972 resultados para Matrix Array Symmetric Key Encryption
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We describe a modification to a previously published pseudorandom number generator improving security while maintaining high performance. The proposed generator is based on the powers of a word-packed block upper triangular matrix and it is designed to be fast and easy to implement in software since it mainly involves bitwise operations between machine registers and, in our tests, it presents excellent security and statistical characteristics. The modifications include a new, key-derived s-box based nonlinear output filter and improved seeding and extraction mechanisms. This output filter can also be applied to other generators.
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The alpha-defensin antimicrobial peptide family is defined by a unique tridisulfide array. To test whether this invariant structural feature determines alpha-defensin bactericidal activity, mouse cryptdin-4 (Crp4) tertiary structure was disrupted by pairs of site-directed Ala for Cys substitutions. In a series of Crp4 disulfide variants whose cysteine connectivities were confirmed using NMR spectroscopy and mass spectrometry, mutagenesis did not induce loss of function. To the contrary, the in vitro bactericidal activities of several Crp4 disulfide variants were equivalent to or greater than those of native Crp4. Mouse Paneth cell alpha-defensins require the proteolytic activation of precursors by matrix metalloproteinase-7 (MMP-7), prompting an analysis of the relative sensitivities of native and mutant Crp4 and proCrp4 molecules to degradation by MMP-7. Although native Crp4 and the alpha-defensin moiety of proCrp4 resisted proteolysis completely, all disulfide variants were degraded extensively by MMP-7. Crp4 bactericidal activity was eliminated by MMP-7 cleavage. Thus, rather than determining alpha-defensin bactericidal activity, the Crp4 disulfide arrangement confers essential protection from degradation by this critical activating proteinase.
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The security and reliability of a class of public-key cryptosystems against attacks by unauthorized parties, who had acquired partial knowledge of one or more of the private key components and/or of the message, were discussed. The standard statistical mechanical methods of dealing with diluted spin systems with replica symmetric considerations were analyzed. The dynamical transition which defined decryption success in practical situation was studied. The phase diagrams which showed the dynamical threshold as a function of the partial acquired knowledge of the private key were also presented.
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Data suggest that for TG2 to be secreted, an intact N-terminal FN binding site (for which TG2 has high affinity) is required, however interaction of TG2 with its high affinity binding partners presents both in the intracellular and extracellular space as well as with specific cell surface receptors may also be involved in this process. Using a site-directed mutagenesis approach, the effects of specific mutations of TG2 on its translocation to the cell surface and secretion into the ECM have been investigated. Mutations include those affecting FN binding (FN1), HSPGs binding (HS1, HS2) GTP/GDP binding site (GTP1, 2) as well as N-terminal and C-terminal domains (TG2 deletion mutants N, and C). By performing transglutaminase activity assays, cell surface protein biotinylation and verifying distribution of TG2 mutants in the ECM we demonstrated that one of the potential heparan sulfate binding site mutants (HS2 mutant) is secreted at the cell surface in a much reduced manner and is less deposited into the ECM than the HS1 mutant. The HS2 mutant showed a low affinity for binding to a heparin sepharose column demonstrating this mutation site may be a potential heparan binding site of TG2. Analogous peptides to this site were shown to have some efficiency in the inhibition of the binding of the FN-TG2 complex to cell surface heparan sulfates in a cell adhesion assay indicating the peptide to be representative of the novel heparin binding site within TG2. The GTP binding site mutants GTP1 and GTP2 exhibited low specific activity however, GTP2 showed more secretion to the cell surface in comparison to GTP1. The FN1 binding mutant did not greatly affect TG2 activity nor did it alter TG2 secretion at the cell surface and deposition into the ECM indicating that fibronectin binding at this site on the enzyme is not an important factor. Interestingly an intact N-terminus (?1-15) appeared to be essential for enzyme externalisation. Removal of the first 15 amino acids (N-terminal mutant) abolished TG2 secretion to the cell surface as well as deposition into the ECM. In addition it reduced the enzymes affinity for binding to heparin. In contrast, deletion of the C-terminal TG2 domain (?594-687) increased enzyme secretion to the cell surface. Consistent with the data presented in this thesis we speculate that TG2 must fulfill two requirements to be successfully secreted from cells. The findings indicate that the closed conformation of the enzyme as well as intact N-terminal tail and a novel HS binding site within the TG2 molecule are key elements for the enzyme’s localisation at the cell surface and its deposition into the extracellular matrix. The importance of understanding the interactions between TG2, heparan sulfates and other TG2 binding partners at the cell surface could have an impact on the design of novel strategies for enzyme inhibition which could be important in the control of extracellular TG2 related diseases.
