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Yoon-Ha Jeong Seong-Kue Jo Bong-Hoon Lee Sugano T. 《Electron Device Letters, IEEE》1995,16(3):109-111
High performance enhancement mode InP MISFET's have been successfully fabricated by using the sulfide passivation for lower interface states and with photo-CVD grown P3N5 film used as gate insulator. The MISFET's thus fabricated exhibited exhibited pinch-off behavior with essentially no hysteresis. Furthermore the device showed a superior stability of drain current. Specifically under the gate bias of 2 V for 104 seconds the room temperature drain current was shown to reduce from the initial value merely by 2.9% at the drain voltage of 4 V. The effective electron mobility and extrinsic transconductance are found to be about 2300 cm 2/V·s and 2.7 mS/mm, respectively. The capacitance-voltage characteristics of the sulfide passivated InP MIS diodes show little hysteresis and the minimum density of interface trap states as low as 2.6×1014/cm2 eV has been attained 相似文献
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The flow and fracture behavior of Be-Al alloys were determined in tension with different levels of superimposed pressure.
The Be-Al alloys were prepared by Brush Wellman, Inc. (Cleveland, OH) from prealloyed powders processed to either a hot isostatically
pressed (“hipped”) or cold isostatically pressed and extruded condition. Significant effects of pressure on both the flow
and ductility have been observed at room temperature, with implications on the formability of these materials. The effects
of changes in processing conditions and stress state on the flow and fracture behavior are summarized in addition to both
optical and scanning electron microscopy (SEM) examination of the fracture surfaces. Separate other studies on the alloy constituents
(e.g., Al and Be) are also reported. The results are also compared to previous works on monolithic materials and composites tested
with high pressure. 相似文献
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MS Oitzl ER de Kloet M Jo?ls W Schmid TJ Cole 《Canadian Metallurgical Quarterly》1997,9(11):2284-2296
Previous studies in rats using the Morris water maze suggested that the processing of spatial information is modulated by corticosteroid hormones through mineralocorticoid and glucocorticoid receptors in the hippocampus. Mineralocorticoid receptors appear to be involved in the modulation of explorative behaviour, while additional activation of glucocorticoid receptors facilitates the storage of information. In the present study we used the water maze task to examine spatial learning and memory in mice homozygous and heterozygous for a targeted disruption of the glucocorticoid receptor gene. Compared with wild-type controls, homozygous and heterozygous mice were impaired in the processing of spatial but not visual information. Homozygous mutants performed variably during training, without specific platform-directed search strategies. The spatial learning disability was partly compensated for by increased motor activity. The deficits were indicative of a dysfunction of glucocorticoid receptors as well as of mineralocorticoid receptors. Although the heterozygous mice performed similarly to wild-type mice with respect to latency to find the platform, their strategy was more similar to that of the homozygous mice. Glucocorticoid receptor-related long-term spatial memory was impaired. The increased behavioural reactivity of the heterozygous mice in the open field points to a more prominent mineralocorticoid receptor-mediated function. The findings indicate that (i) the glucocorticoid receptor is of critical importance for the control of spatial behavioural functions, and (ii) mineralocorticoid receptor-mediated effects on this behaviour require interaction with functional glucocorticoid receptors. Until the development of site-specific, inducible glucocorticoid receptor mutants, glucocorticoid receptor-knockout mice present the only animal model for the study of corticosteroid-mediated effects in the complete absence of a functional receptor. 相似文献
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DJ Benos BH Hahn JK Bubien SK Ghosh NA Mashburn MA Chaikin GM Shaw EN Benveniste 《Canadian Metallurgical Quarterly》1994,91(2):494-498
Infection by human immunodeficiency virus type 1 (HIV-1) is often complicated by a variety of neurological abnormalities. The most common clinical syndrome, termed acquired immunodeficiency syndrome (AIDS) dementia complex, presents as a subcortical dementia with cognitive, motor, and behavioral disturbances and is unique to HIV-1 infection. The pathogenesis of this syndrome is poorly understood but is believed to involve interactions among virally infected macrophages/microglia, astrocytes, and neurons. In this study, we show that exposure of primary rat and human astrocytes to heat-activated HIV-1 virions, or to eukaryotically expressed HIV-1 and HIV-2 envelope glycoproteins (gp120) stimulates amiloride-sensitive Na+/H+ antiport, potassium conductance, and glutamate efflux. These effects are blocked specifically by amiloride, an inhibitor of Na+/H+ antiport and by the selective removal of gp120 with immobilized monoclonal antibody. As a result of modulation of astrocytic function by gp120, the ensuing neuronal depolarization and glutamate exposure could activate both voltage-gated and N-methyl-D-aspartate-regulated Ca2+ channels, leading to increases in intraneuronal Ca2+ and neuronal death. These findings implicate the astrocyte directly in the pathogenesis of AIDS dementia complex. 相似文献
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