Chip and Skim: cloning EMV cards with the pre-play attack

EMV, also known as "Chip and PIN", is the leading system for card payments worldwide. It is used throughout Europe and much of Asia, and is starting to be introduced in North America too. Payment cards contain a chip so they can execute an authentication protocol. This protocol requires point-of-sale (POS) terminals or ATMs to generate a nonce, called the unpredictable number, for each transaction to ensure it is fresh. We have discovered that some EMV implementers have merely used counters, timestamps or home-grown algorithms to supply this number. This exposes them to a "pre-play" attack which is indistinguishable from card cloning from the standpoint of the logs available to the card-issuing bank, and can be carried out even if it is impossible to clone a card physically (in the sense of extracting the key material and loading it into another card). Card cloning is the very type of fraud that EMV was supposed to prevent. We describe how we detected the vulnerability, a survey methodology we developed to chart the scope of the weakness, evidence from ATM and terminal experiments in the field, and our implementation of proof-of-concept attacks. We found flaws in widely-used ATMs from the largest manufacturers. We can now explain at least some of the increasing number of frauds in which victims are refused refunds by banks which claim that EMV cards cannot be cloned and that a customer involved in a dispute must therefore be mistaken or complicit. Pre-play attacks may also be carried out by malware in an ATM or POS terminal, or by a man-in-the-middle between the terminal and the acquirer. We explore the design and implementation mistakes that enabled the flaw to evade detection until now: shortcomings of the EMV specification, of the EMV kernel certification process, of implementation testing, formal analysis, or monitoring customer complaints. Finally we discuss countermeasures

Mechanisms of endothelial cell dysfunction in cystic fibrosis

Although cystic fibrosis (CF) patients exhibit signs of endothelial perturbation, the functions of the cystic fibrosis conductance regulator (CFTR) in vascular endothelial cells (EC) are poorly defined. We sought to uncover biological activities of endothelial CFTR, relevant for vascular homeostasis and inflammation. We examined cells from human umbilical cords (HUVEC) and pulmonary artery isolated from non-cystic fibrosis (PAEC) and CF human lungs (CF-PAEC), under static conditions or physiological shear. CFTR activity, clearly detected in HUVEC and PAEC, was markedly reduced in CF-PAEC. CFTR blockade increased endothelial permeability to macromolecules and reduced trans‑endothelial electrical resistance (TEER). Consistent with this, CF-PAEC displayed lower TEER compared to PAEC. Under shear, CFTR blockade reduced VE-cadherin and p120 catenin membrane expression and triggered the formation of paxillin- and vinculin-enriched membrane blebs that evolved in shrinking of the cell body and disruption of cell-cell contacts. These changes were accompanied by enhanced release of microvesicles, which displayed reduced capability to stimulate proliferation in recipient EC. CFTR blockade also suppressed insulin-induced NO generation by EC, likely by inhibiting eNOS and AKT phosphorylation, whereas it enhanced IL-8 release. Remarkably, phosphodiesterase inhibitors in combination with a β2 adrenergic receptor agonist corrected functional and morphological changes triggered by CFTR dysfunction in EC. Our results uncover regulatory functions of CFTR in EC, suggesting a physiological role of CFTR in the maintenance EC homeostasis and its involvement in pathogenetic aspects of CF. Moreover, our findings open avenues for novel pharmacology to control endothelial dysfunction and its consequences in CF

A Comparison between the Metric Dimension and Zero Forcing Number of Trees and Unicyclic Graphs

The \emph{metric dimension} $\dim(G)$ of a graph $G$ is the minimum number of vertices such that every vertex of $G$ is uniquely determined by its vector of distances to the chosen vertices. The \emph{zero forcing number} $Z(G)$ of a graph $G$ is the minimum cardinality of a set $S$ of black vertices (whereas vertices in $V(G)\!\setminus\!S$ are colored white) such that $V(G)$ is turned black after finitely many applications of "the color-change rule": a white vertex is converted black if it is the only white neighbor of a black vertex. We show that $\dim(T) \leq Z(T)$ for a tree $T$, and that $\dim(G) \le Z(G)+1$ if $G$ is a unicyclic graph, along the way, we characterize trees $T$ attaining $\dim(T)=Z(T)$. For a general graph $G$, we introduce the "cycle rank conjecture". We conclude with a proof of $\dim(T)-2 \leq \dim(T+e) \le \dim(T)+1$ for $e \in E(\overline{T})$.Comment: 15 pages, 14 figure

Chemotherapy treatment of multiple myeloma patients increases circulating levels of endothelial microvesicles

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