Search

Opportunistic spectrum access (OSA), a promising technology to resolve radio spectrum scarcity, is still faced with some challenges, of which one is potentially frequent channel handoff (CH) even handoff blocking (HB) for secondary user (SU) to avoid primary user (PU). Reaccess is a direct way to resolve HB. However, multiple handoff blocking‐then‐reaccess (H‐BTR) are time consuming. Whether it is worthwhile to make multiple H‐BTR, is an interesting but hardly mentioned issue. To this end, the multiple H‐BTR‐based OSA are focused on here. Three key indices, the average transmission probability, handoff delay, and average reaccess times of SU in the H‐BTR‐based OSA, are deduced as close form first. Then, the effects of H‐BTR frequency and service traffic rate of SU on OSA are discussed. Finally, the H‐BTR‐based OSA is compared to two other schemes, the handoff without BTR (HWBTR)‐based OSA and the stop‐and‐waiting (SW)‐based OSA. Theoretical and simulated results show that the H‐BTR‐based OSA performs best among three schemes. Making H‐BTR in moderate frequency according to service traffic rate can increase transmission opportunity while additional delay of SU is tolerable, thus the performance of OSA can be well improved. [ABSTRACT FROM AUTHOR]

Ferroptosis is a new form of regulated cell death caused by iron‐dependent accumulation of lethal polyunsaturated phospholipids peroxidation. It has received considerable attention owing to its putative involvement in a wide range of pathophysiological processes such as organ injury, cardiac ischemia/reperfusion, degenerative disease and its prevalence in plants, invertebrates, yeasts, bacteria, and archaea. To counter ferroptosis, living organisms have evolved a myriad of intrinsic efficient defense systems, such as cyst(e)ine‐glutathione‐glutathione peroxidase 4 system (cyst(e)ine‐GPX4 system), guanosine triphosphate cyclohydrolase 1/tetrahydrobiopterin (BH4) system (GCH1/BH4 system), ferroptosis suppressor protein 1/coenzyme Q10 system (FSP1/CoQ10 system), and so forth. Among these, GPX4 serves as the only enzymatic protection system through the reduction of lipid hydroperoxides, while other defense systems ultimately rely on small compounds to scavenge lipid radicals and prevent ferroptotic cell death. In this article, we systematically summarize the chemical biology of lipid radical trapping process by endogenous chemicals, such as coenzyme Q10 (CoQ10), BH4, hydropersulfides, vitamin K, vitamin E, 7‐dehydrocholesterol, with the aim of guiding the discovery of novel ferroptosis inhibitors. [ABSTRACT FROM AUTHOR]

The internet of things accelerates the wireless connections of massive devices to provide all kinds of new services, and thus intensifies the spectrum scarcity and access delay. Cognitive radio (CR) technology brings a solution for the issue. As a typical CR scheme, opportunistic spectrum access (OSA) has been addressed widely in the past decade. However, the tradeoff between two key indexes, the throughput of cognitive radio network (CRN) and the delay of secondary user (SU), is rarely mentioned so far, which ignites the authors' work in this paper. Taking into account a channel handoff (CH) based multi‐channel OSA scenario, the authors first analyze the opportunistic transmission performance of SU, and model the throughput of CRN as well as the handoff delay of SU. Then, the authors build up a delay‐constraint throughput optimization problem, and thus formulate the throughput‐delay tradeoff for OSA. Finally, the optimal traffic rates of SU for a good throughput‐delay tradeoff are derived according to maximizing the throughput of CRN. Theoretical and simulated results show that to enhance the throughput and to reduce the delay do not conflict always. By well adjusting the traffic rates of SU according to the traffic rates of primary user, the throughput of CRN can be improved while the handoff delay can be kept under a given level. [ABSTRACT FROM AUTHOR]

