Hard Instances of the Constrained Discrete Logarithm Problem

The discrete logarithm problem (DLP) generalizes to the constrained DLP, where the secret exponent $x$ belongs to a set known to the attacker. The complexity of generic algorithms for solving the constrained DLP depends on the choice of the set. Motivated by cryptographic applications, we study sets with succinct representation for which the constrained DLP is hard. We draw on earlier results due to Erd\"os et al. and Schnorr, develop geometric tools such as generalized Menelaus' theorem for proving lower bounds on the complexity of the constrained DLP, and construct sets with succinct representation with provable non-trivial lower bounds

Quantum resource estimates for computing elliptic curve discrete logarithms

We give precise quantum resource estimates for Shor's algorithm to compute discrete logarithms on elliptic curves over prime fields. The estimates are derived from a simulation of a Toffoli gate network for controlled elliptic curve point addition, implemented within the framework of the quantum computing software tool suite LIQ$Ui|\rangle$. We determine circuit implementations for reversible modular arithmetic, including modular addition, multiplication and inversion, as well as reversible elliptic curve point addition. We conclude that elliptic curve discrete logarithms on an elliptic curve defined over an $n$-bit prime field can be computed on a quantum computer with at most $9n + 2\lceil\log_2(n)\rceil+10$ qubits using a quantum circuit of at most $448 n^3 \log_2(n) + 4090 n^3$ Toffoli gates. We are able to classically simulate the Toffoli networks corresponding to the controlled elliptic curve point addition as the core piece of Shor's algorithm for the NIST standard curves P-192, P-224, P-256, P-384 and P-521. Our approach allows gate-level comparisons to recent resource estimates for Shor's factoring algorithm. The results also support estimates given earlier by Proos and Zalka and indicate that, for current parameters at comparable classical security levels, the number of qubits required to tackle elliptic curves is less than for attacking RSA, suggesting that indeed ECC is an easier target than RSA.Comment: 24 pages, 2 tables, 11 figures. v2: typos fixed and reference added. ASIACRYPT 201

Cell loss in the motor and cingulate cortex correlates with symptomatology in Huntington's disease

Huntington's disease is an autosomal dominant inherited neurodegenerative disease with motor symptoms that are variably co-expressed with mood and cognitive symptoms, and in which variable neuronal degeneration is also observed in the basal ganglia and the cerebral cortex. We have recently shown that the variable symptomatology in Huntington's disease correlates with the variable compartmental pattern of GABAA receptor and cell loss in the striatum. To determine whether the phenotypic variability in Huntington's disease is also related to variable neuronal degeneration in the cerebral cortex, we undertook a double-blind study using unbiased stereological cell counting methods to determine the pattern of cell loss in the primary motor and anterior cingulate cortices in the brains of 12 cases of Huntington's disease and 15 controls, and collected detailed data on the clinical symptomatology of the patients with Huntington's disease from family members and clinical records. The results showed a significant association between: (i) pronounced motor dysfunction and cell loss in the primary motor cortex; and (ii) major mood symptomatology and cell loss in the anterior cingulate cortex. This association held for both total neuronal loss (neuronal N staining) and pyramidal cell loss (SMI32 staining), and also correlated with marked dystrophic changes in the remaining cortical neurons. There was also an association between cortical cell loss and striatal neuropathological grade, but no significant association with CAG repeat length in the Huntington's disease gene. These findings suggest that the heterogeneity in clinical symptomatology that characterizes Huntington's disease is associated with variation in the extent of cell loss in the corresponding functional regions of the cerebral cortex whereby motor dysfunction correlates with primary motor cortex cell loss and mood symptomatology is associated with cell loss in the cingulate corte

CROO: A universal infrastructure and protocol to detect identity fraud

Identity fraud (IDF) may be defined as unauthorized exploitation of credential information through the use of false identity. We propose CROO, a universal (i.e. generic) infrastructure and protocol to either prevent IDF (by detecting attempts thereof), or limit its consequences (by identifying cases of previously undetected IDF). CROO is a capture resilient one-time password scheme, whereby each user must carry a personal trusted device used to generate one-time passwords (OTPs) verified by online trusted parties. Multiple trusted parties may be used for increased scalability. OTPs can be used regardless of a transaction’s purpose (e.g. user authentication or financial payment), associated credentials, and online or on-site nature; this makes CROO a universal scheme. OTPs are not sent in cleartext; they are used as keys to compute MACs of hashed transaction information, in a manner allowing OTP-verifying parties to confirm that given user credentials (i.e. OTP-keyed MACs) correspond to claimed hashed transaction details. Hashing transaction details increases user privacy. Each OTP is generated from a PIN-encrypted non-verifiable key; this makes users’ devices resilient to off-line PIN-guessing attacks. CROO’s credentials can be formatted as existing user credentials (e.g. credit cards or driver’s licenses)

