Mitigating Gas Evolution in Electron Beam-Induced Gel Polymer Electrolytes Through Bi-Functional Cross-Linkable Additives.

The current high-capacity lithium-ion batteries (LIBs), reliant on flammable liquid electrolytes (LEs) and nickel-rich cathodes, are plagued by safety hazards, especially the risk of hazardous gas release stemming from internal side reactions. To address these safety concerns, an electron beam (E-beam)-induced gel polymer electrolyte (E-Gel) is introduced, employing dipentaerythritol hexaacrylate (DPH) as a bi-functional cross-linkable additive (CIA). The dual roles of DPH are exploited through a strategically designed E-beam irradiation process. Applying E-beam irradiation on the pre-cycled cells allows DPH to function as an additive during the initial cycle, establishing a protective layer on the surface of the anode and cathode and as a cross-linker during the E-beam irradiation step, forming a polymer framework. The prepared E-Gel with CIA has superior interfacial compatibility, facilitating lithium-ion diffusion at the electrode/E-Gel interface. The electrochemical assessment of 1.2 Ah pouch cells demonstrates that E-Gel substantially reduces gas release by 2.5 times compared to commercial LEs during the initial formation stage and ensures superior reversible capacity retention even after prolonged cycling at 55 °C. The research underscores the synergy of bifunctional CIA with E-beam technology, paving the way for large-scale production of safe, high-capacity, and commercially viable LIBs.

Tailoring Three-Dimensional Cross-Linked Networks Based on Water-Soluble Polymeric Materials for Stable Silicon Anode.

For stable battery operation of silicon (Si)-based anodes, utilizing cross-linked three-dimensional (3D) network binders has emerged as an effective strategy to mitigate significant volume fluctuations of Si particles. In the design of cross-linked network binders, careful selection of appropriate cross-linking agents is crucial to maintaining a balance between the robustness and functionality of the network. Herein, we strategically design and optimize a 3D cross-linked network binder through a comprehensive analysis of cross-linking agents. The proposed network is composed of poly(vinyl alcohol) grafted poly(acrylic acid) (PVA-g-PAA, PVgA) and aromatic diamines. PVgA is chosen as the polymer backbone owing to its high flexibility and facile synthesis using an ecofriendly water solvent. Subsequently, an aromatic diamine is employed as a cross-linker to construct a robust amide network that features a resonance-stabilized high modulus and enhanced adhesion. Comparative investigations of three cross-linkers, 2,2'-bis(trifluoromethyl)benzidine, 3,3'-oxidianiline, and 4,4'-oxybis[3-(trifluoromethyl)aniline] (TFODA), highlight the roles of the trifluoromethyl group (-CF3) and the ether linkage. Consequently, PVgA cross-linked with TFODA (PVgA-TFODA), featuring both -CF3 and -O-, establishes a well-balanced 3D network characterized by heightened elasticity and improved binding forces. The optimized Si and SiOx/graphite composite electrodes with the PVgA-TFODA binder demonstrate impressive structural stability and stable cycling. This study offers a novel perspective on designing cross-linked network binders, showcasing the benefits of a multidimensional approach considering chemical and physical interactions.

Analysis of Training Deep Learning Models for PCB Defect Detection.

Recently, many companies have introduced automated defect detection methods for defect-free PCB manufacturing. In particular, deep learning-based image understanding methods are very widely used. In this study, we present an analysis of training deep learning models to perform PCB defect detection stably. To this end, we first summarize the characteristics of industrial images, such as PCB images. Then, the factors that can cause changes (contamination and quality degradation) to the image data in the industrial field are analyzed. Subsequently, we organize defect detection methods that can be applied according to the situation and purpose of PCB defect detection. In addition, we review the characteristics of each method in detail. Our experimental results demonstrated the impact of various degradation factors, such as defect detection methods, data quality, and image contamination. Based on our overview of PCB defect detection and experiment results, we present knowledge and guidelines for correct PCB defect detection.

Topographical measurement of the attachments of the central band of the interosseous membrane on interosseous crests of the radius and ulna.

