Fluorine-Induced Surface Metallization for Ammonia Synthesis under Photoexcitation up to 1550†nm.

The first observation of surface metallization of TiO2-x induced by fluoride ions is presented. The emerging metallic states are contributed by the 3d orbital of surface Ti and the 2p orbital of surface bridging F, which are intrinsically originated from the strong electron repulsion between F- and adjacent Ti3+ . The metalized TiO2-x with reduced work function and downward band bending possesses high electron-donating power to supported Ru species via atomic-scale ohmic contacts, exhibiting unprecedented photocatalytic performances for ammonia synthesis across the entire solar spectrum region (200-1550 nm) at room temperature. Mechanism and kinetic analysis revealed that the loaded Ru could behave as efficient electron sinks to accumulate photogenerated electrons and that the metallic surface markedly enhanced the dissociation of H2 and N2 by the hot electrons generated by the visible or even infrared light irradiation.

The effect of transversus abdominis plane block on the chronic pain after colorectal surgery: a retrospective cohort study.

BACKGROUND: Chronic postsurgical pain (CPSP) is common and would reduce the quality of life of patients. Transversus abdominal plane (TAP) block has been widely used in lower abdominal surgery and many researches demonstrated that it could improve acute postsurgical pain. We aim to determine whether TAP block could improve chronic postoperative pain at 3 months and 6 months after colorectal surgery. METHODS: A total of 307 patients received selective colorectal surgery under general anesthesia between January, 2015 and January, 2019 in a single university hospital were included: 128 patients received TAP block combined with patient-controlled intravenous analgesia (PCIA) for postsurgical analgesia (group TP) and 179 only administrated with PCIA (group P). Main outcome was the NRS score of pain at 3 months after colorectal surgery. The data was analyzed by two-way repeated measures anova and the chi-square test. RESULTS: The NRS score at rest and during movement was decreased significantly at 24 h after surgery (rest NRS 1.07 ± 1.34 vs 1.65 ± 1.67, movement NRS 3.00 ± 1.45 vs 3.65 ± 1.89; all P = 0.003) in group TP than those of group P. There was no significant difference of NRS score at 48 h after surgery (P > 0.05). At 3 months after surgery, the NRS score during movement was also lower in group TP than that in group P (0.59 ± 1.23 vs 0.92 ± 1.65, P = 0.045). There was no significant difference of NRS score at 6 months after surgery (P > 0.05). The prevalence of CPSP was 19.5% (25/128) in group TP and 20.7% (37/179) in group P at 3 months after surgery. 13.2% (17/128) of patients suffered from CPSP in group TP and 13.9% (25/179) in group P at 6 months after surgery. Both at 3 months and 6 months after surgery, there was no statistical difference of the prevalence of CPSP between the two groups (all P > 0.05) . CONCLUSIONS: TAP block reduced NRS during movement at 3 months after surgery but did not reduce the incidence of CPSP at 3 months and 6 months after selective colorectal surgery.

Atomic-Scale Insights into Surface Lattice Oxygen Activation at the Spinel/Perovskite interface of Co3 O4 /La0.3 Sr0.7 CoO3.

Surface lattice oxygen in transition-metal oxides plays a vital role in catalytic processes. Mastering activation of surface lattice oxygen and identifying the activation mechanism are crucial for the development and design of advanced catalysts. A strategy is now developed to create a spinel Co3 O4 /perovskite La0.3 Sr0.7 CoO3 interface by in situ reconstruction of the surface Sr enrichment region in perovskite LSC to activate surface lattice oxygen. XAS and XPS confirm that the regulated chemical interface optimizes the hybridized orbital between Co 3d and O 2p and triggers more electrons in oxygen site of LSC transferred into lattice of Co3 O4 , leading to more inactive O2- transformed into active O2-x . Furthermore, the activated Co3 O4 /LSC exhibits the best catalytic activities for CO oxidation, oxygen evolution, and oxygen reduction. This work would provide a fundamental understanding to explain the activation mechanism of surface oxygen sites.

The nuclear protein Sam68 is recruited to the cytoplasmic stress granules during enterovirus 71 infection.