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Tissue transglutaminase (TG2) has been reported as a wound response protein. Once over-expressed by cells under stress such as during wound healing or following tissue damage, TG2 can be secreted and deposited into extracellular matrix, where it forms a heterocomplex (TG-FN) with the abundant matrix protein fibronectin (FN). A further cellular response elicited after tissue damage is that of matrix remodelling leading to the release of the Arg-Gly-Asp (RGD) containing matrix fragments by matrix matelloproteinases (MMPs). These peptides are able to block the interaction between integrin cell surface receptors and ECM proteins, leading to the loss of cell adhesion and ultimately Anoikis. This study provides a mechanism for TG2, as a stress-induced matrix protein, in protecting the cells from the RGD-dependent loss of cell adhesion and rescuing the cells from Anoikis. Mouse fibroblasts were used as a major model for this study, including different types of cell surface receptor knockout mouse embryonic fibroblasts (MEFs) (such as syndecan-4, a5, ß1 or ß3 integrins). In addition specific syndecan-2 targetting siRNAs, ß1 integrin and a4ß1 integrin functional blocking antibodies, and a specific targeting peptide against a5ß1 integrin A5-1 were used to investigate the involvement of these receptors in the RGD-independent cell adhesion on TG-FN. Crucial for TG-FN to compensate the RGD-independent cell adhesion and actin cytoskeleton formation is the direct interaction between the heparan sulfate chains of syndecan-4 and TG2, which elicits the inside-out signalling of a5ß1 integrin and the intracellular activation of syndecan-2 by protein kinase C a (PKCa). By using specific inhibitors, a cell-permeable inhibiting peptide and the detection of the phosphorylation sites for protein kinases and/or the translocation of PKCa via Western blotting, the activation of PKCa, focal adhesion kinase (FAK), ERK1/2 and Rho kinase (ROCK) were confirmed as downstream signalling molecules. Importantly, this study also investigated the influence of TG-FN on matrix turnover and demonstrated that TG-FN can restore the RGD-independent FN deposition process via an a5ß1 integrin and syndecan-4/2 co-signalling pathway linked by PKCa in a transamidating-independent manner. These data provide a novel function for TG2 in wound healing and matrix turnover which is a key event in a number of both physiological and pathological processes.
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We have been investigating the cryptographical properties of in nite families of simple graphs of large girth with the special colouring of vertices during the last 10 years. Such families can be used for the development of cryptographical algorithms (on symmetric or public key modes) and turbocodes in error correction theory. Only few families of simple graphs of large unbounded girth and arbitrarily large degree are known. The paper is devoted to the more general theory of directed graphs of large girth and their cryptographical applications. It contains new explicit algebraic constructions of in finite families of such graphs. We show that they can be used for the implementation of secure and very fast symmetric encryption algorithms. The symbolic computations technique allow us to create a public key mode for the encryption scheme based on algebraic graphs.
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Mathematics Subject Classi¯cation 2010: 26A33, 65D25, 65M06, 65Z05.
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2000 Mathematics Subject Classification: 16R50, 16R10.
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The distribution of the secret key is the weakest link of many data encryption systems. Quantum key distribution (QKD) schemes provide attractive solutions [1], however their implementation remains challenging and their range and bit-rate are limited. Moreover, practical QKD systems, employ real-life components and are, therefore, vulnerable to diverse attack schemes [2]. Ultra-Long fiber lasers (UFLs) have been drawing much attention recently because of their fundamentally different properties compared to conventional lasers as well as their unique applications [3]. Here, we demonstrate a 100Bps, practically secure key distribution, over a 500km link, employing Raman gain UFL. Fig. 1(a) depicts a schematic of the UFL system. Each user has an identical set of two wavelength selective mirrors centered at l0 and l 1. In order to exchange a key-bit, each user independently choose one of these mirrors and introduces it as a laser reflector at their end. If both users choose identical mirrors, a clear signal develops and the bits in these cases are discarded. However if they choose complementary mirrors, (1, 0 or 0, 1 states), the UFL remains below lasing threshold and no signal evolves. In these cases, an eavesdropper can only detect noise and is unable to determine the mirror choice of the users, where the choice of mirrors represent a single key bit (e.g. Alice's choice of mirror is the key-bit). These bits are kept and added to the key. The absence of signal in the secure states faxilitates fast measurements to distinguish between the non-secure and the secure states and to determine the key-bit in the later case, Sequentially reapeating the single bit exchange protocol generate the entire keys of any desirable length. © 2013 IEEE.