BACKGROUND: To suggest a reasonable isometric point based on the anatomical consistency of interosseous membrane (IOM) attachment in association with topographic characteristics of the interosseous crests, the footprints of the central band (CB) of the IOM on the radial and ulnar interosseous crests (RIC and UIC) were measured. METHODS: We measured the distance from the CB footprints from each apex of both interosseous crests in 14 cadavers and the angles between the forearm axis of rotation (AOR) and the distal slopes of the RIC and UIC in 33 volunteers. RESULTS: The CB footprints lay on the downslope of both interosseous crests with its upper margin on average 3-mm proximal from the RIC's apex consistently in the radial length, showing normality (p>0.05), and on average 16-mm distal from the UIC's apex on the ulna without satisfying normality (p<0.05). The average angle between the UIC's distal slope and the AOR was 1.3°, and the RIC's distal slope to the AOR was 14.0°, satisfying the normality tests (p>0.05), and there was no side-to-side difference in both forearms (p<0.05). CONCLUSIONS: The CB attached to the downslope just distal to the RIC's apex constrains the radius to the UIC that coincides with the AOR of the forearm circumduction, maintaining itself both isometrically and isotonically.

High Glucose with Insulin Induces Cell Cycle Progression and Activation of Oncogenic Signaling of Bladder Epithelial Cells Cotreated with Metformin and Pioglitazone.

Metformin and pioglitazone are two commonly prescribed oral hypoglycemic agents for diabetes. Recent evidence suggests that these drugs may contribute to bladder cancer. This study investigated molecular mechanism underlying effects of metformin and pioglitazone in bladder epithelial carcinogenesis in type 2 diabetes. The cells derived from human bladder epithelial cells (HBlEpCs) were treated with metformin or pioglitazone with high glucose and insulin. Cell viability and proliferation were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and a bromodeoxyuridine incorporation assay, respectively, while cell cycle regulatory factors and oncogene expression were analyzed using western blotting. Metformin or pioglitazone suppressed cell viability concentration and time dependently, which was reversed by exposure to high glucose with or without insulin. Prolonged exposure to high glucose and insulin enhanced cyclin D, cyclin-dependent kinase 4 (Cdk4), and Cdk2 expression and suppressed cyclin-dependent kinase inhibitors p21 and p15/16 in HBlEpC cotreated with pioglitazone and metformin. Levels of tumor suppressor proteins p53 and cav-1 were downregulated while those of the oncogenic protein as c-Myc were upregulated under high glucose and insulin supplementation in HBlEpC cotreated with pioglitazone and metformin. Prolonged exposure to high glucose with or without insulin downregulated B cell lymphoma 2-associated X (Bax) and failed to enhance the expression of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38MAPK) in drug-treated cells. These results suggest that hyperglycemic and insulinemic conditions promote cell cycle progression and oncogenic signaling in drug-treated bladder epithelial cells and uncontrolled hyperglycemia and hyperinsulinemia are probably greater cancer risk factors than diabetes drugs.

A sensitive electrochemical sensor for in vitro detection of parathyroid hormone based on a MoS2-graphene composite.

This paper reports a biosensor based on a MoS2-graphene (MG) composite that can measure the parathyroid hormone (PTH) concentration in serum samples from patients. The interaction between PTH and MG was analysed via an electrochemical sensing technique. The MG was functionalized using l-cysteine. Following this, PTH could be covalently immobilized on the MG sensing electrode. The properties of MG were evaluated using scanning electron microscopy, high-resolution transmission electron microscopy, X-ray diffraction, Raman spectroscopy, X-ray photoelectron spectroscopy, and Fourier transform infrared spectrometry. Following optimization of immobilized materials-such as MG, PTH, and alkaline phosphatase (ALP)-the performance of the MG sensor was investigated via cyclic voltammetry, to assess its linearity, repeatability, and reproducibility. Electrochemical impedance spectroscopy was performed on graphene oxide (GO) and MG-modified electrodes to confirm the capture of a monoclonal antibody (MAb) targeting PTH. Furthermore, the ALP-PTH-MG sensor exhibits a linear response towards PTH from artificial serum over a range of 1-50 pg mL-1. Moreover, patient sera (n = 30) were evaluated using the ALP-PTH-MG sensor and compared using standard equipment (Roche E 170). The P-value is less than 0.01 when evaluated with a t-test using Welch's correction. This implies that the fabricated sensor can be deployed for medical diagnosis.

Low-temperature growth of layered molybdenum disulphide with controlled clusters.