Our previous study found that the nuclear protein, 68-kDa Src-associated in mitosis protein (Sam68), is translocated to the cytoplasm and forms punctate pattern during enterovirus 71 (EV71) infection [Virus Research, 180 (2014), 1-11]. However, the exact function of this punctate pattern in cytoplasm during EV71 infection remains unknown. In this study, we firstly have examined this punctate pattern of Sam68 re-localization in the cytoplasm, and observed the obvious recruitments of Sam68 to the EV71-induced stress granules (SGs). Sam68, belongs to the KH domain family of RNA binding proteins (RBPs), was then confirmed that its KH domain was essential for this recruitment. Nevertheless, Knockdown of Sam68 expression using ShRNA had no effects on SGs assembly, indicating that Sam68 is not a constitutive component of the SGs during EV71 infection. Lastly, we investigated the importance of microtubulin transport to SGs aggregation, and revealed that microtubule depolymerization inhibited SGs formation, suggesting that EV71-induced SGs move throughout the cytoplasm in a microtubule-dependent manner. Taken together, these results illuminated that EV71 infections can induce SGs formation, and Sam68, as a SGs component, migrates alone with SGs dependent on intact microtubule upon the viral infections. These findings may provide novel underlying mechanism for delineating the role of SGs during EV71 infection.

Enterovirus 71 inhibits cellular type I interferon signaling by inhibiting host RIG-I ubiquitination.

Enterovirus 71 (EV71) is a human pathogen that induces hand, foot, and mouth disease (HFMD) and fatal neurological diseases in young children and infants. Pathogenicity of EV71 is likely related to its ability to evade host innate immunity through inhibiting cellular type I interferon signaling. However, it is less well understood the molecular events governing this process. In this study, we found that EV71 infection suppressed the induction of antiviral immunity by inhibiting the expression levels of IFN-ß and IFN-stimulated genes (ISGs), such as ISG54 and ISG56, at the late stage of viral infection. At the same time, our results showed that EV71 infection significantly inhibited ubiquitination of RIG-I. In contrast, up-regulation of RIG-I ubiquitination promoted expression of IFN-ß and ISGs, suggesting that inhibition of cellular type I interferon signaling was caused by down-regulation of RIG-I ubiquitination during EV71 infection. These results suggest that inhibition of RIG-I-mediated type I IFN responses by EV71 may contribute to the pathogenesis of viral infection.

The optimal dose of oxycodone in PCIA after laparoscopic surgery for gastrointestinal cancer in elderly patients: A randomized controlled trial.

Objective: To explore the optimal bolus dose of oxycodone for patient controlled intravenous analgesia (PCIA) without background dose in elderly patients after laparoscopic surgery for gastrointestinal cancer. Methods: In this prospective, randomized, double-blind, parallel-controlled study, we recruited patients aged 65 years or older. They underwent laparoscopic resection for gastrointestinal cancer and received PCIA after surgery. Eligible patients were randomly divided into 0.01, 0.02, or 0.03 mg/kg group according to the bolus dose of oxycodone in PCIA. The primary outcome was VAS scores of pain on mobilization at 48 h after surgery. Secondary endpoints included the VAS scores of rest pain, the total and effective numbers of press in PCIA, cumulative dose of oxycodone used in PCIA, the incidence of nausea, vomiting and dizziness, as well as patients' satisfaction at 48 h after surgery. Results: A total of 166 patients were recruited and randomly assigned to receive a bolus dose of 0.01 mg/kg (n = 55), 0.02 mg/kg (n = 56) or 0.03 mg/kg (n = 55) of oxycodone in PCIA. The VAS scores of pain on mobilization, the total and effective numbers of press in PCIA in 0.02 mg/kg group and 0.03 mg/kg group were lower than those in 0.01 mg/kg group (P < 0.05). Cumulative dose of oxycodone used in PCIA and patients' satisfaction in 0.02 and 0.03 mg/kg groups were more than those in 0.01 mg/kg group (P < 0.01). The incidence of dizziness in 0.01 and 0.02 mg/kg groups was lower than that in 0.03 mg/kg group (P < 0.01). There were no significant differences in VAS scores of rest pain, the incidence of nausea and vomiting among three groups (P > 0.05). Conclusion: For elderly patients undergoing laparoscopic surgery for gastrointestinal cancer, 0.02 mg/kg bolus dose of oxycodone in PCIA without background infusion may be a better choice.

Efficient full-spectrum driven ammonia synthesis over heterostructured TiO2 nanosheet arrays.

