St.). The cytotoxicity test revealed that impregnation of 5% or higher doses of Ag-SD suppressed the growth of fibroblasts. However, when the artificial dermis impregnated with Ag-SD was implanted into full-thickness skin defects on the backs of guinea pigs, no tissue damage was histologically observed around the implanted site of the dermis. In the in vivo test, the artificial dermis impregnated with 10% Ag-SD, which was grafted on experimentally contaminated wounds in the backs of guinea pigs, macroscopically suppressed degradation of the collagen sponge, and significantly reduced the growth of both Ps. and St., compared with artificial dermis without Ag-SD. We conclude that collagen sponge impregnated with Ag-SD is a promising artificial dermis applicable to treat contaminated wounds.

Animals↗

A novel transrepression pathway of c-Myc. Recruitment of a transcriptional corepressor complex to c-Myc by MM-1, a c-Myc-binding protein.

The protooncogene product c-Myc plays a role in transcription regulation both for activation and repression. While transactivation pathways of c-Myc either from the N-proximal or the C-proximal region that is linked to the chromatin remodeling complex have been identified, a transrepression pathway had been identified only from the C-proximal region via Max and Mad that recruit the histone deacetylase (HDAC) complex. We have reported that a novel c-Myc-binding protein, MM-1, repressed the E-box-dependent transcription activity of c-Myc (Mori, K., Maeda, Y., Kitaura, H., Taira, T., Iguchi-Ariga, S. M. M., and Ariga, H. (1998) J. Biol. Chem. 273, 29794-29800). To clarify the molecular mechanisms of MM-1 toward c-Myc, cDNAs encoding MM-1-binding proteins were screened by the two-hybrid method with MM-1 as a bait using a human HeLa cDNA library, and a cDNA encoding TIF1 beta/KAP1, a transcriptional corepressor, was obtained. MM-1 was found to bind to the central portion of TIF1 beta in vitro and in vivo, and these proteins were found to be colocalized in the nucleus. MM-1 and TIF1 beta complex in human HeLa cells was found to also contain c-Myc, mSin3, and HDAC1. Introduction of the C-terminal half of TIF1 beta as a dominant negative form abrogated the inhibitory activity of MM-1 toward c-Myc and greatly stimulated the transcription activity of c-Myc. Moreover, the inhibitory activity of MM-1 toward c-Myc was canceled by trichostatin A, an inhibitor of HDAC1. These results indicate that MM-1 is a connecting factor that forms a novel transcription repression pathway of c-Myc.

Binding Sites↗

MM-1, a c-Myc-binding protein, is a candidate for a tumor suppressor in leukemia/lymphoma and tongue cancer.

The c-myc oncogene product (c-Myc) is a transcription factor that dimerizes with Max and recognizes the E-box sequence, and it plays key functions in cell proliferation, differentiation, and apoptosis. We previously showed that MM-1 bound to myc box II within the transactivation domain of c-Myc and repressed the E-box-dependent transcriptional activity of c-Myc. Here we report that MM-1 showed features of a tumor suppressor. In an EST data base search for cDNAs homologous to MM-1, we found a frequent substitution of amino acid 157 of MM-1, from alanine to arginine (A157R), and the substitution was observed more in tumor cells than in normal cells. A survey of the A157R mutation of MM-1 in 57 cultured cancer cells and 90 tissues from cancer patients showed that the A157R was present in about 50-60% of leukemia/lymphoma cells and in more than 75% of squamous cell carcinoma of tongue cancer. Although both the A157R and the wild-type MM-1 bound to c-Myc, only A157R lost the activities to repress both the E-box-dependent transcriptional activity of c-Myc and the myc/ras cooperative transforming activity in rat 3Y1 cells. Furthermore, the wild-type MM-1, but not A157R, arrested the growth of 3Y1 cells. The human MM-1 gene was mapped at chromosome 12q12-12q13, where many chromosome abnormalities in cancer cells have been reported. The results suggest that MM-1 is a novel candidate for a tumor suppressor that controls the transcriptional activity of c-Myc.

3T3 Cells↗

AMY-1, a c-Myc-binding protein, is localized in the mitochondria of sperm by association with S-AKAP84, an anchor protein of cAMP-dependent protein kinase.

We have reported that a novel c-Myc-binding protein, AMY-1 (associate of Myc-1), stimulated the transcription activity of c-Myc. To access the molecular function of AMY-1, a two-hybrid screening of cDNAs encoding AMY-1-binding proteins was carried out with AMY-1 as a bait using a human HeLa cDNA library, and a clone encoding cAMP-dependent protein kinase anchor protein 149 (AKAP149), was obtained. AMY-1 was found to bind in vitro and in vivo to the regulatory subunit II binding region of AKAP149 and S-AKAP84, a splicing variant of AKAP149 expressed in the testis. AMY-1 was expressed postmeiotically in the testis, as S-AKAP84 was expressed. Furthermore, S-AKAP84 and regulatory subunit II, a regulatory subunit of cAMP-dependent protein kinase, made a ternary complex in cells, and AMY-1 was localized in the mitochondria of HeLa and sperm in association with AKAP149 and S-AKAP84, respectively. These results suggest that AMY-1 plays a role in spermatogenesis.

A Kinase Anchor Proteins↗

DJ-1 positively regulates the androgen receptor by impairing the binding of PIASx alpha to the receptor.

