Explore the vast range of titles available.

Acute liver failure (ALF) is a severe liver disease caused by disruptions in the body’s immune microenvironment. In the early stages of ALF, Kupffer cells (KCs) become depleted and recruit monocytes derived from the bone marrow or abdomen to replace the depleted macrophages entering the liver. These monocytes differentiate into mature macrophages, which are activated in the immune microenvironment of the liver and polarized to perform various functions. Macrophage polarization can occur in two directions: pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages. Controlling the ratio and direction of M1 and M2 in ALF can help reduce liver injury. However, the liver damage caused by pyroptosis should not be underestimated, as it is a caspase-dependent form of cell death. Inhibiting pyroptosis has been shown to effectively reduce liver damage induced by ALF. Furthermore, macrophage polarization and pyroptosis share common binding sites, signaling pathways, and outcomes. In the review, we describe the role of macrophage polarization and pyroptosis in the pathogenesis of ALF. Additionally, we preliminarily explore the relationship between macrophage polarization and pyroptosis, as well as their effects on ALF.

A bstract We study aspects of the vertex operator algebra (VOA) corresponding to Argyres-Douglas (AD) theories engineered using the 6d N = 2 , 0 theory of type J on a punctured sphere. We denote the AD theories as ( J b [ k ], Y ), where J b [ k ] and Y represent an irregular and a regular singularity respectively. We restrict to the ‘minimal’ case where J b [ k ] has no associated mass parameters, and the theory does not admit any exactly marginal deformations. The VOA corresponding to the AD theory is conjectured to be the W-algebra W k 2 d J , Y , where k 2 d = − h + b b + k with h being the dual Coxeter number of J . We verify this conjecture by showing that the Schur index of the AD theory is identical to the vacuum character of the corresponding VOA, and the Hall-Littlewood index computes the Hilbert series of the Higgs branch. We also find that the Schur and Hall-Littlewood index for the AD theory can be written in a simple closed form for b = h . We also test the conjecture that the associated variety of such VOA is identical to the Higgs branch. The M5-brane construction of these theories and the corresponding TQFT structure of the index play a crucial role in our computations.

HighlightsThis review delves into the recent progress in high-performance and multifunctional neuromorphic devices for artificial intelligence applications from a novel perspective of plasticity modulation.It provides an in-depth discussion on the plasticity modulation strategies by chemical techniques, device structure design and physical signal modulation for advanced neuromorphic applications.It offers the prospects of exploring novel plasticity modulation mechanisms and techniques for scaled neural networks and examining their potentials in multimodal collaborative neuromorphic systems.Manipulating the expression of synaptic plasticity of neuromorphic devices provides fascinating opportunities to develop hardware platforms for artificial intelligence. However, great efforts have been devoted to exploring biomimetic mechanisms of plasticity simulation in the last few years. Recent progress in various plasticity modulation techniques has pushed the research of synaptic electronics from static plasticity simulation to dynamic plasticity modulation, improving the accuracy of neuromorphic computing and providing strategies for implementing neuromorphic sensing functions. Herein, several fascinating strategies for synaptic plasticity modulation through chemical techniques, device structure design, and physical signal sensing are reviewed. For chemical techniques, the underlying mechanisms for the modification of functional materials were clarified and its effect on the expression of synaptic plasticity was also highlighted. Based on device structure design, the reconfigurable operation of neuromorphic devices was well demonstrated to achieve programmable neuromorphic functions. Besides, integrating the sensory units with neuromorphic processing circuits paved a new way to achieve human-like intelligent perception under the modulation of physical signals such as light, strain, and temperature. Finally, considering that the relevant technology is still in the basic exploration stage, some prospects or development suggestions are put forward to promote the development of neuromorphic devices.

