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Quantum secure direct communication (QSDC) can directly transmit secure messages through quantum channel without sharing keys. Three-party (3P) QSDC enables two communication parties synchronously transmit secret messages to a third party through the quantum channels. Previous 3P-QSDC protocols all require ideal and trusted measurement devices, which are hard to realize under current experimental condition. Practical imperfect measurement devices would bring security loophole in the 3P-QSDC. In the paper, we propose a measurement-device-independent (MDI) 3P-QSDC protocol based on the polarization-spatial-mode hyperentanglement, which can resist all possible attacks from practical imperfect measurement devices. Our protocol is unconditionally secure in theory and can enhance 3P-QSDC’s security under practical experimental condition. In one round of communication, two parties can each send 2 bits of secure messages to the third party. Our MDI-3P-QSDC protocol has application potential in future multipartite quantum communication field. [ABSTRACT FROM AUTHOR]

Background Internet gaming disorder (IGD) is a mental health issue that affects individuals worldwide. However, the lack of knowledge about the biomarkers associated with the development of IGD has restricted the diagnosis and treatment of this disorder. Aims We aimed to reveal the biomarkers associated with the development of IGD through resting-state brain network analysis and provide clues for the diagnosis and treatment of IGD. Methods Twenty-six patients with IGD, 23 excessive internet game users (EIUs) who recurrently played internet games but were not diagnosed with IGD and 29 healthy controls (HCs) performed delay discounting task (DDT) and Iowa gambling task (IGT). Resting-state functional magnetic resonance imaging (fMRI) data were also collected. Results Patients with IGD exhibited significantly lower hubness in the right medial orbital part of the superior frontal gyrus (ORBsupmed) than both the EIU and the HC groups. Additionally, the hubness of the right ORBsupmed was found to be positively correlated with the highest excessive internet gaming degree during the past year in the EIU group but not the IGD group; this might be the protective mechanism that prevents EIUs from becoming addicted to internet games. Moreover, the hubness of the right ORBsupmed was found to be related to the treatment outcome of patients with IGD, with higher hubness of this region indicating better recovery when undergoing forced abstinence. Further modelling analysis of the DDT and IGT showed that patients with IGD displayed higher impulsivity during the decision-making process, and impulsivity-related parameters were negatively correlated with the hubness of right ORBsupmed. Conclusions Our findings revealed that the impulsivity-related right ORBsupmed hubness could serve as a potential biomarker of IGD and provide clues for the diagnosis and treatment of IGD. [ABSTRACT FROM AUTHOR]

To elucidate the therapeutic effects and mechanisms of Atractylodes macrocephala extract crystallize (BZEP) and BZEP self-microemulsion (BZEPWR) on metabolic dysfunction-associated fatty liver disease (MAFLD) induced by "high sugar, high fat, and excessive alcohol consumption" based on the gut–liver axis HDL/LPS signaling pathway. In this study, BZEP and BZEPWR were obtained via isolation, purification, and microemulsification. Furthermore, an anthropomorphic MAFLD rat model of "high sugar, high fat, and excessive alcohol consumption" was established. The therapeutic effects of BZEPWR and BZEP on the model rats were evaluated in terms of liver function, lipid metabolism (especially HDL-C), serum antioxidant indexes, and liver and intestinal pathophysiology. To determine the lipoproteins in the serum sample, the amplitudes of a plurality of NMR spectra were derived via deconvolution of the composite methyl signal envelope to yield HDL-C subclass concentrations. The changes in intestinal flora were detected via 16 S rRNA gene sequencing. In addition, the gut–liver axis HDL/LPS signaling pathway was validated using immunohistochemistry, immunofluorescence, and western blot. The findings established that BZEPWR and BZEP improved animal signs, serum levels of liver enzymes (ALT and AST), lipid metabolism (TC, TG, HDL-C, and LDL-C), and antioxidant indexes (GSH, SOD, and ROS). In addition, pathological damage to the liver, colon, and ileum was ameliorated, and the intestinal barrier function of the model rats was restored. At the genus level, BZEPWR and BZEP exerted positive effects on beneficial bacteria, such as Lactobacillus and norank_f__Muribaculaceae , and inhibitory effects on harmful bacteria, such as unclassified_f__Lachnospiraceae and Blautia. Twenty HDL-C subspecies were detected, and their levels were differentially increased in both BZEPWR and BZEP groups, with BZEPWR exhibiting a stronger elevating effect on specific HDL-C subspecies. Also, the gut–liver axis HDL/LPS signaling pathway was studied, which indicated that BZEPWR and BZEP significantly increased the expressions of ABCA1, LXR, occludin, and claudin-1 proteins in the gut and serum levels of HDL-C. Concomitantly, the levels of LPS in the serum and TLR4, Myd88, and NF-κB proteins in the liver were decreased. BZEPWR and BZEP exert restorative and reversal effects on the pathophysiological damage to the gut–liver axis in MAFLD rats, and the therapeutic mechanism may be related to the regulation of the intestinal flora and the HDL/LPS signaling pathway. [Display omitted] • Comparison of the efficacy of BZEP and its microemulsification on MAFLD. • BZEP self-microemulsion is effective in regulating blood lipid levels, especially in raising levels of various HDL subtypes. • BZEP self-microemulsion may improve HDL/LPS signalling pathway through the gut-liver axis for the treatment of MAFLD in rats. [ABSTRACT FROM AUTHOR]

