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The polycrystalline strontium ferrate titanate (SrFe0.1Ti0.9O3, SFTO) thin films have been successfully prepared by chemical solution method. By analyzing the current-voltage (I–V) characteristics, we discuss the conduction mechanism of SFTO. It is found that the number of oxygen vacancy defects is increased by Fe ion doping, making SFTO be with better resistive switching property. Fe ion doping can also enhance the absorption of strontium titanate to be exposed to visible light, which is associated with the change of energy band. The band gap width (2.84 eV) of SFTO films is figured out, which is less than that of pure strontium titanate. Due to more oxygen vacancy defects caused by Fe ion doping, the band gap width of strontium titanate was reduced slightly. The defect types of SFTO thin films can be determined by electron paramagnetic resonance spectroscopy. In addition, we analyzed the energy band and state density of SFTO by first-principles calculation based on density functional theory, and found that Fe ion doping can reduce the band gap width of strontium titanate with micro-regulation on the band structure. A chemical state of SFTO was analyzed by X-ray photo electron spectroscopy. At the same time, the structure and morphology of SFTO were characterized by X-ray diffraction and scanning electron microscope. This study deepens further understanding of the influence of Fe ion doping on the structure and properties of strontium ferrate titanate, which is expected to be a functional thin film material for memristor devices.

Though there are many advantages of pegylated interferon-α (PegIFN-α) treatment to chronic hepatitis B (CHB) patients, the response rate of PegIFN-α is only 30 ~ 40%. Therefore, it is important to explore predictors at baseline and establish models to improve the response rate of PegIFN-α.We randomly divided 260 HBeAg-positive CHB patients who were not previously treated and received PegIFN-α monotherapy (180 μg/week) into a training dataset (70%) and testing dataset (30%). The intersect features were extracted from 50 routine laboratory variables using the recursive feature elimination method algorithm, Boruta algorithm, and Least Absolute Shrinkage and Selection Operator Regression algorithm in the training dataset. After that, based on the intersect features, eight machine learning models including Logistic Regression, k-Nearest Neighbors, Support Vector Machine, Decision Tree, Random Forest, Gradient Boosting, Extreme Gradient Boosting (XGBoost), and Naïve Bayes were applied to evaluate HBeAg seroconversion in HBeAg-positive CHB patients receiving PegIFN-α monotherapy in the training dataset and testing dataset.XGBoost model showed the best performance, which had largest AUROC (0.900, 95% CI: 0.85-0.95 and 0.910, 95% CI: 0.84-0.98, in training dataset and testing dataset, respectively), and the best calibration curve performance to predict HBeAg seroconversion. The importance of XGBoost model indicated that treatment time contributed greatest to HBeAg seroconversion, followed by HBV DNA(log), HBeAg, HBeAb, HBcAb, ALT, triglyceride, and ALP.XGBoost model based on common laboratory variables had good performance in predicting HBeAg seroconversion in HBeAg-positive CHB patients receiving PegIFN-α monotherapy.

Genetically engineered bacterial cancer therapy presents several advantages over conventional therapies. However, the anticancer effects of bacterium-based therapies remain insufficient, and serious side effects may be incurred with the increase in therapeutic dosages. Photodynamic therapy (PDT) suppresses tumor growth by producing reactive oxygen species (ROS) through specific laser-activated photosensitizers (PSs). Tumor-specific PS delivery and activatable ROS generation are two critical aspects for PDT advancement. Here, we propose PDT-enhanced oncolytic bacterial immunotherapy (OBI) by using genetically engineered avirulent Salmonella expressing a fluorogen-activating protein (FAP). Upon binding to a fluorogen, FAP could be activated and generate fluorescence and ROS. The instant activation of persistent fluorescence was detected in tumors through bacterium-based imaging. In a colon cancer model, PDT-OBI showed an enhanced tumor inhibition effect and prolonged animal survival. Mechanically, PDT generated ROS, resulting in the killing of cancer cells and over-accumulated bacteria. The pathogen-associated molecular patterns and damage-associated molecular patterns released from the destroyed bacteria and cancer cells recruited and activated immune cells (macrophages, neutrophils, and dendritic cells), which released additional proinflammatory cytokines (TNF-α and IL-1β); reduced anti-inflammatory cytokines (IL-10); and further enhanced immune cell infiltration in a positive-feedback manner, thus reducing bacterium-induced side effects and improving anticancer activities. This synergistic therapy has promising potential for cancer immunotherapy.

