Real-Time Pricing Strategy Based on the Stability of Smart Grid for Green Internet of Things

The ever increasing demand of energy efficiency and the strong awareness of environment have led to the enhanced interests in green Internet of things (IoTs). How to efficiently deliver power, especially, with the smart grid based on the stability of network becomes a challenge for green IoTs. Therefore, in this paper we present a novel real-time pricing strategy based on the network stability in the green IoTs enabled smart grid. Firstly, the outage is analyzed by considering the imbalance of power supply and demand as well as the load uncertainty. Secondly, the problem of power supply with multiple-retailers is formulated as a Stackelberg game, where the optimal price can be obtained with the maximal profit for retailers and users. Thirdly, the stability of price is analyzed under the constraints. In addition, simulation results show the efficiency of the proposed strategy

Searching for the scalar meson a0(1817)a_{0}(1817) in kaon induced reactions

In this study, we comprehensively investigate the production of isovector scalar meson $a_{0}(1817)$ using the effective Lagrangian approach. Specifically, we employ the Reggeized $t$-channel Born term to calculate the total and differential cross sections for the reaction $K^{-}p \rightarrow a_{0}(1817)\Lambda$. Our analysis reveals that the optimal energy range for detecting the $a_{0}(1817)$ meson lies between $W=3.4$ MeV and $W=3.6$ MeV, where the predicted total cross section reaches a minimum value of 112 nb. Notably, the $t$ channel, as predicted by the Regge model, significantly enhances the differential cross sections, particularly at extreme forward angles. Furthermore, we investigate the Dalitz processes of $2\rightarrow 3$ and discuss the feasibility of detecting the $a_{0}(1817)$ meson in experiments such as J-PARC.Comment: 6 pages, 6 figure

Advances in the etiology and neuroimaging of children with attention deficit hyperactivity disorder

Attention deficit hyperactivity disorder (ADHD) is the most common neurodevelopmental disorder in children, characterized by age-inappropriate inattention, hyperactivity, and impulsivity, which can cause extensive damage to children's academic, occupational, and social skills. This review will present current advancements in the field of attention deficit hyperactivity disorder, including genetics, environmental factors, epigenetics, and neuroimaging features. Simultaneously, we will discuss the highlights of promising directions for further study

Suppression of experimental arthritis through AMP-activated protein kinase activation and autophagy modulation

Autophagy plays a central role in various disease processes. However, its contribution to inflammatory arthritides such as rheumatoid arthritis (RA) is unclear. We observed that autophagy is engaged in the K/BxN serum transfer model of RA but autophagic flux is severely impaired. Metformin is an anti-diabetic drug that has been shown to stimulate autophagy. Induction of autophagic flux, through metformin-mediated AMP-activated protein kinase (AMPK) activation and interruption of mammalian target of rapamycin (mTOR) signaling mitigated the inflammation in experimental arthritis. Further investigation into the effects of metformin suggest that the drug directly activates AMPK and dose-dependently suppressed the release of TNF-α, IL-6, and MCP-1 by macrophages while enhancing the release of IL-10 in vitro. In vivo, metformin treatment significantly suppressed clinical arthritis and inflammatory cytokine production. Mechanistic studies suggest that metformin exerts its anti-inflammatory effects by correcting the impaired autophagic flux observed in the K/BxN arthritis model and suppressing NF-κB-mediated signaling through selective degradation of IκB kinase (IKK). These findings establish a central role for autophagy in inflammatory arthritis and argue that autophagy modulators such as metformin may represent potential therapeutic agents for the treatment of RA

Understanding the Passivation Mechanisms and Opto-Electronic Spectral Response in Methylammonium Lead Halide Perovskite Single Crystals

Attaining control over the surface traps in halide perovskites is critical for the tunability of ultimate device characteristics. Here, we present a study on the modulation of photophysical properties, surface traps, and recombination in MAPbI(3) single crystals (MSCs) with methylamine (MA) vapor surface treatment. Transient photoluminescence spectroscopy in conjunction with density functional theory calculations reveals that nonradiative recombination related to Pb2+ becomes mitigated after MA vaporing while radiative recombination via bimolecular path tends to increase, which originates from the passivation of Pb ions with the Lewis base nitrogen in MA. In contrast to the broad photoresponse in the pristine MSC photodiodes, application of MA surface treatments leads to a spectral narrowing effect (SNE) in MSCs with the response peak width</p

A chalcone derivative reactivates latent HIV-1 transcription through activating P-TEFb and promoting Tat-SEC interaction on viral promoter.

The principal barrier to the eradication of HIV/AIDS is the existence of latent viral reservoirs. One strategy to overcome this barrier is to use latency-reversing agents (LRAs) to reactivate the latent proviruses, which can then be eliminated by effective anti-retroviral therapy. Although a number of LRAs have been found to reactivate latent HIV, they have not been used clinically due to high toxicity and poor efficacy. In this study, we report the identification of a chalcone analogue called Amt-87 that can significantly reactivate the transcription of latent HIV provirses and act synergistically with known LRAs such as prostratin and JQ1 to reverse latency. Amt-87 works by activating the human transcriptional elongation factor P-TEFb, a CDK9-cyclin T1 heterodimer that is part of the super elongation complex (SEC) used by the viral encoded Tat protein to activate HIV transcription. Amt-87 does so by promoting the phosphorylation of CDK9 at the T-loop, liberating P-TEFb from the inactive 7SK snRNP, and inducing the formation of the Tat-SEC complex at the viral promoter. Together, our data reveal chalcones as a promising category of compounds that should be further explored to identify effective LRAs for targeted reversal of HIV latency