A cotton endoreduplication gene, GaTOP6B, regulates trichome branching development.

Trichomes are specialized epidermal structures that protect plants from biotic and abiotic stresses by synthesizing, storing, and secreting defensive compounds. This study investigates the role of the Gossypium arboreum DNA topoisomerase VI subunit B gene (GaTOP6B) in trichome development and branching. Sequence alignment revealed a high similarity between GaTOP6B and AtTOP6B, suggesting a conserved function in trichome regulation. Although AtTOP6B acts as a positive regulator of trichome development, functional analyses showed contrasting effects: Virus-induced gene silencing (VIGS) of GaTOP6B in cotton increased trichome density, while its overexpression in Arabidopsis decreased trichome density but enhanced branching. This demonstrates that GaTOP6B negatively regulates trichome number, indicating species-specific roles in trichome initiation and branching between cotton and Arabidopsis. Overexpression of the GaTOP6B promotes jasmonic acid synthesis, which in turn inhibits the G1/S or G2/M transitions, stalling the cell cycle. On the other hand, it suppresses brassinolide synthesis and signaling while promoting cytokinin degradation, further inhibiting mitosis. These hormonal interactions facilitate the transition of cells from the mitotic cycle to the endoreduplication cycle. As the level of endoreduplication increases, trichomes develop an increased number of branches. These findings highlight GaTOP6B's critical role as a regulator of trichome development, providing new genetic targets for improving cotton varieties in terms of enhanced adaptability and resilience.

Photodetector with a metalens packaging module for visible light communication based on RGBY illumination LED light source.

A novel, to the best of our knowledge, photodetector with a metalens packaging module used as the visible light communication (VLC) receiver is proposed and designed. An LED consisting of red, green, blue, and yellow chips (RGBY-LED) is adopted as the transmitter for intensity modulation direct detection VLC systems. A metalens array with a numerical aperture (NA) of 0.707 used as a polarization-insensitive planar lens of the VLC system receiver is designed at wavelengths of 457, 523, 592, and 623 nm corresponding to blue, green, yellow, and red for high efficiency. Compared with a traditional Fresnel lens positive-intrinsic-negative (PIN) photodetector module as the VLC receiver, the introduction of a metalens module can decrease the form factor of the VLC receiver module and, in particular, it is much thinner. The combination of the multi-color LED transmitter and photodetector metalens packaging module receiver can increase the modulation bandwidth due to four different wavelengths used for the VLC system. Finite-difference time domain (FDTD) simulations are performed to validate the performance of the photodetector with a metalens module. It is revealed that the corresponding efficiencies of 57.5%, 55.4%, 57%, and 56.3% were achieved at wavelengths of 623, 592, 523, and 457 nm, respectively, based on a metalens array with a 0.707 NA and 2.5 µm radius of the active area of the photodetector. It is a promising technology for indoor VLC systems such as those for smart phones and other Internet of Things devices due to the need for compact packaging for the receiver.

Nonstructural Protein A238L of the African Swine Fever Virus (ASFV) Enhances Antiviral Immune Responses by Activating the TBK1-IRF3 Pathway.

African swine fever virus (ASFV) is a double-stranded DNA virus with an envelope. ASFV has almost the largest genome among all DNA viruses, and its mechanisms of immune evasion are complex. Better understanding of the molecular mechanisms of ASFV genes will improve vaccine design. A238L, a nonstructural protein of ASFV, inhibits NF-κB activation by suppressing the HAT activity of p300. Whether A238L also affects the transcriptional activity of IRF3 remains unexplored. Here we first confirmed the ability of A238L to suppress NF-κB-activity in L929 cells. A238L inhibits the expression of proinflammatory cytokine genes. In contrast, A238L increased the phosphorylation levels of TBK1 and IRF3 in three different cell lines. A238L increases the IRF3-driven promoter activity and induces IRF3 nuclear translocation. Furthermore, A238L enhanced innate antiviral immunity in the absence or presence of poly d (A:T) or poly (I:C) stimulation, or herpes simplex virus type 1 (HSV-1) or Sendai virus (SeV) infection. This study reveals a previously unrecognized role of A238L in promoting antiviral immune responses by TBK1-IRF3 pathway activation.

