39,716 research outputs found

    Generation and recovery of strain in (28)Si-implanted pseudomorphic GeSi films on Si(100)

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    Effects of ion implantation of 320 keV Si-28 at room temperature in pseudomorphic metastable GexSi1-x (x almost-equal-to 0.04, 0.09, 0.13) layers approximately 170 nm thick grown on Si(100) wafers were characterized by x-ray double-crystal diffractometry and MeV He-4 channeling spectrometry. The damage induced by implantation produces additional compressive strain in the GexSi1-x layers, superimposed on the intrinsic compressive strain of the heterostructures. This strain rises with the dose proportionally for doses below several times 10(14) Si-28/cm2. Furthermore, for a given dose, the strain increases with the Ge content in the layer. Upon thermal processing, the damage anneals out and the strain recovers to the value before implantation. Amorphized samples (doses of greater than 2 x 10(15) Si-28/cm2) regrow poorly

    Defect production in Si(100) by 19F, 28Si, 40Ar, and 131Xe implantation at room temperature

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    We used x-ray double-crystal diffractometry and MeV 4He channeling spectrometry to study quantitatively the damage produced in Si(100) at room temperature by 230-keV 19F, 230-keV 28Si, 250-keV 40Ar, or 570-keV 131Xe implantation. The measured defect concentration and the perpendicular strain have the same depth profile, and both are depleted near the surface compared to the Frenkel pair concentration calculated from computer simulation. The perpendicular strain is proportional to the defect concentration with a coefficient of B~0.01 common to all implanted species. The maximum value of the perpendicular strain and of the defect concentration rises nonlinearly with the dose for all species. The damage produced by different implanted species depends on the dose in approximately the same way save for a scaling factor of the dose. In the regime of low damage, the strain and the defect concentration rise linearly with increasing dose. The slope of this rise with dose increases with the square of the Frenkel pairs produced per unit dose of incident ions, as calculated from computer simulations. This fact means that stable defects produced by room-temperature implantation in Si(100) cannot be predicted by a linear cascade model

    Defects production and annealing in self-implanted Si

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    230-keV 28Si ions were implantated into Si(100) at room temperature with doses from 1014 to 1015/cm2. The samples were analyzed by x-ray double crystal diffractometry and 2-MeV 4He ion channeling spectrometry. The implanted layer has a parallel lattice spacing equal to that of the unimplanted substrate. The perpendicular lattice spacing is larger than that of the unimplanted substrate and is proportional to the defect concentration extracted from the channeling measurement. Both the perpendicular lattice spacing and the defect concentration increase nonlinearly with ion dose. The defect concentration initially increases slowly with dose until a critical value (~15%, at 4×1014/cm2), then rises rapidly, and finally a continuous amorphous layer forms. The initial sluggish increase of the damage is due to the considerable recombination of point defects at room temperature. The rapid growth of the defect concentration is attributed to the reduction of the threshold energy for atomic displacement in a predamaged crystal. The amorphization is envisioned as a cooperative process initiated by a spontaneous collapse of heavily damaged crystalline regions. The annealing behavior of the damaged layer reveals various stages of defect recovery, indicating that the damage consists of a hierarchy of various defect structures of vacancy and interstitial aggregates

    Damage production and annealing in 28Si-implanted CoSi2/Sim(111) heterostructures

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    The damage in epitaxial CoSi2 films 500 nm thick grown on Si(111) produced by room-temperature implantation of 150 keV 28Si were investigated by 2-MeV 4He channeling spectrometry, double-crystal x-ray diffractometry, and electrical resistivity measurements. The damage in the films can be categorized into two types. In lightly (heavily) damaged CoSi2 the damage is in the form of point-like (extended) defects. The resistivity of lightly damaged CoSi2 films rises with the dose of implantation. Electrical defects correlate well with structural ones in lightly damaged films. The resistivity of heavily damaged films flattens off while the structural defects continue to rise with the dose, so that resistivity no longer correlates with structural defects. Upon thermal annealing, lightly damaged films can fully recover structurally and electrically, whereas heavily damaged films do so only electrically. A residual structural damage remains even after annealing at 800 °C for 60 min

    Black hole evaporation based upon a q-deformation description

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    A toy model based upon the qq-deformation description for studying the radiation spectrum of black hole is proposed. The starting point is to make an attempt to consider the spacetime noncommutativity in the vicinity of black hole horizon. We use a trick that all the spacetime noncommutative effects are ascribed to the modification of the behavior of the radiation field of black hole and a kind of q-deformed degrees of freedom are postulated to mimic the radiation particles that live on the noncommutative spacetime, meanwhile the background metric is preserved as usual. We calculate the radiation spectrum of Schwarzschild black hole in this framework. The new distribution deviates from the standard thermal spectrum evidently. The result indicates that some correlation effect will be introduced to the system if the noncommutativity is taken into account. In addition, an infrared cut-off of the spectrum is the prediction of the model.Comment: 13 pages, 2 figure

    Hepatitis C virus 3'UTR regulates viral translation through direct interactions with the host translation machinery.

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    The 3' untranslated region (3'UTR) of hepatitis C virus (HCV) messenger RNA stimulates viral translation by an undetermined mechanism. We identified a high affinity interaction, conserved among different HCV genotypes, between the HCV 3'UTR and the host ribosome. The 3'UTR interacts with 40S ribosomal subunit proteins residing primarily in a localized region on the 40S solvent-accessible surface near the messenger RNA entry and exit sites. This region partially overlaps with the site where the HCV internal ribosome entry site was found to bind, with the internal ribosome entry site-40S subunit interaction being dominant. Despite its ability to bind to 40S subunits independently, the HCV 3'UTR only stimulates translation in cis, without affecting the first round translation rate. These observations support a model in which the HCV 3'UTR retains ribosome complexes during translation termination to facilitate efficient initiation of subsequent rounds of translation
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