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This study investigates the impact of warm-rolling and subsequent annealing on the microstructure and tensile properties of a dual-phase Al0.45CoCrFeNiTi0.25 high-entropy alloy (HEA) containing both face-centered cubic and body-centered cubic phases. The HEA underwent warm-rolling at temperatures of 450, 600, and 750 °C with a 50% reduction in thickness, followed by annealing at various temperatures. Higher warm-rolling temperatures facilitated the precipitation of B2 particles, significantly influencing the alloy's phase distribution. Throughout the experiments, no new phases emerged, and annealing maintained the alloy's original phase composition.Warm-rolling at 450 °C, followed by annealing at 1200 °C, led to substantial microstructural changes, including the formation of distinctive annealed twins. These microstructural changes enhanced ductility significantly, increasing elongation to 13.4% (a 538% improvement over the as-cast state) while maintaining a fracture strength of 983 MPa. Overall, this comprehensive analysis demonstrates that optimizing the warm-rolling and annealing parameters can significantly enhance the properties of dual-phase HEA.

This study investigated the microstructure and mechanical properties of GdxCoCrFeNiV0.4 alloys. Various techniques such as XRD, SEM, EBSD, and TEM were utilized, alongside hardness and compression tests at room temperature. The findings revealed that the high-entropy alloy without Gd element exhibited a single face-centered cubic (FCC) phase. Upon the introduction of Gd element, the phase composition shifted to FCC + hexagonal structure (HS) phases, and further addition of Gd resulted in the presence of FCC + HS + body-centered cubic (BCC) phases. Additionally, the inclusion of Gd element led to the precipitation of Gd-rich particles within the alloy. The Vickers hardness test results revealed a significant increase in alloy hardness as the Gd content rose, from 177.5 HV for Gd0 to 848.4 HV for Gd0.4. This suggests that the presence of the HS phase and BCC phase notably influences alloy hardness. Furthermore, compressive test outcomes demonstrated that the alloy's yield strength rose from 173.74 MPa for Gd0 to 1356.17 MPa for Gd0.3 with increasing Gd content. However, the excessive addition of Gd elements results in significant precipitation of V and Cr elements, leading to grain coarsening, adversely affecting its mechanical properties. The high strength of Gd-containing high-entropy alloys can be attributed to various strengthening mechanisms, such as solid solution strengthening, the presence of the HS phase, the precipitation of a small number of Gd-rich particles, and the grain refinement caused by the addition of Gd.

Abstract Joint sensing and communications systems have gained significant research interest by merging sensing capabilities with communication functionalities. However, few works have examined the case of multiple users. This work investigates a dual‐user joint sensing and communications system, focusing on the interference between the users that explores the optimal performance trade‐offs through a time‐division approach. Bi‐static radar setting is considered. Two typical strategies under this approach are studied: one in which both users follow the same order of communications and then sensing, and the other in which the tasks are performed in opposite order at two users. In each strategy, the sum rate and the detection probability are evaluated and optimized. The results show that the opposite order strategy offers superior performance to the same order strategy, and they also quantify their performance difference. This research highlights the potential benefits of time‐division strategies and multiple users in joint sensing and communications systems.