Layered molybdenum disulphide was grown at a low-temperature of 350 °C using chemical vapour deposition by elaborately controlling the cluster size. The molybdenum disulphide grown under various sulphur-reaction-gas to molybdenum-precursor partial-pressure ratios were examined. Using spectroscopy and microscopy, the effect of the cluster size on the layered growth was investigated in terms of the morphology, grain size, and impurity incorporation. Triangular single-crystal domains were grown at an optimized sulphur-reaction-gas to molybdenum-precursor partial-pressure ratio. Furthermore, it is proved that the nucleation sites on the silicon-dioxide substrate were related with the grain size. A polycrystalline monolayer with the 100-nm grain size was grown on a nucleation site confined substrate by high-vacuum annealing. In addition, a field-effect transistor was fabricated with a MoS2 monolayer and exhibited a mobility and on/off ratio of 0.15 cm(2) V(-1) s(-1) and 10(5), respectively.

Controlled MoS2 layer etching using CF4 plasma.

A few-layered molybdenum disulfide (MoS2) thin film grown by plasma enhanced chemical vapor deposition was etched using a CF4 inductively coupled plasma, and the possibility of controlling the MoS2 layer thickness to a monolayer of MoS2 over a large area substrate was investigated. In addition, damage and contamination of the remaining MoS2 layer surface after etching and a possible method for film recovery was also investigated. The results from Raman spectroscopy and atomic force microscopy showed that one monolayer of MoS2 was etched by exposure to a CF4 plasma for 20 s after an initial incubation time of 20 s, i.e., the number of MoS2 layers could be controlled by exposure to the CF4 plasma for a certain processing time. However, XPS data showed that exposure to CF4 plasma induced a certain amount of damage and contamination by fluorine of the remaining MoS2 surface. After exposure to a H2S plasma for more than 10 min, the damage and fluorine contamination of the etched MoS2 surface could be effectively removed.

Transforming growth factor-ß1 regulates human renal proximal tubular epithelial cell susceptibility to natural killer cells via modulation of the NKG2D ligands.

Transforming growth factor-ß (TGF-ß) has a significant role in the response to injury and tissue repair, and it has been detected in various cell types. However, the mechanism by which it regulates the response to ischemia­reperfusion injury (IRI) and manipulates natural killer (NK) cells is not well understood. In the present study, TGF­ß modulated NK cell function, thereby promoting recovery from renal IRI. Human renal proximal tubular epithelial cells (HK­2) treated with TGF­ß exhibited increased surface and intracellular expression of the NK group 2 member D (NKG2D) ligand MICA. This increased surface expression of MICA inhibited NK cell cytotoxicity to the HK­2 cells. In addition, an enzyme­linked immunosorbent assay revealed that TGF­ß treatment evidently increased the amount of soluble MICA released into the culture supernatant from HK­2 cells. Taken together, these findings suggest that TGF­ß­induced release of soluble MICA leads to downregulation of NKG2D, thereby preventing NK cell­mediated cytotoxicity toward renal proximal tubular epithelial cells in renal IRI, which in turn improves the survival of these cells.

Pectin Micro- and Nano-capsules of Retinyl Palmitate as Cosmeceutical Carriers for Stabilized Skin Transport.

Retinyl palmitate (RP)-loaded pectinate micro- and nano-particles (PMP and PNP) were designed for stabilization of RP that is widely used as an anti-wrinkle agent in anti-aging cosmeceuticals. PMP/PNP were prepared with an ionotropic gelation method, and anti-oxidative activity of the particles was measured with a DPPH assay. The stability of RP in the particles along with pectin gel and ethanolic solution was then evaluated. In vitro release and skin permeation studies were performed using Franz diffusion cells. Distribution of RP in each skin tissue (stratum corneum, epidermis, and dermis) was also determined. PMP and PNP could be prepared with mean particle size diameters of 593~843 µm (PMP) and 530 nm (i.e., 0.53 µm, PNP). Anti-oxidative activity of PNP was greater than PMP due largely to larger surface area available for PNP. The stability of RP in PMP and PNP was similar but much greater than RP in pectin bulk gels and ethanolic solution. PMP and PNP showed the abilities to constantly release RP and it could be permeated across the model artificial membrane and rat whole skin. RP was serially deposited throughout the skin layers. This study implies RP loaded PMP and PNP are expected to be advantageous for improved anti-wrinkle effects.

