P2P soft security: On evolutionary dynamics of P2P incentive mechanism

This paper thoroughly investigates the evolutionary dynamics of soft security mechanism, namely, reciprocity-based incentive mechanism, in P2P systems based on Evolutionary Game Theory (EGT). By soft security mechanism, it means social control mechanisms to overcome peers’ selfish (rational) behaviors, and encourage cooperation in P2P systems. Specifically, there exist three strategies in P2P systems: always cooperative (ALLC), always defect (ALLD) and reciprocator (R). Instead of existing work which take it for granted that, like ALLC users, R users did not bear any information-seeking cost, we assume small reciprocation cost, and study generalized mutation-selection dynamics. Our contributions are threefold: firstly, we prove and illustrate that, in a well-mixed P2P structure, ALLD is the only strict Nash equilibrium; secondly, we infer the specific condition under which evolution dynamics exhibits rock-scissors-paper oscillation in a structured P2P population. That is, the population cycles from ALLD to R to ALLC and back to ALLD; finally, we theoretically illustrate that the intensity of selection plays an important role in the evolutionary dynamics of P2P incentive mechanism. That is, when the intensity of selection is relatively weak and reciprocation cost limits to zero, the time average can be mostly concentrated on reciprocator. In brief, considering the existence of reciprocation cost and the small mutation in P2P incentive mechanisms, unlike existing work, it is impossible to simply achieve the “absolute cooperative” in P2P incentive mechanisms. On the other hand, stochastic evolution in P2P incentive mechanism with finite population and network structure still favor reciprocation.     

A Linear Algorithm for Computing the Homography from Conics in Correspondence

This paper presents a study, based on conic correspondences, on the relationship between two perspective images acquired by an uncalibrated camera. We show that for a pair of corresponding conics, the parameters representing the conics satisfy a linear constraint. To be more specific, the parameters that represent a conic in one image are transformed by a five-dimensional projective transformation to the parameters that represent the corresponding conic in another image. We also show that this transformation is expressed as the symmetric component of the tensor product of the transformation based on point/line correspondences and itself. In addition, we present a linear algorithm for uniquely determining the corresponding point-based transformation from a given conic-based transformation up to a scale factor. Accordingly, conic correspondences enable us to easily handle both points and lines in uncalibrated images of a planar object.     

Microstructure and yield strength of UDIMET 720LI alloyed with Co-16.9 Wt Pct Ti

We proposed a new method for developing Ni-base turbine disc alloy for application at temperatures above 700 °C by mixing a Ni-base superalloy U720LI with a two-phase alloy Co-16.9 wt pct Ti in various contents. The microstructure and phase stability of the alloys were analyzed using an optical microscope, a scanning electron microscope, energy-dispersive spectroscopy, and an X-ray diffractometer. The yield strength was studied by compression tests at temperatures ranging from 25 °C to 1200 °C. The results show that all the alloys had a dendritic structure. Ni₃Ti (η) phase was formed in the interdendritic region in the alloys with the addition of Co-16.9 wt pct Ti, and its volume fraction increased with the increase in the addition of Co-16.9 wt pct Ti. The results of exposure at 750 °C show that the addition of Co-16.9 wt pct Ti to U720LI had a great effect on suppressing the formation of σ phase due to the reduced Cr content in the γ matrix. Compared to U720LI, the alloys with the addition of Co-16.9 wt pct Ti possessed higher yield strength. The solid-solution strengthening of γ and γ′ and higher volume fraction of γ′ were assumed to cause this strength increase.     

On the computational power of insertion-deletion systems

Gene insertion and deletion are basic phenomena found in DNA processing or RNA editing in molecular biology. The genetic mechanism and development based on these evolutionary transformations have been formulated as a formal system with two operations of insertion and deletion, called insertion-deletion systems (Kari and Thierrin, 1996; Kari et al., 1997).We investigate the generative power of insertion-deletion systems (InsDel systems), and show that the family INS ¹ ₁ DEL ¹ ₁ is equal to the family of recursively enumerable languages. This gives a positive answer to an open problem posed in Kari et al. (1997) where it was conjectured contrary. This revised version was published online in June 2006 with corrections to the Cover Date.     

Complete Mining of Frequent Patterns from Graphs: Mining Graph Data

Basket Analysis, which is a standard method for data mining, derives frequent itemsets from database. However, its mining ability is limited to transaction data consisting of items. In reality, there are many applications where data are described in a more structural way, e.g. chemical compounds and Web browsing history. There are a few approaches that can discover characteristic patterns from graph-structured data in the field of machine learning. However, almost all of them are not suitable for such applications that require a complete search for all frequent subgraph patterns in the data. In this paper, we propose a novel principle and its algorithm that derive the characteristic patterns which frequently appear in graph-structured data. Our algorithm can derive all frequent induced subgraphs from both directed and undirected graph structured data having loops (including self-loops) with labeled or unlabeled nodes and links. Its performance is evaluated through the applications to Web browsing pattern analysis and chemical carcinogenesis analysis.     