Abstract Background Pulmonary fibrosis (PF) is an aging-related progressive lung disorder. The aged lung undergoes functional and structural changes termed immunosenescence and inflammaging, which facilitate the occurrence of fibrosis. Interleukin-10 (IL-10) is a potent anti-inflammatory and immunoregulatory cytokine, yet it remains unclear how IL-10 deficiency-induced immunosenescence participates in the development of PF. Methods Firstly we evaluated the susceptibility to fibrosis and IL-10 expression in aged mice. Then 13-month-old wild-type (WT) and IL-10 knockout (KO) mice were subjected to bleomycin(BLM) and analyzed senescence-related markers by PCR, western blot and immunohistochemistry staining of p16, p21, p53, as well as DHE and SA-β-gal staining. We further compared 18-month-old WT mice with 13-month-old IL-10KO mice to assess aging-associated cell senescence and inflamation infiltration in both lung and BALF. Moreover, proliferation and apoptosis of alveolar type 2 cells(AT2) were evaluated by FCM, immunofluorescence, TUNEL staining, and TEM analysis. Recombinant IL-10 (rIL-10) was also administered intratracheally to evaluate its therapeutic potential and related mechanism. For the in vitro experiments, 10-week-old naïve pramily lung fibroblasts(PLFs) were treated with the culture medium of 13-month PLFs derived from WT, IL-10KO, or IL-10KO + rIL-10 respectively, and examined the secretion of senescence-associated secretory phenotype (SASP) factors and related pathways. Results The aged mice displayed increased susceptibility to fibrosis and decreased IL-10 expression. The 13-month-old IL-10KO mice exhibited significant exacerbation of cell senescence compared to their contemporary WT mice, and even more severe epithelial-mesenchymal transition (EMT) than that of 18 month WT mice. These IL-10 deficient mice showed heightened inflammatory responses and accelerated PF progression. Intratracheal administration of rIL-10 reduced lung CD45 + cell infiltration by 15%, including a 6% reduction in granulocytes and a 10% reduction in macrophages, and increased the proportion of AT2 cells by approximately 8%. Additionally, rIL-10 significantly decreased α-SMA and collagen deposition, and reduced the expression of senescence proteins p16 and p21 by 50% in these mice. In vitro analysis revealed that conditioned media from IL-10 deficient mice promoted SASP secretion and upregulated senescence genes in naïve lung fibroblasts, which was mitigated by rIL-10 treatment. Mechanistically, rIL-10 inhibited TGF-β-Smad2/3 and PTEN/PI3K/AKT/ERK pathways, thereby suppressing senescence and fibrosis-related proteins. Conclusions IL-10 deficiency in aged mice leads to accelerated cell senescence and exacerbated fibrosis, with IL-10KO-PLFs displaying increased SASP secretion. Recombinant IL-10 treatment effectively mitigates these effects, suggesting its potential as a therapeutic target for PF. Graphical Abstract

Abstract Background Molecular signatures of chronic rhinosinusitis with nasal polyps (CRSwNP) related to macrophages remain unclear. This study aimed to develop a macrophage‐associated diagnostic signature for CRSwNP. Methods Transcriptome data from 54 patients with CRSwNP and 37 healthy controls across GSE136825, GSE36830, and GSE72713 were used to identify differentially expressed genes (DEGs) between two groups. Gene Set Enrichment Analysis and Weighted Gene Co‐Expression Network Analysis pinpointed crucial pathways and gene clusters. A diagnostic model was created from these analyses and receiver operating characteristic curve (ROC), and further validated in our transcriptome data from 29 samples. Immune cell infiltration analysis was performed and linked those diagnostic genes to macrophages and verified by single‐cell RNA sequencing data. Immunofluorescence co‐staining of CD163 and HMOX1 was performed in nasal tissues. Mouse bone marrow‐derived macrophage (BMDMs) cultures were used in functional experiments. Correlations between the expression of HMOX1 and eotaxin genes were investigated. Results DEGs of CRSwNP versus control group were enriched in the INTERLEUKIN_4_AND_13_SIGNALING pathways. A four‐gene diagnostic model (HMOX1, ALOX5, F13A1 and ITGB2) was developed and demonstrated high diagnostic precision with an area under ROC curve of 0.980 for training dataset and 0.895 for test dataset. M2 macrophage presence and HMOX1 expression significantly correlated with CRSwNP (p