Discovery of Kinetin in inhibiting colorectal cancer progression via enhancing PSMB1-mediated RAB34 degradation.

Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide. Understanding the underlying mechanism driving CRC progression and identifying potential therapeutic drug targets are of utmost urgency. We previously utilized LC-MS-based proteomic profiling to identify proteins associated with postoperative progression in stage II/III CRC. Here, we revealed that proteasome subunit beta type-1 (PSMB1) is an independent predictor for postoperative progression in stage II/III CRC. Mechanistically, PSMB1 binds directly to onco-protein RAB34 and promotes its proteasome-dependent degradation, potentially leading to the inactivation of the MEK/ERK signaling pathway and inhibition of CRC progression. To further identify potential anticancer drugs, we screened a library of 2509 FDA-approved drugs using computer-aided drug design (CADD) and identified Kinetin as a potentiating agent for PSMB1. Functional assays confirmed that Kinetin enhanced the interaction between PSMB1 and RAB34, hence facilitated the degradation of RAB34 protein and decreased the MEK/ERK phosphorylation. Kinetin suppresses CRC progression in patient-derived xenograft (PDX) and liver metastasis models. Conclusively, our study identifies PSMB1 as a potential biomarker and therapeutic target for CRC, and Kinetin as an anticancer drug by enhancing proteasome-dependent onco-protein degradation.

New model for predicting the development of pancreatic pseudocyst secondary to acute pancreatitis.

Pancreatic pseudocyst (PPC) increases the risk of a poor prognosis in in patients with acute pancreatitis (AP). Currently, an efficient tool is not available for predicting the risk of PPC in patients with AP. Therefore, this research aimed to explore the risk factors associated with PPC secondary to AP and to develop a model based on clinical information for predicting PPC secondary to AP. This study included 400 patients with acute pancreatitis and pancreatic pseudocyst secondary to acute pancreatitis admitted to the emergency department and gastroenterology department of The First Affiliated Hospital of the University of Science and Technology of China from January 2019 to June 2022. Participants were divided into no PPCs (321 cases) and PPCs (79 cases). Independent factors of PPC secondary to AP were analyzed using univariate and multivariate logistic regression. The nomogram model was constructed based on multivariate logistic regression analyses, which included all risk factors, and evaluated using R. We enrolled 400 eligible patients and allocated 280 and 120 to the training and test sets, respectively. Clinical features, including severe pancreatitis history [odds ratio (OR) = 4.757; 95% confidence interval (CI): 1.758-12.871], diabetes mellitus (OR = 6.919; 95% CI: 2.084-22.967), history of biliary surgery (OR = 9.232; 95% CI: 3.022-28.203), hemoglobin (OR = 0.974; 95% CI: 0.955-0.994), albumin (OR = 0.888; 95% CI: 0.825-0.957), and body mass index (OR = 0.851; 95% CI: 0.753-0.962), were significantly associated with the incidence of PPC after AP in the training sets. Additionally, the individualized nomogram demonstrated good discrimination in the training and validation samples with good calibration, The area under the curve and 95% CI of the nomogram were 0.883 (0.839-0.927) in the training dataset and 0.839 (0.752-0.925) in the validation set. We developed a nomogram model of PPC secondary to AP using R Studio. This model has a good predictive value for PPC in patients with AP and can help improve clinical decision-making.

Effects of cavitation erosion-induced surface damage on the corrosion behaviour of TA31 Ti alloy.

This study used electrochemical noise technology to analyse the effects of surface damage induced by cavitation erosion (CE) on the pitting and passivation behaviours of TA31 Ti alloy. According to the results, TA31 Ti alloy exhibited high corrosion resistance in NaCl solutions. However, the residual tensile stress layer generated during grinding and polishing reduced its passivation ability. Subsequently, the residual tensile stress layer was eliminated after CE for 1 h, improving the passivation ability of the material. Thereafter, pitting corrosion was initiated on the material surface. Increasing the CE time from 1 h to 2 h gradually decreased the passivation ability of the alloy. A large number of CE holes promoted the transition from pitting initiation to metastable pitting growth. which gradually dominated the surface of TA31 Ti alloy. The damage mechanism of uniform thinning increased the passivation ability and stability of the alloy with the increase in CE time from 2 h to 6 h. Therefore, the surface of TA31 Ti alloy was dominated by the initiation of pitting corrosion.

