16 research outputs found
Influence of a thin amorphous surface layer on de-channeling during aluminum implantation at different temperatures into 4H-SiC
Ion implantation is an important technique in semiconductor processing and has become a key technology for 4H-SiC devices. Today, aluminum (Al) implantations are routinely used for p-type contacts, p+-emitters, terminations and many other applications. However, in all crystalline materials, quite a few ions find a path along a crystal channel, so-called channeling, and these ions travel deep into the crystal. This paper reports on the channeling phenomenon during Al implantation into 4H-SiC, and in particular, the influence of a thin native oxide will be discussed in detail. The effects of thermal lattice vibrations for implantations performed at elevated temperatures will also be elucidated. 100 keV Al ions have been implanted along the [000-1] direction employing samples with 4° miscut. Before implantation, the samples have been aligned using the blocking pattern of backscattered protons. Secondary ion mass spectrometry has been used to record the Al depth distribution. To predict implantation profiles and improve understanding of the role of crystal structure, simulations were performed using the Monte-Carlo binary collision approximation code SIIMPL. Our results show that a thin surface layer of native oxide, less than 1 nm, has a decisive role for de-channeling of aligned implantations. Further, as expected, for implantations at elevated temperatures, a larger degree of de-channeling from major axes is present due to increased thermal vibrations and the penetration depth of channeled aluminum ions is reduced. The values for the mean-square atomic displacements at elevated temperatures have been extracted from experimental depth profiles in combination with simulations
Ion-implantation-induced extended defect formation in (0001) and (11(2)over-bar0) 4H-SiC
Generation of Defects in Heavily Al-Doped 4H-SiC Epitaxial Layers Grown by the Low-Temperature Halo-Carbon Method
Cross-sectional investigation of radiation damage of 2 MeV proton-irradiated silicon carbide
Compound Semiconductor Heterostructures by Smart Cut™: SiC On Insulator, QUASIC™ Substrates, InP and GaAs Heterostructures on Silicon
Effects of glutamine and hyperoxia on pulmonary oxygen uptake and muscle deoxygenation kinetics.
The aim of the present study was to determine whether glutamine ingestion, which has been shown to enhance the exercise-induced increase in the tricarboxylic acid intermediate (TCAi) pool size, resulted in augmentation of the rate of increase in oxidative metabolism at the onset of exercise. In addition, the potential interaction with oxygen availability was investigated by completing exercise in both normoxic and hyperoxic conditions. Eight male cyclists cycled for 6 min at 70% VO2max following consumption of a drink (5 ml kg body mass(-1)) containing a placebo or 0.125 g kg body mass(-1) of glutamine in normoxic (CON and GLN respectively) and hyperoxic (HYP and HPG respectively) conditions. Breath-by-breath pulmonary oxygen uptake and continuous, non-invasive muscle deoxygenation (via near infrared spectroscopy: NIRS) data were collected throughout exercise. The time constant of the phase II component of pulmonary oxygen uptake kinetics was unchanged between trials (CON: 21.5 +/- 3.0 vs. GLN: 18.2 +/- 1.3 vs. HYP: 18.9 +/- 2.0 vs. HPG: 18.6 +/- 1.2 s). There was also no alteration of the kinetics of relative muscle deoxygenation as measured via NIRS (CON: 5.9 +/- 0.7 vs. GLN: 7.3 +/- 0.8 vs. HYP: 6.5 +/- 0.9 vs. HPG: 5.2 +/- 0.4 s). Conversely, the mean response time of pulmonary oxygen uptake kinetics was faster (CON: 33.4 +/- 1.2 vs. GLN: 29.8 +/- 2.3 vs. HYP: 33.2 +/- 2.6 vs. HPG: 31.6 +/- 2.6 s) and the time at which muscle deoxygenation increased above pre-exercise values was earlier (CON: 9.6 +/- 0.9 vs. GLN: 8.7 +/- 1.1 vs. HYP: 8.5 +/- 0.8 vs. HPG: 8.4 +/- 0.7 s) following glutamine ingestion. In normoxic conditions, plasma lactate concentration was lower following glutamine ingestion compared to placebo. Whilst the results of the present study provide some support for the present hypothesis, the lack of any alteration in the time constant of pulmonary oxygen uptake and muscle deoxygenation kinetics suggest that the normal exercise induced expansion of the TCAi pool size is not limiting to oxidative metabolism at the onset of cycle exercise at 70% VO2max