Abstract Background Numerous studies have confirmed the involvement of extracellular vesicles (EVs) in various physiological processes, including cellular death and tissue damage. Recently, we reported that EVs derived from ischemia-reperfusion heart exacerbate cardiac injury. However, the role of EVs from healthy heart tissue (heart-derived EVs, or cEVs) on myocardial ischemia-reperfusion (MI/R) injury remains unclear. Results Here, we demonstrated that intramyocardial administration of cEVs significantly enhanced cardiac function and reduced cardiac damage in murine MI/R injury models. cEVs treatment effectively inhibited ferroptosis and maintained mitochondrial homeostasis in cardiomyocytes subjected to ischemia-reperfusion injury. Further results revealed that cEVs can transfer ATP5a1 into cardiomyocytes, thereby suppressing mitochondrial ROS production, alleviating mitochondrial damage, and inhibiting cardiomyocyte ferroptosis. Knockdown of ATP5a1 abolished the protective effects of cEVs. Furthermore, we found that the majority of cEVs are derived from cardiomyocytes, and ATP5a1 in cEVs primarily originates from cardiomyocytes of the healthy murine heart. Moreover, we demonstrated that adipose-derived stem cells (ADSC)-derived EVs with ATP5a1 overexpression showed much better efficacy on the therapy of MI/R injury compared to control ADSC-derived EVs. Conclusions These findings emphasized the protective role of cEVs in cardiac injury and highlighted the therapeutic potential of targeting ATP5a1 as an important approach for managing myocardial damage induced by MI/R injury.

Path tracking is an essential stage for vehicle safety control. The study proposes an optimal control method for path tracking problem. Firstly, a nonlinear 4-DOF vehicle model is established. Secondly, the path optimization problem of vehicle is transformed into a nonlinear programming problem(NLP) by discretizing both control variables and state variables using the local collocation method. Then, in order to improve the efficiency of solving the NLP, an efficient calculation method for partial derivatives is established. Finally, a real vehicle test is executed to verify the rationality of the proposed model and methodology. The results show that by decomposing the partial derivative of the NLP into the partial derivative of the original path optimization problem the computational complexity of the first order partial derivative of NLP is significantly reduced improving computational efficiency even more significantly.

In this study, the microstructure and mechanical properties of Al0.45CoCrFeNiTix (x = 0, 0.25, 0.5, 0.75, 1.0) high-entropy alloys were investigated. Various techniques including XRD, SEM, EBSD, and TEM were employed, along with hardness tests, compressive tests, and tensile tests conducted at room temperature. Our findings reveal that the alloy's microstructure changes from FCC + BCC to FCC + BCC + L21 phase as the Ti content increases. Specifically, the BCC content increases from 0.9 % to 62.3 %. This alteration in microstructure leads to a significant enhancement in the compressive yield strength of the alloy, from 305.96 MPa to 1492.53 MPa. The observed strengthening effect can be attributed to the increased BCC content and the formation of the L21 phase within the alloy. The results of the tensile experiments demonstrate that the Ti0.25 alloy exhibits the most favorable overall properties, possessing a yield strength of 619 MPa. This represents a significant increase of 64.6 % when compared to Ti0. The strengthening mechanism of the Al0.45CoCrFeNiTix high-entropy alloy is thoroughly discussed. The main strengthening mechanisms of the alloy system are fine grain strengthening, solid solution strengthening and second phase strengthening. This study achieves a balance between strength and ductility by modulating the phase composition of the alloy, laying the foundation for further development and research into the properties of the high-entropy alloys.

Abstract Background Extracellular vesicles (EVs) derived from various cell sources exert cardioprotective effects during cardiac ischemic injury. Our previous study confirmed that EVs derived from ischemic-reperfusion injured heart tissue aggravated cardiac inflammation and dysfunction. However, the role of EVs derived from normal cardiac tissue in myocardial ischemic injury remains elusive. Results In the present study, normal heart-derived EVs (cEVs) and kidney-derived EVs (nEVs) were isolated and intramyocardially injected into mice after myocardial infarction (MI). We demonstrated that administration of both cEVs and nEVs significantly improved cardiac function, reduced the scar size, and alleviated inflammatory infiltration into the heart. In addition, cardiomyocyte apoptosis was inhibited, whereas angiogenesis was enhanced in the hearts receiving cEVs or nEVs treatment. Moreover, intramyocardial injection of cEVs displayed much better cardiac protective efficacy than nEVs in murine MI models. RNA-seq and protein-protein interaction (PPI) network analysis revealed the protective mRNA clusters in both cEVs and nEVs. These mRNAs were involved in multiple signaling pathways, which may synergistically orchestrate to prevent the heart from further damage post MI. Conclusions Collectively, our results indicated that EVs derived from normal heart tissue may represent a promising strategy for cardiac protection in ischemic heart diseases.