Interleukin-35 dampens T helper 22 phenotype shift in CD4+CD25+CD127dim/- regulatory T cells in primary biliary cholangitis.

The phenotype shift in regulatory T cells (Tregs) contributes to immunopathogenesis of autoimmune diseases. The current study was aimed to investigate the regulatory function of interleukin-35 (IL-35) to T helper 22 (Th22) cell phenotype shift in Tregs in primary biliary cholangitis (PBC). Fifty-five PBC patients and twenty-four controls were enrolled. CD4+CD25+CD127dim/- Tregs and Th22 cells were investigated by flow cytometry. Forkhead box P3 (FoxP3) and aryl hydrocarbon receptor (AhR) mRNA levels were assessed by real-time polymerase chain reaction. Plasma IL-10 and IL-22 levels were measured by ELISA. Purified Tregs were stimulated with exogenous IL-35, and were co-cultured with autologous CD4+CD25- T cells. Cellular proliferation and cytokine production was measured. Purified Tregs were also cultured into Th22 condition in the presence or absence of exogenous IL-35, and Th22 phenotype were assessed. PBC patients had lower levels of Treg percentage, FoxP3 mRNA, and plasma IL-10, while had higher levels of Th22 proportion, AhR mRNA, and plasma IL-22. Tregs from PBC patients showed reduced immunosuppressive activity, which presented as increased cellular proliferation, interferon-γ production and decreased IL-35/IL-10 secretion in co-culture system. Tregs shifted into Th22 phenotype in PBC patients with elevated CCR4, CCR6, and CCR10 expression as well as increased IL-22 production. IL-35 not only enhanced inhibitory function of Tregs but also suppressed phenotype shift of Tregs into Th22 phenotype in PBC patients. This process was accompanied by elevation of IL-10 and transforming growth factor-ß1 secretion by Tregs from PBC patients. The present data suggested that reduced IL-35 might be insufficient to maintain Tregs function and phenotype shift from Tregs into Th22 phenotype in PBC patients.

LncRNA LINC00649 aggravates the progression of cervical cancer through sponging miR-216a-3p.

AIM: Increasing studies have revealed the participation of lncRNAs in the occurrence and development of cervical cancer. This study explored the influence of lncRNA LINC00649 in cervical cancer. METHODS: Expression of LINC00649 and miR-216a-3p in cervical cancer was detected by reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The Kaplan-Meier curve and Cox regression analyses were conducted to evaluate the clinical value of LINC00649 in cervical cancer. The roles of LINC00649 in cervical cancer cells were detected by transfecting siRNA through cellular function assays. RESULTS: LINC00649 expression was increased in cervical cancer tissues, especially in squamous histology, positive lymph node metastasis, and high-FIGO stage tissues. The higher expression of LINC00649 predicted a shorter survival rate for patients. LINC00649 could bind directly with miR-216a-3p. Silence of LINC00649 could enhance the expression of miR-216a-3p and suppress the cervical cancer cell proliferation abilities, migration capacities, and invasion power. Whereas, transfection of miR-216a-3p inhibitor partially reverses the above cellular activities changes in cervical cancer cells. CONCLUSIONS: The LINC00649 expression may act as a prognostic predictor and may aggravate cervical cancer progression by targeting miR-216a-3p, providing potential therapeutic targets for patients with cervical cancer.

A novel thiolysis-high-performance liquid chromatography method for the determination of proanthocyanidins in grape seeds.