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2000 Mathematics Subject Classification: Primary 60J45, 60J50, 35Cxx; Secondary 31Cxx.
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Multiple myeloma is characterized by genomic alterations frequently involving gains and losses of chromosomes. Single nucleotide polymorphism (SNP)-based mapping arrays allow the identification of copy number changes at the sub-megabase level and the identification of loss of heterozygosity (LOH) due to monosomy and uniparental disomy (UPD). We have found that SNP-based mapping array data and fluorescence in situ hybridization (FISH) copy number data correlated well, making the technique robust as a tool to investigate myeloma genomics. The most frequently identified alterations are located at 1p, 1q, 6q, 8p, 13, and 16q. LOH is found in these large regions and also in smaller regions throughout the genome with a median size of 1 Mb. We have identified that UPD is prevalent in myeloma and occurs through a number of mechanisms including mitotic nondisjunction and mitotic recombination. For the first time in myeloma, integration of mapping and expression data has allowed us to reduce the complexity of standard gene expression data and identify candidate genes important in both the transition from normal to monoclonal gammopathy of unknown significance (MGUS) to myeloma and in different subgroups within myeloma. We have documented these genes, providing a focus for further studies to identify and characterize those that are key in the pathogenesis of myeloma.
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In this paper a new type of architecture for secure wireless key establishment is proposed. A retrodirective array (RDA) that is configured to receive and re-transmit at different frequencies is utilized as a relay node. The RDA is able to respond in ‘real-time’, reducing the required number of time slots to two. More importantly, in this architecture equivalent reciprocal wireless channels between legitimate keying nodes can be randomly updated within one channel coherence time period, leading to greatly increased key generation rates (KGRs) in slow fading environment. The secrecy performance of this RDA assisted key generation system is evaluated under several eavesdropping strategies and it is shown that it outperforms previous relay key generation systems.
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Encryption of personal data is widely regarded as a privacy preserving technology which could potentially play a key role for the compliance of innovative IT technology within the European data protection law framework. Therefore, in this paper, we examine the new EU General Data Protection Regulation’s relevant provisions regarding encryption – such as those for anonymisation and pseudonymisation – and assess whether encryption can serve as an anonymisation technique, which can lead to the non-applicability of the GDPR. However, the provisions of the GDPR regarding the material scope of the Regulation still leave space for legal uncertainty when determining whether a data subject is identifiable or not. Therefore, we inter alia assess the Opinion of the Advocate General of the European Court of Justice (ECJ) regarding a preliminary ruling on the interpretation of the dispute concerning whether a dynamic IP address can be considered as personal data, which may put an end to the dispute whether an absolute or a relative approach has to be used for the assessment of the identifiability of data subjects. Furthermore, we outline the issue of whether the anonymisation process itself constitutes a further processing of personal data which needs to have a legal basis in the GDPR. Finally, we give an overview of relevant encryption techniques and examine their impact upon the GDPR’s material scope.
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The human brain stores, integrates, and transmits information recurring to millions of neurons, interconnected by countless synapses. Though neurons communicate through chemical signaling, information is coded and conducted in the form of electrical signals. Neuroelectrophysiology focus on the study of this type of signaling. Both intra and extracellular approaches are used in research, but none holds as much potential in high-throughput screening and drug discovery, as extracellular recordings using multielectrode arrays (MEAs). MEAs measure neuronal activity, both in vitro and in vivo. Their key advantage is the capability to record electrical activity at multiple sites simultaneously. Alzheimer’s disease (AD) is the most common neurodegenerative disease and one of the leading causes of death worldwide. It is characterized by neurofibrillar tangles and aggregates of amyloid-β (Aβ) peptides, which lead to the loss of synapses and ultimately neuronal death. Currently, there is no cure and the drugs available can only delay its progression. In vitro MEA assays enable rapid screening of neuroprotective and neuroharming compounds. Therefore, MEA recordings are of great use in both AD basic and clinical research. The main aim of this thesis was to optimize the formation of SH-SY5Y neuronal networks on MEAs. These can be extremely useful for facilities that do not have access to primary neuronal cultures, but can also save resources and facilitate obtaining faster high-throughput results to those that do. Adhesion-mediating compounds proved to impact cell morphology, viability and exhibition of spontaneous electrical activity. Moreover, SH-SY5Y cells were successfully differentiated and demonstrated acute effects on neuronal function after Aβ addition. This effect on electrical signaling was dependent on Aβ oligomers concentration. The results here presented allow us to conclude that the SH-SY5Y cell line can be successfully differentiated in properly coated MEAs and be used for assessing acute Aβ effects on neuronal signaling.