Silencing of galectin-3 represses osteosarcoma cell migration and invasion through inhibition of FAK/Src/Lyn activation and ß-catenin expression and increases susceptibility to chemotherapeutic agents.

Galectin-3 is involved in tumor cell proliferation, adhesion, angiogenesis and metastasis. Galectin-3 promotes ß-catenin/Wnt signaling, and ß-catenin-related oncogenesis has been frequently reported in osteosarcoma. However, the correlation between galectin-3 and ß­catenin signaling in osteosarcoma is poorly defined. We hypothesized that galectin-3 may control the migration and invasion of cancer cells and that silencing of galectin-3 would therefore, suppress motility in osteosarcoma cells. In the present study, we show that galectin-3 silencing in cultured human osteosarcoma cells had decreased cell migration and invasion capabilities; reduced the expression and activation of FAK, Src, Lyn, PI3K/Akt, ERK1/2 and ß-catenin, which are key mediators of invasion; inhibited the expression and secretion of VEGF, MCP-1, IL-8, IL-6, MMP2/9 and phospho-Stat3; and potentiated sensitivity to cisplatin. Our results suggest that galectin-3 may be a feasible therapeutic target for osteosarcoma.

Silencing of PKCη induces cycle arrest of EBV(+) B lymphoma cells by upregulating expression of p38-MAPK/TAp73/GADD45α and increases susceptibility to chemotherapeutic agents.

PKCη is involved in proliferation, differentiation, and drug resistance. However, PKCη function in EBV(+) B lymphoma remains poorly understood. Gene silencing of PKCη through siRNA knockdown inhibited cellular proliferation, induced cell cycle arrest in G0/G1 and G2/M phases, and sensitized cells to chemotherapeutic drugs. Upon PKCη knockdown, expression levels of p21, GADD45α, and TAp73 were all increased, whereas expression levels of CDK2, CDK4, CDK6, cyclin E, cyclin B1, and cdc2 were all downregulated. PKCη silencing also activated p38-MAPK, which in turn contributed to the expression of cell cycle arrest-related molecules. These results suggest that siRNA-mediated silencing of PKCη can be a potent tool to complement existing chemotherapy regimens for treating EBV(+) B lymphoma.

Antibody ligation of CM1 on cisplatin-exposed HeLa cells induces apoptosis through reactive oxygen species-dependent Fas ligand expression.

Centrocyte/centroblast marker 1 (CM1) has been identified as a pro-apoptosis molecule on B-cell lymphoma cells as well as several types of cancer cells. In this study, we investigated its signaling mechanism in HeLa cells after treatment with cisplatin in order to potentially identify a new therapeutic target. The CM1 molecule was induced on the surface of cisplatin-exposed HeLa cells. In these cells, ligation of CM1 with anti-CM1 monoclonal antibodies inhibited cell proliferation and produced reactive oxygen species. Fas ligand (FasL) expression was upregulated without upregulating Fas in cisplatin-exposed HeLa cells after CM1 stimulation. Pretreatment with N-acetylcysteine, a pan-capase inhibitor, and ZB4, an antagonistic anti-Fas antibody, effectively inhibited the apoptotic effect triggered by CM1. CM1 ligation induced apoptosis through disruption of the mitochondrial membrane potential, decreased Bcl-2 and phosphorylated ERK expression. These findings identify CM1 as a potential new therapeutic target related to cisplatin-exposed cervical cancer.

Enhanced In Vitro Skin Deposition Properties of Retinyl Palmitate through Its Stabilization by Pectin.

The purpose of this study was to examine the effect of stabilization of retinyl palmitate (RP) on its skin permeation and distribution profiles. Skin permeation and distribution study were performed using Franz diffusion cells along with rat dorsal skin, and the effect of drug concentration and the addition of pectin on skin deposition profiles of RP was observed. The skin distribution of RP increased in a concentration dependent manner and the formulations containing 0.5 and 1 mg of pectin demonstrated significantly increased RP distributions in the epidermis. Furthermore, it was found that skin distribution of RP could be further improved by combined use of pectin and ascorbyl palmitate (AP), due largely to their anti-oxidative effect. These results clearly demonstrate that the skin deposition properties of RP can be improved by stabilizing RP with pectin. Therefore, it is strongly suggested that pectin could be used in the pharmaceutical and cosmetic formulations as an efficient stabilizing agent and as skin penetration modulator.