Pegylated interferon-alpha (PegIFNα) therapy has limited effectiveness in hepatitis B e-antigen (HBeAg)-positive chronic hepatitis B (CHB) patients. However, the mechanism underlying this failure is poorly understood. We aimed to investigate the influence of bile acids (BAs), especially taurocholic acid (TCA), on the response to PegIFNα therapy in CHB patients. Here, we used mass spectrometry to determine serum BA profiles in 110 patients with chronic HBV infection and 20 healthy controls (HCs). We found that serum BAs, especially TCA, were significantly elevated in HBeAg-positive CHB patients compared with those in HCs and patients in other phases of chronic HBV infection. Moreover, serum BAs, particularly TCA, inhibited the response to PegIFNα therapy in HBeAg-positive CHB patients. Mechanistically, the expression levels of IFN-γ, TNF-α, granzyme B, and perforin were measured using flow cytometry to assess the effector functions of immune cells in patients with low or high BA levels. We found that BAs reduced the number and proportion and impaired the effector functions of CD3+CD8+ T cells and natural killer (NK) cells in HBeAg-positive CHB patients. TCA in particular reduced the frequency and impaired the effector functions of CD3+CD8+ T and NK cells in vitro and in vivo and inhibited the immunoregulatory activity of IFN-α in vitro. Thus, our results show that BAs, especially TCA, inhibit the response to PegIFNα therapy by impairing the effector functions of CD3+CD8+ T and NK cells in HBeAg-positive CHB patients. Our findings suggest that targeting TCA could be a promising approach for restoring IFN-α responsiveness during CHB treatment.

PbxSr1-xTiO3 (PST) (x = 0.3, 0.35 and 0.40, abbreviated as PST30, PST35 and PST40, respectively) ceramics were prepared by solid-state reaction route. Coexistence of tetragonal and cubic phase of ceramics is confirmed by X-ray diffraction pattern at room temperature (RT). Temperature-dependent dielectric permittivity εr measurements showed that Pb2+ doping increased the phase transition temperature of ferroelectric (FE) to paraelectric (PE) phase. The temperature-related polarization-electric field (P-E) measurements were performed to study the FE properties of PST ceramics. Phase transition from FE to PE was observed in P-E measurements. Furthermore, pyroelectric energy harvesting performance was evaluated based on Olsen cycle. The calculated results of pyroelectric energy harvesting density (ND) showed that PST35 ceramic with ND = 283 kJ/m3 (∆T = 70°C, EL = 2.5 kV and EH = 40 kV) is most potential for pyroelectric energy harvesting application near RT among all samples.

The ability to harness innate immunity is a promising solution for improving cancer immunotherapy. Interferon (IFN) induces expression of IFN-stimulated genes (ISGs) by activating the JAK-STAT signaling pathway to promote innate immunity and inhibit malignant tumor growth, but the functions and mechanisms of most ISGs in cancer regulation are unknown. As an innate immune effector, ISG12a promotes the innate immune response to viral infection. In this study, ISG12a was found to be expressed at low levels in gastrointestinal cancer, represented by hepatocellular cancer (HCC) and gastric cancer (GC), and it identified as a tumor suppressor that affects clinical prognosis. ISG12a silencing accelerated the malignant transformation and epithelial–mesenchymal transition of cancer cells. Mechanistically, ISG12a promoted β-catenin proteasomal degradation by inhibiting the degradation of ubiquitinated Axin, thereby suppressing the canonical Wnt/β-catenin signaling pathway. Notably, β-catenin was identified as a transcription factor for PD-L1. Inhibition of Wnt/β-catenin signaling by ISG12a suppressed expression of the immune checkpoint PD-L1, rendering cancer cells sensitive to NK cell-mediated killing. This study reveals a mechanism underlying the anticancer effects of IFN. Some ISGs, as represented by ISG12a, may be useful in cancer therapy and prevention. The identified interrelations among innate immunity, Wnt/β-catenin signaling, and cancer immunity may provide new insight into strategies that will improve the efficiency of immunotherapy.

