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941.
An experimental 1.5-V 64-Mb DRAM   总被引:1,自引:0,他引:1  
Low-voltage circuit technologies for higher-density dynamic RAMs (DRAMs) and their application to an experimental 64-Mb DRAM with a 1.5-V internal operating voltage are presented. A complementary current sensing scheme is proposed to reduce data transmission delay. A speed improvement of 20 ns was achieved when utilizing a 1.5-V power supply. An accurate and speed-enhanced half-VCC voltage generator with a current-mirror amplifier and tri-state buffer is proposed. With it, a response time reduction of about 1.5 decades was realized. A word-line driver with a charge-pump circuit was developed to achieve a high boost ratio. A ratio of about 1.8 was obtained from a power supply voltage as low as 1.0 V. A 1.28 μm2 crown-shaped stacked-capacitor (CROWN) cell was also made to ensure a sufficient storage charge and to minimize data-line interference noise. An experimental 1.5 V 64 Mb DRAM was designed and fabricated with these technologies and 0.3 μm electron-beam lithography. A typical access time of 70 ns was obtained, and a further reduction of 50 ns is expected based on simulation results. Thus, a high-speed performance, comparable to that of 16-Mb DRAMs, can be achieved with a typical power dissipation of 44 mW, one tenth that of 16-Mb DRAMs. This indicates that a low-voltage battery operation is a promising target for future DRAMs  相似文献   
942.
943.
A 1 Mb 5 V-only EEPROM (electrically erasable programmable ROM) with metal-oxide-nitride-oxide-semiconductor (MONOS) memory cells specifically designed for a semiconductor disk application is described. The memory has high endurance to write/erase cycles and a relatively low programming voltage of ±9 V. These advantages result from the structure and the characteristics of the MONOS memory cell. A newly developed dual-gate-type MONOS memory cell has a small unit cell area of 18.4 μm2 with 1.2 μm lithography, and the die size of the fabricated chip is 5.3 mm×6.3 mm. A new programming scheme called multiblock erase solved the problem of slow programming speed. A programming speed of up to 1.1 μs/B equivalent (140 ms/chip) was obtained  相似文献   
944.
Mechanical properties of linear thermoplastic polyurethanes (TPUs) prepared by polyaddition reaction using a polycarbonate diol (PCD), 1,4‐butanediol (a chain extender) and 4,4'‐diphenylmethane diissocyanate were investigated. Chemical composition among these three components was kept constant. Primary attention was directed to how chain length of an alkylene group in the PCD affected the mechanical properties of the resultant TPU. To clarify this effect, the PCDs were synthesized using 1,6‐hexanediol and 1,12‐dodecanediol. In addition, the TPUs from copolycarbonate diols containing these two components were also produced, and then extensively examined and further compared to the ones from the corresponding blended PCDs. From a practical point of view, weatherability and solubility in a polar solvent were also evaluated.  相似文献   
945.
The authors present their experiences in assisting the government of Niger to develop automated information systems for health care management. They discuss the structure of the health system, the role of donor assistance, the process of initiating automated systems, and the technical requirements and costs of the system. Finally, they draw general conclusions that may be useful for those attempting similar efforts.  相似文献   
946.
947.
Bluetongue virus (BTV) cores consist of the viral genome and five proteins, including two major components (VP3 and VP7) and three minor components (VP1, VP4, and VP6). VP3 proteins form an inner scaffold for the deposition on the core of the surface layer of VP7. VP3 also encapsidates and interacts with the three minor proteins. The BTV VP3 protein consists of 901 amino acids and has a sequence that is a highly conserved among BTV serotypes and other orbiviruses (e.g., epizootic hemorrhagic disease virus and African horse sickness virus). To locate sites of interaction between VP3 and the other structural proteins, we have analyzed the effects of a number of VP3 deletion mutants representing conserved regions of the protein, using as an assay the formation of core-like particles (CLPs) expressed by recombinant baculoviruses. Five of the VP3 deletion mutants interacted with the coexpressed VP7 and made CLPs. These CLPs also incorporated the three minor proteins. One mutant, lacking VP3 amino acid residues 499 to 508, failed to make CLPs. Further mutational analyses have demonstrated that a methionine at residue 500 of VP3 and an arginine at residue 502 were both required for CLP formation.  相似文献   
948.
949.
950.
Although microglial cells are well known to become activated in the pathological brain, mechanisms underlying the microglial activation are not fully understood. In the present study, with an aim to elucidate whether neurons are involved in the microglial activation, we compared the morphology and the superoxide anion (O2-)-generating activity of rat microglial cells in pure culture with those of cells cocultured with rat primary cortical neurons. Microglial cells in pure culture in serum-free Eagle's minimum essential medium on poly-L-lysine-coated coverslips displayed ramified morphology and suppressed activity of O2- generation. In contrast, microglial cells in neuron-microglia coculture under the same conditions as those for the pure culture displayed ameboid shape and upregulated activity of O2- generation. Electron microscopic observation revealed that microglial cells in coculture were more abundant in Golgi apparatus and secretory granules than those in pure culture and that some of microglial cells in the vicinity of neurites exhibited membrane specialization reminiscent of a junctional apparatus with high electron density between a microglial soma and a neurite. Microglial cells in coculture tended to tie neurites in bundles by extending processes. Medium conditioned by neurons significantly enhanced O2- generation by microglia, but microglial cells in contact with or in close apposition to cocultured neurons were much more intensely activated than those remote from the neurons. Furthermore, the membrane fraction of cortical neurons activated microglial cells, and this effect was abolished by treating the neuronal membrane with trypsin or neuraminidase. In conclusion, neuronal-microglial contact may be necessary to mediate microglial activation. The present findings suggest that the contact of microglia with damaged neurons in the brain is a plausible cause to activate microglia in the neuropathological processes.  相似文献   
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