Engineering a small system

“Do it right first time” is the slogan of systems engineering. The approach can benefit all types of development projects, from smaller commercial products to large government projects, because the objective is the same: to design a high-quality product as fast and efficiently as possible. The author describes how the key to this process is translating a customer's need into a set of specifications that drive the system's design     

Drain structure optimization for highly reliable deep submicrometern-channel MOSFET

A guideline for n^- fully gate overlapped (FOLD) structure design optimization has been studied. From the viewpoint of reliability, the greatest reduction in substrate current directly leads to the most reliable n^- design for the FOLD structure. The current path modulation phenomenon due to the trapped charge at the n ^- extension region dominates the hot-carrier induced characteristics change for conventional lightly doped drain (LDD) structure with side-wall spacer. This phenomenon is minimized in the FOLD structure due to its higher controllability of the gate electrode than the LDD structure at the n^- extension region. Furthermore, it was also confirmed that the 0.3 μm optimized FOLD structure can achieve high circuit performance at 3.3 V operation, maintaining hot-carrier resistance     

Distribution of total uptime during a given time interval

The distribution of total uptime during a given time interval for a repairable system is obtained. The total uptime is the total amount of time the system is up (in operation) during the interval. It is assumed that: (1) the system starts to operate at the beginning of the interval and alternately takes only the two states, up and down (under repair); (2) repair restores the system to “like-new”. A simple approximation to the distribution function of total uptime for a shorter interval is presented     

Thyroid doses resulting from the Ukraine Chernobyl accident--Part I: Dose estimates for the population of Kiev

In the context of the radiation exposure of the Ukrainian population resulting from the Chernobyl accident, the quantification of the thyroid doses due to iodine incorporation is of special interest. This first part of a series of planned publications deals with the dose and risk estimation for Kiev citizens. Although these doses are expected to be considerably lower than those for some other regions of Ukraine, the investigations started with this population because the quantification of the thyroid doses due to iodine incorporation is of special interest. This first part of a series of planned publications deals with the dose and risk estimation for Kiev citizens. Although these doses are expected to be considerably lower than those for some other regions of Ukraine, the investigations started with this population because of the availability of rather reliable measurements and because of the size of this population. The methods developed allowed the estimation of individual thyroid doses. The average values of individual thyroid doses for five age groups (birth years 1983-1986, 1979-1982, 1975-1978, 1971-1974, and < 1971) are 104, 62, 19, 18, and 41 mGy, respectively. The collective thyroid doses were estimated as 83 x 10(3) person-Gy for those born before 1971 and as 38 x 10(3) person-Gy for younger inhabitants. The numbers of expected thyroid cancers in the whole Kiev population are 66 and 130, respectively.     

Sequences present in the cytoplasmic domain of CD4 are necessary and sufficient to confer sensitivity to the human immunodeficiency virus type 1 Vpu protein

CD4 is an integral membrane glycoprotein which functions as the human immunodeficiency virus receptor for infection of human host cells. We have recently demonstrated that Vpu, a human immunodeficiency virus type 1-encoded integral membrane phosphoprotein, induces rapid degradation of CD4 in the endoplasmic reticulum. Using an in vitro model system, we demonstrated that Vpu targets specific sequences in the cytoplasmic domain of CD4 to promote its degradation. In this report, we have further delineated regions within CD4 which are required for susceptibility to Vpu. Transfer of the CD4 cytoplasmic region into a heterologous protein, CD8, rendered the chimeric protein sensitive to Vpu-dependent degradation. In contrast, substitution of the CD8 transmembrane domain with the analogous region from CD4 did not confer sensitivity to Vpu. Finally, mutant forms of the CD4 protein containing the extracellular region alone or the extracellular and transmembrane regions linked to a heterologous cytoplasmic domain were not targeted by Vpu. Thus, sequences present in the cytoplasmic domain of CD4 are necessary and sufficient to confer sensitivity to Vpu.     

Toxicity of an antitumor ribonuclease to Purkinje neurons

Purkinje cell toxicity is one of the characteristic features of the Gordon phenomenon, a syndrome manifested by ataxia, muscular rigidity, paralysis, and tremor that may lead to death (Gordon, 1933). Two members of the RNase superfamily found in humans, EDN (eosinophil-derived neurotoxin) and ECP (eosinophil cationic protein), cause the Gordon phenomenon when injected intraventricularly into guinea pigs or rabbits. We have found that another member of the RNase superfamily, an antitumor protein called onconase, isolated from Rana pipiens oocytes and early embryos, will also cause the Gordon phenomenon when injected into the cerebrospinal fluid of guinea pigs at a dose similar to that of EDN (LD50, 3-4 micrograms). Neurologic abnormalities of onconase-treated animals were indistinguishable from those of EDN-treated animals, and histology showed dramatic Purkinje cell loss in the brains of onconase-treated animals. The neurotoxic activity of onconase correlates with ribonuclease activity. Onconase modified by iodoacetic acid to eliminate 70% and 98% of the ribonuclease activity of the native enzyme displays a similar decrease in ability to cause the Gordon phenomenon. In contrast, the homologous bovine pancreatic RNase A injected intraventricularly at a dose 5000 times greater than the LD50 dose of EDN or onconase is not toxic and does not cause the Gordon phenomenon. A comparison of the RNase activities of EDN, onconase, and bovine pancreatic RNase A using three pancreatic RNA substrates demonstrates that onconase is orders of magnitude less active enzymatically than EDN and RNase A. Thus, another member of the RNase superfamily in addition to EDN and ECP can cause the Gordon phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)