Background and aim Recently, the role of albumin-bilirubin (ALBI) score in chronic hepatitis B (CHB) has not been well-understood. We aimed to investigate the association of ALBI score with natural history of chronic HBV infection and treatment response of CHB patients. Methods The ALBI score in a cohort of 849 individuals including 721 chronic HBV-infected patients naive to anti-HBV treatment in different phases and 128 healthy controls were estimated. Additionally, the dynamic changes of ALBI score of 243 hepatitis B e antigen (HBeAg)-positive CHB patients treated with pegylated interferon-alpha (PEG-IFN-α) or nucleos(t)ide analogues (NAs) were tested for 72 weeks. Results ALBI score differed among phases, with the highest score in HBeAg-positive CHB patients, followed by HBeAg-negative CHB patients, HBeAg-positive chronic HBV infection, and HBeAg-negative chronic HBV infection. Besides, CHB patients harbouring high baseline ALBI score exhibited a relatively stronger therapeutic response to PEG-IFN-α or NAs. Moreover, the rate of HBeAg and HBsAg loss in patients with ALBI grade 2 was persistently higher than that in patients with ALBI grade 1 throughout the course of treatment. Furthermore, ALBI score was an independent predictor of sustained response achievement. The combined use of ALBI score, HBeAg and ALT could enhance the predictive value of treatment response. Conclusions ALBI score differed significantly across the natural course of chronic HBV infection and was correlated with PEG-IFN-α and NAs treatment response in HBeAg-positive CHB patients, which suggested that ALBI score could be useful as an auxiliary clinical factor to determine the initiation of therapy and predict stronger antiviral treatment response.

Background: There are limited data regarding the efficacy of addition of entecavir (ETV) or tenofovir disoproxil fumarate (TDF) to Peg-IFNα-2b in HBeAg positive chronic hepatitis B (CHB) patients without early response to Peg-IFNα-2b. In this study, we aimed to evaluate the efficacy of ETV and TDF in HBeAg positive CHB patients who had a poor response to Peg-INFα-2b at the end of 12 weeks of monotherapy. Methods: A total of 40 HBeAg-positive CHB patients who were naive to antiviral therapy were recruited. The patients received a subcutaneous injection of Peg-IFNα-2b (180 µg) once a week for 12 weeks. However, the patients had a poor response to Peg-INFα-2b at the end of the 12-week-period monotherapy. The patients were then divided into two therapeutic protocol groups: (1) Group A: Patients received Peg-IFNα-2b (180 µg) subcutaneously weekly and ETV (0.5 mg) orally once daily for 48 weeks; (2) Group B: Patients received Peg-IFNα-2b (180 µg) subcutaneously weekly and TDF (300 mg) orally once daily for 48 weeks. The therapeutic efficacy was evaluated. Blood samples were collected at baseline and every 12 weeks. Routine biochemical tests including ALT, AST, etc. were measured by automated biochemical technique. HBV DNA was quantified using the TaqMan PCR assay. The levels of HBsAg, HBsAb, HBeAg, HBeAb and HBcAb were measured using a commercial chemiluminescent microparticle immunoassay. Results: The HBsAg level declined rapidly in both two treatment groups during the first 12 weeks and declined gradually in the next 36 weeks. At week 48, the mean ΔHBsAg level in Peg-IFNα-2b+TDF group was significantly higher than that in Peg-IFNα-2b +ETV group (-1.799 ± 0.3063 vs. -1.078 ± 0.2028, P=0.0491). The HBeAg loss rate was significantly higher in TDF add-on group than that in ETV add-on group at week 48 (40% vs. 10%, P=0.028). At week 48, the proportions of patients with undetectable HBV DNA (

