477 research outputs found
Nicolas Standaert, L'«autre» dans la mission. Leçons à partir de la Chine, 2003
No full textSoetens Claude. Nicolas Standaert, L'«autre» dans la mission. Leçons à partir de la Chine, 2003. In: Revue théologique de Louvain, 35ᵉ année, fasc. 3, 2004. pp. 413-416
A Combined Design-Time/Test-Time Study of the Vulnerability of Sub-Threshold Devices to Low Voltage Fault Attacks
No full textThe continuous scaling of VLSI technology and the possibility to run circuits in subthreshold voltage range make it possible to implement standard cryptographic primitives within the very limited circuit and power budget of RFID devices. However, such cryptographic implementations raise concerns regarding their vulnerability to both active and passive side-channel attacks. In particular, when focusing on RFID targeted designs, it is important to evaluate their resistance against low cost physical attacks. A low cost fault injection attack can be mounted, for example, by lowering the supply voltage of the chip with the goal of causing setup time violations. In this paper, we provide an in-depth characterization of a chip implementation of the AES cipher. The chip has been designed using a 65nm low power standard cell library and operates in a subthreshold voltage range. We first show that it is possible to inject faults (through lowering the supply voltage) compliant with the fault models required to perform attacks against the AES cipher. We then investigate the possibility of predicting, at design time, which parts of the chip are more likely to be sensitive to such fault injection attacks and produce the desirable (from the point of view of the attacker) faulty behavior. Identifying such sensitive logic signals allows us to suggest to the designer a tailored countermeasure strategy for thwarting these attacks, with a minimal impact on the circuit’s performance
Association of AMPA receptors with a subset of glutamate receptor-interacting protein in vivo
No full textThe NMDA and AMPA classes of ionotropic glutamate receptors are concentrated at postsynaptic sites in excitatory synapses. NMDA receptors interact via their NR2 subunits with PSD-95/SAP90 family proteins, whereas AMPA receptors bind via their GluR2/3 subunits to glutamate receptor-interacting protein (GRIP), AMPA receptor-binding protein (ABP), and protein interacting with C kinase 1 (PICK1). We report here a novel cDNA (termed ABP-L/GRIP2) that is virtually identical to ABP except for additional GRIP-like sequences at the N-terminal and G-terminal ends. Like GRIP (which we now term GR(PI), AEP-L/GRIP2 contains a seventh PDZ domain at its C terminus. Using antibodies that recognize both these proteins, we examined the subcellular localization of GRIP1 and ABP-L/GRIP2 (collectively termed GRIP) and their biochemical association with AMPA receptors. Immunogold electron microscopy revealed the presence of GRIP at excitatory synapses and also at nonsynaptic membranes and within intracellular compartments. The association of native GRIP and AMPA receptors was confirmed biochemically by coimmunoprecipitation from rat brain extracts. A majority of detergent-extractable GluR2/3 was complexed with GRIP in the brain. However, only approximately half of GRIP was associated with AMPA receptors. Unexpectedly, immunocytochemistry of cultured hippocampal neurons and rat brain at the light microscopic level showed enrichment of GRIP in GABAergic neurons and in GABAergic nerve terminals. Thus GRIP is associated with inhibitory as well as excitatory synapses. Collectively, these findings support a role for GRIP in the synaptic anchoring of AMPA receptors but also suggest that GRIP has additional functions unrelated to the binding of AMPA receptors
Analytical fuel cell modelling and exergy analysis of fuel cells
No full textMechanical Maritime and Materials Engineerin
A Belgian flat income tax: effects on labour supply and income distribution
No full textThe adverse distributional effects of a flat tax are well known and have been documented by empirical research in several countries, including Belgium. Advocates of the flat tax argue, correctly, that these studies do not take into account agents’ behavioural reactions and possible feed back effects. One of the important effects in this context is the potential increase in labour supply and the resulting increase in the taxable base and decrease in unemployment allowances. In this study we calculate the cost recovery based on a micro-simulation model that includes a labour supply model. We find that there is indeed a clearly positive effect on labour supply and hence also on the tax base. By introducing a revenue-neutral flat tax, labour supply increases by approximately 47,000 full-time equivalents. However, the effect is limited because, compared to a static scenario the cost recovery only allows the revenue-neutral flat tax to decrease from 38.5% to 37%. Furthermore, there is little or no impact of these employment effects on the strongly regressive nature of a flat tax reform.