Ti/Al laminated composites embedded with Al0.5CoCrFeNi high entropy alloy particles were prepared by vacuum hot press sintering process at temperatures of 660 °C and 730 °C. The microstructure of the material was initially examined using XRD, SEM, EDS, EBSD, and TEM techniques. The results of microstructural characterisation show that Al3Ti is the only newly generated phase in the materials prepared at two temperatures. The Al3Ti generated at the temperature of 660 °C is concentrated at the Ti/Al interface position. The Al3Ti generated at a temperature of 730 °C is dispersed in the Al matrix, leading to the formation of numerous Al3Ti/Al interfaces. The residual HEA particles were observed at the sites of oxide aggregation, potentially enhancing the connectivity of the weak interfaces. Following that, the flexural strength and fracture toughness of the composites were evaluated. The results indicate that the materials prepared at a temperature of 730 °C exhibit superior properties. The flexural strength perpendicular to the layer direction reaches 515.89 MPa, while the flexural strength parallel to the layer direction reaches 487.1 MPa. These findings demonstrate clear anisotropy in the flexural performance. Additionally, the material exhibits excellent resistance to crack extension, with a fracture toughness of 32.67 MPa√m.

In this paper, classical molecular dynamics simulations were used to explore the impact of deposition temperature and bias voltage on the growth of Al2O3 thin films through magnetron sputtering. Ion energy distributions were derived from plasma mass spectrometer measurements. The fluxes of deposited particles (Ar+, Al+, and O−) were categorized into low, medium, and high energies, and the results show that the films are dominated by amorphous Al2O3 at low incident energies without applying bias. As the deposition temperature increased, the crystallinity of the films also increased, with the crystals predominantly consisting of γ-Al2O3. The crystal content of the deposited films increased when biased with −20 V compared to when no bias was applied. Crystalline films were successfully obtained at a deposition temperature of 773 K with a −20 V bias. When biased with −40 V, crystals could be obtained at a lower deposition temperature of 573 K. Increasing the bias enables the particles to have higher energy to overcome the nucleation barrier of the crystallization process, leading to a greater degree of film crystallization. At this stage, the average bond length between Al-O is measured to be approximately 1.89 Å to 1.91 Å, closely resembling that of the crystal.

Abstract Extracellular vesicles (EVs) exist throughout our bodies. We recently revealed the important role of intracardiac EVs induced by myocardial ischemia/reperfusion on cardiac injury and dysfunction. However, the role of EVs isolated from normal tissues remains unclear. Here we found that EVs, derived from murine heart, lung, liver and kidney have similar effects on macrophages and regulate the inflammation, chemotaxis, and phagocytosis of macrophages. Interestingly, EV‐treated macrophages showed LPS resistance with reduced expressions of inflammatory cytokines and enhanced phagocytic activity. Furthermore, we demonstrated that the protein content in EVs contributed to the activation of inflammation, while the RNA component mainly limited the excessive inflammatory response of macrophages to LPS. The enrichment of miRNAs, including miR‐148a‐3p, miR‐1a‐3p and miR‐143‐3p was confirmed in tissue EVs. These EV‐enriched miRNAs contributed to the inflammation remission in LPS induced macrophages through multiple pathways, including STAT3, P65 and SAPK/JNK. Moreover, administration of both EVs and EV‐educated macrophages attenuated septic injury and cytokine storm in murine CLP models. Taken together, the present study disclosed that EVs from normal tissues can orchestrate the homeostasis of macrophages and attenuate inflammatory injury of sepsis. Therefore, tissue derived EVs or their derivatives may serve as potential therapeutic strategies in inflammatory diseases.

