Breaking a Chaotic Cryptographic Scheme Based on Composition Maps

Recently, a chaotic cryptographic scheme based on composition maps was proposed. This paper studies the security of the scheme and reports the following findings: 1) the scheme can be broken by a differential attack with $6+\lceil\log_L(MN)\rceil$ chosen-plaintext, where $MN$ is the size of plaintext and $L$ is the number of different elements in plain-text; 2) the scheme is not sensitive to the changes of plaintext; 3) the two composition maps do not work well as a secure and efficient random number source.Comment: 9 pages, 7 figure

Non-relativistic metrics with extremal limits

We present solutions of type IIB supergravity with z=2 Schrodinger asymptotics that admit an extremal limit, i.e. the black hole horizon has a double zero. These solutions are obtained as TsT transformations of the charged planar black hole in AdS_5 \times S^5. Unlike the uncharged solution, the Ramond-Ramond two-form is turned on. We study the thermodynamic properties of these new solutions, and we show that the ratio of shear viscosity to entropy density is 1/4\pi even in the extremal limit. We also consider the TsT-transformed soliton and show that, for a special radius of the compact circle, there is a confinement-deconfinement phase transition at zero temperature between the soliton and black hole phases.Comment: 23 pages, references and clarifications added, typos corrected, restriction in phase transition due to equation 6.5 emphasized; published versio

Probing the Thermal Deoxygenation of Graphene Oxide using High Resolution In Situ X-Ray based Spectroscopies

Despite the recent developments in Graphene Oxide due to its importance as a host precursor of Graphene, the detailed electronic structure and its evolution during the thermal reduction remain largely unknown, hindering its potential applications. We show that a combination of high resolution in situ X-ray photoemission and X-ray absorption spectroscopies offer a powerful approach to monitor the deoxygenation process and comprehensively evaluate the electronic structure of Graphene Oxide thin films at different stages of the thermal reduction process. It is established that the edge plane carboxyl groups are highly unstable, whereas carbonyl groups are more difficult to remove. The results consistently support the formation of phenol groups through reaction of basal plane epoxide groups with adjacent hydroxyl groups at moderate degrees of thermal activation (~400 {\deg}C). The phenol groups are predominant over carbonyl groups and survive even at a temperature of 1000 {\deg}C. For the first time a drastic increase in the density of states (DOS) near the Fermi level at 600 {\deg}C is observed, suggesting a progressive restoration of aromatic structure in the thermally reduced graphene oxideComment: Pagona Papakonstantinou as Corresponding author, E-mail: [email protected]

Stimulus responsive graphene scaffolds for tissue engineering

Tissue engineering (TE) is an emerging area that aims to repair damaged tissues and organs by combining different scaffold materials with living cells. Recently, scientists started to engineer a new generation of nanocomposite scaffolds able to mimic biochemical and biophysical mechanisms to modulate the cellular responses promoting the restoration of tissue structure or function. Due to its unique electrical, topographical and chemical properties, graphene is a material that holds a great potential for TE, being already considered as one of the best candidates for accelerating and guiding stem cell differentiations. Although this is a promising field there are still some challenges to overcome, such as the efficient control of the differentiation of the stem cells, especially in graphene-based microenvironments. Hence, this chapter will review the existing research related to the ability of graphene and its derivatives (graphene oxide and reduced graphene oxide) to induce stem cell differentiation into diverse lineages when under the influence of electrical, mechanical, optical and topographic stimulations

Clean thermal decomposition of tertiary-alkyl metal thiolates to metal sulfides: Environmentally-benign, non-polar inks for solution-processed chalcopyrite solar cells