Environmentally adaptive power generation is attractive for the development of next-generation energy sources. Here we develop a heterogeneous moisture-enabled electric generator (HMEG) based on a bilayer of polyelectrolyte films. Through the spontaneous adsorption of water molecules in air and induced diffusion of oppositely charged ions, one single HMEG unit can produce a high voltage of ~0.95 V at low (25%) relative humidity (RH), and even jump to 1.38 V at 85% RH. A sequentially aligned stacking strategy is created for large-scale integration of HMEG units, to offer a voltage of more than 1,000 V under ambient conditions (25% RH, 25 °C). Using origami assembly, a small section of folded HMEGs renders an output of up to 43 V cm −3 . Such integration devices supply sufficient power to illuminate a lamp bulb of 10 W, to drive a dynamic electronic ink screen and to control the gate voltage for a self-powered field effect transistor. A power generator exhibits enhanced output due to a dual-charge-carrier design. The voltage produced is constant yet competitive even under low relative humidity.

Circular RNAs (circRNAs) have been implicated in cancer progression through largely unknown mechanisms. Herein, we identify an N 6 -methyladenosine (m 6 A) modified circRNA, circNSUN2, frequently upregulated in tumor tissues and serum samples from colorectal carcinoma (CRC) patients with liver metastasis (LM) and predicts poorer patient survival. The upregulated expression of circNSUN2 promotes LM in PDX metastasis models in vivo and accelerates cancer cells invasion in vitro. Importantly, N 6 -methyladenosine modification of circNSUN2 increases export to the cytoplasm. By forming a circNSUN2/IGF2BP2/ HMGA2 RNA-protein ternary complex in the cytoplasm, circNSUN2 enhances the stability of HMGA2 mRNA to promote CRC metastasis progression. Clinically, the upregulated expressions of circNSUN2 and HMGA2 are more prevalent in LM tissues than in primary CRC tissues. These findings elucidate that N 6 -methyladenosine modification of circNSUN2 modulates cytoplasmic export and stabilizes HMGA2 to promote CRC LM, and suggest that circNSUN2 could represent a critical prognostic marker and/or therapeutic target for the disease. Liver metastasis of colorectal cancer leads to poor prognosis. Here the authors report that an N 6 -methyladenosine modified circular RNA is upregulated in colorectal cancer and promotes liver metastasis by enhancing the stability of HMGA2 mRNA.

One can derive a large class of new$$ \\mathcal{N} $$N = 1 SCFTs by turning on$$ \\mathcal{N} $$N = 1 preserving deformations for$$ \\mathcal{N} $$N = 2 Argyres-Dougals theories. In this work, we use$$ \\mathcal{N} $$N = 2 superconformal indices to get indices of$$ \\mathcal{N} $$N = 1 SCFTs, then use these indices to derive chiral rings of$$ \\mathcal{N} $$N = 1 SCFTs. For a large class of$$ \\mathcal{N} $$N = 2 theories, we find that the IR theory contains only free chirals if we deform the parent$$ \\mathcal{N} $$N = 2 theory using the Coulomb branch operator with smallest scaling dimension. Our results provide interesting lessons on studies of$$ \\mathcal{N} $$N = 1 theories, such as a -maximization, accidental symmetries, chiral ring, etc.

Background Circular RNAs (circRNAs) regulate various biological activities and have been shown to play crucial roles in hepatocellular carcinoma (HCC) progression. However, only a few coding circRNAs have been identified in cancers, and their roles in HCC remain elusive. This study aimed to identify coding circRNAs and explore their function in HCC. Methods CircMAP3K4 was selected from the CIRCpedia database. We performed a series of experiments to determine the characteristics and coding capacity of circMAP3K4. We then used in vivo and in vitro assays to investigate the biological function and mechanism of circMAP3K4 and its protein product, circMAP3K4-455aa, in HCC. Results We found circMAP3K4 to be an upregulated circRNA with coding potential in HCC. IGF2BP1 recognized the circMAP3K4 N6-methyladenosine modification and promoted its translation into circMAP3K4-455aa. Functionally, circMAP3K4-455aa prevented cisplatin-induced apoptosis in HCC cells by interacting with AIF, thus protecting AIF from cleavage and decreasing its nuclear distribution. Moreover, circMAP3K4-455aa was degraded through the ubiquitin–proteasome E3 ligase MIB1 pathway. Clinically, a high level of circMAP3K4 is an independent prognostic factor for adverse overall survival and adverse disease-free survival of HCC patients. Conclusions CircMAP3K4 is a highly expressed circRNA in HCC. Driven by m6A modification, circMAP3K4 encoded circMAP3K4-455aa, protected HCC cells from cisplatin exposure, and predicted worse prognosis of HCC patients. Targeting circMAP3K4-455aa may provide a new therapeutic strategy for HCC patients, especially for those with chemoresistance. Graphical Abstract CircMAP3K4 is a highly expressed circRNA in HCC. Driven by m6A modification, IGF2BP1 facilitates circMAP3K4 peptide translation, then the circMAP3K4 peptide inhibits AIF cleavage and nuclear distribution, preventing HCC cells from cell death under stress and promoting HCC progression.