Dynamic and real-time hepatitis B virus (HBV) DNA, genotype, and reverse transcriptase mutation analysis plays an important role in diagnosing and monitoring chronic hepatitis B (CHB) and in assessing the therapeutic response. We established a highly sensitive coamplification at lower denaturation temperature PCR (COLD-PCR) coupled with probe-based fluorescence melting curve analysis (FMCA) for precision diagnosis of CHB patients. The imprecision with %CV and detection limit of HBV DNA detected by COLD-PCR/FMCA were 2.58% to 4.42% and 500 IU/mL, respectively. For mutation, the imprecision and detection limit were 3.35% to 6.49% and 1%, respectively. Compared with Sanger sequencing, the coincidence rates of genotype and mutation were 96.0% and 82.5%, respectively, whereas the inconsistent data resulted from a low proportion (20%) of mixed genotypes or mixed mutations. The mutation ratio in HBV infection patients was as follows: hepatitis B e antigen (HBeAg)-positive infection (0/0.0%) HBeAg-negative infection (16/4.5%) HBeAg-positive hepatitis (30/5.5%) HBeAg-negative hepatitis (36/6.5%). In patients with entecavir therapy, the proportion of mutation at baseline or week 4 in virologic response (VR) group was4%, whereas in the partial VR group, it was mostly ≥4%. COLD-PCR/FMCA provides a novel tool with high sensitivity, convenience, and practicability for the simultaneous quantification of HBV DNA, genotype, and mutation. It might be used for distinguishing the different phases of HBV infection and predicting VR of CHB patients.

Innate immunity is an essential way for host cells to resist viral infection through the production of interferons (IFNs) and proinflammatory cytokines. Interferon regulatory factor 3 (IRF3) plays a critical role in the innate immune response to viral infection. However, the role of IRF1 in innate immunity remains largely unknown. In this study, we found that IRF1 is upregulated through the IFN/JAK/STAT signaling pathway upon viral infection. The silencing of IRF1 attenuates the innate immune response to viral infection. IRF1 interacts with IRF3 and augments the activation of IRF3 by blocking the interaction between IRF3 and protein phosphatase 2A (PP2A). The DNA binding domain (DBD) of IRF1 is the key functional domain for its interaction with IRF3. Overall, our study reveals a novel mechanism by which IRF1 promotes the innate immune response to viral infection by enhancing the activation of IRF3, thereby inhibiting viral infection. IMPORTANCE The activation of innate immunity is essential for host cells to restrict the spread of invading viruses and other pathogens. IRF3 plays a critical role in the innate immune response to RNA viral infection. However, whether IRF1 plays a role in innate immunity is unclear. In this study, we demonstrated that IRF1 promotes the innate immune response to viral infection. IRF1 is induced by viral infection. Notably, IRF1 targets and augments the phosphorylation of IRF3 by blocking the interaction between IRF3 and PP2A, leading to the upregulation of innate immunity. Collectively, the results of our study provide new insight into the regulatory mechanism of IFN signaling and uncover the role of IRF1 in the positive regulation of the innate immune response to viral infection.

Summary Our previous study revealed that Yin Yang 1(YY1) played an important part in promoting interleukin (IL)-6 production in rheumatoid arthritis (RA). However, whether YY1 has any role in regulation of IL-8 in RA remains unclear. YY1 and IL-8 expression in RA patients were analyzed by real-time polymerase chain reaction (PCR). Ingenuity pathway analysis (IPA) was used to analyze the signaling pathway involved in YY1-induced IL-8 production. The expression of YY1 and proteins involved in the pathway were detected by Western blot and enzyme-linked immunosorbent assay (ELISA). Migration of neutrophils was performed by chemotaxis assay. In this study, we found that high expression of IL-8 was positively associated with YY1 expression in RA. Blocking YY1 expression by YY1-short hairpin (sh)RNA lentivirus reduced IL-8 production. Mechanistically, we showed YY1 activated IL-8 production via the phosphatidylinositol-3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway. Further, using a co-culture system consisting of peripheral blood mononuclear cells (PBMC) and neutrophils, we found that migration of neutrophils would be inhibited by YY1 RNA interference. Finally, using the collagen-induced arthritis animal model, we showed that treatment with the YY1-shRNA lentivirus led to reduction of IL-8 levels and attenuation of inflammation and neutrophil infiltration in vivo. Our results reveal a role of YY1 involved in neutrophil infiltration in RA via the PI3K/Akt/mTOR/IL-8 signaling pathway. YY1 may be a new therapeutic target for treatment of RA.