Cold spraying was used to prepare Al/Al2O3 composite coatings. The Al2O3 content was controlled to increase the mechanical property and corrosion resistance of the composite coating. The inclusion of Al2O3 particles results in considerable plastic deformation of Al particles and grain size refinement in the coating. Additionally, the coating’s surface roughness decreased from 24.63 μm to 9.02 μm, and the porosity decreased from 6.34% to 2.07%. The increase in microhardness of the composite coatings was attributed to the combined effect of residual compressive stress, second phase strengthening of Al2O3, and plastic hardening of Al particles. The electrochemical test results indicate that the mass fractions of Al2O3 significantly affected the corrosion resistance of the Al/Al2O3 composite coating. Compared to the Al coating, the composite coating exhibited improved corrosion resistance, with a reduction in corrosion current density from 1.09 × 10−3 A/cm2 to 2.67 × 10−6 A/cm2 and an increase in corrosion potential from −1.57 V to −1.14 V. However, when the alumina particle content exceeded 17.7%, it led to more Al2O3 particle breakage, increasing the weak bonding interfaces in the composite coating, and consequently reducing its corrosion resistance.

Abstract Mitochondrial dysfunction is considered to be a key contributor to the development of heart failure. Replacing injured mitochondria with healthy mitochondria to restore mitochondrial bioenergy in myocardium holds great promise for cardioprotection after infarction. This study aimed to investigate whether direct transplantation of exogenous mitochondria derived from mesenchymal stem cells (MSC‐mt) is beneficial and superior in protecting cardiac function in a mouse model of myocardial infarction (MI) compared to mitochondria derived from skin fibroblast (FB‐mt) and to explore the underlying mechanisms from their effects on the endothelial cells. The isolated MSC‐mt presented intact mitochondrial morphology and activity, as determined by electron microscopy, JC‐1 mitochondrial membrane potential assay, and seahorse assay. Direct injection of MSC‐mt into the peri‐infarct region in a mouse MI model enhanced blood vessel density, inhibited cardiac remodeling and apoptosis, thus improving heart function compared with FB‐mt group. The injected MSC‐mt can be tracked in the endothelial cells. In vitro, the fluorescence signal of MSC‐mt can be detected in human umbilical vein endothelial cells (HUVECs) by confocal microscopy and flow cytometry after coculture. Compared to FB‐mt, MSC‐mt more effectively protected the HUVECs from oxidative stress‐induced apoptosis and reduced mitochondrial production of reactive oxygen species. MSC‐mt presented superior capacity in inducing tube formation, enhancing SCF secretion, ATP content and cell proliferation in HUVECs compared to FB‐mt. Mechanistically, MSC‐mt administration alleviated oxidative stress‐induced endothelial senescence via activation of ERK pathway. These findings suggest that using MSCs as sources of mitochondria is feasible and that proangiogenesis could be the mechanism by which MSC‐mt transplantation attenuates MI. MSC‐mt transplantation might serve as a new therapeutic strategy for treating MI.

Novel HEAp-Ti/Al laminated composites embedded with particles of the high-entropy alloy Al0.5CoCrFeNi (HEA) were fabricated by vacuum hot-press sintering at 730 °C. The phase composition and microstructure of the composites were studied with X-ray diffractometer (XRD), scanning electron microscope SEM, energy dispersive spectrometer (EDS), transmission electron microscope (TEM), and electron backscattering diffraction (EBSD) techniques. At this temperature, it has been observed that Al3Ti intermetallic compound is the favored phase and the reaction results in the dispersion of Al3Ti in the original Al layer. A large number of interfaces are formed between Al3Ti and Al. The deformed Al3Ti grains are concentrated in the interface near the Ti side. The mechanical properties, including tensile and compressive properties at room temperature, were analyzed. The tensile test results indicate that the composite exhibited an average tensile strength of 258 MPa and an average yield strain of 9.86%. Compression test results show that when a load perpendicular to the layer is applied, the yield strain and yield stress of the material are 9.67% and 474.09 MPa, respectively. Moreover, under a load parallel to the layer, the material fails due to interfacial debonding.

