A Number-Theoretic Error-Correcting Code

In this paper we describe a new error-correcting code (ECC) inspired by the Naccache-Stern cryptosystem. While by far less efficient than Turbo codes, the proposed ECC happens to be more efficient than some established ECCs for certain sets of parameters. The new ECC adds an appendix to the message. The appendix is the modular product of small primes representing the message bits. The receiver recomputes the product and detects transmission errors using modular division and lattice reduction

Regular graphs of large girth and arbitrary degree

For every integer d > 9, we construct infinite families {G_n}_n of d+1-regular graphs which have a large girth > log_d |G_n|, and for d large enough > 1,33 log_d |G_n|. These are Cayley graphs on PGL_2(q) for a special set of d+1 generators whose choice is related to the arithmetic of integral quaternions. These graphs are inspired by the Ramanujan graphs of Lubotzky-Philips-Sarnak and Margulis, with which they coincide when d is prime. When d is not equal to the power of an odd prime, this improves the previous construction of Imrich in 1984 where he obtained infinite families {I_n}_n of d+1-regular graphs, realized as Cayley graphs on SL_2(q), and which are displaying a girth > 0,48 log_d |I_n|. And when d is equal to a power of 2, this improves a construction by Morgenstern in 1994 where certain families {M_n}_n of 2^k+1-regular graphs were shown to have a girth > 2/3 log_d |M_n|.Comment: (15 pages) Accepted at Combinatorica. Title changed following referee's suggestion. Revised version after reviewing proces

Low-Cost Body Biasing Injection (BBI) Attacks on WLCSP Devices

Body Biasing Injection (BBI) uses a voltage applied with a physical probe onto the backside of the integrated circuit die. Compared to other techniques such as electromagnetic fault injection (EMFI) or Laser Fault Injection (LFI), this technique appears less popular in academic literature based on published results. It is hypothesized being due to (1) moderate cost of equipment, and (2) effort required in device preperation. This work demonstrates that BBI (and indeed many other backside attacks) can be trivially performed on Wafer-Level Chip-Scale Packaging (WLCSP), which inherently expose the die backside. A low-cost ($15) design for the BBI tool is introduced, and validated with faults introduced on a STM32F415OG against code flow, RSA, and some initial results on various hardware block attacks are discussed

DIGITAL EARTH OBSERVATION INFRASTRUCTURES AND INITIATIVES: A REVIEW FRAMEWORK BASED ON OPEN PRINCIPLES

Recent years have seen a tremendous increase of digital Earth Observation (EO) infrastructures, which provide web-based environments for accessing and processing data in a highly automated and scalable way. However, the current landscape of EO infrastructures and initiatives is fragmented, with various levels of user on-boarding and uptake success. The current work aims to make sense of this complex landscape by providing two main contributions. First, it offers a classification scheme used to review and analyse more than 150 EO infrastructures and initiatives. Then, adopting a user-centric perspective, the main limitations and obstacles currently faced by users when working with the existing EO platforms are identified. For each of these limitations, we propose a number of good practices that could benefit, from a user point of view, the design and functioning of EO platforms. Some technological enablers, i.e. specific resources (such as software components, standards and data encodings) that emerged from the analysis as holding a great potential for improving the usability of existing EO platforms, are finally listed. The work aims to provide a first scientific insight on how to best design and operate EO platforms to maximise the benefits of their user communities

Template-based Fault Injection Analysis of Block Ciphers

We present the first template-based fault injection analysis of FPGA-based block cipher implementations. While template attacks have been a popular form of side-channel analysis in the cryptographic literature, the use of templates in the context of fault attacks has not yet been explored to the best of our knowledge. Our approach involves two phases. The first phase is a profiling phase where we build templates of the fault behavior of a cryptographic device for different secret key segments under different fault injection intensities. This is followed by a matching phase where we match the observed fault behavior of an identical but black-box device with the pre-built templates to retrieve the secret key. We present a generic treatment of our template-based fault attack approach for SPN block ciphers, and illustrate the same with case studies on a Xilinx Spartan-6 FPGA-based implementation of AES-128

The penicillin receptor in Streptomyces

Kinetics and optical studies of Streptomyces DD-carboxypeptidases-transpeptidases led to the conclusion that the donor, acceptor, and penicillin sites on these enzymes are different but not independent and that penicillin acts as a modifier of the conformation of the protein. In the presence of penicillin, the penicillin-sensitive enzymes would be frozen in a conformation that prevents catalytic activity

Genesis of Neuronal and Glial Progenitors in the Cerebellar Cortex of Peripuberal and Adult Rabbits

