Behavior of the resonant absorption area of a 57Fe-doped Ni/C catalyst during sulfidation

In-situ Moessbauer spectroscopy measurements down to 4.2 K were performed on a 57Fe-doped Ni/C catalyst after various successive sulfidation treatments. After exposure of the catalysts to the H2S/H2 gas mixt. at room temp., part of the 57Fe becomes sulfidic. The rest is present as a sulfate-like intermediate species. The interaction between this intermediate species and the carbon support material is influenced by water. A

Pore Formation During Solidification of Aluminum: Reconciliation of Experimental Observations, Modeling Assumptions, and Classical Nucleation Theory

An in-depth discussion of pore formation is presented in this paper by first reinterpreting in situ observations reported in the literature as well as assumptions commonly made to model pore formation in aluminum castings. The physics of pore formation is reviewed through theoretical fracture pressure calculations based on classical nucleation theory for homogeneous and heterogeneous nucleation, with and without dissolved gas, i.e., hydrogen. Based on the fracture pressure for aluminum, critical pore size and the corresponding probability of vacancies clustering to form that size have been calculated using thermodynamic data reported in the literature. Calculations show that it is impossible for a pore to nucleate either homogeneously or heterogeneously in aluminum, even with dissolved hydrogen. The formation of pores in aluminum castings can only be explained by inflation of entrained surface oxide films (bifilms) under reduced pressure and/or with dissolved gas, which involves only growth, avoiding any nucleation problem. This mechanism is consistent with the reinterpretations of in situ observations as well as the assumptions made in the literature to model pore formation

Association between Vitamin D Levels and Nonalcoholic Fatty Liver Disease: Potential Confounding Variables

Nonalcoholic fatty liver disease (NAFLD), historically considered to be the hepatic component of the metabolic syndrome, is a spectrum of fat-associated liver conditions, in the absence of secondary causes, that may progress to nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. Disease progression is closely associated with body weight or fatness, dyslipidemia, insulin resistance, oxidative stress, and inflammation. Recently, vitamin D deficiency has been linked to the pathogenesis and severity of NAFLD because of vitamin D "pleiotropic" functions, with roles in immune modulation, cell differentiation and proliferation, and regulation of inflammation. Indeed, several studies have reported an association between vitamin D and NAFLD/NASH. However, other studies have failed to find an association. Therefore, we sought to critically review the current evidence on the association between vitamin D deficiency and NAFLD/NASH, and to analyze and discuss some key variables that may interfere with this evaluation, such as host-, environment-, and heritability-related factors regulating vitamin D synthesis and metabolism; definitions of deficient or optimal vitamin D status with respect to skeletal and nonskeletal outcomes including NAFLD/NASH; methods of measuring 25(OH)D; and methods of diagnosing NAFLD as well as quantifying adiposity, the cardinal link between vitamin D deficiency and NAFLD