Here, we report that efficient photocatalytic ammonia synthesis was realized across the entire solar spectrum by using Ru modified anatase/TiO2(B) heterostructured nanosheet arrays. The superior NH3 production rates of 2004 µg h-1 g-1 and 521 µg h-1 g-1 were achieved under visible light (400 nm) and near-infrared-light (1550 nm) irradiation, respectively.

Organic anion transporting polypeptide 1A2 mediates fentanyl uptake in cultured cells.

Individual differences in the response to fentanyl, which may be caused by different concentrations of the drug in the central nervous system, can complicate analgesic treatment. It has been reported that the organic anion transporting polypeptide (OATP) at the blood­brain barrier (BBB) in Sprague­Dawley rats may serve an important role in the transport of fentanyl across the BBB. However, whether human OATP can transport fentanyl has thus far not been reported. The present study aimed to establish a 293 cell line stably overexpressing OATP1A2, and to determine whether OATP1A2 is able to transport fentanyl across the plasma membrane. Initially, 293 cells were transfected with an OATP1A2­expressing plasmid (referred to as 293­OATP1A2 cells), and single colonies were selected and characterized following geneticin treatment. Subsequently, reverse transcription­quantitative polymerase chain reaction and western blot analyses were conducted to verify the transfection efficiency. Furthermore, treatment of 293­OATP1A2 cells with different concentrations of fexofenadine (FEX) and fentanyl was performed to investigate the transport function of OATP1A2 in 293 cells. FEX and fentanyl uptake experiments were also performed with naringenin, an inhibitor of OATP1A2. The results indicated that FEX and fentanyl uptake was significantly increased in 293­OATP1A2 cells compared with that in the control­transfected cells. The 293­OATP1A2­mediated uptake of FEX at concentration of 100 nM FEX was ~10­fold higher than that of 293­VC cells. The 293­OATP1A2­mediated uptake of fentanyl (100 nM) was 5.1­fold higher compared with that in 293­VC cells. In 293­OATP1A2 cells, the uptake of FEX without OATP1A2 inhibitor naringenin (100 µg/ml) was 2.8­fold higher compared with that in the presence of naringenin, and the uptake of fentanyl without naringenin was 7.3­fold higher compared with that in the presence of naringenin (100 µg/ml). In conclusion, 293 cells that overexpressed OATP1A2 were successfully constructed, and OATP1A2 was revealed to mediate fentanyl uptake in the cultured cells.

Correction: Identification of Optimal Insertion Site in Recombinant Newcastle Disease Virus (rNDV) Vector Expressing Foreign Gene to Enhance Its Anti-Tumor Effect.

[This corrects the article DOI: 10.1371/journal.pone.0164723.].

Identification of Optimal Insertion Site in Recombinant Newcastle Disease Virus (rNDV) Vector Expressing Foreign Gene to Enhance Its Anti-Tumor Effect.

Recombinant Newcastle disease virus (rNDV) is tumor selective and intrinsically oncolytic, which has been developed as a vector to express exogenous genes to enhance its oncolytic efficacy. Our previous studies found that insertion sites of foreign gene in rNDV vector affected its expression and anti-tumor activities. However, the optimal insertion site for foreign genes remains unknown. In this study, we inserted the enhanced green fluorescence protein (EGFP) and IL2 genes into four different intergenic regions of the rNDV using reverse genetics technology. Recombinants rNDV-EGFPs and rNDV-IL2s were successfully rescued, which displayed the similar growth kinetics with parental virus. Both EGFP mRNA and protein levels were most abundant in HepG2 cells, when EGFP gene was inserted between the NP/P site of the rNDV. Similarly, the IL-2 expressed by HepG2 cells infected with rNDV-IL2 was highest, when IL2 was inserted into NP/P site. To test whether these rNDVs that express higher foreign genes could induce stronger anti-tumor response, we treated the H22-oxter-tumor-bearing C57BL/6J mice with rNDV-IL2s and then examined the oncolytic efficacy. The results showed that rNDV-IL2-NP/P had the strongest inhibition of murine hepatoma carcinoma tumors. The splenocytes isolated from the mice treated with rNDV-IL2-NP/P reached the highest degrees of CD4+ T and CD8+ T cells. In addition, animals' survival rate in rNDV-IL2-NP/P-treated group was higher than that of other groups. Taken together, these results demonstrate that NP and P gene junction in rNDV is the optimal insertion site for foreign genes expression to enhance rNDV's anti-tumor effects.

