Theoretical insight into the promotion effect of potassium additive on the water-gas shift reaction over low-coordinated Au catalysts.

CONTEXT: How to elucidate the effect of alkali metal promoters on gold-catalyzed water-gas shift reaction intrinsically remains a challenging, because that the complex synergy effects such as strong metal-support interactions, interfacial effects, and charge transfer of supported metal catalysts makes people difficulty in the understanding the alkali promotion phenomenon in nature. Herein, we report a systematically study of whole water-gas shift reaction mechanism on pure and the K-modified defected-Au(211) (i.e., by removing one surface Au atom from perfect Au(211) and make one model with the Au-Au coordination number is six) by using the microkinetic modeling based on first principles. Our results indicate that the presence of K can increase the adsorption ability of oxygen-containing species via the attractive coulomb interaction, has no significant effect on the adsorption of H species, but inhibits the adsorption of CO due to the steric effect. K promoter stabilizes the water adsorption by ~0.3 eV, which results in one order increasing of whole reaction rate. Interestingly, the strong promotion effect of the K can be assigned to the significant direct space interaction between K and the adsorbate H2O* through the inducted electric field, which can be further confirmed by the posed negative electric field on the unpromoted D-Au(211). Microkinetic modeling results revealed that the carboxyl mechanism is the most likely to occur, redox mechanism is the next one, and the formate mechanism is the least likely to occur. For different kinds of alkali metal additives, the adsorption strength of water molecules gradually weakens from Li to Cs, but Na shows the best promoter behavior at the low temperature. By considering the effect of K contents on the reactivity of water-gas shift reaction, we found that the K with the medium coverage (~0.2~0.3 ML) has the strongest promoting effect. It is expected that the conclusion of this work can be extended to other WGSR catalytic systems like Cu(or Pt). METHODS: All calculations were performed by using the plane-wave based periodic method implemented in Vienna ab initio simulation package (VASP, version 5.4.4), where the ionic cores are described by the projector augmented wave (PAW) method. The exchange and correlation energies were computed using the Perdew, Burke and Ernzerhof functional with the vdw correction (PBE-D3). The transition states (TSs) were searched using the climbing image nudged elastic band (CI-NEB) method. Some electronic structure properties like work function was predicated by the DS-PAW software. Microkinetic simulation was carried out using MKMCXX software.

AKT3 deficiency in M2 macrophages impairs cutaneous wound healing by disrupting tissue remodeling.

AKT signaling and M2 macrophage-guided tissue repair are key factors in cutaneous wound healing. A delay in this process threatens human health worldwide. However, the role of AKT3 in delayed cutaneous wound healing is largely unknown. In this study, histological staining and transcriptomics demonstrated that prolonged tissue remodeling delayed wound healing. This delay was accompanied by defects in AKT3, collagen alpha-1(I) chain (COL1A1), and collagen alpha-1(XI) chain (COL11A1) expression and AKT signaling. The defect in AKT3 expression was M2 macrophage-specific, and decreased AKT3 protein levels were observed in CD68/CD206-positive macrophages from delayed wound tissue. Downregulation of AKT3 in M2 macrophages did not influence cell polarization but impaired collagen organization by inhibiting COL1A1 and COL11A1 expression in human skin fibroblasts (HSFs). Moreover, a co-culture model revealed that the downregulation of AKT3 in the human monocytic cell line (THP-1)-derived M2 macrophages impaired HSF proliferation and migration. Finally, cutaneous wound healing in AKT3-/- mice was much slower than that of AKT3+/+ mice, and F4/80 macrophages from the AKT3-/- mice had an impaired ability to promote wound healing. Thus, the downregulation of AKT3 in M2 macrophages prolonged tissue remodeling and delayed cutaneous wound healing.

Identification of Fe and Zr oxide phases in an iron-zirconium binary oxide and arsenate complexes adsorbed onto their surfaces.