Melphalan-induced apoptosis of EBV-transformed B cells through upregulation of TAp73 and XAF1 and nuclear import of XPA.

Melphalan (Mel) is widely used to treat patients with hematologic cancer, including multiple myeloma, but its mechanism of action in EBV-transformed B cells is poorly described. In this study, we demonstrate a novel mechanism by which transcriptionally active p73 (TAp73) induces translocation of X-linked inhibitor of apoptosis protein-associated factor 1 (XAF1) and xeroderma pigmentosum group A (XPA) during apoptosis caused by Mel treatment. We observed that Mel induced significant generation of reactive oxygen species (ROS) and subsequent apoptosis, as well as an early phosphorylation of p38 MAPK that preceded expression of the mitochondria membrane potential disruption-related molecules and the cleavage of caspases. In particular, Mel led to upregulation of TAp73, XAF1, and Puma and induced XPA nuclear import and translocation of Bax into mitochondria. Mel-induced apoptosis was inhibited by pretreatment with the ROS scavenger 4-amino-2,4-pyrrolidine-dicarboxylic acid (APDC) and the p38 MAPK inhibitor SB203580. We supposed that ROS generation might be the first event in Mel-induced apoptosis, because APDC blocked the increase in ROS, p38 MAPK, and TAp73, but SB203580 did not block ROS generation. Moreover, Mel elicited activation of ATR, and APDC inhibited phosphorylation of ATR but not SB203580. APDC and SB203580 completely blocked XPA and Bax translocation. We conclude that Mel promotes TAp73-mediated XAF1 and Puma expression via ROS generation and ATR/p38 MAPK pathway activation, thereby triggering apoptosis. Our results provide evidence of a novel alternate regulatory mechanism of TAp73 and reveal that Mel may be a therapeutic drug for curing EBV-related malignancies.

Anti-oxidative activity of pectin and its stabilizing effect on retinyl palmitate.

The purpose of this study was to examine the anti-oxidative activity of pectin and other polysaccharides in order to develop a cosmeceutical base having anti-oxidative effects towards retinyl palmitate (RP). The anti-oxidative stabilizing effects of pectin and other polysaccharides on RP were evaluated by DPPH assay and then the stabilizing effect of pectin on RP was examined as a function of time. Among the polysaccharides we examined, pectin exhibited a considerably higher anti-oxidative activity, with an approximately 5-fold greater DPPH radical scavenging effect compared to other polysaccharides. The DPPH radical scavenging effect of pectin increased gradually with increasing concentrations of pectin. At two different RP concentrations, 0.01 and 0.1% in ethanol, addition of pectin improved the stability of RP in a concentration dependent manner. The stabilizing effect of pectin on RP was more effective for the lower concentration of RP (0.01%, v/v). Further, degradation of RP was reduced following the addition of pectin as measured over 8 hours. From the results obtained, it can be suggested that pectin may be a promising ingredient for cosmeceutical bases designed to stabilize RP or other pharmacological agents subject to degradation by oxidation.

Development of estimation methods of skin oxidation and evaluation of anti-oxidative effects of genistein in topical formulations.

The objective of the present study was to establish the method of measurement of hydrogen peroxide and to estimate the anti-oxidative effect of genistein in the skin. UVB induced skin oxidation and anti-oxidative effect of genistein formulations were evaluated by determining levels of hydrogen peroxide. The mechanism involved in the determination of hydrogen peroxide is based on a color reaction between ferric ion (Fe(3+)) and xylenol orange, often called FOX assay and subsequent monitoring of absorbance values of the reactant at 540 nm. The reaction was to some extent pH-dependent and detection sensitivity was greatest at pH 1.75. Genistein liposomal gel demonstrated better anti-oxidative effect with regard to lowering hydrogen peroxide levels elevated by UVB irradiation compared to genistein-suspended gel. A linear relationship has been observed between anti-oxidative effect of genistein and drug deposition in the skin tissue. Genistein liposomal gel resulting in the localization of the drug in the deeper skin led to improved anti-oxidative effect compared to genistein gel. The suggested method for evaluation of oxidation of the skin can be used as a tool to screen effective anti-oxidative agents and their delivery systems acting on the skin.

