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The Metaverse is a multi-user virtual world that combines physical reality with digital virtual reality. The three basic technologies for building the Metaverse are immersive technologies, artificial intelligence, and blockchain. Companies are subsequently making significant investments into creating an artificially intelligent Metaverse, with the consequence that cybersecurity has become more crucial. As cybercrime increases exponentially, it is evident that a comprehensive study of Metaverse security based on artificial intelligence is lacking. A growing number of distributed denial-of-service attacks and theft of user identification information makes it necessary to conduct comprehensive and inclusive research in this field in order to identify the Metaverse’s vulnerabilities and weaknesses. This article provides a summary of existing research on AI-based Metaverse cybersecurity and discusses relevant security challenges. Based on the results, the issue of user identification plays a very important role in the presented works, for which biometric methods are the most commonly used. While the use of biometric data is considered the safest method, due to their uniqueness, they are also susceptible to misuse. A cyber-situation management system based on artificial intelligence should be able to analyze data of any volume with the help of algorithms. To prepare researchers who will pursue this topic in the future, this article provides a comprehensive summary of research on cybersecurity in the Metaverse based on artificial intelligence.

Low-density lipoprotein receptor-related protein 6 (LRP6) is a coreceptor of the β-catenin-dependent Wnt signaling pathway. The LRP6 ectodomain binds Wnt proteins, as well as Wnt inhibitors such as sclerostin (SOST), which negatively regulates Wnt signaling in osteocytes. Although LRP6 ectodomain 1 (E1) is known to interact with SOST, several unresolved questions remain, such as the reason why SOST binds to LRP6 E1E2 with higher affinity than to the E1 domain alone. Here, we present the crystal structure of the LRP6 E1E2–SOST complex with two interaction sites in tandem. The unexpected additional binding site was identified between the C-terminus of SOST and the LRP6 E2 domain. This interaction was confirmed by in vitro binding and cell-based signaling assays. Its functional significance was further demonstrated in vivo using Xenopus laevis embryos. Our results provide insights into the inhibitory mechanism of SOST on Wnt signaling. The low-density lipoprotein receptor-related protein 6 (LRP6) is a co-receptor of the β-catenin-dependent Wnt signaling pathway and interacts with the Wnt inhibitor sclerostin (SOST). Here the authors present the crystal structure of SOST in complex with the LRP6 E1E2 ectodomain construct, which reveals that the SOST C-terminus binds to the LRP6 E2 domain, and further validate this binding site with in vitro and in vivo experiments.

Cellular senescence is a state of terminal growth arrest associated with the upregulation of different cell cycle inhibitors, mainly p16 and p21, structural and metabolic alterations, chronic DNA damage responses, and a hypersecretory state known as the senescence-associated secretory phenotype (SASP). The SASP is the major mediator of the paracrine effects of senescent cells in their tissue microenvironment and of various local and systemic biological functions. In this Review, we discuss the composition, dynamics and heterogeneity of the SASP as well as the mechanisms underlying its induction and regulation. We describe the various biological properties of the SASP, its beneficial and detrimental effects in different physiological and pathological settings, and its impact on overall health span. Finally, we discuss the use of the SASP as a biomarker and of SASP inhibitors as senomorphic interventions to treat cancer and other age-related conditions.The senescence-associated secretory phenotype (SASP) mediates the tissue effects of senescent cells. This Review discusses the composition, regulation and various biological implications of the SASP and its uses as a biomarker and a target of senomorphic drugs to treat cancer and other age-related conditions.

Prefrontal brain areas are implicated in the control of fear behavior. However, how prefrontal circuits control fear response to innate threat is poorly understood. Here, we show that the anterior cingulate cortex (ACC) and its input to the basolateral nucleus of amygdala (BLA) contribute to innate fear response to a predator odor in mice. Optogenetic inactivation of the ACC enhances freezing response to fox urine without affecting conditioned freezing. Conversely, ACC stimulation robustly inhibits both innate and conditioned freezing. Circuit tracing and slice patch recordings demonstrate a monosynaptic glutamatergic connectivity of ACC-BLA but no or very sparse ACC input to the central amygdala. Finally, our optogenetic manipulations of the ACC-BLA projection suggest its inhibitory control of innate freezing response to predator odors. Together, our results reveal the role of the ACC and its projection to BLA in innate fear response to olfactory threat stimulus. Brain circuits that control innate fear response are essential for an animal’s survival. Here, the authors report how the anterior cingulate cortex and its projection to amygdala control the innate fear response in mice.

Background Metastasis causes the vast majority of colorectal carcinoma (CRC)-related deaths. However, little is known about the specific traits and underlying mechanisms of metastasis-initiating cells in primary CRC. And whether or not circular RNAs (circRNAs) take part in this particular event remain not adequately stated yet. Methods A screening method based on Transwell assay was first applied to build CRC subgroups with different metastatic potential. High throughput RNA sequencing was used to find out novel metastatic drivers in CRC metastasis-initiating step. A series of in vitro and in vivo assays were further applied to elucidate the functions and underlying molecular mechanisms of circRNAs in CRC metastasis. Results A circRNA consisting of exon 8–11 of LONP2, termed as circLONP2, was upregulated in metastasis-initiating CRC subgroups. Aberrant higher expression of circLONP2 was observed in primary CRC tissues with established metastasis, and along the invasive margin in metastatic site. High expression of circLONP2 predicted unfavorable overall survival. Functional studies revealed that circLONP2 could enhance the invasiveness of CRC cells in vitro, and targeting circLONP2 through anti-sense oligonucleotide (ASO) dramatically reduced the penetrance of metastasis to foreign organs in vivo . Mechanically, circLONP2 directly interacted with and promoted the processing of primary microRNA-17 (pri-miR-17), through recruiting DiGeorge syndrome critical region gene 8 (DGCR8) and Drosha complex in DDX1-dependent manner. Meanwhile, upregulated mature miR-17-5p could be assembled into exosomes and internalized by neighboring cells to enhance their aggressiveness. Conclusions Our data indicate that circLONP2 acts as key metastasis-initiating molecule during CRC progression through modulating the intracellular maturation and intercellular transfer of miR-17, resulting in dissemination of metastasis-initiating ability in primary site and acceleration of metastasis formation in foreign organs. circLONP2 could serve as an effective prognostic predictor and/or novel anti-metastasis therapeutic target in CRC treatment.

Wind forcing injects energy into mesoscale eddies and near-inertial waves (NIWs) in the ocean, and the NIWs are believed to solve the puzzle of mesoscale energy budget by absorbing energy from mesoscale eddies. This work studies the turbulent energy transfer in the NIW–quasigeostrophic mean mesoscale eddy coupled system based on a previously derived two-dimensional model which inherits conserved quantities in Boussinesq equations (Xie & Vanneste, J. Fluid Mech., vol. 774, 2015, pp. 147–169). The conservation of energy, potential enstrophy and wave action implies the existence of phase transition with a change of the relative strength between NIW and mean-flow, quantified by a parameter $R$. By running forced-dissipative numerical simulations, we justify the existence of second-order phase transition around a critical value $R_c$. When $0R_c$, energy transfers downscale, wave action transfers bidirectionally and vortex filaments are dominant. We find the catalytic wave induction mechanism where the NIW induces a downscale energy flux of the mean flow, which differs from the stimulated loss of balance mechanism observed in inertial value problems. In the parameter regime $0

Journal Article

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