Understanding the process of protein–RNA interaction is essential for structural biology. The thermodynamic process is an important part to uncover the protein–RNA interaction mechanism. The regulatory networks between protein and RNA in organisms are dominated by the binding or dissociation in the cells. Therefore, determining the binding affinity for protein–RNA complexes can help us to understand the regulation mechanism of protein–RNA interaction. Since it is time‐consuming and labor‐intensive to determine the binding affinity for protein–RNA complexes by experimental methods, it is necessary and urgent to develop computational methods to predict that. To develop a binding affinity prediction model, first we update the dataset of protein–RNA binding affinity benchmark (PRBAB), which includes 145 complexes now. Second, we extract the structural features based on complex structure, and then we analyze and select the representative structural features to train the regression model. Third, we random select the subset from the PRBAB2.0 to fit the protein–RNA binding affinity determined by experiment. In the end, we tested our model on the nonredundant PDBbind dataset, and the results showed that Pearson correlation coefficient r =.57 and RMSE = 2.51 kcal/mol. The Pearson correlation coefficient achieves 0.7 while removing 5 complex structures with modified residues/nucleotides and metal ions. While testing on ProNAB, the results showed that 71.60% of the prediction achieves Pearson correlation coefficient r =.61 and RMSE = 1.56 kcal/mol with experiment values. [ABSTRACT FROM AUTHOR]

Human learners are capable to acquire foreign language vocabulary at an impressive speed even in adulthood. Previous studies have examined the neural mechanisms underlying rapid acquisition of Latin-alphabet vocabulary and revealed dynamic changes in several event-related potential (ERP) components during novel word learning. However, scant attention has been paid to the acquisition of Russian words. The present study used ERP and examined dynamic brain responses to rapid Russian word acquisition in 53 native Chinese speakers with no prior knowledge of Russian language. Behavioral data showed robust individual differences in Russian word acquisition, with most participants being able to rapidly learn a subset of novel Russian words in a few exposures. ERP results revealed significant learning effects in the P200, N400, and P600 amplitudes. Moreover, P600 amplitude changes predicted participants' word acquisition after learning. These findings demonstrated dynamic brain responses to rapid Russian word learning and suggested that the P600 component may serve as a bio-marker for individual learning ability in Russian word acquisition. [ABSTRACT FROM AUTHOR]

Rhenium disulfide (ReS2) with low structural symmetry and highly spontaneous, exhibits some unique optical and electrical anisotropy properties for developing optoelectronic devices. This work studies the hydrothermal synthesis and the excitonic effects in the linear and nonlinear optical properties of 1T′ phase ReS2. The growth is controlled by adjusting experimental conditions, and its growth mechanism is revealed. The varying degrees of Re vacancy are characterized. They cause the growth direction of ReS2 nanosheets from lateral to agglomeration and the stacks into self‐assembly micro‐nanospheres. The density functional theory explains the electronic and bonding properties of Re vacancy, where the existent defects reduce the band gap and change the states density. Re vacancy increases the conductivity and results in the metallization of ReS2. The photoluminescence intensity of defect emission peak is negatively correlated with the defect level for the enriching vacancies. However, compared with intrinsic peak, it will increase monotonically with the number of bound excitons in defects. Furthermore, the nonlinear absorption properties are obtained by picosecond Z‐scan technique. By adjusting temperature, different degrees of saturation absorption and reverse saturation absorption characteristics appear due to the vacancy effect. The synthesized ReS2 has broad application in photodetectors and optical devices with optical amplitude limiting. [ABSTRACT FROM AUTHOR]