Cholinergic dysregulation produced by selective inactivation of the dystonia-associated protein torsinA
No full textDYT1 dystonia, a common and severe primary dystonia, is caused by a 3-bp deletion in TOR1A which encodes torsinA, a protein found in the endoplasmic reticulum. Several cellular functions are altered by the mutant protein, but at a systems level the link between these and the symptoms of the disease is unclear. The most effective known therapy for DYT1 dystonia is the use of anticholinergic drugs. Previous studies have revealed that in mice, transgenic expression of human mutant torsinA under a non-selective promoter leads to abnormal function of striatal cholinergic neurons. To investigate what pathological role torsinA plays in cholinergic neurons, we created a mouse model in which the Dyt1 gene, the mouse homolog of TOR1A, is selectively deleted in cholinergic neurons (ChKO animals). These animals do not have overt dystonia, but do have subtle motor abnormalities. There is no change in the number or size of striatal cholinergic cells or striatal acetylcholine content, uptake, synthesis, or release in ChKO mice. There are, however, striking functional abnormalities of striatal cholinergic cells, with paradoxical excitation in response to D2 receptor activation and loss of muscarinic M2/M4 receptor inhibitory function. These effects are specific for cholinergic interneurons, as recordings from nigral dopaminergic neurons revealed normal responses. Amphetamine stimulated dopamine release was also unaltered. These results demonstrate a cell-autonomous effect of Dyt1 deletion on striatal cholinergic function. Therapies directed at modifying the function of cholinergic neurons may prove useful in the treatment of the human disorder
Evaluation of AZD1446 as a Therapeutic in DYT1 Dystonia
No full textDYT1 dystonia is an early-onset, hyperkinetic movement disorder caused by a deletion in the gene TOR1A, which encodes the protein torsinA. Several lines of evidence show that in animal models of DTY1 dystonia, there is impaired basal dopamine (DA) release and enhanced acetylcholine tone. Clinically, anticholinergic drugs are the most effective pharmacological treatment for DYT1 dystonia, but the currently used agents are non-selective muscarinic antagonists and associated with side effects. We used a DYT1 ∆GAG knock-in mouse model (DYT1 KI) to investigate whether nicotine and/or a non-desensitizing nicotinic agonist, AZD1446, would increase DA output in DYT1 dystonia. Using in vivo microdialysis, we found that DYT1 KI mice showed significantly increased DA output and greater sensitivity to nicotine compared to wild type (WT) littermate controls. In contrast, neither systemic injection (0.25–0.75 mg/kg) or intrastriatal infusion (30 μM–1 mM) of AZD1446 had a significant effect on DA efflux in WT or DYT1 KI mice. In vitro, we found that AZD1446 had no effect on the membrane properties of striatal spiny projection neurons (SPNs) and did not alter the spontaneous firing of ChI interneurons in either WT or DYT1 KI mice. We did observe that the firing frequency of dopaminergic neurons was significantly increased by AZD1446 (10 μM), an effect blocked by dihydro-beta-erythroidine (DHβE 3 μM), but the effect was similar in WT and DYT1 KI mice. Our results support the view that DYT1 models are associated with abnormal striatal cholinergic transmission, and that the DYT1 KI animals have enhanced sensitivity to nicotine. We found little effect of AZD1446 in this model, suggesting that other approaches to nicotinic modulation should be explored
De rol van emoties en symbolische merkassociaties in het adoptieproces van de elektrische auto
No full textIndustrial DesignIndustrial Design Engineerin
Don't mind the gap: sinology as an art of in-betweenness
No full text© 2015 The Author(s) Philosophy Compass © 2015 John Wiley & Sons Ltd. (New) Sinology is like a Chinese ritual dance: the key is not the movement, but rather the positions (shi), the moments of non-action 'in between', that make rhythm and transformation possible. (New) Sinology itself occupies an in-between position in the landscape of academic disciplines, though it is not the only one to undertake this dance, as various disciplines engage themselves into a similar quest. Its distinctiveness as intellectual inquiry is to point at intervals, interstices, gaps, cracks, pauses, poses, in-between moments or zones in culture and human life. In that sense, Sinology does 'mind' gaps.status: Publishe
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