A novel thiolysis-high-performance liquid chromatography method for the quantitative determination of total proanthocyanidins and the mean degree of polymerization in grape seeds has been developed. Following thiolysis with formic acid and benzyl mercaptan, reaction products were separated and purified. Three proanthocyanidin monomers and three derivatives were obtained and their structures were identified by liquid chromatography-mass spectrometry, FTIR spectroscopy, and NMR spectroscopy. A decomposition model of the thiolysis products and a correction formula for proanthocyanidins concentration were established. This thiolysis-high-performance liquid chromatography method displayed good calibration linearity (R2  > 0.999 over the concentration range 0.01 to 10 mg/mL), excellent accuracy (recoveries of 97.9-99.6%), and precision (repeatability relative standard deviations of 0.45-0.75%). This method is suitable for the quantitative analysis of proanthocyanidins in grape seed products.

Overexpression of ascitic interleukin-35 induces CD8+ T cell exhaustion in liver cirrhotic patients with spontaneous bacterial peritonitis.

Interleukin (IL) -35 induces immunotolerance by suppression of CD8+ T cells during chronic infections and cancers. In the present study, we amined to investigate the role of IL-35-mediated regulation of CD8+ T cells in patients with liver cirrhosis. Seventy-one patients with liver cirrhosis (46 patients with untainted ascites and 25 patients with spontaneous bacterial peritonitis [SBP]) and 22 controls were enrolled. Plasma and ascitic IL-35 levels were measured using ELISA. Peripheral and ascitic CD4+ and CD8+ T cells were purified to investigate their functional phenotypes. IL-35-stimulated CD8+ T cells were cultured with HepG2 cells in direct and indirect contact systems. Lactate dehydrogenase expression and cytokine secretion were measured to determine the cytotoxicity of CD8+ T cells. Plasma IL-35 was elevated in patients with liver cirrhosis, and ascitic IL-35 levels were higher in the SBP group than in the untainted ascites group. No significant differences in transcription factor expression or cytokine production in peripheral and ascitic CD4+ T cells were observed among groups. In the SBP group, ascitic CD8+ T cells expressed decreased cytotoxic molecules, along with the reduced secretion of interferon-γ and tumor necrosis factor-α when compared with the untainted ascites group. IL-35 stimulation suppressed ascitic CD8+ T cell cytotoxicity and cytokine production in both direct and indirect contact culture systems. This process was accompanied by decreased cytotoxic molecule expression and increased immune-checkpoint molecules in ascitic CD8+ T cells. The present findings revealed that overexpression of ascitic IL-35 dampened the cytotoxicity of CD8+ T cells in liver cirrhotic patients with SBP.

The Role of RAB GTPases and Its Potential in Predicting Immunotherapy Response and Prognosis in Colorectal Cancer.

Background: Colorectal cancer (CRC) is the third most common cancer worldwide, in which aberrant activation of the RAS signaling pathway appears frequently. RAB proteins (RABs) are the largest Ras small GTPases superfamily that regulates intracellular membrane trafficking pathways. The dysregulation of RABs have been found in various diseases including cancers. Compared with other members of Ras families, the roles of RABs in colorectal cancer are less well understood. Methods: We analyzed the differential expression and clinicopathological association of RABs in CRC using RNA sequencing and genotyping datasets from TCGA samples. Moreover, the biological function of RAB17 and RAB34 were investigated in CRC cell lines and patient samples. Results: Of the 62 RABs we analyzed in CRC, seven (RAB10, RAB11A, RAB15, RAB17, RAB19, RAB20, and RAB25) were significantly upregulated, while six (RAB6B, RAB9B, RAB12, RAB23, RAB31, and RAB34) were significantly downregulated in tumor tissues as compared to normal. We found that the upregulated-RABs, which were highly expressed in metabolic activated CRC subtype (CMS3), are associated with cell cycle related pathways enrichment and positively correlated with the mismatch repair (MMR) genes in CRC, implying their role in regulating cell metabolism and tumor growth. While, high expression of the downregulated-RABs were significantly associated with poor prognostic CRC mesenchymal subtypes (CMS4), immune checkpoint genes, and tumor infiltrating immune cells, indicating their role in predicting prognosis and immunotherapy efficacy. Interestingly, though RAB34 mRNA is downregulated in CRC, its high expression is significantly associated with poor prognosis. In vitro experiments showed that RAB17 overexpression can promote cell proliferation via cell cycle regulation. While, RAB34 overexpression can promote cell migration and invasion and is associated with PD-L1/PD-L2 expression increase in CRC cells. Conclusions: Our study showed that RABs may play important roles in regulating cell cycle and immune-related pathways, therefore might be potential biomarkers in predicting prognosis and immunotherapy response in CRC.

