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Implanted B and P dopants in Si exhibit transient enhanced diffusion (TED) during initial annealing, due to Si interstitials being emitted from the region of the implant damage. The structural source of these interstitials has not previously been identified. Quantitative transmission electron microscopy measurements of extended defects are used to demonstrate that TED is caused by the emission of interstitials from specific defects. The defects are rodlike defects running along 〈110〉 directions, which consist of interstitials precipitating on {311} planes as a single monolayer of hexagonal Si. We correlate the evaporation of {311} defects during annealing at 670 and 815 °C with the length of the diffusion transient, and demonstrate a link between the number of interstitials emitted by the defects, and the flux of interstitials driving TED. Thus not only are {311} defects contributing to the interstitial flux, but the contribution attributable to {311} defect evaporation is sufficient to explain the whole of the observed transient. The {311} defects are the source of the interstitials.

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Copper centers in copper-diffused n-type silicon measured by photoluminescence and deep-level transient spectroscopy Appl. Phys. Lett. 101, 042113 (2012) Bonding and diffusion of nitrogen in the InSbN alloys fabricated by two-step ion implantation Appl. Phys. Lett. 101, 021905 (2012) Shift of Ag diffusion profiles in CdTe by metal/semiconductor interfaces Appl. Phys. Lett. 100, 171915 (2012) Diffusion of co-implanted carbon and boron in silicon and its effect on excess self-interstitials Implanted B and P dopants in Si exhibit transient enhanced diffusion ͑TED͒ during annealing which arises from the excess interstitials generated by the implant. In order to study the mechanisms of TED, transmission electron microscopy measurements of implantation damage were combined with B diffusion experiments using doping marker structures grown by molecular-beam epitaxy ͑MBE͒. Damage from nonamorphizing Si implants at doses ranging from 5ϫ10 12 to 1ϫ10 14 /cm 2 evolves into a distribution of ͕311͖ interstitial agglomerates during the initial annealing stages at 670-815°C. The excess interstitial concentration contained in these defects roughly equals the implanted ion dose, an observation that is corroborated by atomistic Monte Carlo simulations of implantation and annealing processes. The injection of interstitials from the damage region involves the dissolution of ͕311͖ defects during Ostwald ripening with an activation energy of 3.8Ϯ0.2 eV. The excess interstitials drive substitutional B into electrically inactive, metastable clusters of presumably two or three B atoms at concentrations below the solid solubility, thus explaining the generally observed immobile B peak during TED of ion-implanted B. Injected interstitials undergo retarded diffusion in the MBE-grown Si with an effective migration energy of ϳ3.5 eV, which arises from trapping at substitutional C. The concept of trap-limited diffusion provides a stepping stone for understanding the enormous disparity among published values for the interstitial diffusivity in Si. The population of excess interstitials is strongly reduced by incorporating substitutional C in Si to levels of ϳ10 19 /cm 3 prior to ion implantation. This provides a promising method for suppressing TED, thus enabling shallow junction formation in future Si devices through dopant implantation. The present insights have been implemented into a process simulator, allowing for a significant improvement of the predictive modeling of TED.

We have investigated the fundamental mechanism underlying the hydrogen-induced exfoliation of silicon, using a combination of spectroscopic and microscopic techniques. We have studied the evolution of the internal defect structure as a function of implanted hydrogen concentration and annealing temperature and found that the mechanism consists of a number of essential components in which hydrogen plays a key role. Specifically, we show that the chemical action of hydrogen leads to the formation of (100) and (111) internal surfaces above 400 °C via agglomeration of the initial defect structure. In addition, molecular hydrogen is evolved between 200 and 400 °C and subsequently traps in the microvoids bounded by the internal surfaces, resulting in the build-up of internal pressure. This, in turn, leads to the observed “blistering” of unconstrained silicon samples, or complete layer transfer for silicon wafers joined to a supporting (handle) wafer which acts as a mechanical “stiffener.”

A membrane consisting of multiwall carbon nanotubes embedded in a silicon nitride matrix was fabricated for fluid mechanics studies on the nanometer scale. Characterization by tracer diffusion and scanning electron microscopy suggests that the membrane is free of large voids. An upper limit to the diffusive flux of D 2 O of 2.4x10 -8 mole/m 2 -s was determined, indicating extremely slow transport. By contrast, hydrodynamic calculations of water flow across a nanotube membrane of similar specifications predict a much higher molar flux of 1.91 mole/m 2 -s, suggesting that the nanotubes produced possess a "bamboo" morphology. The carbon nanotube membranes were used to make nanoporous silicon nitride membranes, fabricated by sacrificial removal of the carbon. Nitrogen flow measurements on these structures give a membrane permeance of 4.7x10 -4 mole/m 2 -s-Pa at a pore density of 4x10 10 cm -2 .Using a Knudsen diffusion model, the average pore size of this membrane is estimated to be 66 nm, which agrees well with TEM observations of the multiwall carbon nanotube outer diameter. These membranes are a robust platform for the study of confined molecular transport, with applications in separations and chemical sensing.

A comprehensive model for B implantation, diffusion and clustering is presented. The model, implemented in a Monte Carlo atomistic simulator, successfully explains and predicts the behavior of B under a wide variety of implantation and annealing conditions by invoking the formation of immobile precursors of B clusters, prior to the onset of transient enhanced diffusion. The model also includes the usual mechanisms of Si self-interstitial diffusion and B kick-out. The immobile B cluster precursors, such as BI2 (a B atom with two Si self-interstitials) form during implantation or in the very early stages of the annealing, when the Si interstitial supersaturation is very high. They then act as nucleation centers for the formation of B-rich clusters during annealing. The B-rich clusters constitute the electrically inactive B component, so that the clustering process greatly affects both junction depth and doping level in high-dose implants.