Actuación en zonas antiguas de pueblos y ciudades

Actuación en zonas antiguas de pueblos y ciudade

On lattice profile of the elliptic curve linear congruential generators

Lattice tests are quality measures for assessing the intrinsic structure of pseudorandom number generators. Recently a new lattice test has been introduced by Niederreiter and Winterhof. In this paper, we present a general inequality that is satisfied by any periodic sequence. Then, we analyze the behavior of the linear congruential generators on elliptic curves (EC-LCG) under this new lattice test and prove that the EC-LCG passes it up to very high dimensions. We also use a result of Brandstätter and Winterhof on the linear complexity profile related to the correlation measure of order k to present lower bounds on the linear complexity profile of some binary sequences derived from the EC-LCG

Incidence of childhood leukaemia in the vicinity of nuclear sites in France, 1990–1998

Overall, 670 cases (O) of childhood leukaemia were diagnosed within 20 km of the 29 French nuclear installations between 1990 and 1998 compared to an expected number (E) of 729.09 cases (O/E=0.92, 95% confidence interval (CI)=[0.85-0.99]). Each of the four areas defined around the sites showed non significant deficits of cases (0-5 km: O=65, O/E=0.87, CI=[0.67-1.10]; 5-10 km: O=165, O/E=0.95, CI=[0.81-1.10]; 10-15 km: O=220, O/E=0.88, CI=[0.77-1.00]; 15-20 km: O=220, O/E=0.96, CI=[0.84-1.10]). There was no evidence of a trend in standardised incidence ratio with distance from the sites for all children or for any of the three age groups studied. Similar results were obtained when the start-up year of the electricity-generating nuclear sites and their electric nuclear power were taken into account. No evidence was found of a generally increased risk of childhood leukaemia around the 29 French nuclear sites under study during 1990-1998

B-RAF Mutant Alleles Associated with Langerhans Cell Histiocytosis, a Granulomatous Pediatric Disease

Langerhans cell histiocytosis (LCH) features inflammatory granuloma characterised by the presence of CD1a+ dendritic cells or 'LCH cells'. Badalian-Very et al. recently reported the presence of a canonical (V600E)B-RAF mutation in 57% of paraffin-embedded biopsies from LCH granuloma. Here we confirm their findings and report the identification of two novel B-RAF mutations detected in LCH patients.Mutations of B-RAF were observed in granuloma samples from 11 out of 16 patients using 'next generation' pyrosequencing. In 9 cases the mutation identified was (V600E)B-RAF. In 2 cases novel polymorphisms were identified. A somatic (600DLAT)B-RAF insertion mimicked the structural and functional consequences of the (V600E)B-RAF mutant. It destabilized the inactive conformation of the B-RAF kinase and resulted in increased ERK activation in 293 T cells. The (600DLAT)B-RAF and (V600E)B-RAF mutations were found enriched in DNA and mRNA from the CD1a+ fraction of granuloma. They were absent from the blood and monocytes of 58 LCH patients, with a lower threshold of sequencing sensitivity of 1%-2% relative mutation abundance. A novel germ line (T599A)B-RAF mutant allele was detected in one patient, at a relative mutation abundance close to 50% in the LCH granuloma, blood monocytes and lymphocytes. However, (T599A)B-RAF did not destabilize the inactive conformation of the B-RAF kinase, and did not induce increased ERK phosphorylation or C-RAF transactivation.Our data confirmed presence of the (V600E)B-RAF mutation in LCH granuloma of some patients, and identify two novel B-RAF mutations. They indicate that (V600E)B-RAF and (600DLAT)B-RAF mutations are somatic mutants enriched in LCH CD1a(+) cells and absent from the patient blood. Further studies are needed to assess the functional consequences of the germ-line (T599A)B-RAF allele

Unifying Leakage Models: From Probing Attacks to Noisy Leakage

A recent trend in cryptography is to formally show the leakage resilience of cryptographic implementations in a given leakage model. One of the most prominent leakage models -- the so-called bounded leakage model -- assumes that the amount of leakage is a-priori bounded. Unfortunately, it has been pointed out that the assumption of bounded leakages is hard to verify in practice. A more realistic assumption is to assume that leakages are sufficiently noisy, following the engineering observation that real-world physical leakages are inherently noisy. While the noisy leakage assumption has first been studied in the seminal work of Chari et al. (CRYPTO 99), the recent work of Prouff and Rivain (Eurocrypt 2013) provides the first analysis of a full masking scheme under a physically motivated noise model. In particular, the authors show that a block-cipher implementation that uses an additive masking scheme is secure against noisy leakages. Unfortunately, the security analysis of Prouff and Rivain has three important shortcomings: (1) it requires leak-free gates, (2) it considers a restricted adversarial model (random message attacks), and (3) the security proof has limited application for cryptographic settings. In this work, we provide an alternative security proof in the same noisy model that overcomes these three challenges. We achieve this goal by a new reduction from noisy leakage to the important theoretical model of probing adversaries (Ishai et al~ -- CRYPTO 2003). Our work can be viewed as a next step of closing the gap between theory and practice in leakage resilient cryptography: while our security proofs heavily rely on concepts of theoretical cryptography, we solve problems in practically motivated leakage models

EAPP: Gatekeeper at the crossroad of apoptosis and p21-mediated cell-cycle arrest

We previously identified and characterized E2F-associated phospho-protein (EAPP), a nuclear phosphoprotein that interacts with the activating members of the E2F transcription factor family. EAPP levels are frequently elevated in transformed human cells. To examine the biological relevance of EAPP, we studied its properties in stressed and unstressed cells. Overexpression of EAPP in U2OS cells increased the fraction of G1 cells and lead to heightened resistance against DNA damage- or E2F1-induced apoptosis in a p21-dependent manner. EAPP itself becomes upregulated in confluent cells and after DNA damage and stimulates the expression of p21 independently of p53. It binds to the p21 promoter and seems to be required for the assembly of the transcription initiation complex. RNAi-mediated knockdown of EAPP expression brought about increased sensitivity towards DNA damage and resulted in apoptosis even in the absence of stress. Our results indicate that the level of EAPP is critical for cellular homeostasis. Too much of it results in G1 arrest and resistance to apoptosis, which, paradoxically, might favor cellular transformation. Too little EAPP seems to retard the expression not only of the p21 gene, but also of a number of other genes and ultimately results in apoptosis