Background: The steam reforming of dimethyl ether (DME) is one of the promising technologies for high‐efficiency hydrogen production. The key issue for the steam reforming of DME is the development of catalysts with higher performance. In this study, a series of X‐Cu/Acid‐MMT (X = Co, Ni, Zr, Ce) catalysts were prepared via the impregnation method using Acid‐MMT obtained by montmorillonite activated with nitric acid (20 wt%) at 80 °C for 12 h as the support and metallic nitrate as precursor. The catalysts were characterized by XRD, H2‐TPR, XPS, N2O titration and N2 adsorption–desorption at low temperature. Results: The introduction of promoter X could reduce the interaction between Cu and the support, and more CuO was reduced to Cu0; meanwhile, it was beneficial for improving the dispersion of Cu. This would enhance the reaction rate of steam reforming of DME. Therefore, the introduction of promoter X significantly increased DME conversion, especially Ni‐Cu/Acid‐MMT presented the maximum DME conversion. However, Ni‐Cu/Acid‐MMT exhibited low H2 yield, high selectivity of CO and CH4 due to reverse water gas shift reaction and methanation reaction. Co‐Cu/Acid‐MMT catalyst presented the maximum H2 yield, high conversion of DME, relatively low selectivity of CH4 and better stability. Conclusions: The introduction of promoters to Cu/Acid‐MMT catalyst improved the catalyst performance for the steam reforming of DME. Among these catalysts, Co‐Cu/Acid‐MMT exhibited remarkable catalytic performance, which is expected to be a potential catalyst for steam reforming of DME. © 2022 Society of Chemical Industry (SCI). [ABSTRACT FROM AUTHOR]

This work proposes a microwave angular displacement sensor with wideband matching based on a wideband impedance transformer. According to the design requirement of the microstrip impedance transformer (load‐to‐source impedance of 250‐to‐50 Ω, centre frequency of 2.40 GHz) with Chebyshev frequency response, the proposed angular displacement sensor is explored for the high bandwidth sensitivity of 11.18 MHz/degree. [ABSTRACT FROM AUTHOR]

Background and Purpose: Interleukin‐36 is induced by proinflammatory cytokines and promotes inflammatory responses, creating an IL‐36‐based inflammation loop. Although hepatocytes, produce IL‐36 responses to drug‐induced liver injury, little is known about the mechanistic role of IL‐36 signalling during the progression of alcoholic steatohepatitis (ASH). Regarding IL‐36/IL‐36R and P2X7R coregulating the inflammatory response, we elucidated that modulation of IL‐36R‐P2X7R‐TLR axis affected hepatocyte steatosis as well as the IL‐36‐based inflammatory feedback loop that accompanies the onset of ASH. Experimental Approach: C57BL/6J mice were subjected to either chronic‐plus‐binge ethanol feeding or acute gavage with multiple doses of ethanol to establish ASH, followed by pharmacological inhibition or genetic silencing of IL‐36R and P2X7R. AML12 cells or mouse primary hepatocytes were stimulated with alcohol, LPS plus ATP or Poly(I:C) plus ATP, followed by silencing of IL‐36γ, IL‐36R or P2X7R. Key Results: P2X7R and IL‐36R deficiency blocked the inflammatory loop, specifically initiated by IL‐36 cytokines, in hepatocytes of mice suffering from ASH. Pharmacological inhibition to P2X7R or IL‐36R alleviated lipid accumulation and inflammatory response in ASH. IL‐36R was indispensable for P2X7R modulated NLRP3 inflammasome activation in ASH, and IL‐36 led to a vicious cycle of P2X7R‐driven inflammation in alcohol‐treated hepatocytes. TLR ligands promoted IL‐36γ production in hepatocytes, based on synergism with P2X7R. Conclusions and Implications: Blockade of IL‐36 based inflammatory feedback loop, via IL‐36R‐P2X7R‐TLRs‐modulated NLRP3 inflammasome activation, circumvented steatosis and inflammation that accompanies the onset of ASH, suggesting that targeting IL‐36 can serve as a novel therapeutic approach to combat ASH. [ABSTRACT FROM AUTHOR]

