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

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

Reasoning about Card Tears and Transactions in Java Card

Contains fulltext : 60616.pdf (author's version ) (Open Access

From Finite State Machines To Provably Correct Java Card Applets

Contains fulltext : 112456.pdf (preprint version ) (Open Access)5 p

Implementing a formally verifiable security protocol in Java Card

Contains fulltext : 60536.pdf (preprint version ) (Open Access

Reasoning about Card Tears and Transactions in Java Card

The Java dialect Java Card for programming smartcards contains some features which do not exist in Java. Java Card distinguishes persistent and transient data (data stored in EEPROM and RAM, respectively). Because power to a smartcard can suddenly be interrupted by a so-called card tear, by someone removing the smartcard from the reader, Java Card provides a notion of transaction to ensure that updates of multiple fields in persistent memory can be performed atomically. This paper describes a way to reason about these Java Card specific language features

Transactions and non-atomic API calls in Java Card: specification ambiguity and strange implementation behaviours

Item does not contain fulltext22 p

Blackboard Security Assessment

Contains fulltext : 117321.pdf (publisher's version ) (Open Access)31 p