Cosmological Tests with the Joint Lightcurve Analysis

We examine whether a comparison between wCDM and R_h=ct using merged Type Ia SN catalogs produces results consistent with those based on a single homogeneous sample. Using the Betoule et al. (2014) joint lightcurve analysis (JLA) of a combined sample of 613 events from SNLS and SDSS-II, we estimate the parameters of the two models and compare them. We find that the improved statistics can alter the model selection in some cases, but not others. In addition, based on the model fits, we find that there appears to be a lingering systematic offset of ~0.04-0.08 mag between the SNLS and SDSS-II sources, in spite of the cross-calibration in the JLA. Treating wCDM, LCDM and R_h=ct as separate models, we find in an unbiased pairwise statistical comparison that the Bayes Information Criterion (BIC) favors the R_h=ct universe with a likelihood of 82.8% versus 17.2% for wCDM, but the ratio of likelihoods is reversed (16.2% versus 83.8%) when w_de=-1 (i.e., LCDM) and strongly reversed (1.0% versus 99.0%) if in addition k=0 (i.e., flat LCDM). We point out, however, that the value of k is a measure of the net energy (kinetic plus gravitational) in the Universe and is not constrained theoretically, though some models of inflation would drive k to 0 due to an expansion-enforced dilution. Since we here consider only the basic LCDM model, the value of k needs to be measured and, therefore, the pre-assumption of flatness introduces a significant bias into the BIC.Comment: 7 pages, 4 figures, 2 tables. Accepted for publication in EP

The MEKK1 PHD ubiquitinates TAB1 to activate MAPKs in response to cytokines.

Unlike the other MAP3Ks, MEKK1 (encoded by Map3k1) contains a PHD motif. To understand the role of this motif, we have created a knockin mutant of mouse Map3k1 (Map3k1(m) (PHD)) with an inactive PHD motif. Map3k1(m) (PHD) ES cells demonstrate that the MEKK1 PHD controls p38 and JNK activation during TGF-β, EGF and microtubule disruption signalling, but does not affect MAPK responses to hyperosmotic stress. Protein microarray profiling identified the adaptor TAB1 as a PHD substrate, and TGF-β- or EGF-stimulated Map3k1(m) (PHD) ES cells exhibit defective non-canonical ubiquitination of MEKK1 and TAB1. The MEKK1 PHD binds and mediates the transfer of Lys63-linked poly-Ub, using the conjugating enzyme UBE2N, onto TAB1 to regulate TAK1 and MAPK activation by TGF-β and EGF. Both the MEKK1 PHD and TAB1 are critical for ES-cell differentiation and tumourigenesis. Map3k1(m) (PHD) (/+) mice exhibit aberrant cardiac tissue, B-cell development, testis and T-cell signalling

miRNAs Reshape Immunity and Inflammatory Responses in Bacterial Infection

Pathogenic bacteria cause various infections worldwide, especially in immunocompromised and other susceptible individuals, and are also associated with high infant mortality rates in developing countries. MicroRNAs (miRNAs), small non-coding RNAs with evolutionarily conserved sequences, are expressed in various tissues and cells that play key part in various physiological and pathologic processes. Increasing evidence implies roles for miRNAs in bacterial infectious diseases by modulating inflammatory responses, cell penetration, tissue remodeling, and innate and adaptive immunity. This review highlights some recent intriguing findings, ranging from the correlation between aberrant expression of miRNAs with bacterial infection progression to their profound impact on host immune responses. Harnessing of dysregulated miRNAs in bacterial infection may be an approach to improving the diagnosis, prevention and therapy of infectious diseases

Mutual regulation between deubiquitinase CYLD and retroviral oncoprotein Tax

<p>Abstract</p> <p>Background</p> <p>Oncoprotein Tax, encoded by the human T-cell leukemia virus type 1 (HTLV1), persistently induces NF-κB activation, which contributes to HTLV1-mediated T-cell transformation. Recent studies suggest that the signaling function of Tax requires its ubiquitination, although how the Tax ubiquitination is regulated remains unclear.</p> <p>Results</p> <p>We show here that the deubiquitinase CYLD physically interacts with Tax and negatively regulates the ubiquitination of this viral protein. This function of CYLD is associated with inhibition of Tax-mediated activation of IKK although not that of Tak1. Interestingly, CYLD undergoes constitutive phosphorylation in HTLV1-transformed T cells, a mechanism known to inactivate the catalytic activity of CYLD. Consistently, a phospho-mimetic CYLD mutant fails to inhibit Tax ubiquitination.</p> <p>Conclusion</p> <p>These findings suggest that CYLD negatively regulates the signaling function of Tax through inhibition of Tax ubiquitination. Conversely, induction of CYLD phosphorylation may serve as a mechanism by which HTLV1 overrides the inhibitory function of CYLD, leading to the persistent activation of NF-κB.</p

Decision Engineering Analysis of Fraud Information Disclosure after China's Share-Splitting Reform

AbstractThis paper outlines a dynamic game model to analyze the fraud information disclosure by listed companies in China since the share-splitting reform in 2005. By analyzing the conditions of coalition-proof Nash equilibrium between large shareholders and the manager, exogenous variables’ effects on the equilibrium as well as the first-order condition of the maximum utility of the supervisory department, it is concluded that efficient capital markets require a high supervising probability and intensity of penalty to the “insider” and shortened the intervals between supervising conducts as well. Moreover, there exists a unique optimum incentive stock option ratio over which fraud information disclosure becomes more rampant. This results in a higher intensity of penalty to the manager given more stock option incentive and, in contrast, a higher intensity of penalty to large shareholders of a well managed and efficiently capital-structured company once fraud information disclosure is detected. The model's conclusions are consistent with the facts of listed companies in China. Finally, the model makes sharp suggestions for the mechanism design of stock option incentive as well as suggestions for the supervisory department to achieve efficiency of capital markets in China

An Intermediate-field Fast Radio Burst Model and the Quasi-periodic Oscillation

Quasi-periodic oscillation (QPO) signals are discovered in some fast radio bursts (FRBs) such as FRB 20191221A, as well as in the X-ray burst associated with the galactic FRB from SGR 1935+2154. We revisit the intermediate-field FRB model where the radio waves are generated as fast-magnetosonic waves through magnetic reconnection near the light cylinder. The current sheet in the magnetar wind is compressed by a low frequency pulse emitted from the inner magnetosphere to trigger magnetic reconnection. By incorporating the wave dynamics of the magnetosphere, we demonstrate how the FRB frequency, the single pulse width, and luminosity are determined by the period, magnetic field, QPO frequency and quake energetics of the magnetar. We find that this model can naturally and self-consistently interpret the X-ray/radio event from SGR 1935+2154 and the QPO in FRB 20191221A. It can also explain the observed wide energy range of repeating FRBs in a narrow bandwidth.Comment: 10 pages, 1 figure, accepted to RAA, Figure 1 is updated with a clearer description of the mode