Serum HBV large surface protein (HBV-LP) is an envelope protein that has a close relationship with HBV DNA level. This study is to explore the prediction value of HBV-LP in different phase of HBV infection and during antiviral therapy in chronic hepatitis B (CHB) patients.A retrospective study was conducted in 2033 individuals, which included 1677 HBV infected patients in different phases and 356 healthy controls. HBV-LP, HBV serum markers and HBV DNA were detected by ELISA, CMIA and qRT-PCR, respectively. 85 CHB patients receiving PegIFNα or ETV were divided into virological response (VR) and partial virological response (PVR). The dynamic changes of HBV DNA and HBV-LP were observed.The level of HBV-LP in 2033 individuals was shown as: HBeAg-positive hepatitis HBeAg-positive infection HBeAg-negative hepatitis HBeAg-negative infection healthy controls. HBV-LP was positive in all patients whose HBV DNA 1.0E + 06 IU/ml. When HBsAg was0.05 IU/ml or1000 IU/ml, HBV DNAs were all negative if HBV-LP 1.0 S/CO. When HBsAg was between 0.05 IU/ml and 1000 IU/ml, the consistency of HBV-LP with HBV DNA was 100% in case of HBV-LP 4.0 S/CO in HBeAg-positive patients and HBV-LP 2.0 S/CO in HBeAg-negative ones. During antiviral therapy, baseline HBV-LP was lower in VR patients than that in PVR patients. The optimal cut-off points to predict VR by baseline HBV-LP were 32.4 and 28.6 S/CO for HBeAg-positive and HBeAg-negative hepatitis patients, respectively.HBV-LP may be a useful marker for distinguishing the different phases of HBV infection. Moreover, baseline HBV-LP level can be used for predicting VR of CHB patients.

AIM Sodium taurocholate co-transporting polypeptide (NTCP) plays an important role in the enterohepatic circulation of bile acids. Recently, NTCP was identified as a hepatitis B virus (HBV) receptor. The aim of this study is to investigate the association of NTCP polymorphisms with HBV clinical outcomes and investigate the relationship between NTCP polymorphisms and the serum bile acid level in a Chinese Han population. METHODS The single nucleotide polymorphisms rs2296651 and rs4646285 were genotyped in 1619 Chinese Han individuals. Improved multiple ligase detection reaction was utilized to genotype. The level of bile acids was measured by the enzymatic cycling method. Quantitative polymerase chain reaction analysis was carried out to analyze the potential function. RESULTS In logistic regression analysis, the frequency of rs2296651 (S267F) CT genotype was higher in HBV immune recovery and healthy control groups than in the chronic HBV infection group (P = 0.001 and P

Background Recent studies suggest that serum lipids are associated with pegylated interferon-alpha (PEG-IFN-α) treatment response in chronic hepatitis C patients. However, the role of serum lipids in influencing the outcome of HBV treatment is not well understood. This study aims to investigate the association of serum lipids with the response to interferon-alpha treatment for chronic hepatitis B (CHB) patients. Methods We dynamically measured 11 clinical serum lipid parameters of 119 hepatitis B e antigen (HBeAg)-positive CHB patients, including 53 patients who achieved sustained response (SR) and 66 patients who achieved non-response (NR) induced by PEG-IFN-α treatment for 48 weeks. Results The dynamic analysis showed that the baseline serum total cholesterol (TCHO) level was higher in the NR group than that in the SR group ( P=0.004). Moreover, the correlation analysis demonstrated a significant positive correlation between TCHO and hepatitis B surface antigen (HBsAg) at baseline ( P=0.009). In addition, CHB patients with high baseline TCHO levels exhibited higher HBV DNA, HBsAg, HBeAg and hepatitis B e antibody (HBeAb) levels during early treatment periods (weeks 0, 4, 12 and 24) than those with the low TCHO levels. Furthermore, the logistic regression analysis identified that baseline serum TCHO was a risk factor for NR achievement (OR=4.94; P=0.047). Conclusions: Our results indicated that serum TCHO was associated with PEG-IFN-α therapeutic response in HBeAg-positive CHB patients which suggested that serum TCHO could be useful as an auxiliary clinical factor to predict poor efficacy of PEG-IFN-α therapy.