Adult neurogenesis in mammals is restricted to some brain regions, in contrast with other vertebrates in which the genesis of new neurons is more widespread in different areas of the nervous system. In the mammalian cerebellum, neurogenesis is thought to be limited to the early postnatal period, coinciding with end of the granule cell genesis and disappearance of the external granule cell layer (EGL). We recently showed that in the rabbit cerebellum the EGL is replaced by a proliferative layer called ‘subpial layer’ (SPL) which persists beyond puberty on the cerebellar surface. Here we investigated what happens in the cerebellar cortex of peripuberal rabbits by using endogenous and exogenously-administered cell proliferation antigens in association with a cohort of typical markers for neurogenesis. We show that cortical cell progenitors extensively continue to be generated herein. Surprisingly, this neurogenic process continues to a lesser extent in the adult, even in the absence of a proliferative SPL. We describe two populations of newly generated cells, involving neuronal cells and multipolar, glia-like cells. The genesis of neuronal precursors is restricted to the molecular layer, giving rise to cells immunoreactive for GABA, and for the transcription factor Pax2, a marker for GABAergic cerebellar interneuronal precursors of neuroepithelial origin that ascend through the white matter during early postnatal development. The multipolar cells are Map5+, contain Olig2 and Sox2 transcription factors, and are detectable in all cerebellar layers. Some dividing Sox2+ cells are Bergmann glia cells. All the cortical newly generated cells are independent from the SPL and from granule cell genesis, the latter ending before puberty. This study reveals that adult cerebellar neurogenesis can exist in some mammals. Since rabbits have a longer lifespan than rodents, the protracted neurogenesis within its cerebellar parenchyma could be a suitable model for studying adult nervous tissue permissiveness in mammals

Models of Traumatic Cerebellar Injury

Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Studies of human TBI demonstrate that the cerebellum is sometimes affected even when the initial mechanical insult is directed to the cerebral cortex. Some of the components of TBI, including ataxia, postural instability, tremor, impairments in balance and fine motor skills, and even cognitive deficits, may be attributed in part to cerebellar damage. Animal models of TBI have begun to explore the vulnerability of the cerebellum. In this paper, we review the clinical presentation, pathogenesis, and putative mechanisms underlying cerebellar damage with an emphasis on experimental models that have been used to further elucidate this poorly understood but important aspect of TBI. Animal models of indirect (supratentorial) trauma to the cerebellum, including fluid percussion, controlled cortical impact, weight drop impact acceleration, and rotational acceleration injuries, are considered. In addition, we describe models that produce direct trauma to the cerebellum as well as those that reproduce specific components of TBI including axotomy, stab injury, in vitro stretch injury, and excitotoxicity. Overall, these models reveal robust characteristics of cerebellar damage including regionally specific Purkinje cell injury or loss, activation of glia in a distinct spatial pattern, and traumatic axonal injury. Further research is needed to better understand the mechanisms underlying the pathogenesis of cerebellar trauma, and the experimental models discussed here offer an important first step toward achieving that objective

Remyelination after chronic spinal cord injury is associated with proliferation of endogenous adult progenitor cells after systemic administration of guanosine

Axonal demyelination is a consistent pathological sequel to chronic brain and spinal cord injuries and disorders that slows or disrupts impulse conduction, causing further functional loss. Since oligodendroglial progenitors are present in the demyelinated areas, failure of remyelination may be due to lack of sufficient proliferation and differentiation of oligodendroglial progenitors. Guanosine stimulates proliferation and differentiation of many types of cells in vitro and exerts neuroprotective effects in the central nervous system (CNS). Five weeks after chronic traumatic spinal cord injury (SCI), when there is no ongoing recovery of function, intraperitoneal administration of guanosine daily for 2 weeks enhanced functional improvement correlated with the increase in myelination in the injured cord. Emphasis was placed on analysis of oligodendrocytes and NG2-positive (NG2+) cells, an endogenous cell population that may be involved in oligodendrocyte replacement. There was an increase in cell proliferation (measured by bromodeoxyuridine staining) that was attributable to an intensification in progenitor cells (NG2+ cells) associated with an increase in mature oligodendrocytes (determined by Rip+ staining). The numbers of astroglia increased at all test times after administration of guanosine whereas microglia only increased in the later stages (14 days). Injected guanosine and its breakdown product guanine accumulated in the spinal cords; there was more guanine than guanosine detected. We conclude that functional improvement and remyelination after systemic administration of guanosine is due to the effect of guanosine/guanine on the proliferation of adult progenitor cells and their maturation into myelin-forming cells. This raises the possibility that administration of guanosine may be useful in the treatment of spinal cord injury or demyelinating diseases such as multiple sclerosis where quiescent oligodendroglial progenitors exist in demyelinated plaques

Deletion of the Chd6 exon 12 affects motor coordination

Members of the CHD protein family play key roles in gene regulation through ATP-dependent chromatin remodeling. This is facilitated by chromodomains that bind histone tails, and by the SWI2/SNF2-like ATPase/helicase domain that remodels chromatin by moving histones. Chd6 is ubiquitously expressed in both mouse and human, with the highest levels of expression in the brain. The Chd6 gene contains 37 exons, of which exons 12-19 encode the highly conserved ATPase domain. To determine the biological role of Chd6, we generated mouse lines with a deletion of exon 12. Chd6 without exon 12 is expressed at normal levels in mice, and Chd6 Exon 12 −/− mice are viable, fertile, and exhibit no obvious morphological or pathological phenotype. Chd6 Exon 12 −/− mice lack coordination as revealed by sensorimotor analysis. Further behavioral testing revealed that the coordination impairment was not due to muscle weakness or bradykinesia. Histological analysis of brain morphology revealed no differences between Chd6 Exon 12 −/− mice and wild-type (WT) controls. The location of CHD6 on human chromosome 20q12 is overlapped by the linkage map regions of several human ataxias, including autosomal recessive infantile cerebellar ataxia (SCAR6), a nonprogressive cerebrospinal ataxia. The genomic location, expression pattern, and ataxic phenotype of Chd6 Exon 12 −/− mice indicate that mutations within CHD6 may be responsible for one of these ataxias