Roles of Endothelial Motilin Receptor and Its Signal Transduction Pathway in Motilin-Induced Left Gastric Artery Relaxation in Dogs.

Background: Motilin increases left gastric artery (LGA) blood flow in dogs via the endothelial motilin receptor (MLNR). This article investigates the signaling pathways of endothelial MLNR. Methods: Motilin-induced relaxation of LGA rings was assessed using wire myography. Nitric oxide (NO), and cyclic guanosine monophosphate (cGMP) levels were measured using an NO assay kit and cGMP ELISA kit, respectively. Results: Motilin concentration-dependently (EC50=9.1±1.2×10-8M) relaxed LGA rings precontracted with U46619 (thromboxane A2 receptor agonist). GM-109 (MLNR antagonist) significantly inhibited motilin-induced LGA relaxation and the production of NO and cGMP. N-ethylmaleimide (NEM; G-protein antagonist), U73122 [phospholipase C (PLC) inhibitor], and 2-aminoethyl diphenylborinate [2-APB; inositol trisphosphate (IP3) blocker] partially or completely blocked vasorelaxation. In contrast, chelerythrine [protein kinase C (PKC) inhibitor] and H89 [protein kinase A (PKA) inhibitor] had no such effect. Low-calcium or calcium-free Krebs solutions also reduced vasorelaxation. N-nitro-L-arginine methyl ester [L-NAME; nitric oxide synthase (NOS) inhibitor] and ODQ [soluble guanylyl cyclase (sGC) inhibitor] completely abolished vasodilation and synthesis of NO and cGMP. Indomethacin (cyclooxygenase inhibitor), 18α-glycyrrhetinic acid [18α-GA; myoendothelial gap junction (MEGJ) inhibitor], and K+ channel inhibition through high K+ concentrations or tetraethylammonium (TEA-Cl; KCa channel blocker) partially decreased vasorelaxation, whereas glibenclamide (KATP channel blocker) had no such effect. Conclusion: The current study suggests that motilin-induced LGA relaxation is dependent on endothelial MLNR through the G protein-PLC-IP3 pathway and Ca2+ influx. The NOS-NO-sGC-cGMP pathway, prostacyclin, MEGJ, and K+ channels (especially KCa) are involved in endothelial-dependent relaxation of vascular smooth muscle (VSM) cells.

Interleukin-35 suppresses the activity of natural killer-like B cells in patients with hepatocellular carcinoma.

Natural killer-like B (NKB) cells are newly identified lymphocyte subset, which present immunomodulatory property in infectious diseases through secretion of interleukin-18 (IL-18). However, the role of NKB cells function and its regulation in hepatocellular carcinoma (HCC) is not elucidated. Seventy-two HCC patients and twenty-five controls were enrolled. Peripheral and liver-infiltrating CD3-CD19+CD56+NKp46+ cells were investigated by flow cytometry. Serum IL-35 and NKB cell-secreting cytokine level was measured by ELISA. The regulatory activity of IL-35 to peripheral and liver-infiltrating NKB cells was assessed in direct co-culture system between CD8+ T cells and HepG2 cells. Peripheral NKB cells and IL-18 secretion were reduced in HCC patients, while liver-infiltrating NKB cells and IL-18 secretion were also decreased in HCC tumor sites. Increased IL-35 level was negatively correlated with NKB cell percentage and IL-18 production in HCC. NKB cells induced the elevation of CD8+ T cell cytotoxicty, and this enhancement could be inhibited by IL-18 binding protein. IL-35 stimulation dampened NKB cell percentage and IL-18 production, leading to the suppression of NKB cell-mediated CD8+ T cell cytotoxicity in HCC patients. Our current data revealed that IL-35 might suppress NKB cell activity in HCC patients.