Enhancement on resistive switching characteristics of Bismuth ferrite (BFO) has attracted persistent interest in the past decades due to the inimitable interior structure. In the work, the amorphous and the polycrystalline Bismuth ferrite thin films have been successfully prepared via sol–gel method. We utilize X-ray diffraction, Transmission Electron Microscope and absorption spectrum to characterize the internal structure and calculate the band gap of Bismuth ferrite thin film samples. By comparing the current–voltage (I-V) characteristics between the amorphous and the polycrystalline sample, we investigate the amorphous sample has better resistive switching performance (switching ratio is 104) than that of polycrystalline (1 0 1) bismuth ferrite thin film devices. However, the polycrystalline Bismuth ferrite sample exhibits favorable switchable photovoltaic response and good stability. Additionally, we discuss the conduction mechanism via the double logarithm fitting of amorphous Bismuth ferrite sample. The article also indicates that resistive switching property is closely related with the defects such as oxygen vacancies. The article deepens the comprehension of resistive switching properties of amorphous and polycrystalline Bismuth ferrite thin film which would have further potential applications in advanced electronic devices such as new resistive memory.

Recent studies have demonstrated a potential link between mitochondrial DNA (mtDNA) content and cirrhosis or hepatocellular carcinoma (HCC). However, there are few studies evaluating mtDNA content as a noninvasive marker of chronic hepatitis B infection (CHB). In this study, we conducted a case-control study to determine mtDNA content in peripheral blood leukocyte (PBL) samples from 76 CHB cases naive to antivirus therapy and 96 healthy controls, and then evaluated the association between mtDNA content and baseline serum concentration of HBV markers. Consequently, CHB cases had significantly higher mtDNA content than healthy controls (1052.85 vs 618.98, P

The mechanism for the co-existence of hepatitis B surface antigen (HBsAg) and antibodies to HBsAg (anti-HBs) in chronic HBV infected patients remains controversial. This study aimed to explore the role of HBV S gene mutation and anti-HBs subtype-nonspecificity in patients with simultaneous HBsAg/anti-HBs positivity. Chronic HBV infections with (n = 145, group I) and without (n = 141, group II) anti-HBs were included. The S gene was amplified and sequenced. The neutralization experiment was used in group I patients' sera to determine the specificity of anti-HBs. Additionally, the HBV vaccinated persons' sera were used to estimate the neutralize capacity of anti-HBs against HBsAg in group I patients. Results showed that 2.63% (145/5513) chronic HBV infected patients had positive results for anti-HBs. HBsAg amino acid (aa) substitution rate in 35 patients of group I was significantly higher than that in 58 patients of group II (1.89% vs 0.95%, P

The Src-associated in mitosis 68-kDa (Sam68) protein is a highly conserved nuclear protein and is involved in a series of cellular processes, including transcription and signal transduction. Sam68 is comprised of 443 amino acids and contains an RGG box domain, a KH domain, and a tyrosine-rich domain. Its role in hepatitis C virus (HCV) replication is unknown. Here, we find that Sam68 promotes HCV replication without affecting viral translation. The RNA immunoprecipitation experiments show that the positive strand of HCV RNA interacts with Sam68. HCV infection triggers the translocation of the Sam68 protein from the nucleus to the cytoplasm, where it interacts with the HCV genome. Further study shows that the region of Sam68 spanning amino acids 1 to 157 is the pivotal domain to interact with the stem-loop 2 of the HCV 5′ untranslated region (5′ UTR) and is responsible for the enhancement of HCV replication. These data suggested that Sam68 may serve as a proviral factor of HCV to facilitate viral replication through interaction with the viral genome. IMPORTANCE Hepatitis C virus (HCV) is a member of the Flaviviridae family, and its infection causes chronic hepatitis, liver cirrhosis, and even hepatocellular carcinoma. No vaccine is available. Many host factors may be implicated in the pathogenesis of HCV-related diseases. This study discloses a new host factor that binds to the HCV 5′ UTR and promotes HCV replication. Sam68 may play an important role in HCV-related diseases, and further investigation is highly encouraged to explore its specific actions in HCV pathogenesis.