A bstract We study S-duality of Argyres-Douglas theories obtained by compactification of 6d (2,0) theories of ADE type on a sphere with irregular punctures. The weakly coupled descriptions are given by the degeneration limit of auxiliary Riemann sphere with marked points, among which three punctured sphere represents isolated superconformal theories. We also discuss twisted irregular punctures and their S-duality.

The Great Wall Villages (GWVs) are linked to the Great Wall in history, culture, and ecology. The cultural landscape resilience of Great Wall Villages (CLRGWVs) is distinctly significant. However, it is influenced by urbanization, pollution, and a lack of awareness of cultural landscape protection. Therefore, conservation and development practices still lack scientific strategies and guidance. This study proposes a new assessment system to quantify CLRGWVs, an analysis of the main influencing factors of resilience, and optimization paths to maintain sustainable development. Based on the socio-ecological system, this research designed the assessment with three criteria, eleven factors, and thirty-three indexes from the perspective of CLRGWVs. Furthermore, a demonstration test was constructed in Ningyuanbao Village, Dushikou Village, and Longmensuo Village in Chicheng County, Hebei Province, China. The results showed that there is some disparity between the three GWVs, with the resilience score of Dushikou Village being the highest in terms of resistance and learning. In contrast, Ningyuanbao Village’s resilience score is the lowest since resistance, recovery, and learning capacity are lower than in Dushikou and Longmensuo. Some influencing factors were found to be highly related to adaptive capacity. Lastly, some low-resilience aspects were identified as critical improvement targets for which corresponding optimization strategies should be proposed. This could be applied to streamline resilience optimization paths according to local conditions. This paper provides new ideas and directions for dealing with the sustainable development of villages and the conservation of cultural landscapes. It will also help villages deal with the relationship between socio-economic development and the conservation of cultural landscapes.

Although 5-methylcytosine (m 5 C) is a widespread modification in RNAs, its regulation and biological role in pathological conditions (such as cancer) remain unknown. Here, we provide the single-nucleotide resolution landscape of messenger RNA m 5 C modifications in human urothelial carcinoma of the bladder (UCB). We identify numerous oncogene RNAs with hypermethylated m 5 C sites causally linked to their upregulation in UCBs and further demonstrate YBX1 as an m 5 C ‘reader’ recognizing m 5 C-modified mRNAs through the indole ring of W65 in its cold-shock domain. YBX1 maintains the stability of its target mRNA by recruiting ELAVL1. Moreover, NSUN2 and YBX1 are demonstrated to drive UCB pathogenesis by targeting the m 5 C methylation site in the HDGF 3′ untranslated region. Clinically, a high coexpression of NUSN2, YBX1 and HDGF predicts the poorest survival. Our findings reveal an unprecedented mechanism of RNA m 5 C-regulated oncogene activation, providing a potential therapeutic strategy for UCB. Chen et al. provide an m 5 C landscape in bladder cancer and show m 5 C enrichment at oncogene mRNAs that promotes tumour progression. They identify YBX1 as the m 5 C ‘reader’ that recruits ELAVL1 to stabilize mRNAs.