Synthesis and Optical Properties of In2S3-Hosted Colloidal Zn-Cu-In-S Nanoplatelets.

High-efficiency photoluminescence quaternary hexagon Zn-Cu-In-S (ZCIS) nanoplatelets (NPls) have been synthesized by a two-step cation exchange method, which starts with the In2S3 NPls followed by the addition of Cu and Zn. It is the first time that In2S3 NPls are used as templates to synthesize ZCIS NPls. In this paper, the reaction temperature of In2S3 is essential for the formation of NPls. The photoluminescence wavelength of NPls can be tuned by adjusting the temperature of Cu addition. To enhance the stability of the resulting NPls and to improve their optical properties, we introduced Zn2+ and obtained ZCIS NPls by cation exchange on the surface. It is worth noting that the obtained ZCIS NPls show a shorter fluorescence lifetime than other ternary copper sulfide-based NPls. This work provides a new way to synthesize high-efficiency, nontoxic, and no byproduct ZCIS NPls.

The Mechanism of Interleukin-35 in Chronic Hepatitis B.

Interleukin-35 (IL-35) is a newly identified inhibitory cytokine. It has recently been found to play an extremely important role in chronic hepatitis B disease, which makes it likely to be a target for new therapies for hepatitis B malady. IL-35 modulates a variety of immune mechanisms to cause persistent viral infections, such as affecting the ratio of helper T cells, reducing the activity of cytotoxic T cells, hindering the antigen presentation capacity for dendritic cells, and increasing the transcription level of hepatitis B virus. On the other hand, IL-35 can control the inflammation caused by hepatitis B liver injury. Therefore, to seek a breakthrough in curing hepatitis B disease, the contradictory part of IL-35 in the occurrence and development of this sickness is worthy of further discussion and research. This article will systematically review the biological effects of IL-35 and the specific mechanisms affecting the disease.

Differential expression of motilin receptors on the endothelium of dog gastrointestinal arteries and motilin-induced motilin receptor dependent relaxation of corresponding arteries.

BACKGROUND: Motilin's role in the regulation of vascular tone and hemodynamic besides gastrointestinal motility is concerned. This study aimed to investigate the expression of motilin receptors in gastrointestinal arteries and motilin-induced relaxation. MATERIAL AND METHODS: The expression of motilin receptors in the left gastric artery (LGA), superior mesenteric artery (SMA), and inferior mesenteric artery (IMA) of adult dogs (1.5-5 years old) were analyzed by immunochemistry, RT-PCR, and western blotting. Motilin's effects on the gastrointestinal arteries were evaluated in a multi-wire myograph system. RESULTS: Immunohistochemical staining showed that motilin receptor was expressed on the membranes of endothelial cells with the fluorescence intensity LGA > SMA > IMA (P < 0.01). The motilin receptor's mRNA and protein expression levels shared the same distribution patterns as it in fluorescence intensity (P < 0.01). In isolated LGA preparations precontracted with U46619 (a thromboxaneA2 analog), motilin induced a concentration-dependent relaxation, and the EC50 was 8.8 × 10-8 ± 0.9 × 10-8 M. Motilin-induced relaxation on the three arteries also shared the same pattern as it in fluorescence intensity (P < 0.01) and inhibited by denuded-endothelium and GM-109 (a motilin receptor antagonist) but not by atropine (a muscarinic receptor antagonist). CONCLUSIONS: Motilin receptors are expressed differentially on the membranes of endothelial cells in dog gastrointestinal arteries with a significantly high expression in the LGA. Motilin-induced relaxation is endothelium- and motilin receptor-dependent. The motilin receptor expressed on the endothelial cell membrane of the LGA is the molecular basis for motilin regulating gastric blood flow under physiological conditions in dogs.

Interleukin-35 Suppresses Interleukin-9-Secreting CD4+ T Cell Activity in Patients With Hepatitis B-Related Hepatocellular Carcinoma.