Ruddlesden–Popper (RP) phase Sr2TiO4 thin film is deposited successfully on FTO/glass substrate by spin coating. X-ray diffraction (XRD) pattern shows high-intensity (00 l) (l = 2, 4, and 6) peaks. The device shows bipolar resistive switching (RS) effect. Analysis on current–voltage (I-V) characteristic shows that conduction mechanism is dominated by Schottky emission in both low resistive state (LRS) and high resistive state (HRS). A variation (~0.12 eV) in Schottky barrier height (SBH) is observed between HRS and LRS. Thus, RS at electrode-Sr2TiO4 interface is the main mechanism. In general, variation of SBH is induced by accumulation of interfacial charges. Polarization-voltage (P-V) measurement shows hysteresis loop, which indicates the accumulation of interfacial charges. Formation and migration of charged oxygen vacancies and ions is proposed to be a possible mechanism of interfacial charges accumulation. This study paves the avenue for exploring RS application based on RP phase Sr2TiO4 perovskite oxide.

Inflammatory cytokine gene polymorphisms may influence the hepatic and extrahepatic HBV-related disease. In this study, we aimed to investigate the relationship between polymorphisms of IL-17, IL-21 gene and HBV related hepatocellular carcinoma in Chinese Han population.We performed a multi-center study comprised 866 HBV-related hepatocellular carcinoma (HCC) patients and 1086 unrelated patients with a diagnosis of chronic hepatitis B (CHB) as control to evaluate the effects of IL-17 (rs4711998), IL-21 SNPs (rs12508721, rs13143866 and rs2221903) and the susceptibility of HCC. MassARRAY technology was utilized to genotype. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum IL-17 and IL-21 level. Quantitative real time polymerase chain reaction (qRT-PCR) was used to analyze the serum viral loads.In logistic regression analysis, our results showed the frequency of rs4711998 allele G in CHB group was significantly higher than that in HCC group (P = 0.042, 0.859(0.743-0.994)), and it is present only among females. Compared to HCC group, rs13143866 A allele was more likely to appear in HCC group (P = 0.015, 1.268 (1.049-1.532)). The frequency of AA also showed different between HCC group and CHB groups (P = 0.011, 3.135 (1.292-7.603)), which showed strong sex-specific relationships. ELISA showed a higher serum IL-17 and IL-21 expression in HCC patients compared to CHB patients (P all0.05). Haplotype rs12508721C/rs13143866A/rs2221903T in male HCC group was statistically higher than in male CHB group(P = 0.013) but not in females (P 0.05).We suggested rs4711998 allele A as risk factors for women to develop HBV related-HCC in Chinese Han population. rs13143866 allele A as risk factors to develop HBV related-HCC in Chinese male population. Male patients with haplotype rs12508721C/rs13143866A/rs2221903T may with 1.3-fold risk for HBV-related HCC.

A molecular-level insight into the nature of reactive oxygen species involved in dihydrogen (H2 ) dissociation is of great importance to understand gold catalysis. In this study, laser ablation generated and mass-selected AuNbO4+ oxide cluster cations could dissociate H2 in an ion-trap reactor. The reaction has been characterized by time-of-flight mass spectrometric experiments and density functional calculations. The lowest energy isomer of AuNbO4+ contains two lattice oxygen (O2- ) and one superoxide (O2.- ) species. The gold atom anchors the H2 molecule in the first step and then delivers one hydrogen atom to the O2- ion in H2 dissociation. At the same time, O2.- is reduced into a peroxide unit that can accept the second hydrogen atom of H2 with the generation of a hydroxyl radical as the main product. In this study, the important roles of the O2.- unit in the dissociation of H2 have been identified.

Analog-type resistive switching (RS) behavior of Au/HfO2/ZnO thin film deposited on flexible Mica substrate is studied. ZnO thin film is deposited on insulating Mica substrate as bottom electrode and buffer layer by magnetron sputtering. And then HfO2 thin film is fabricated by chemical solution deposition method. The device shows diode-like current-voltage (I-V) characteristic, and its conductivity decreases gradually with consecutive sweeping of applied bias. Such resistive switching behavior is similar to the learning process of biological synapse. A model of mobile charges migration and accumulation at interface is constructed to understand the resistive switching mechanism. It is suggested that the change of Schottky barrier height (SBH) is responsible for resistive switching. This study provides guidance to develop HfO2-based memristor for electronic synapse device, but also provides the theoretical model for understanding the physical mechanism of analog-type resistive switching.