Abstract. Objective:. The aim of this study was to analyze the outcomes and complications of endoscopic tympanoplasties and review the strategies for endoscopic revision surgeries. Methods:. Revision endoscopic surgeries are performed on patients with unsatisfactory outcomes after endoscopic tympanoplasties. This study was approved by the Ethics Committee of Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, China (approval No. 2020-0045-1). Results:. Residual or recurrent tympanic membrane marginal perforation is treated by autogenous fat and cartilage grafting; graft collapse is treated using tissue from the tragus; and graft displacement is treated by endoscopic fixation of the cartilage–perichondrium complex. Lateral healing of the tympanic membrane, prosthesis fracture, prosthesis extrusion, middle ear adhesions, and recurrent perforation also required revision surgeries. Conclusion:. Residual or recurrent tympanic membrane marginal perforation is the most common cause of unsatisfactory outcomes after endoscopic tympanoplasty; fat grafting is effective only for small perforations. Small cartilage grafts are an effective means of dealing with residual marginal perforation; the cartilage and perichondrium complex should be fixed securely. Patients with prosthesis implants require regular examination.

PurposeThis study aimed to construct a prognostic signature consisting of immune-related RNA-binding proteins (RBPs) to predict the prognosis of patients with head and neck squamous cell carcinoma (HNSCC) effectively.MethodsThe transcriptome and clinical data of HNSCC were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. First, we ascertained the immunological differences in HNSCC, through single-sample gene set enrichment analysis, stromal and immune cells in malignant tumor tissues using expression data (ESTIMATE), and cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT) deconvolution algorithm. Then we used univariate proportional hazards (Cox) regression analysis and least absolute shrinkage and selection operator (LASSO) Cox regression analysis to screen immune-related RBPs and acquire the risk score of each sample. Subsequently, we further investigated the difference in prognosis, immune status, and tumor mutation burden in high- and low-risk groups. Finally, the efficacy of immunotherapy was measured by the tumor immune dysfunction and exclusion (TIDE) score.ResultsWe derived 15 immune-related RBPs, including FRMD4A, ASNS, RAB11FIP1, FAM120C, CFLAR, CTTN, PLEKHO1, SELENBP1, CHCHD2, NPM3, ATP2A3, CFDP1, IGF2BP2, NQO1, and DENND2D. There were significant differences in the prognoses of patients in the high- and low-risk groups in the training set (p < 0.001) and the validation set (p < 0.01). Furthermore, there were statistical differences between the high-risk group and low-risk group in immune cell infiltration and pathway and tumor mutation load (p < 0.001). In the end, we found that patients in the low-risk group were more sensitive to immunotherapy (p < 0.001), and then we screened 14 small-molecule chemotherapeutics with higher sensitivity to the high-risk group (p < 0.001).ConclusionThe study constructed a prognostic signature of HNSCC, which might guide clinical immunotherapy in the future.

Better understanding the mechanism of cisplatin-induced ototoxicity is of great significance for clinical prevention and treatment of cisplatin-related hearing loss. However, the mechanism of cisplatin-induced inflammatory response in cochlear stria vascularis and the mechanism of marginal cell (MC) damage have not been fully clarified. In this study, a stable model of cisplatin-induced MC damage was established in vitro, and the results of PCR and Western blotting showed increased expressions of NLRP3, Caspase-1, IL-1β, and GSDMD in MCs. Incomplete cell membranes including many small pores appearing on the membrane were also observed under transmission electron microscopy and scanning electron microscopy. In addition, downregulation of NLRP3 by small interfering RNA can alleviate cisplatin-induced MC pyroptosis, and reducing the expression level of TXNIP possesses the inhibition effect on NLRP3 inflammasome activation and its mediated pyroptosis. Taken together, our results suggest that NLRP3 inflammasome activation may mediate cisplatin-induced MC pyroptosis in cochlear stria vascularis, and TXNIP is a possible upstream regulator, which may be a promising therapeutic target for alleviating cisplatin-induced hearing loss.

Sensorineural hearing loss is a common sensory impairment in humans caused by abnormalities in the inner ear. The stria vascularis is regarded as a major cochlear structure that can independently degenerate and influence the degree of hearing loss. This review summarizes the current literature on the role of the stria vascularis in the pathogenesis of sensorineural hearing loss resulting from different etiologies, focusing on both molecular events and signaling pathways, and further attempts to explore the underlying mechanisms at the cellular and molecular biological levels. In addition, the deficiencies and limitations of this field are discussed. With the rapid progress in scientific technology, new opportunities are arising to fully understand the role of the stria vascularis in the pathogenesis of sensorineural hearing loss, which, in the future, will hopefully lead to the prevention, early diagnosis, and improved treatment of sensorineural hearing loss.