Background: Alcadeinα (Alcα) is a neuronal membrane protein that colocalizes with the Alzheimer's amyloid-β precursor protein (APP). Successive cleavage of APP by β- and γ-secretases generates the aggregatable amyloid-β peptide (Aβ), while cleavage of APP or Alcα by α- and γ-secretases generates non-aggregatable p3 or p3-Alcα peptides. Aβ and p3-Alcα can be recovered from human cerebrospinal fluid (CSF). We have previously reported alternative processing of APP and Alcα in the CSF of some patients with sporadic mild cognitive impairment (MCI) and AD (SAD). Results: Using the sandwich enzyme-linked immunosorbent assay (ELISA) system that detects total p3-Alcα, we determined levels of total p3-Alcα in CSF from subjects in one of four diagnostic categories (elderly controls, MCI, SAD, or other neurological disease) derived from three independent cohorts. Levels of Aβ40 correlated with levels of total p3-Alcα in all cohorts. Conclusions: We confirm that Aβ40 is the most abundant Aβ species, and we propose a model in which CSF p3- Alcα can serve as a either (1) a nonaggregatable surrogate marker for γ-secretase activity; (2) as a marker for clearance of transmembrane domain peptides derived from integral protein catabolism; or (3) both. We propose the specification of an MCI/SAD endophenotype characterized by co-elevation of levels of both CSF p3-Alcα and Aβ40, and we propose that subjects in this category might be especially responsive to therapeutics aimed at modulation of γ-secretase function and/or transmembrane domain peptide clearance. These peptides may also be used to monitor the efficacy of therapeutics that target these steps in Aβ metabolism. [ABSTRACT FROM AUTHOR]

The neural type I membrane protein Alcadein α (Alcα), is primarily cleaved by amyloid β-protein precursor (APP) α-secretase to generate a membrane-associated carboxyl-terminal fragment (Alcα CTF), which is further cleaved by γ-secretase to secrete p3-Alcα peptides and generate an intracellular cytoplasmic domain fragment (Alcα ICD) in the late secretory pathway. By association with the neural adaptor protein X11L (X11-like), Alcα and APP form a ternary complex that suppresses the cleavage of both Alcα and APP by regulating the transport of these membrane proteins into the late secretory pathway where secretases are active. However, it has not been revealed how Alcα and APP are directed from the ternary complex formed largely in the Golgi into the late secretory pathway to reach a nerve terminus. Using a novel transgenic mouse line expressing excess amounts of human Alcα CTF (hAlcα CTF) in neurons, we found that expression of hAlcα CTF induced excess production of hAlcα ICD, which facilitated APP transport into the nerve terminus and enhanced APP metabolism, including Aβ generation. In vitro cell studies also demonstrated that excess expression of Alcα ICD released both APP and Alcα from the ternary complex. These results indicate that regulated intramembrane proteolysis of Alcα by γ-secretase regulates APP trafficking and the production of Aβ in vivo. [ABSTRACT FROM AUTHOR]

Splicing the shredded paper means the technology that, according the paper, which has been shredded to design a particular Algorithm to splice and recover the original paper. This paper introduced the algorithm of splicing the shredded paper based on the matching to texture feature. By means of this algorithm, we modeled for the problem of splicing the shredded paper and solved it. And, we used the algorithm to splice both pieces of English shredded paper and Chinese shredded paper. The recovered paper had proved the accuracy of the algorithm. [ABSTRACT FROM AUTHOR]