Characterization of in-depth cavity distribution after thermal annealing of helium-implanted silicon and gallium nitride

Single-crystalline silicon wafers covered with sacrificial oxide layer and epitaxially grown gallium nitride layers were implanted with high-fluence helium ions (2-6 × 1016 cm- 2) at energies of 20-30 keV. Thermal annealings at 650-1000 °C, 1 h were performed on the Si samples and rapid thermal annealings at 600-1000 °C, 120 s under N2 were performed on the GaN samples. The as-implanted samples and the near-surface cavity distributions of the annealed samples were investigated with variable angle spectroscopic ellipsometry. In-depth defect profiles and cavity profiles can be best described with multiple independent effective medium sublayers of varying ratio of single-crystal/void. The number of sublayers was chosen to maximize the fit quality without a high parameter cross-correlation. The dependence of the implantation fluence, oxide layer thickness and annealing temperature on the cavity distribution was separately investigated. The ellipsometric fitted distributions were compared and cross-checked with analyses of transmission electron micrographs where the average surface cavity was determined sublayer by sublayer. The in-depth profiles were also compared with simulations of He and vacancy distributions

PAC-Bayesian Bounds for Randomized Empirical Risk Minimizers

The aim of this paper is to generalize the PAC-Bayesian theorems proved by Catoni in the classification setting to more general problems of statistical inference. We show how to control the deviations of the risk of randomized estimators. A particular attention is paid to randomized estimators drawn in a small neighborhood of classical estimators, whose study leads to control the risk of the latter. These results allow to bound the risk of very general estimation procedures, as well as to perform model selection

Low temperature (down to 450° C) annealed TiAl contacts on N-type gallium nitride characterized by differential scanning calorimetry

International audienceThis work reports on Differential Scanning Calorimetry (DSC) measurements performed on Ti-Al metallic layers stacks deposited on n+-GaN. The aim is to get better understanding of the mechanisms leading to ohmic contact formation during the annealing stage. Two exothermic peaks were found, one below 500°C and the other one around 660°C. They can be respectively attributed to Al3Ti and Al2Ti compounds formation. The locations of these peaks provide clear evidence of solid-solid reac-tions. Lowest contact resistance is well correlated with the presence of Al3Ti compound, corresponding to Al(200nm)/Ti(50nm) stoichiometric ratio. Subsequently, Al(200 nm)Ti(50 nm) stacks on n+-GaN were annealed from 400°C to 650°C. Specific Contact Resistivity (SCR) values stay in the mid 10-5 Ω.cm² range for annealing temperatures between 450°C and 650°C. Such low-temperature annealed contacts on n+-GaN may open new device processing routes, simpler and cheaper, in which Ohmic and Schottky contacts are annealed together

Distribution of exogenous 25-hydroxycholesterol in Hep G2 cells between two different pools

AbstractBinding of [26,27-3H]25-hydroxycholesterol (25HC) to human hepatoma Hep G2 cells was saturated within 120 min. Two intracellular pools of 25HC were identified in a pulse-chase experiment: (i) an exchangeable pool which was in dynamic equilibrium with 25HC in the medium (t1/2 of reversible exchange 15 min) and (ii) an unexchangeable pool which remained in cells during incubation in medium containing LPDS. 25HC from the exchangeable pool inhibits cholesterol biosynthesis, decreases the HMG CoA reductase mRNA level and stimulates cholesterol acylation. 25HC from the unexchangeable pool was partially bound to cytosolic proteins and apparently utilized for metabolic transformation. Incubation of Hep G2 cells with [26,27-3H]25HC in the presence of a 30-fold molar excess of 3β-hydroxy-5α-cholest-8(14)-en-15-one was found to cause (i) 2-fold decrease in the binding of [26,27-3H]25HC to cytosolic proteins (sedimentation constant of radioactive complex was 4–5 S) and (ii) the 35% inhibition of 25HC transformation to polar metabolites

Ca2+/Calmodulin-Dependent Protein Kinase Kinase Is Not Involved in Hypothalamic AMP-Activated Protein Kinase Activation by Neuroglucopenia

Hypoglycemia and neuroglucopenia stimulate AMP-activated protein kinase (AMPK) activity in the hypothalamus and this plays an important role in the counterregulatory responses, i.e. increased food intake and secretion of glucagon, corticosterone and catecholamines. Several upstream kinases that activate AMPK have been identified including Ca2+/Calmodulin-dependent protein kinase kinase (CaMKK), which is highly expressed in neurons. However, the involvement of CaMKK in neuroglucopenia-induced activation of AMPK in the hypothalamus has not been tested. To determine whether neuroglucopenia-induced AMPK activation is mediated by CaMKK, we tested whether STO-609 (STO), a CaMKK inhibitor, would block the effects of 2-deoxy-D-glucose (2DG)-induced neuroglucopenia both ex vivo on brain sections and in vivo. Preincubation of rat brain sections with STO blocked KCl-induced α1 and α2-AMPK activation but did not affect AMPK activation by 2DG in the medio-basal hypothalamus. To confirm these findings in vivo, STO was pre-administrated intracerebroventricularly (ICV) in rats 30 min before 2DG ICV injection (40 µmol) to induce neuroglucopenia. 2DG-induced neuroglucopenia lead to a significant increase in glycemia and food intake compared to saline-injected control rats. ICV pre-administration of STO (5, 20 or 50 nmol) did not affect 2DG-induced hyperglycemia and food intake. Importantly, activation of hypothalamic α1 and α2-AMPK by 2DG was not affected by ICV pre-administration of STO. In conclusion, activation of hypothalamic AMPK by 2DG-induced neuroglucopenia is not mediated by CaMKK