Background: N6-methyladenosine (m6A), 5-methylcytosine (m5C) and N1-methyladenosine (m1A) are the main RNA methylation modifications involved in the progression of cancer. However, it is still unclear whether m6A/m5C/m1A-related long non-coding RNAs (lncRNAs) affect the prognosis of head and neck squamous cell carcinoma (HNSCC).Methods: We summarized 52 m6A/m5C/m1A-related genes, downloaded 44 normal samples and 501 HNSCC tumor samples with RNA-seq data and clinical information from The Cancer Genome Atlas (TCGA) database, and then searched for m6A/m5C/m1A-related genes co-expressed lncRNAs. We adopt the least absolute shrinkage and selection operator (LASSO) Cox regression to obtain m6A/m5C/m1A-related lncRNAs to construct a prognostic signature of HNSCC.Results: This prognostic signature is based on six m6A/m5C/m1A-related lncRNAs (AL035587.1, AC009121.3, AF131215.5, FMR1-IT1, AC106820.5, PTOV1-AS2). It was found that the high-risk subgroup has worse overall survival (OS) than the low-risk subgroup. Moreover, the results showed that most immune checkpoint genes were significantly different between the two risk groups (p < 0.05). Immunity microenvironment analysis showed that the contents of NK cell resting, macrophages M2, and neutrophils in samples of low-risk group were significantly lower than those of high-risk group (p < 0.05), while the contents of B cells navie, plasma cells, and T cells regulatory (Tregs) were on the contrary (p < 0.05). In addition, patients with high tumor mutational burden (TMB) had the worse overall survival than those with low tumor mutational burden.Conclusion: Our study elucidated how m6A/m5C/m1A-related lncRNAs are related to the prognosis, immune microenvironment, and TMB of HNSCC. In the future, these m6A/m5C/m1A-related lncRNAs may become a new choice for immunotherapy of HNSCC.

A wristwatch-style wearable dielectric resonator antenna (DRA) is proposed for the 2.45-GHz ISM band and sub-6 GHz 5G NR bands around 2.5 GHz, such as the commercial band for China Mobile Communications Corporation. The antenna is designed for applications on forearms and ankles. Practical concerns, including the aligning method, platform size, specific absorption rate, and user effects are investigated. Coplanar feeding structure is applied for alignment and isolation. Analysis of the watchband-like substrate is highlighted to avoid performance degradation. Given that platform configurations are not discretionary in actual devices, parasitic loading is introduced to attain desirable substrate effects and suppress unwanted ones. The user-device interplay is studied in light of actual application scenarios. The specific absorption rate is calculated through multilayer biological tissue models. Meanwhile, radiation variation caused by users is estimated based on human phantom models and measurements.

PurposeTo construct a prognostic signature composed of DNA repair genes to effectively predict the prognosis of patients with head and neck squamous cell carcinoma (HNSCC).MethodsAfter downloading the transcriptome and clinical data of HNSCC from the Cancer Genome Atlas (TCGA), 499 patients with HNSCC were equally divided into training and testing sets. In the training set, 13 DNA repair genes were screened using univariate proportional hazard (Cox) regression analysis and least absolute shrinkage and selection operator (LASSO) Cox regression analysis to construct a risk model, which was validated in the testing set.ResultsIn the training and testing sets, there were significant differences in the clinical outcomes of patients in the high- and low-risk groups showed by Kaplan-Meier survival curves (P < 0.001). Univariate and multivariate Cox regression analyses showed that the risk score had independent prognostic predictive ability (P < 0.001). At the same time, the immune cell infiltration, immune score, immune-related gene expression, and tumor mutation burden (TMB) of patients with HNSCC were also different between the high- and low-risk groups (P < 0.05). Finally, we screened several chemotherapeutics for HNSCC, which showed significant differences in drug sensitivity between the high- and low-risk groups (P < 0.05).ConclusionThis study constructed a 13-DNA-repair-gene signature for the prognosis of HNSCC, which could accurately and independently predict the clinical outcome of the patient. We then revealed the immune landscape, TMB, and sensitivity to chemotherapy drugs in different risk groups, which might be used to guide clinical treatment decisions.

