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1.
Rev Sci Instrum ; 81(2): 02A719, 2010 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-20225405

RESUMEN

Voltage holding capability of JT-60 negative ion source that has a large electrostatic negative ion accelerator with 45 cm x 1.1 m acceleration grids was experimentally examined and improved to realize 500 keV, 22 A, and 100 s D- ion beams for JT-60 Super Advanced. The gap lengths in the acceleration stages were extended to reduce electric fields in a gap between the large grids and at the corner of the support flanges from the original 4-5 to 3-4 kV/mm. As a result, the voltage holding capability without beam acceleration has been successfully improved from 400 to 500 kV. The pulse duration to hold 500 kV reached 40 s of the power supply limitation.

2.
Rev Sci Instrum ; 79(2 Pt 2): 02A519, 2008 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-18315140

RESUMEN

The first long pulse production of high power D(-) ion beams has been demonstrated in the JT-60 U negative ion sources, each of which was designed to produce 22 A, 500 keV D(-) ion beams. Voltage holding capability and the grid power loading were examined for long pulse production of high power D(-) ion beams. From the correlation between voltage holding and the light intensity of cathodoluminescence from the Fiber Reinforced Plastic insulators, the acceleration voltage for stable voltage holding capability was found to be less than 320-340 kV where the light was sufficiently suppressed. By tuning the extraction voltage, the grid power loadings in the ion sources were decreased to the allowable levels for long pulse injection without a significant reduction of the beam power. After tuning the acceleration and extraction voltages, D(-) ion beams of 12.5 and 9.8 A were produced at 340 keV with cesium seeding at a rate of approximately 14 microg/s into the ion sources. The pulse duration of these D(-) ion beams was extended step by step, and then was successfully extended up to 18 s without degradation of the negative ion production. The D(-) ion beams were neutralized to yield 3.6 MW D(0) beams by a gas cell, and then injected into the JT-60 U plasma. Further, a slight reduction of D(-) ion beam power allowed the longer injection duration of 21 s at a D(0) beam power of 3.2 MW. The success in the long pulse production of a high power D(-) ion beam shows that negative ion beams can be produced during a few tens of seconds without degradations of negative ion production and the voltage holding in a large Cs-seeded negative ion source.

3.
J Phys Condens Matter ; 20(6): 064231, 2008 Feb 13.
Artículo en Inglés | MEDLINE | ID: mdl-21693892

RESUMEN

Optical properties in conjugated polymers such as poly(p-phenylenevinylene) and poly(9,9-dialkyl-fluorene) have been studied using time-dependent density functional theory. In the calculations of the optical properties, real-space and real-time techniques are employed. We follow the linear responses of the systems under externally applied perturbations in the real time. To estimate the polymer spectra, we have calculated the responses of oligomers of different lengths and obtained the extrapolated values. The estimated polymer spectra agree with the experiments reasonably well.

4.
Phys Rev E Stat Nonlin Soft Matter Phys ; 63(4 Pt 1): 041706, 2001 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-11308866

RESUMEN

We present large-scale molecular-dynamics simulations of a nematic-isotropic interface in a system of repulsive ellipsoidal molecules, focusing in particular on the capillary-wave fluctuations of the interfacial position. The interface anchors the nematic phase in a planar way, i.e., the director aligns parallel to the interface. Capillary waves in the direction parallel and perpendicular to the director are considered separately. We find that the spectrum is anisotropic, the amplitudes of capillary waves being larger in the direction perpendicular to the director. In the long-wavelength limit, however, the spectrum becomes isotropic and compares well with the predictions of a simple capillary-wave theory.

5.
Vaccine ; 14(1): 28-36, 1996 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-8821646

RESUMEN

Replication-deficient recombinant adenoviruses expressing structural proteins of hepatitis C virus (HCV) were constructed. Each recombinant lacks adenoviral E1A and E3 genes and bears expression units for HCV structural proteins. The expression units contain HCV cDNAs coding for either the protein or core, one of two envelopes (E1 and E2) or all of these structural proteins (core, E1 and E2) under the control of the SR alpha promoter. In HeLa or HepG2 cells, the recombinants can express efficiently HCV genes after infection without replication of the recombinants. We detected 22-kDa core, 35-kDa E1 and 58-kDa E2 proteins of HCV in these cells. The recombinant expressing all three HCV structural proteins was inoculated into mice. Antibodies to each of the three HCV proteins were detected in all of the ten mice tested. The results indicate that the recombinant adenoviruses efficiently express HCV genes and induce specific antibody against the expressed HCV proteins in animals.


Asunto(s)
Adenoviridae/genética , Vectores Genéticos/inmunología , Hepacivirus/inmunología , Anticuerpos contra la Hepatitis C/biosíntesis , Antígenos de la Hepatitis C/inmunología , Vacunas Sintéticas/inmunología , Vacunas contra Hepatitis Viral/inmunología , Proteínas Estructurales Virales/inmunología , Adenoviridae/inmunología , Animales , Línea Celular , Hepacivirus/química , Humanos , Masculino , Ratones , Ratones Endogámicos BALB C , Factores de Tiempo , Proteínas del Núcleo Viral/biosíntesis , Proteínas del Envoltorio Viral/biosíntesis , Proteínas del Envoltorio Viral/inmunología
6.
Neuroreport ; 6(8): 1101-4, 1995 May 30.
Artículo en Inglés | MEDLINE | ID: mdl-7662886

RESUMEN

Arachidonic acid (AA) showed profound toxicity against primary neuronal cultures prepared from fetal rat striatum. This toxicity was attenuated by nordihydroguaiaretic acid but not by indomethacin, indicating that lipoxygenase pathway of AA metabolism is involved in the toxicity. Furthermore, the neurotoxic action of AA was abolished by antioxidants butylated hydroxyanisole or N-acetylcysteine. In contrast, treatment with forskolin or high K+, which have been shown to prevent neuronal death induced by MPP+ or high oxygen conditions, showed no protection against AA toxicity. These results suggest that, although oxygen free radicals generated through lipoxygenase metabolism is responsible for the neurotoxicity, distinct mechanisms from those of other oxidative stress are operative in AA-induced neuronal injury.


Asunto(s)
Antioxidantes/farmacología , Ácidos Araquidónicos/toxicidad , Neuronas/efectos de los fármacos , Animales , Muerte Celular/efectos de los fármacos , Células Cultivadas , Cuerpo Estriado/citología , Cuerpo Estriado/efectos de los fármacos , AMP Cíclico/farmacología , Relación Dosis-Respuesta a Droga , Indometacina/farmacología , Potasio/farmacología , Ratas , Ratas Wistar
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