Rank-based model selection for multiple ions quantum tomography

The statistical analysis of measurement data has become a key component of many quantum engineering experiments. As standard full state tomography becomes unfeasible for large dimensional quantum systems, one needs to exploit prior information and the "sparsity" properties of the experimental state in order to reduce the dimensionality of the estimation problem. In this paper we propose model selection as a general principle for finding the simplest, or most parsimonious explanation of the data, by fitting different models and choosing the estimator with the best trade-off between likelihood fit and model complexity. We apply two well established model selection methods -- the Akaike information criterion (AIC) and the Bayesian information criterion (BIC) -- to models consising of states of fixed rank and datasets such as are currently produced in multiple ions experiments. We test the performance of AIC and BIC on randomly chosen low rank states of 4 ions, and study the dependence of the selected rank with the number of measurement repetitions for one ion states. We then apply the methods to real data from a 4 ions experiment aimed at creating a Smolin state of rank 4. The two methods indicate that the optimal model for describing the data lies between ranks 6 and 9, and the Pearson $\chi^{2}$ test is applied to validate this conclusion. Additionally we find that the mean square error of the maximum likelihood estimator for pure states is close to that of the optimal over all possible measurements.Comment: 24 pages, 6 figures, 3 table

Chronic exposure to KATP channel openers results in attenuated glucose sensing in hypothalamic GT1-7 neurons

Individuals with Type 1 diabetes (T1D) are often exposed to recurrent episodes of hypoglycaemia. This reduces hormonal and behavioural responses that normally counteract low glucose in order to maintain glucose homeostasis, with altered responsiveness of glucose sensing hypothalamic neurons implicated. Although the molecular mechanisms are unknown, pharmacological studies implicate hypothalamic ATP-sensitive potassium channel (KATP) activity, with KATP openers (KCOs) amplifying, through cell hyperpolarization, the response to hypoglycaemia. Although initial findings, using acute hypothalamic KCO delivery, in rats were promising, chronic exposure to the KCO NN414 worsened the responses to subsequent hypoglycaemic challenge. To investigate this further we used GT1-7 cells to explore how NN414 affected glucose-sensing behaviour, the metabolic response of cells to hypoglycaemia and KATP activity. GT1-7 cells exposed to 3 or 24 h NN414 exhibited an attenuated hyperpolarization to subsequent hypoglycaemic challenge or NN414, which correlated with diminished KATP activity. The reduced sensitivity to hypoglycaemia was apparent 24 h after NN414 removal, even though intrinsic KATP activity recovered. The NN414-modified glucose responsiveness was not associated with adaptations in glucose uptake, metabolism or oxidation. KATP inactivation by NN414 was prevented by the concurrent presence of tolbutamide, which maintains KATP closure. Single channel recordings indicate that NN414 alters KATP intrinsic gating inducing a stable closed or inactivated state. These data indicate that exposure of hypothalamic glucose sensing cells to chronic NN414 drives a sustained conformational change to KATP, probably by binding to SUR1, that results in loss of channel sensitivity to intrinsic metabolic factors such as MgADP and small molecule agonists.We thank Novo Nordisk for providing NN414. This study was funded by grants from Diabetes UK (to MLJA, RJM) and the Juvenile Diabetes Research Foundation (postdoctoral fellowship 3-576-2010 to CB and 1-2008-728 to RJM)

Enhanced Fatty Acid Oxidation and FATP4 Protein Expression after Endurance Exercise Training in Human Skeletal Muscle

FATP1 and FATP4 appear to be important for the cellular uptake and handling of long chain fatty acids (LCFA). These findings were obtained from loss- or gain of function models. However, reports on FATP1 and FATP4 in human skeletal muscle are limited. Aerobic training enhances lipid oxidation; however, it is not known whether this involves up-regulation of FATP1 and FATP4 protein. Therefore, the aim of this project was to investigate FATP1 and FATP4 protein expression in the vastus lateralis muscle from healthy human individuals and to what extent FATP1 and FATP4 protein expression were affected by an increased fuel demand induced by exercise training. Eight young healthy males were recruited to the study. All subjects were non smokers and did not participate in regular physical activity (<1 time per week for the past 6 months, VO2peak 3.4±0.1 l O2 min−1). Subjects underwent an 8 week supervised aerobic training program. Training induced an increase in VO2peak from 3.4±0.1 to 3.9±0.1 l min−1 and citrate synthase activity was increased from 53.7±2.5 to 80.8±3.7 µmol g−1 min−1. The protein content of FATP4 was increased by 33%, whereas FATP1 protein content was reduced by 20%. Interestingly, at the end of the training intervention a significant association (r2 = 0.74) between the observed increase in skeletal muscle FATP4 protein expression and lipid oxidation during a 120 min endurance exercise test was observed. In conclusion, based on the present findings it is suggested that FATP1 and FATP4 proteins perform different functional roles in handling LCFA in skeletal muscle with FATP4 apparently more important as a lipid transport protein directing lipids for lipid oxidation