High reward enhances perceptual learning.

Studies of perceptual learning have revealed a great deal of plasticity in adult humans. In this study, we systematically investigated the effects and mechanisms of several forms (trial-by-trial, block, and session rewards) and levels (no, low, high, subliminal) of monetary reward on the rate, magnitude, and generalizability of perceptual learning. We found that high monetary reward can greatly promote the rate and boost the magnitude of learning and enhance performance in untrained spatial frequencies and eye without changing interocular, interlocation, and interdirection transfer indices. High reward per se made unique contributions to the enhanced learning through improved internal noise reduction. Furthermore, the effects of high reward on perceptual learning occurred in a range of perceptual tasks. The results may have major implications for the understanding of the nature of the learning rule in perceptual learning and for the use of reward to enhance perceptual learning in practical applications

Diammonium aqua­(ethyl­ene­diamine­tetra­acetato)iron(II) trihydrate

In the title compound, (NH4)2[Fe(C10H12N2O8)(H2O)]·3H2O, the FeII center is in a distorted penta­gonal-bipyramidal geometry. Two carboxyl­ate O and two N atoms from the ethyl­enediaminetetra­acetate (EDTA) ion and one O atom from coordinated water comprise the equatorial plane. Two other carboxyl­ate O atoms from the EDTA ion occupy the apical sites. Both ammonium cations and all water mol­ecules function as hydrogen-bond donors, and ten N—H⋯O and nine O—H⋯O hydrogen bonds form a three-dimensional network between the complex anions, cations and the water mol­ecules

Transcriptional up-regulation of relaxin-3 by Nur77 attenuates β-adrenergic agonist-induced apoptosis in cardiomyocytes.

The relaxin family peptides have been shown to exert several beneficial effects on the heart, including anti-apoptosis, anti-fibrosis, and anti-hypertrophy activity. Understanding their regulation might provide new opportunities for therapeutic interventions, but the molecular mechanism(s) coordinating relaxin expression in the heart remain largely obscured. Previous work demonstrated a role for the orphan nuclear receptor Nur77 in regulating cardiomyocyte apoptosis. We therefore investigated Nur77 in the hopes of identifying novel relaxin regulators. Quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) data indicated that ectopic expression of orphan nuclear receptor Nur77 markedly increased the expression of latexin-3 (RLN3), but not relaxin-1 (RLN1), in neonatal rat ventricular cardiomyocytes (NRVMs). Furthermore, we found that the -adrenergic agonist isoproterenol (ISO) markedly stimulated RLN3 expression, and this stimulation was significantly attenuated in Nur77 knockdown cardiomyocytes and Nur77 knockout hearts. We showed that Nur77 significantly increased RLN3 promoter activity via specific binding to the RLN3 promoter, as demonstrated by electrophoretic mobility shift assay (EMSA) and chromatin immuno-precipitation (ChIP) assays. Furthermore, we found that Nur77 overexpression potently inhibited ISO-induced cardiomyocyte apoptosis, whereas this protective effect was significantly attenuated in RLN3 knockdown cardiomyocytes, suggesting that Nur77-induced RLN3 expression is an important mediator for the suppression of cardiomyocyte apoptosis. These findings show that Nur77 regulates RLN3 expression, therefore suppressing apoptosis in the heart, and suggest that activation of Nur77 may represent a useful therapeutic strategy for inhibition of cardiac fibrosis and heart failure. © 2018 You et al

Non-TAL Effectors From Xanthomonas oryzae pv. oryzae Suppress Peptidoglycan-Triggered MAPK Activation in Rice

Xanthomonas oryzae pv. oryzae, the causal pathogen of bacterial blight of rice, depends on its type III secretion system and associated effector proteins to grow and colonize the vascular tissues of rice plants. The type III effectors include a family of closely related transcription activator-like (TAL) effectors and the rest of diverse effectors, so-called non-TAL effectors. Our understanding of non-TAL effectors for pathogenesis in rice blight is still limited. Here we report a feasible method to rapidly detect the activation of mitogen-activated protein kinase pathway in rice mesophyll protoplasts by the X. oryzae pv. oryzae derived peptidoglycan and screen for virulent effectors that can suppress the pathogen-associated molecular pattern triggered immunity (PTI) response. Amongst 17 non-TAL effectors transiently expressed in rice cells, we found that three effectors (XopZ, XopN, and XopV) were able to suppress the peptidoglycan-triggered MAPK activation. The triple mutant of the X. oryzae pv. oryzae strain PXO99A lacking XopZ, XopN, and XopV showed additively reduced virulence. Adding back either of genes restored the virulence of the triple mutant. Our results demonstrate the collective and redundant ability of defense suppression by non-TAL effectors in causing bacterial blight of rice