We report the preparation of Cu2S, In2S3, CuInS2 and Cu(In,Ga)S2 semiconducting films via the spin coating and annealing of soluble tertiary-alkyl thiolate complexes. The thiolate compounds are readily prepared via the reaction of metal bases and tertiary-alkyl thiols. The thiolate complexes are soluble in common organic solvents and can be solution processed by spin coating to yield thin films. Upon thermal annealing in the range of 200-400 ??C, the tertiary-alkyl thiolates decompose cleanly to yield volatile dialkyl sulfides and metal sulfide films which are free of organic residue. Analysis of the reaction byproducts strongly suggests that the decomposition proceeds via an SN1 mechanism. The composition of the films can be controlled by adjusting the amount of each metal thiolate used in the precursor solution yielding bandgaps in the range of 1.2 to 3.3 eV. The films form functioning p-n junctions when deposited in contact with CdS films prepared by the same method. Functioning solar cells are observed when such p-n junctions are prepared on transparent conducting substrates and finished by depositing electrodes with appropriate work functions. This method enables the fabrication of metal chalcogenide films on a large scale via a simple and chemically clear process.ope

Disordered protein-graphene oxide co-assembly and supramolecular biofabrication of functional fluidic devices

Supramolecular chemistry offers an exciting opportunity to assemble materials with molecular precision. However, there remains an unmet need to turn molecular self-assembly into functional materials and devices. Harnessing the inherent properties of both disordered proteins and graphene oxide (GO), we report a disordered protein-GO co-assembling system that through a diffusion-reaction process and disorder-to-order transitions generates hierarchically organized materials that exhibit high stability and access to non-equilibrium on demand. We use experimental approaches and molecular dynamics simulations to describe the underlying molecular mechanism of formation and establish key rules for its design and regulation. Through rapid prototyping techniques, we demonstrate the system's capacity to be controlled with spatio-temporal precision into well-defined capillary-like fluidic microstructures with a high level of biocompatibility and, importantly, the capacity to withstand flow. Our study presents an innovative approach to transform rational supramolecular design into functional engineering with potential widespread use in microfluidic systems and organ-on-a-chip platforms

The N–Terminal Tail of hERG Contains an Amphipathic α–Helix That Regulates Channel Deactivation

The cytoplasmic N–terminal domain of the human ether–a–go–go related gene (hERG) K+ channel is critical for the slow deactivation kinetics of the channel. However, the mechanism(s) by which the N–terminal domain regulates deactivation remains to be determined. Here we show that the solution NMR structure of the N–terminal 135 residues of hERG contains a previously described Per–Arnt–Sim (PAS) domain (residues 26–135) as well as an amphipathic α–helix (residues 13–23) and an initial unstructured segment (residues 2–9). Deletion of residues 2–25, only the unstructured segment (residues 2–9) or replacement of the α–helix with a flexible linker all result in enhanced rates of deactivation. Thus, both the initial flexible segment and the α–helix are required but neither is sufficient to confer slow deactivation kinetics. Alanine scanning mutagenesis identified R5 and G6 in the initial flexible segment as critical for slow deactivation. Alanine mutants in the helical region had less dramatic phenotypes. We propose that the PAS domain is bound close to the central core of the channel and that the N–terminal α–helix ensures that the flexible tail is correctly orientated for interaction with the activation gating machinery to stabilize the open state of the channel

Graphene Oxide-Gallic Acid Nanodelivery System for Cancer Therapy

Despite the technological advancement in the biomedical science, cancer remains a life-threatening disease. In this study, we designed an anticancer nanodelivery system using graphene oxide (GO) as nanocarrier for an active anticancer agent gallic acid (GA). The successful formation nanocomposite (GOGA) was characterized using XRD, FTIR, HRTEM, Raman, and UV/Vis spectroscopy. The release study shows that the release of GA from the designed anticancer nanocomposite (GOGA) occurs in a sustained manner in phosphate-buffered saline (PBS) solution at pH 7.4. In in vitro biological studies, normal fibroblast (3T3) and liver cancer cells (HepG2) were treated with different concentrations of GO, GOGA, and GA for 72 h. The GOGA nanocomposite showed the inhibitory effect to cancer cell growth without affecting normal cell growth. The results of this research are highly encouraging to go further for in vivo studies

