RIES: Internet voting in action

RIES stands for Rijnland Internet Election System. It is an online voting system that was developed by one of the Dutch local authorities on water management. The system has been used twice in the fall of 2004 for in total approximately two million potential voters. In this paper we describe how this system works. Furthermore we do not only describe how the outcome of the elections can be verified but also how it has been verified by us. To conclude the paper we describe some possible points for improvement

Combatting electoral traces: the Dutch tempest discussion and beyond

In the Dutch e-voting debate, the crucial issue leading to the abandonment of all electronic voting machines was compromising radiation, or tempest. Other countries, however, do not seem to be bothered by this risk. In this paper, we use actor-network theory to analyse the socio-technical origins of the Dutch tempest issue in e-voting, and its consequences for e-voting beyond the Netherlands. We introduce the term electoral traces to denote any physical, digital or social evidence of a voter's choices in an election. From this perspective, we provide guidelines for risk analysis as well as an overview of countermeasures

A Polynomial Counterexample to the Markus–Yamabe Conjecture

AbstractWe give a polynomial counterexample to both the Markus–Yamabe conjecture and the discrete Markus–Yamabe problem for all dimensions ⩾3

Formally based semi-automatic implementation of an open security protocol

International audienceThis paper presents an experiment in which an implementation of the client side of the SSH Transport Layer Protocol (SSH-TLP) was semi-automatically derived according to a model-driven development paradigm that leverages formal methods in order to obtain high correctness assurance. The approach used in the experiment starts with the formalization of the protocol at an abstract level. This model is then formally proved to fulfill the desired secrecy and authentication properties by using the ProVerif prover. Finally, a sound Java implementation is semi-automatically derived from the verified model using an enhanced version of the Spi2Java framework. The resulting implementation correctly interoperates with third party servers, and its execution time is comparable with that of other manually developed Java SSH-TLP client implementations. This case study demonstrates that the adopted model-driven approach is viable even for a real security protocol, despite the complexity of the models needed in order to achieve an interoperable implementation

IBMPFD disease-causing mutant VCP/p97 proteins are targets of autophagic-lysosomal degradation

The ubiquitin-proteasome system (UPS) degrades soluble proteins and small aggregates, whereas macroautophagy (autophagy herein) eliminates larger protein aggregates, tangles and even whole organelles in a lysosome-dependent manner. VCP/p97 was implicated in both pathways. VCP/p97 mutations cause a rare multisystem disease called IBMPFD (Inclusion Body Myopathy with Paget's Disease and Frontotemporal Dementia). Here, we studied the role IBMPFD-related mutants of VCP/p97 in autophagy. In contrast with the wild-type VCP/p97 protein or R155C or R191Q mutants, the P137L mutant was aggregate-prone. We showed that, unlike commonly studied R155C or R191Q mutants, the P137L mutant protein stimulated both autophagosome and autolysosome formation. Moreover, P137L mutant protein itself was a substrate of autophagy. Starvation- and mTOR inhibition-induced autophagy led to the degradation of the P137L mutant protein, while preserving the wild-type and functional VCP/p97. Strikingly, similar to the P137L mutant, other IBMPFD-related VCP/p97 mutants, namely R93C and G157R mutants induced autophagosome and autolysosome formation; and G157R mutant formed aggregates that could be cleared by autophagy. Therefore, cellular phenotypes caused by P137L mutant expression were not isolated observations, and some other IBMPFD disease-related VCP/p97 mutations could lead to similar outcomes. Our results indicate that cellular mechanisms leading to IBMPFD disease may be various, and underline the importance of studying different disease-associated mutations in order to better understand human pathologies and tailor mutation-specific treatment strategies

Cubic similarity in dimension five

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