DJ-1 was first identified as a novel candidate of the oncogene product that transformed mouse NIH3T3 cells in cooperation with an activated ras. Later DJ-1 was also found to be an infertility-related protein that was reduced in rat sperm treated with sperm toxicants that cause infertility in rats. To determine the functions of DJ-1, cDNAs encoding DJ-1-binding proteins were screened by the yeast two-hybrid method. Of several proteins identified, PIASx alpha/ARIP3, a modulator of androgen receptor (AR), was first characterized as the DJ-1-binding protein in this study. DJ-1 directly bound to the AR-binding region of PIASx alpha by an in vitro coimmunoprecipitation assay and also bound to PIASx alpha in human 293T cells. Both proteins were co-localized in the nuclei. PIASx alpha inhibited the AR transcription activity in a dose-dependent manner in cotransfected monkey CV1 cells with an androgen responsive element-luciferase reporter. Introduction of DJ-1 into CV1 cells in a state of inhibition of AR activity by PIASx alpha restored AR transcription activity by absorbing PIASx alpha from the AR-PIASx alpha complex, while a DJ-1 mutant harboring an amino acid substitution at number 130 from lysine to arginine did not restore it. These results indicate that DJ-1 is a positive regulator of the androgen receptor.

3T3 Cells↗

Molecular cloning of human and mouse DJ-1 genes and identification of Sp1-dependent activation of the human DJ-1 promoter.

DJ-1 has been identified as a novel oncogene that transforms mouse NIH3T3 cells in cooperation with activated ras. Subsequently, two other groups have identified SP22 or CAP-1, rat homologs of human DJ-1, as a sperm protein targeted by some toxicants leading to male infertility, and another group has also reported that RS, the same as human DJ-1, is a component of an RNA-binding protein complex. To characterize the expression or functional importance of DJ-1, the genomic DNAs of both human and mouse DJ-1 were cloned and characterized. Both genomic DNAs comprise 7 exons spanning about 16-24 kb, in which 2-6 exons encode the DJ-1 protein. The human DJ-1 gene was mapped at chromosome 1p36.2-p36.3, a region that has been shown to be a hot spot of chromosome abnormalities in several tumor cells. To analyze the promoter of the human DJ-1 gene, a series of deletion constructs of the region upstream of exon 2 were linked to the luciferase gene, and their luciferase activities were measured in human HeLa cells. Of the many putative transcription regulatory sequences, the Sp1 site present at -100 from the transcription initiation site contributed to the major promoter activity, and Sp1 was identified as a protein binding to this site by a mobility shift assay using HeLa nuclear extract.

Amino Acid Sequence↗

Enhanced hippocampal long-term potentiation in mice lacking heparin-binding growth-associated molecule.

Heparin-binding growth-associated molecule (HB-GAM) (pleiotrophin) is a highly conserved extracellular matrix-associated protein implicated in a diverse range of developmental processes, including the formation and plasticity of neuronal connections. Using gene targeting, we have in the present study created HB-GAM-deficient mice that are viable and fertile and show no gross anatomical abnormalities. The hippocampal structure as well as basal excitatory synaptic transmission in the area CA1 appear normal in the mice lacking HB-GAM. However, hippocampal slices from HB-GAM-deficient mice display a lowered threshold for induction of long-term potentiation (LTP), which reverts back to the wild-type level by application of HB-GAM. HB-GAM expression in hippocampus is activity-dependent and upregulated in several neuropathological conditions. Thus, we suggest that HB-GAM acts as an inducible signal to inhibit LTP in hippocampus.

Animals↗

Immunohistochemical localization of amelogenin in human odontogenic tumors, using a polyclonal antibody against bovine amelogenin.

In the present study, we investigated the localization of amelogenin in odontogenic tumors, using an anti-amelogenin polyclonal antibody. In order to make the antibody, antisera against an amelogenin fraction obtained from the enamel matrix of unerupted bovine tooth was raised in rabbits. By Western blot analysis, a main band of 25 kDa and six minor bands (6.8, 12, 18, 20, 23, and 27 kDa) were detected under nonreducing conditions. Immunoreactivity for the amelogenin was observed in ameloblasts and in the immature enamel matrix of 4-day-old rats. In odontogenic tumors, positive reactions for amelogenin were localized in limited areas in adenomatoid odontogenic tumor, calcifying odontogenic cyst, primary intraosseous carcinoma and odontoma. The strongest immunoreactions were shown in enamel matrices in odontomas. Small mineralized foci in epithelial nests showed positive reactions, and a few reactions were observed in epithelium adjacent to the mineralized foci. In calcifying odontogenic cysts, some ghost cells in the lining epithelium were strongly stained. The results indicate that the present antibody for amelogenin is useful for the determination of odontogenic tumors, especially in those in which small mineralized foci are present in the epithelial nests.

Amelogenin↗

Purification and characterization of a lectin from the mushroom Mycoleptodonoides aitchisonii.

A lectin was isolated from the mushroom Mycoleptodonoides aitchisonii by means of affinity chromatography on bovine submaxillary mucin (BSM)-Toyopearl and gel filtration on Superose 12 HR10/30 using a FPLC system. This lectin is composed of four identical 16 kDa subunits and the molecular mass of the intact lectin was estimated to be 64 kDa by gel filtration. In a hemagglutination inhibition assay, it exhibited strong sugar-binding specificity towards asialo-BSM among the mono- or oligo-saccharides and glycoproteins tested. The binding specificity of the lectin was also examined by surface plasmon resonance analysis.

Agaricales↗