Trafficking Defect and Proteasomal Degradation Contribute to the Phenotype of a Novel KCNH2 Long QT Syndrome Mutation

The Kv11.1 (hERG) K+ channel plays a fundamental role in cardiac repolarization. Missense mutations in KCNH2, the gene encoding Kv11.1, cause long QT syndrome (LQTS) and frequently cause channel trafficking-deficiencies. This study characterized the properties of a novel KCNH2 mutation discovered in a LQT2 patient resuscitated from a ventricular fibrillation arrest. Proband genotyping was performed by SSCP and DNA sequencing. The electrophysiological and biochemical properties of the mutant channel were investigated after expression in HEK293 cells. The proband manifested a QTc of 554 ms prior to electrolyte normalization. Mutation analysis revealed an autosomal dominant frameshift mutation at proline 1086 (P1086fs+32X; 3256InsG). Co-immunoprecipitation demonstrated that wild-type Kv11.1 and mutant channels coassemble. Western blot showed that the mutation did not produce mature complex-glycosylated Kv11.1 channels and coexpression resulted in reduced channel maturation. Electrophysiological recordings revealed mutant channel peak currents to be similar to untransfected cells. Co-expression of channels in a 1∶1 ratio demonstrated dominant negative suppression of peak Kv11.1 currents. Immunocytochemistry confirmed that mutant channels were not present at the plasma membrane. Mutant channel trafficking rescue was attempted by incubation at reduced temperature or with the pharmacological agents E-4031. These treatments did not significantly increase peak mutant currents or induce the formation of mature complex-glycosylated channels. The proteasomal inhibitor lactacystin increased the protein levels of the mutant channels demonstrating proteasomal degradation, but failed to induce mutant Kv11.1 protein trafficking. Our study demonstrates a novel dominant-negative Kv11.1 mutation, which results in degraded non-functional channels leading to a LQT2 phenotype

Trafficking Defect and Proteasomal Degradation Contribute to the Phenotype of a Novel KCNH2 Long QT Syndrome Mutation

The Kv11.1 (hERG) K+ channel plays a fundamental role in cardiac repolarization. Missense mutations in KCNH2, the gene encoding Kv11.1, cause long QT syndrome (LQTS) and frequently cause channel trafficking-deficiencies. This study characterized the properties of a novel KCNH2 mutation discovered in a LQT2 patient resuscitated from a ventricular fibrillation arrest. Proband genotyping was performed by SSCP and DNA sequencing. The electrophysiological and biochemical properties of the mutant channel were investigated after expression in HEK293 cells. The proband manifested a QTc of 554 ms prior to electrolyte normalization. Mutation analysis revealed an autosomal dominant frameshift mutation at proline 1086 (P1086fs+32X; 3256InsG). Co-immunoprecipitation demonstrated that wild-type Kv11.1 and mutant channels coassemble. Western blot showed that the mutation did not produce mature complex-glycosylated Kv11.1 channels and coexpression resulted in reduced channel maturation. Electrophysiological recordings revealed mutant channel peak currents to be similar to untransfected cells. Co-expression of channels in a 1∶1 ratio demonstrated dominant negative suppression of peak Kv11.1 currents. Immunocytochemistry confirmed that mutant channels were not present at the plasma membrane. Mutant channel trafficking rescue was attempted by incubation at reduced temperature or with the pharmacological agents E-4031. These treatments did not significantly increase peak mutant currents or induce the formation of mature complex-glycosylated channels. The proteasomal inhibitor lactacystin increased the protein levels of the mutant channels demonstrating proteasomal degradation, but failed to induce mutant Kv11.1 protein trafficking. Our study demonstrates a novel dominant-negative Kv11.1 mutation, which results in degraded non-functional channels leading to a LQT2 phenotype