Interfacial impregnation chemistry in the synthesis of nickel catalysts supported on titania.

The interfacial chemistry of the impregnation step involved in the preparation of nickel catalysts supported on titania is presented. Several methodologies based on deposition data, pH measurements, potentiometric mass titrations, and microelectrophoresis have been used in conjunction with diffuse reflectance UV/Vis/NIR spectroscopy, simulations, and semiempirical quantum chemical calculations. Three mononuclear inner-sphere complexes were formed at the compact layer of the "titania/electrolyte solution" interface: A monosubstituted, dihydrolyzed complex above a terminal oxo group, a disubstituted, dihydrolyzed complex above two terminal adjacent oxo groups, and a disubstituted, nonhydrolyzed complex above one terminal and one bridging adjacent oxo groups. The monosubstituted, dihydrolyzed complex predominates. The contribution of the disubstituted configurations is also important at very low Ni(II) surface concentration, but it decreases as the Ni(II) surface concentration increases. In addition, bi- and trinuclear inner-sphere complexes were formed. The receptor site involves one bridging and two terminal oxo groups in the first case and two bridging and three terminal oxo groups in the second case. The relative surface concentrations of these configurations increase initially with Ni(II) surface concentration and then remain practically constant. The understanding of these interfacial processes at a molecular level is very important to shift the catalytic synthesis from an art to a science as well as to obtain strict control of the impregnation step and, to some extent, of the whole preparative sequence. This study is very relevant to the synthesis of submonolayer/monolayer nickel catalysts supported on TiO(2) following equilibrium deposition filtration (otherwise called equilibrium adsorption).

Reduction of CD55 and/or CD59 in red blood cells of patients with HIV infection.

BACKGROUND: Anemia is a common feature in HIV infection. An increased sensitivity of lymphocytes from HIV patients to lysis by complement has been correlated with a decreased expression of CD55 and CD59 in their surface. The aim of this study was to evaluate CD55/CD59 presence in red cells of HIV patients and explore possible correlations with clinical parameters. MATERIAL/METHODS: CD55/CD59 expression was evaluated in erythrocytes of 37 patients (30M/7F, median age: 39 years) with HIV infection (25 also having hemophilia), 121 controls, and 8 PNH patients using the sephacryl-gel microtyping system. Ham and sucrose tests were also performed. RESULTS: Anemia was present in 14/37 (37%) HIV patients. Interestingly, all HIV patients had deficient CD55 and/or CD59 erythrocytes: 8 (21%) for both CD55 andCD59 and 29 (78%) isolated CD55 and/or CD59 negativity. Deficient erythrocytes did not account for more than 10% of the total in the vast majority of patients. In controls, only 2 (1%) had red cells with double CD55/CD59 negativity and 3 (2%) had isolated deficiency. All PNH patients had a simultaneous CD55/CD59 deficiency. Positive Ham and sucrose tests were found only in PNH. There was no correlation between the presence of deficient CD55/CD59 erythrocytes and anemia, hemolysis, antiretroviral therapy, CD4+ counts, viral load, or concomitant hepatitis C infection in HIV patients. CONCLUSIONS: This study provides evidence supporting the presence of erythrocytes with CD55 and/or CD59 deficiency in HIV. Further studies using molecular techniques will be required to clarify the exact role of this deficiency in HIV patients.