The Fe-Zr binary oxide adsorbents have higher arsenic adsorptive capacities than either iron oxide or zirconium oxide alone, indicating a strong synergistic effect exists between Fe and Zr oxides. However, no generally accepted in-depth explanations have been reached on the origin of this better performance. In the present study, the component phases, the active surface sites, the structure of the adsorbed As(V) surface species, and the mechanism of the synergistic effect, were investigated and elucidated using multiple advanced experimental techniques combined with quantum chemical calculations. Goethite and lepidocrocite were identified as the main Fe oxide components while amorphous zirconium hydroxide was the main Zr oxide component, respectively. A monodentate-mononuclear complex and a bidentate-binuclear complex were revealed to be dominant on the surface, respectively, when at lower and higher initial As(V) concentrations. Density functional theory calculations indicated that As(V) preferred to bind with Zr-OH rather than Fe-OH. This was verified with the As K-edge EXAFS results and XPS observations. The synergistic effect was due to a short-range ordering state, the enlarged contents of amorphous and poorly-crystalline fractions, and increased hydroxyl surface site density. These results lead to the realization that the above properties are preferred in future adsorbent preparations.

Periodic density functional theory analysis of direct methane conversion into ethylene and aromatic hydrocarbons catalyzed by Mo4C2/ZSM-5.

Mo/ZSM-5-catalyzed methane conversion into aromatic hydrocarbons is an important reaction to produce ethylene and benzene, but the detailed reaction mechanism has not been investigated due to its high complexity. In the present study, density functional theory combined with a periodic model was used to investigate the reaction mechanism of direct methane conversion into aromatic hydrocarbons catalyzed by Mo/ZSM-5. The calculation results show that the active phase for Mo is Mo4C2 instead of MoOx. The whole reaction processes processed via the following steps: the C-H bond in methane was first activated by Mo4C2 with an energy barrier of 1.01 eV and then converted into ethylene species via the coupling of two CH3 species as well as two successive dehydrogenation steps (2CH3 → C2H6 → C2H4 + 2H). The rate-controlling step for the processes to form ethylene is the coupling of two methyl species with a barrier of 1.22 eV. The produced ethylene species then react with each other to produce C6H8via the reaction of 3C2H4 → C3H8 + 2H2, and molecular benzene is formed by successive dehydrogenation of C6H8. The rate-limiting step for benzene formation from ethylene is the cyclization step of chain C6H8 with an energy barrier of 1.21 eV. Additionally, molecular propane (C3H8) is formed by the reaction of C2H4 + CH4 → C3H8, and the controlling step C3H7 + H → C3H8 has a barrier of 1.46 eV. Molecular C10H12 is produced via coupling of C6H8 and C2H4, where the limiting step is the dehydrogenation step of C8H12 with an energy barrier of 1.44 eV. Our present calculation results indicate that the selectivity of benzene was the largest among the possible products, that is, C2H4, C3H6, C6H6 and C10H12, based on the corresponding controlling step barrier. Importantly, the rate-controlling step for the whole reaction process from methane to benzene is the dissociative adsorption of methane (CH4 → CH3 + H) with an energy barrier of 1.83 eV when considering entropy contribution. The present study may help people design a good catalyst for the formation of benzene from methane; in other words, the catalyst should have a good ability to activate the C-H bond of molecular methane.

A density functional theory study of ethylene hydrogenation on MgO- and γ-Al2O3-supported carbon-containing Ir4 clusters.

Density functional theory was used to investigate the reaction mechanisms of ethylene hydrogenation on MgO(100)- and γ-Al2O3(110)-supported carbon-containing Ir4 clusters. The cluster supported on γ-Al2O3(110) is more active than that on MgO(100), which is consistent with experimental observations. The present calculations show that the binding energies of reactants on the carbon-containing Ir4 cluster are weaker on the γ-Al2O3 supported catalysts compared to the MgO supported Ir cluster. This relatively weak adsorption energy of ethylene on the γ-Al2O3 surface means that ethylene desorption is easier, hence a higher catalytic activity is achieved. To gain further understanding, the energy decomposition method and micro-kinetic analysis are also introduced.