Chronic hepatitis B virus (HBV) infection induces dysfunction of immune response and chronic liver damage. However, the mechanisms that account for HBV-related hepatocellular carcinoma (HCC) are poorly understood. The aim of present study was to investigate the modulatory role of interleukin (IL)-35, an immunosuppressive cytokine, to IL-9-secreting T cells in hepatitis B-related HCC. Twenty-two HBV-related HCC patients, twenty-seven chronic hepatitis B (CHB) patients, and eleven controls were enrolled. Serum IL-35 and IL-9 concentration was measured by ELISA. Peripheral and liver-infiltrating non-specific and HBV-specific Th9 and Tc9 cells were assessed by flow cytometry. The regulatory activity of IL-35 to peripheral and liver-infiltrating Th9 cells was assessed in co-culture system between CD8+ T cells and HepG2.2.15 cells. Serum IL-35 was up-regulated, while IL-9 was down-regulated in HBV-related HCC patients compared with in CHB patients and controls. Peripheral non-specific and HBV-specific Th9 cells, but not Tc9 cells, were decreased in HBV-related HCC patients. Liver-infiltrating non-specific and HBV-specific Th9 cells were also reduced in HCC tumor sites. CD8+ T cells from CHB and HBV-related HCC patients revealed decreased cytotoxicity compared with those from controls. Autologous Th9 cells mediated the elevation of CD8+ T cell cytotoxicity, and this process was depending on IL-9 secretion. Recombinant IL-35 stimulation inhibited IL-9 secretion and PU.1 mRNA expression in non-specific and HBV-specific Th9 cells, leading to the suppression of Th9-mediated CD8+ T cell cytotoxicity in CHB and HBV-related HCC patients. Our current data indicated that IL-35 might dampen non-specific and HBV-specific Th9 cells activity in HBV-related HCC patients.

Hybrid MgCl2/AlCl3/Mg(TFSI)2 Electrolytes in DME Enabling High-Rate Rechargeable Mg Batteries.

Rechargeable magnesium batteries (RMBs) are considered as one of the most promising next-generation secondary batteries due to their low cost, safety, dendrite-free nature, as well as high volumetric energy density. However, the lack of suitable cathode material and electrolyte is the greatest challenge facing practical RMBs. Herein, a hybrid electrolyte MgCl2/AlCl3/Mg(TFSI)2 (MACT) in dimethyl ether (DME) is developed and exhibits excellent electrochemical performance. The high ionic conductivity (6.82 mS cm-1) and unique solvation structure of [Mg2(µ-Cl)2(DME)4]2+ promote the fast Mg kinetics and favorable thermodynamics in hybrid Mg salts and DME electrolyte, accelerating mass transport and the charge transfer process. Therefore, the great rate capability can be realized both in symmetric Mg/Mg cell and in CuS/Mg full cell.

Effect of γ' Phase Elements on Oxidation Behavior of Nanocrystalline Coatings at 1050 °C.

To study the effect of γ' phase elements on the oxidation behavior of nanocrystalline coatings, two comparable nanocrystalline coating systems were established and prepared by magnetron sputtering. The oxidation experiments of the nanocrystalline coatings on the K38G and N5 superalloys were carried at 1050 °C for 100 h, respectively. The chemical composition of the above coatings is the same as the substrate alloy, including the γ' elements, such as Al, Ta, and Ti. After serving at a high temperature for certain periods, their oxides participated and then affected the oxidation behavior of the coatings. The Al2O3 scale can be formed on the N5 coating, which cannot be formed on the K38G coating. Tantalum and titanium oxides can be detected on the oxide scale, which ruin its purity and integrity.

Effect of Iron Ion on Corrosion Behavior of Inconel 625 in High-Temperature Water.

The corrosion behavior of an ultralow iron nickel-based alloy Inconel 625 under high-temperature water has been evaluated. The results show that surface oxidation and pitting were the principal corrosion mechanisms of Inconel 625 during the initial immersion period. The surface layer of the oxide film is first Ni-enriched and then Fe-enriched as immersion time increases. The iron ions dissolved from the autoclave could lead to the formation of NiFe2O4 and have a great influence on the oxidation behavior of Inconel 625. The oxides nucleated by solid-state reactions with selective dissolution of Fe and Ni and then grew up through precipitation of cations from solution.