L-kynurenine-induced apoptosis in human NK cells is mediated by reactive oxygen species.

Recent studies have shown that indoleamine 2,3-dioxygenase (IDO) plays a pivotal role in the modulation of immune response against tumor and virus infection. Here we demonstrate the pro-apoptotic effect of L-kynurenine, a tryptophan catabolite of IDO, on human NK cell line, NK92 MI. Treatment with L-kynurenine dose-dependently induced growth inhibition and apoptosis in NK92 MI cells. Treatment with the antioxidant NAC completely protected cells from L-kynurenine-induced apoptosis. Moreover, we found that treatment with Z-VAD-fmk and ZB4 slightly inhibited L-kynurenine-induced apoptosis, suggesting that L-kynurenine-induced apoptosis in NK cells occurs primarily through an ROS mediated pathway. We observed that the presence of NAC blocks cytochrome c release and activation of caspase-3 during L-kynurenine-induced apoptosis. Overall, we conclude that L-kynurenine resulting from IDO can cause cell death via ROS pathway in NK cells. Our findings provide a new insight into the interaction between NK cells and IDO positive cancer cells in regulating immune responses.

IDO metabolite produced by EBV-transformed B cells inhibits surface expression of NKG2D in NK cells via the c-Jun N-terminal kinase (JNK) pathway.

Natural Killer cells are known to play a major role in the innate immune response against viral infections and tumor cells. Several viruses, such as CMV, EBV and HIV-1, have acquired strategies to escape elimination by NK cells. In this study, we observed that EBV infection increased expression of IDO on B cells. To evaluate the function of IDO associated with EBV infection, we investigated whether EBV-induced IDO could modulate expression of NK cell-activation receptor, NKG2D. When NK cells were co-incubated with EBV transformed B cells, surface expression of NKG2D was significantly reduced in NK cells. Incubation with L-kynurenine, an IDO metabolite, down-modulated NKG2D expression in NK cells in a dose- and time-dependent manner. Incubation with the JNK inhibitor SP600125 also inhibited NKG2D expression in NK cells. In addition, we observed that the effect of L-kynurenine was blocked by JNK agonist, anisomycin, suggesting the involvement of the JNK pathway in the signal transduction of L-kynurenine-reduced NKG2D expression. Furthermore, IL-18 significantly reduced L-kynurenine-induced down-regulation of NKG2D expression in NK cells. Taken together, these data indicate that down-regulation of NKG2D by EBV-induced IDO metabolite provides a potential mechanism by which EBV escapes NKG2D-mediated attack by immune cells.

Cell cycle arrest induced by engagement of B7-H4 on Epstein-Barr virus-positive B-cell lymphoma cell lines.

B7-H4 is a recently discovered B7 family member that has inhibitory effects on T-cell immunity. However, the reverse signalling mechanism of the B7-H4-expressing cells remains unclear. Previous work has shown that B7-H4 expression was enhanced on B cells following Epstein-Barr virus (EBV) infection, and engagement of cell-surface-expressed B7-H4 induces cell death of EBV-transformed B cells. Here we found that B7-H4 was constitutively expressed on EBV-positive lymphoma cells, Raji and IM-9 cells, but was not expressed on EBV-negative lymphoma cells (Ramos). Engagement of B7-H4 significantly reduced cell growth of Raji and IM-9 cells and resulted in cell cycle arrest at G0-G1 phase in a dose- and time-dependent manner. To clarify the mechanism of cell cycle arrest via activation of B7-H4, cell cycle regulatory factors were examined by reverse transcription-polymerase chain reaction and immunoblotting. We found that B7-H4 triggered down-regulation of CDK4/6 and up-regulation of p21 expression at both protein and RNA levels. Furthermore, CDK2 and cyclin E/D expression was down-regulated by B7-H4 triggering. Additionally, the down-regulation of phospho-AKT and phospho-cyclin E were clearly detected in B7-H4-activated Raji cells, but the phosphorylation of p53 was constitutively maintained. These results indicate that B7-H4-mediated signalling on EBV-positive B-cell lymphoma cells modulates the cell cycle through down-regulation of the AKT pathway. Consequently, B7-H4 may be a new potential target for use in EBV-positive lymphoma therapy.