Evaluation of varying ductile fracture criteria for 42CrMo steel by compressions at different temperatures and strain rates.

Fracturing by ductile damage occurs quite naturally in metal forming processes, and ductile fracture of strain-softening alloy, here 42CrMo steel, cannot be evaluated through simple procedures such as tension testing. Under these circumstances, it is very significant and economical to find a way to evaluate the ductile fracture criteria (DFC) and identify the relationships between damage evolution and deformation conditions. Under the guidance of the Cockcroft-Latham fracture criteria, an innovative approach involving hot compression tests, numerical simulations, and mathematic computations provides mutual support to evaluate ductile damage cumulating process and DFC diagram along with deformation conditions, which has not been expounded by Cockcroft and Latham. The results show that the maximum damage value appears in the region of upsetting drum, while the minimal value appears in the middle region. Furthermore, DFC of 42CrMo steel at temperature range of 1123~1348 K and strain rate of 0.01~10 s(-1) are not constant but change in a range of 0.160~0.226; thus, they have been defined as varying ductile fracture criteria (VDFC) and characterized by a function of temperature and strain rate. In bulk forming operations, VDFC help technicians to choose suitable process parameters and avoid the occurrence of fracture.

Induction of polyploidy by histone deacetylase inhibitor: a pathway for antitumor effects.

Histone deacetylase (HDAC) inhibitors can induce various transformed cells to undergo growth arrest and/or death. Suberoylanilide hydroxamic acid (SAHA) is an HDAC inhibitor which is in phase I/II clinical trials and has shown antitumor activity in hematologic and solid tumors at doses well tolerated by patients. HDAC is the target for SAHA, but the mechanisms of the consequent induced death of transformed cells are not completely understood. In this study, we report that SAHA induced polyploidy in human colon cancer cell line HCT116 and human breast cancer cell lines, MCF-7, MDA-MB-231, and MBA-MD-468, but not in normal human embryonic fibroblast SW-38 and normal mouse embryonic fibroblasts. The polyploid cells lost the capacity for proliferation and committed to senescence. The induction of polyploidy was more marked in HCT116 p21WAF1-/- or HCT116 p53-/- cells than in wild-type HCT116. The development of senescence of SAHA-induced polyploidy cells was similar in all colon cell lines. The present findings indicate that the HDAC inhibitor could exert antitumor effects by inducing polyploidy, and this effect is more marked in transformed cells with nonfunctioning p21WAF1 or p53 genes.

[Roles of mitochondria in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells].

OBJECTIVE: In order to investigate the roles of mitochondria in vitamin E succinate (VES)-induced apoptosis in human gastric cancer SGC-7901 cells. METHODS: Mitochondrial transmembrane potential (deltapsi(m)) was observed by confocal laser scanning microscopy, while the expression of cytochrome c in cytosol and caspase-3 was measured by western blotting after the cells were treated with VES at 5, 10, 20 microg/ml. RESULTS: VES obviously decreased deltapsi(m) with dose- and time-dependent relationship, increased the expression of cytochrome c in cytosol and caspase-3 and activated caspase-3 as well. CONCLUSION: VES-induced apoptosis in SGC-7901 cells might involve mitochondrial permeability transition, release of cytochrome c and activation of caspase-3 downstream.

c-Jun N-terminal kinase is required for vitamin E succinate-induced apoptosis in human gastric cancer cells.