Data on sofosbuvir‐based therapy for pregnant women and infants with severe chronic hepatitis C (CHC) are lacking. Two late pregnant women and one female infant with severe CHC were enrolled for treatment. Pregnant Women 1 and 2 and Infant 3 were 30, 33, and 1.2 years old, respectively; the gestational ages of pregnant Women 1 and 2 were 31 and 26 weeks, respectively. Notably, pregnant Women 1 and 2 and Infant 3 had hepatitis C virus (HCV) RNA levels of 139 000, 198 000, and 8 450 000 IU/ml; alanine aminotransferase levels of 420, 781, and 220 U/L; and received sofosbuvir/ledipasvir, sofosbuvir/velpatasvir, and sofosbuvir/ledipasvir for 12 weeks, respectively. All three patients were safely cured with favorable tolerance, and two newborns were both breastfeeding and were consistently negative for the anti‐HCV antibody during the 1‐year follow‐up after birth. Additionally, two newborns and Infant 3 had normal growth parameters during the follow‐up year one. In conclusion, this case series study found that sofosbuvir‐based therapy for pregnant women and infants with severe CHC is safe and effective. The data may fill the gap and provide evidence of the use of sofosbuvir‐based therapy as a reference when similar severe CHC situations are encountered during clinical practice. [ABSTRACT FROM AUTHOR]

The mega‐infrastructural development project provides easy access to remarkable tourism destinations and keeps attracting tourists. Tourist data from the tourism department of Gilgit‐Baltistan (GB), Pakistan, show that the China–Pakistan Economic Corridor (CPEC) project's impact positively relates to tourism demand. GB is at the early stage of tourism development, and residents show a willingness to support tourism even though tourism costs outweigh benefits. Besides, the existing tourism policy of Gilgit‐Baltistan focuses explicitly on economic sustainability but overlooks the socio‐cultural and environmental concerns. Therefore, the present study based on the stakeholder theory provides policy implications to minimize adverse effects on socio‐cultural and ecological resources and achieve sustainable tourism. [ABSTRACT FROM AUTHOR]

With proteomic analysis, we identified 379 egg surface proteins from an endoparasitoid, Cotesia chilonis. Proteins containing conserved enzymatic domains constitute a large proportion of egg surface components. Some proteins, such as superoxidase dismutase, homolog of C. rubecula 32‐kDa protein, and immunoevasive protein‐2A, are classical parasitism factors that have known functions in host immunity regulation. Melanization assays revealed that a novel egg surface protein, C. chilonis egg surface serpin domain‐containing protein had the same function as a C. chilonis venom serpin, as both suppressed host melanization in a dose‐dependent manner. C. chilonis egg surface serpin domain‐containing protein is mainly transcribed in C. chilonis oocytes with follicular cells, and it is located on both the anterior and posterior sides of the mature egg surface. Additionally, we used LC‐MS/MS to identify 586 binding proteins sourced from C. suppressalis plasma located on the eggshell surface of C. chilonis, which included some immunity‐related proteins. These results not only indicate that C. chilonis uses its egg surface proteins to reduce the immune response of its host but also imply that endoparasitoid egg surface proteins might be a new parasitism factor involved in host immune regulation. [ABSTRACT FROM AUTHOR]

The subcellular localization and intracellular trafficking of Toll‐like receptors (TLRs) critically regulate TLRs‐mediated antimicrobial immunity and autoimmunity. Here, it is demonstrated that the E3 ubiquitin ligase RNF115 inhibits the post‐endoplasmic reticulum (ER) trafficking of TLRs and TLRs‐mediated immune responses by catalyzing ubiquitination of the small GTPases RAB1A and RAB13. It is shown that the 14‐3‐3 chaperones bind to AKT1‐phosphorylated RNF115 and facilitate RNF115 localizing on the ER and the Golgi apparatus. RNF115 interacts with RAB1A and RAB13 and catalyzes K11‐linked ubiquitination on the Lys49 and Lys61 residues of RAB1A and on the Lys46 and Lys58 residues of RAB13, respectively. Such a modification impairs the recruitment of guanosine diphosphate (GDP) dissociation inhibitor 1 (GDI1) to RAB1A and RAB13, a prerequisite for the reactivation of RAB proteins. Consistently, knockdown of RAB1A and RAB13 in Rnf115+/+ and Rnf115−/− cells markedly inhibits the post‐ER and the post‐Golgi trafficking of TLRs, respectively. In addition, reconstitution of RAB1AK49/61R or RAB13K46/58R into Rnf115+/+ cells but not Rnf115−/− cells promotes the trafficking of TLRs from the ER to the Golgi apparatus and from the Golgi apparatus to the cell surface, respectively. These findings uncover a common and step‐wise regulatory mechanism for the post‐ER trafficking of TLRs. [ABSTRACT FROM AUTHOR]