Dimethyl Fumarate Induces Apoptosis via Inhibition of NF-κB and Enhances the Effect of Paclitaxel and Adriamycin in Human TNBC Cells

Triple-negative breast cancer (TNBC) has the poorest prognosis of all breast cancer subtypes. Recently, the activation of NF-κB, which is involved in the growth and survival of malignant tumors, has been demonstrated in TNBC, suggesting that NF-κB may serve as a new therapeutic target. In the present study, we examined whether dimethyl fumarate (DMF), an NF-κB inhibitor, induces apoptosis in TNBC cells and enhances the apoptosis-inducing effect of paclitaxel and adriamycin. Cell survival was analyzed by the trypan blue assay and apoptosis assay. Protein detection was examined by immunoblotting. The activation of NF-κB p65 was correlated with poor prognosis in patients with TNBC. DMF induced apoptosis in MDA-MB-231 and BT-549 cells at concentrations that were non-cytotoxic to the normal mammary cell line MCF-10A. Furthermore, DMF inhibited NF-κB nuclear translocation and Survivin, XIAP, Bcl-xL, and Bcl-2 expression in MDA-MB-231 and BT-549 cells. Moreover, DMF enhanced the apoptosis-inducing effect of paclitaxel and adriamycin in MDA-MB-231 cells. These findings suggest that DMF may be an effective therapeutic agent for the treatment of TNBC, in which NF-κB is constitutively active. DMF may also be useful as an adjuvant therapy to conventional anticancer drugs.     

Functional and Structural Insights into Human PPARα/δ/γ Subtype Selectivity of Bezafibrate,Fenofibric Acid,and Pemafibrate

Among the agonists against three peroxisome proliferator-activated receptor (PPAR) subtypes, those against PPARα (fibrates) and PPARγ (glitazones) are currently used to treat dyslipidemia and type 2 diabetes, respectively, whereas PPARδ agonists are expected to be the next-generation metabolic disease drug. In addition, some dual/pan PPAR agonists are currently being investigated via clinical trials as one of the first curative drugs against nonalcoholic fatty liver disease (NAFLD). Because PPARα/δ/γ share considerable amino acid identity and three-dimensional structures, especially in ligand-binding domains (LBDs), clinically approved fibrates, such as bezafibrate, fenofibric acid, and pemafibrate, could also act on PPARδ/γ when used as anti-NAFLD drugs. Therefore, this study examined their PPARα/δ/γ selectivity using three independent assays—a dual luciferase-based GAL4 transactivation assay for COS-7 cells, time-resolved fluorescence resonance energy transfer-based coactivator recruitment assay, and circular dichroism spectroscopy-based thermostability assay. Although the efficacy and efficiency highly varied between agonists, assay types, and PPAR subtypes, the three fibrates, except fenofibric acid that did not affect PPARδ-mediated transactivation and coactivator recruitment, activated all PPAR subtypes in those assays. Furthermore, we aimed to obtain cocrystal structures of PPARδ/γ-LBD and the three fibrates via X-ray diffraction and versatile crystallization methods, which we recently used to obtain 34 structures of PPARα-LBD cocrystallized with 17 ligands, including the fibrates. We herein reveal five novel high-resolution structures of PPARδ/γ–bezafibrate, PPARγ–fenofibric acid, and PPARδ/γ–pemafibrate, thereby providing the molecular basis for their application beyond dyslipidemia treatment.     

An Antisense Oligonucleotide against a Splicing Enhancer Sequence within Exon 1 of the MSTN Gene Inhibits Pre-mRNA Maturation to Act as a Novel Myostatin Inhibitor

Antisense oligonucleotides (ASOs) are agents that modulate gene function. ASO-mediated out-of-frame exon skipping has been employed to suppress gene function. Myostatin, encoded by the MSTN gene, is a potent negative regulator of skeletal muscle growth. ASOs that induce skipping of out-of-frame exon 2 of the MSTN gene have been studied for their use in increasing muscle mass. However, no ASOs are currently available for clinical use. We hypothesized that ASOs against the splicing enhancer sequence within exon 1 of the MSTN gene would inhibit maturation of pre-mRNA, thereby suppressing gene function. To explore this hypothesis, ASOs against sequences of exon 1 of the MSTN gene were screened for their ability to reduce mature MSTN mRNA levels. One screened ASO, named KMM001, decreased MSTN mRNA levels in a dose-dependent manner and reciprocally increased MSTN pre-mRNA levels. Accordingly, KMM001 decreased myostatin protein levels. KMM001 inhibited SMAD-mediated myostatin signaling in rhabdomyosarcoma cells. Remarkably, it did not decrease GDF11 mRNA levels, indicating myostatin-specific inhibition. As expected, KMM001 enhanced the proliferation of human myoblasts. We conclude that KMM001 is a novel myostatin inhibitor that inhibits pre-mRNA maturation. KMM001 has great promise for clinical applications and should be examined for its ability to treat various muscle-wasting conditions.     

Correction and evaluation of the effect due to parasitic motion on primary accelerometer calibration

Primary accelerometer calibration is carried out under the assumption that a vibration exciter gives a rectilinear motion to an accelerometer to be calibrated. However practical vibration given by the vibration exciter includes parasitic motion such as transverse, rocking, and bending motion. Such parasitic motion would give two serious effects on primary calibration results, transverse motion effect and vibration distribution effect. Transverse motion effect is caused by an inner product of the vectors of both transverse motion and transverse sensitivity. On the other hand, the vibration distribution effect is caused by relative motion between a sensing point of accelerometer and a spot sensed by the interferometer. As these effects have close interaction between parasitic motion and measuring instruments, it would be very difficult to evaluate them by measuring independently each component.     

A Method for Reducing the Dead‐Time Voltage and Impedance Voltage in a Series Voltage Compensator

Many research groups are developing series voltage compensators. In a series converter, since a transformer is used in series in the power system, the power system current flows into the voltage source inverter through the transformer. The inverter current, which is determined by the transformation ratio, gives rise to an error voltage that consists of a dead‐time voltage and an impedance voltage. The error voltage is generated even when the reference voltage is zero. This paper describes the mechanism by which the error voltage occurs and proposes a method for reducing the error voltage. © 2013 Wiley Periodicals, Inc. Electr Eng Jpn, 186(3): 85–93, 2014; Published online in Wiley Online Library ( wileyonlinelibrary.com ). DOI 10.1002/eej.22333