AIM: To investigate the roles of c-Jun N-terminal kinase (JNK) signaling pathway in vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells. METHODS: Human gastric cancer cell lines (SGC-7901) were treated with vitamin E succinate (VES) at 5, 10, 20 mg/L. Succinic acid and vitamin E were used as vehicle controls and condition medium only as an untreated (UT) control. Apoptosis was observed by 4', 6-diamidine-2'-phenylindole dihydrochloride (DAPI) staining for morphological changes and by DNA fragmentation for biochemical alterations. Western blot analysis was applied to measure the expression of JNK and phosphorylated JNK. After the cells were transiently transfected with dominant negative mutant of JNK (DN-JNK) followed by treatment of VES, the expression of JNK and c-Jun protein was determined. RESULTS: The apoptotic changes were observed after VES treatment by DNA fragmentation. DNA ladder in the 20 mg/L VES group was more clearly seen than that in 10 mg/L VES group and was not detected following treatment of UT control, succinate and vitamin E. VES at 5, 10 and 20 mg/L increased the expression of p-JNK by 2.5-, 2.8- and 4.2-fold, respectively. VES induced the phosphorylation of JNK beginning at 1.5 h and produced a sustained increase for 24 h with the peak level at 12 h. Transient transfection of DN-JNK blocked VES-triggered apoptosis by 52%. DN-JNK significantly increased the level of JNK, while decreasing the expression of VES-induced c-Jun protein. CONCLUSION: VES-induced apoptosis in human gastric cancer SGC-7901 cells involves JNK signaling pathway via c-Jun and its downstream transcription factor.

Combined therapy of allantoin, metronidazole, dexamethasone on the prevention of intra-abdominal adhesion in dogs and its quantitative analysis.

AIM: To observe the preventive effects of combined therapy of AMD (allantoin, metronidazolem and dexamethasone in combination) on intra-abdominal adhesion in dogs. METHODS: 20 dogs of both sexes were used in this study. After laparotomy under anesthesia, 2 cm section of cecal end was clamped and ligated, then 1 cm cecum section was cut and another 1 cm was kept. The cecum stump was closed with purse-string suture. Both parietal and visceral peritonea were stripped for an area of about 3X4 cm(2). Before the skin closure, the animals were divided into two groups randomly. The abdominal cavities in Group AMD (n=10) were rinsed by 200 ml of AMD solution, and with 50 ml left, whereas the control (n=10) received the equal volume of normal saline. After 7 d, the degree of intra-abdominal adhesions was evaluated by using the score method of ultrasonography and traditional dissection. RESULTS: Compared with the control, both the ultrasonography and traditional dissection scores in Group AMD were significantly decreased that marked as 2.0+/-1.25 vs 3.3+/-0.82 and 1.91+/-0.83 vs 3.3+/-0.82 respectively (P<0.01). CONCLUSION: The combined therapy of AMD is an effective way to prevent intra-abdominal adhesion, and ultrasonography is an useful tool to diagnose intra-abdominal adhesion.

Mechanism of Differentiation of HEL Cells Induced by Hydroxyurea.

HEL cells, a human erythroleukemia cell line, mainly express fetal globin gene(gamma) and small amount of the embryonic(epsilon) globin gene, but not the adult (beta) globin gene. Our previous studies demonstrated that hydroxyurea could induce HEL cells to express adult (beta) globin gene and induce HEL cells to terminal differentiation. In order to reveal the differentiation mechanism of HEL cells induced by hydroxyurea, GMSA was performed to examine the binding of nuclear extracts from hydroxyurea induced and uninduced HEL cells to the positive control region in the 5'-flanking sequence of human beta-globin gene and to the synthesized GATA oligonucleotides. Our results showed that, in the nuclear proteins from the induced HEL cells, the binding of GATA-1 to GATA motif was increased. However, the binding of GATA-2 to GATA motif was decreased. Besides, our data showed that a YY1-like protein was decreased quickly in hydroxyurea induced HEL cells. Western blotting analysis was used to analyze variation of GATA proteins in nuclei of HEL cells. Results revealed that the amount of GATA-2 was significantly decreased while the amount of GATA-1 was increased after HEL cells were induced for 12 h. These results indicate that GATA-1 may play a critical role in inducing HEL cells to terminal differentiation. The YY1-like protein and GATA-2 might inhibit HEL cells from terminal differentiation.