Human Gyrovirus Apoptin shows a similar subcellular distribution pattern and apoptosis induction as the chicken anaemia virus derived VP3/Apoptin

The chicken anaemia virus-derived protein Apoptin/VP3 (CAV-Apoptin) has the important ability to induce tumour-selective apoptosis in a variety of human cancer cells. Recently the first human Gyrovirus (HGyV) was isolated from a human skin swab. It shows significant structural and organisational resemblance to CAV and encodes a homologue of CAV-Apoptin/VP3. Using overlapping primers we constructed a synthetic human Gyrovirus Apoptin (HGyV-Apoptin) fused to green fluorescent protein in order to compare its apoptotic function in various human cancer cell lines to CAV-Apoptin. HGyV-Apoptin displayed a similar subcellular expression pattern as observed for CAV-Apoptin, marked by translocation to the nucleus of cancer cells, although it is predominantly located in the cytosol of normal human cells. Furthermore, expression of either HGyV-Apoptin or CAV-Apoptin in several cancer cell lines triggered apoptosis at comparable levels. These findings indicate a potential anti-cancer role for HGyV-Apoptin

Smad4 promotes diabetic nephropathy by modulating glycolysis and OXPHOS

Diabetic nephropathy (DN) is the leading cause of end‐stage kidney disease. TGF‐β1/Smad3 signalling plays a major pathological role in DN; however, the contribution of Smad4 has not been examined. Smad4 depletion in the kidney using anti‐Smad4 locked nucleic acid halted progressive podocyte damage and glomerulosclerosis in mouse type 2 DN, suggesting a pathogenic role of Smad4 in podocytes. Smad4 is upregulated in human and mouse podocytes during DN. Conditional Smad4 deletion in podocytes protects mice from type 2 DN, independent of obesity. Mechanistically, hyperglycaemia induces Smad4 localization to mitochondria in podocytes, resulting in reduced glycolysis and oxidative phosphorylation and increased production of reactive oxygen species. This operates, in part, via direct binding of Smad4 to the glycolytic enzyme PKM2 and reducing the active tetrameric form of PKM2. In addition, Smad4 interacts with ATPIF1, causing a reduction in ATPIF1 degradation. In conclusion, we have discovered a mitochondrial mechanism by which Smad4 causes diabetic podocyte injury

Periaxonal and nodal plasticities modulate action potential conduction in the adult mouse brain

Central nervous system myelination increases action potential conduction velocity. However, it is unclearhow myelination is coordinated to ensure the temporally precise arrival of action potentials and facilitate information processing within cortical and associative circuits. Here, we show that myelin sheaths, supportedby mature oligodendrocytes, remain plastic in the adult mouse brain and undergo subtle structural modifications to influence action potential conduction velocity. Repetitive transcranial magnetic stimulation andspatial learning, two stimuli that modify neuronal activity, alter the length of the nodes of Ranvier and thesize of the periaxonal space within active brain regions. This change in the axon-glial configuration is independent of oligodendrogenesis and robustly alters action potential conduction velocity. Because aptitudein the spatial learning task was found to correlate with action potential conduction velocity in the fimbriafornix pathway, modifying the axon-glial configuration may be a mechanism that facilitates learning in theadult mouse brain

A low-memory algorithm for finding short product representations in finite groups

We describe a space-efficient algorithm for solving a generalization of the subset sum problem in a finite group G, using a Pollard-rho approach. Given an element z and a sequence of elements S, our algorithm attempts to find a subsequence of S whose product in G is equal to z. For a random sequence S of length d log_2 n, where n=#G and d >= 2 is a constant, we find that its expected running time is O(sqrt(n) log n) group operations (we give a rigorous proof for d > 4), and it only needs to store O(1) group elements. We consider applications to class groups of imaginary quadratic fields, and to finding isogenies between elliptic curves over a finite field.Comment: 12 page