Newcastle disease virus chimeras expressing the Hemagglutinin- Neuraminidase protein of mesogenic strain exhibits an enhanced anti-hepatoma efficacy.

Newcastle disease virus (NDV) is an intrinsically tumor-specific virus, many researchers have reported that lentogenic NDV is a safe and effective agent for human cancer therapy. It had been demonstrated that the amino acid sequence of the fusion protein cleavage site is a major factor in the pathogenicity and anti-tumor efficacy of rNDV. However, the role of Hemagglutinin-Neuraminidase (HN) gene that contributes to virulence and anti-tumor efficacy remains undefined. To assess the role of HN gene in virus pathogenicity and anti-tumor efficacy, a reverse genetic system was developed using the lentogenic NDV Clone30 strain to provide backbone for gene exchange. Chimeric virus (rClone30-Anh(HN)) created by exchange of the HN gene of lentogenic strain Clone30 with HN gene of mesogenic strain produce no significant changes in virus pathogenicity as assessed by conducting the mean death time (MDT) and intracerebral pathogenicity index (ICPI) assays. In vitro, infection with chimeras could induce the formation of syncytium relative significantly in HepG2 cells. Furthermore, chimeras was shown to induce the cell apoptosis via MTT and Annexin V-PI assays, reduce mitochondrial membrane potential and increase the mRNA transcription level of caspase 3. In vivo, ICR mice carrying tumor of hepatoma H22 cells were treated via intratumoral injection of chimeric virus. The treatment of chimera shows an obvious suppression in tumor volume. These results suggest that it could be an ideal approach to enhance the antitumor ability of Newcastle disease virus and highlighted the potential therapeutic application of rClone30-Anh(HN) as a viral vector to deliver foreign genes for treatment of cancers.

Activation of PI3K/Akt pathway limits JNK-mediated apoptosis during EV71 infection.

Apoptosis is frequently induced to inhibit virus replication during infection of Enterovirus 71 (EV71). On the contrary, anti-apoptotic pathway, such as PI3K/Akt pathway, is simultaneously exploited by EV71 to accomplish the viral life cycle. The relationship by which EV71-induced apoptosis and PI3K/Akt signaling pathway remains to be elucidated. In this study, we demonstrated that EV71 infection altered Bax conformation and triggered its redistribution from the cytosol to mitochondria in RD cells. Subsequently, cytochrome c was released from mitochondria to cytosol. We also found that c-Jun NH2-terminal kinase (JNK) was activated during EV71 infection. The JNK specific inhibitor significantly inhibited Bax activation and cytochrome c release, suggesting that EV71-induced apoptosis was involved into a JNK-dependent manner. Meanwhile, EV71-induced Akt phosphorylation involved a PI3K-dependent mechanism. Inhibition of the PI3K/Akt pathway enhanced JNK phosphorylation and the JNK-mediated apoptosis upon EV71 infection. Moreover, PI3K/Akt pathway phosphorylated apoptosis signal-regulating kinase 1 (ASK1) and negatively regulated the ASK1 activity. Knockdown of ASK1 significantly decreased JNK phosphorylation, which implied that ASK1 phosphorylation by Akt inhibited ASK1-mediated JNK activation. Collectively, these data reveal that activation of the PI3K/Akt pathway limits JNK-mediated apoptosis by phosphorylating and inactivating ASK1 during EV71 infection.

Analysis of synonymous codon usage in enterovirus 71.

Enterovirus 71 (EV71) is the major cause of hand-foot-and-mouth disease in children. In our study, using the complete genome sequences of 42 EV71 representing all three genotypes, we analyzed synonymous codon usage and the relative dinucleotide abundance in EV71 genome. The general correlation between base composition and codon usage bias suggests that mutational pressure rather than natural selection is the main factor that determines the codon usage bias in EV71 genome. Furthermore, we observed that the relative abundance of dinucleotides in EV71 is independent of the overall base composition but is still the result of differential mutational pressure, which also shapes codon usage. In addition, other factors, such as hydrophobicity and aromaticity, also influence the codon usage variation among the genomes of EV71. This study represents the most comprehensive analysis of EV71 codon usage patterns and provides a basic understanding of the mechanisms for codon usage bias.