Various conventional and novel fixing strategies for dielectric resonator antennas (DRAs) in K band and beyond are presented and investigated. Their effects on DRAs are studied in depth and explained theoretically through the perturbation theory and basic principles of DRAs. Multifunctional fixtures which achieve different antenna performance are then proposed and discussed. Their mechanisms for offering flexible bandwidth, miniaturization, frequency diversity, low cross polarization, and circular polarization are explained. In practical applications, glue is used besides fixtures to increase reliability, and its influence on antenna performance is difficult to predict. By considering various glue distributions in simulation beforehand, potential performance degradation is successfully mitigated. For validation, a four-element DRA array for 24-GHz automotive radars is fabricated. The results demonstrate that the proposed fixing strategy provides superior characteristics such as shock-resistance, fabrication and assembly simplicity, and robust antenna performance.

Ground effects on arc-shaped conformal dielectric resonator antennas (DRAs) working in the TE11δz mode are investigated and utilized to attain various radiation performances. Manipulation of directivity patterns are achieved with the help of the three-dimensional curved metal ground. The backlobe, beamwidth, broadside gain, backscattering, and cross-polarization level of the antenna are all readily controllable. The geometric theory of diffraction is applied to provide an intuitional explanation for the radiation changes. Detailed analysis is then conducted from the perspective of ground current. It is found that the current distribution is affected by configurations of both the arc DRA and ground plane. Based on this, analytical methods are developed to calculate the ground effects exclusively for conformal arc-shaped DRAs. Next, the design theory of arc DRAs with curved ground is proposed. To demonstrate it, two conformal DRAs owning directional and wide beams, respectively, are designed as paradigms. At last, a prototype is fabricated and measured for validation.

Compact arc-shaped conformal dielectric resonator antennas (DRAs) loaded by metal plates and high-dielectric-constant (HiK) patches are investigated. Their miniaturizing principles are analyzed from different aspects. Closed-form expressions are derived to characterize the function of the conformal ground in size reduction. Difference between the conventional flat ground and conformal one is discussed. As to lateral metal loading, its influence on radiation patterns are utilized to acquire additional function. Next, to replace the metallic structure, HiK patches are used as perfect electric conductor (PEC) walls. Their working mechanisms are analyzed through the electromagnetic theory in layered media, and waveguide-based simulation methods. As validation, a dielectric-loaded arc DRA is proposed. By working like a PEC, the thin dielectric patch reduces the DRA size to one half. Similar characteristics are observed between the dielectric- and metal-loaded antennas. Finally, a bare DRA and a miniaturized one are fabricated and measured. This research expands the miniaturizing theory of conformal arc DRAs.

In this work, a novel superelastic NiTi fiber reinforced NiTi/(Al _3 Ti+Al _3 Ni) metal-intermetallic laminated (SFR-MIL) composites was fabricated via vacuum hot pressing method. In order to accurately determine the reaction products of the fabrication process, the microstructure and phase constituents were analyzed and determined using scanning electron microscopy (SEM), energy dispersive spectroscope (EDS) and x-ray diffraction (XRD). Results showed that Al _3 Ti and Al _3 Ni were formed during fabrication process. In addition, the quasi-static tensile testing results indicated the average UTS and failure strain of SFR-MIL composite are 377.0 MPa and 15.4%, respectively. The compressive tests of SFR-MIL composites manifested that the average peak compressive strength of this class of materials with load perpendicular to layers is 1114.3 MPa, equivalent to or higher than that of some other laminated composites. Then, the fracture mechanisms are discussed, and the results showed that the reaction band is the possible crack initiation due to the stress concentration, and the major fracture mechanisms are intergranular and transgranular fracture modes.