The genetic variants from genes proposed by American College of Medical Genetics and Genomics (ACMG) should be reported to clinician as secondary findings if the annotation suggested pathogenic or likely pathogenic.1 With the increasing application of DNA sequencing in the clinic, the ACMG updated the SF v3.0 list to 73 genes in 2021.2 Ethnic disparities exist in allele frequency of pathogenic variants. In conclusion, we found that approximately 17.37% (778/4480) of Chinese individuals carried at least one reported P/LP variant in the 73 genes recommended by ACMG, and 295 P/LP genetic variants were detected in our WBBC pilot cohort. Following the variant classification standard (Figure 1 and Supporting Information), we identified 295 P/LP variants (99 pathogenic and 196 likely pathogenic variants, Table S2), accounting for 3.15% of the variants. [Extracted from the article]

Metabolite‐protein interactions (MPIs) play key roles in cancer metabolism. However, our current knowledge about MPIs in cancers remains limited due to the complexity of cancer cells. Herein, the authors construct an integrative MPI network and propose a MPI network based hepatocellular carcinoma (HCC) subtyping and mechanism exploration workflow. Based on the expressions of hub proteins on the MPI network, two prognosis‐distinctive HCC subtypes are identified. Meanwhile, multiple interdependent features of the poor prognostic subtype are observed, including hypoxia, DNA hypermethylation of metabolic pathways, fatty acid accumulation, immune pathway up‐regulation, and exhausted T‐cell infiltration. Notably, the immune pathway up‐regulation is probably induced by accumulated unsaturated fatty acids which are predicted to interact with multiple immune regulators like SRC and TGFB1. Moreover, based on tumor microenvironment compositions, the poor prognostic subtype is further divided into two sub‐populations showing remarkable differences in metabolism. The subtyping shows a strong consistency across multiple HCC cohorts including early‐stage HCC. Overall, the authors redefine robust HCC prognosis subtypes and identify potential MPIs linking metabolism to immune regulations, thus promoting understanding and clinical applications about HCC metabolism heterogeneity. [ABSTRACT FROM AUTHOR]

It is widely accepted that redox reprogramming participates in malignant transformation of lung adenocarcinoma (LUAD). However, the source of excessive reactive oxygen species (ROS) and the downstream signaling regulatory mechanism are complicated and unintelligible. In the current study, we newly identified the aquaporin 3 (AQP3) as a LUAD oncogenic factor with capacity to transport exogenous hydrogen peroxide (H2O2) and increase intracellular ROS levels. Subsequently, we demonstrated that AQP3 was necessary for the facilitated diffusion of exogenous H2O2 in LUAD cells and that the AQP3‐dependent transport of H2O2 accelerated cell growth and inhibited rapamycin‐induced autophagy. Mechanistically, AQP3‐mediated H2O2 uptake increased intracellular ROS levels to inactivate PTEN and activate the AKT/mTOR pathway to subsequently inhibit autophagy and promote proliferation in LUAD cells. Finally, we suggested that AQP3 depletion retarded subcutaneous tumorigenesis in vivo and simultaneously decreased ROS levels and promoted autophagy. These findings underscore the importance of AQP3‐induced oxidative stress in malignant transformation and suggest a therapeutic target for LUAD. [ABSTRACT FROM AUTHOR]