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The activity and adsorption behavior of oxygen on rutile TiO2(110) (RTiO2(110)) were investigated using the temperature programmed desorption (TPD) method with methanol (CH3OH) as the probe molecule. By controlling the coverage of molecular O2 on the surface via increasing or decreasing O2 exposure, two chemisorbed O2 species on the surface are confirmed, one at the bridging oxygen vacancy (OV) site (O22-/Ov) and the other at the five-fold coordinated titanium (Ti5c) site (O22--/Ti5c). At low O2 exposure, O22--/OV is the main species on the surface, which only leads to the O–H bond cleavage of CH3OH, producing methoxy groups (CH3O). However, after the OV sites are nearly filled by O2 at about 0.1 L O2 exposure, O2/Ti5c species begins to appear on R-TiO2(110) surface, resulting in the formation of formaldehyde (CH2O) via the reaction of O2/Ti5c species with CH3OH or CH3O to break the C-H bond at low surface temperature. Moreover, the yield of CH2O increases linearly with that of H2O. In addition, when the 1 L O2 covered surface is irradiated with 355 nm UV irradiation to desorb and dissociate O2/Ti5c species, the yield of CH2O decreases linearly with that of H2O. Further analysis suggests that the charge state of O2/Ti5c may not change as the exposure of O2 changes on the R-TiO2(110) surface, and O2 is most likely to adsorb on the Ti5c sites in the form of O22-, not O2−. The result not only advances our understanding on the adsorption state of O2 on TiO2, but also provides clues for low temperature C–H bond activation with O2 on TiO2. [ABSTRACT FROM AUTHOR]

Understanding the mechanism of hydrogen (H 2 ) formation from the conversion of water (H 2 O) and renewables on TiO 2 surfaces with cocatalysts via either photocatalysis or other catalytic processes is of significant importance to the successful design of efficient catalysts. Herein, we have investigated H 2 production from H 2 O, CH 3 OH, and C 2 H 5 OH on a Pt cluster covered rutile (R)-TiO 2 (110) surface (Pt clut /R-TiO 2 (110)) to address the mechanism of H 2 production. Experimental results demonstrate that surface adsorbates not only help H atom diffusion on Pt clut /R-TiO 2 (110) but also take part in H 2 production directly. Further density functional theory (DFT) calculations suggest that H 2 production on Pt clut /R-TiO 2 (110) occurs via a synergistic catalysis process between Pt clusters and interfacial adsorbates rather than a recombination reaction of H atoms on Pt clusters. This work provides new insight into H 2 production from H 2 O and renewables with Pt/TiO 2 catalysts, which may be applicable to H 2 production on other Pt cluster deposited metal oxide catalysts.

Ethyl acetate (EA) production from sequential ethanol (EtOH) photooxidation on a rutile(R)-TiO 2 (110) surface has been investigated by the temperature-programmed desorption (TPD) method at 355 and 266 nm. Significant EA product is detected under 266 nm irradiation, which is most likely to be formed via cross-coupling of primary dissociation products, aldehyde (CH 3 CHO) and ethoxy groups. On the contrary, EA formation at 355 nm is negligible. In addition, the initial rate of EA formation from EtOH at 266 nm is nearly 2 orders of magnitude faster than that at 355 nm. Quantitative analysis suggests that EA formation from sequential EtOH photooxidation on R-TiO 2 (110) is strongly dependent on photon energy or the energy of hot holes. This experimental result raises doubt about the traditional photocatalysis model on TiO 2 where charge carriers relax to their respective band edges prior to charge transfer to adsorbates during the photocatalytic process, leading to no dependence on photon energy in TiO 2 photocatalysis.

Muscle wasting is the hallmark of cancer cachexia and is associated with poor quality of life and increased mortality. Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, has important biological effects in the treatment of muscular dystrophy. To verify whether VPA could ameliorate muscle wasting induced by cancer cachexia, we explored the role of VPA in two cancer cachectic mouse models [induced by colon-26 (C26) adenocarcinoma or Lewis lung carcinoma (LLC)] and atrophied C2C12 myotubes [induced by C26 cell conditioned medium (CCM) or LLC cell conditioned medium (LCM)]. Our data demonstrated that treatment with VPA increased the mass and cross-sectional area of skeletal muscles in tumor-bearing mice. Furthermore, treatment with VPA also increased the diameter of myotubes cultured in conditioned medium. The skeletal muscles in cachectic mice or atrophied myotubes treated with VPA exhibited reduced levels of CCAAT/enhancer binding protein beta (C/EBPβ), resulting in atrogin1 downregulation and the eventual alleviation of muscle wasting and myotube atrophy. Moreover, atrogin1 promoter activity in myotubes was stimulated by CCM via activating the C/EBPβ-responsive cis-element and subsequently inhibited by VPA. In contrast to the effect of VPA on the levels of C/EBPβ, the levels of inactivating forkhead box O3 (FoxO3a) were unaffected. In summary, VPA attenuated muscle wasting and myotube atrophy and reduced C/EBPβ binding to atrogin1 promoter locus in the myotubes. Our discoveries indicate that HDAC inhibition by VPA might be a promising new approach for the preservation of skeletal muscle in cancer cachexia., (Copyright © 2016 the American Physiological Society.)

Background: Environmental and genetic factors are thought to be involved in the pathogenesis of multiple sclerosis (MS). Polymorphisms of tumor necrosis factor (TNF)-α -308 were implicated in MS risk in several case-control association studies. However, the studies have shown inconsistent results., Objectives: To address the association of G/A polymorphisms of TNF-α -308 with MS risk by meta-analysis., Methods: Thirteen studies were included. Pooled odds ratios (ORs) together with 95% confidence intervals (CIs) were calculated., Results: A total of 1870 cases and 2769 controls were included in the meta-analysis. The pooled result indicated that -308 A allele is significantly associated with reduced risk of MS compared with -308 G allele (A vs. G, p=0.022). The same pattern of the result was also obtained in the contrasts of AA+ GA vs. GG (p=0.008) and GA vs. GG (p=0.007). For AA vs. GG or AA vs. GA + GG, no significant association was detected most likely caused by very low frequency or non-availability of homozygote genotype AA for all of the studies., Conclusions: TNF-α -308 A allele is associated with reduced risk of MS.