ABSTRACT
A series of in situ-prepared catalytic systems incorporating RuII precursors and bidentate phosphine ligands has been probed in the reductive carboxylation of ethylene in the presence of triethylsilane as reductant. The catalytic production of propionate and acrylate silyl esters was evidenced by high-throughput screening (HTS) and implemented in batch reactor techniques. The most promising catalyst systems identified were made of Ru(H)(Cl)(CO)(PPh3 )3 and 1,4-bis(dicyclohexylphosphino)butane (DCPB) or 1,1'-ferrocene-diyl-bis(cyclohexylphosphine) (DCPF). A marked influence of water on the acrylate/propionate selectivity was noted. Turnover numbers [mol mol(Ru)-1 ] up to 16 for acrylate and up to 68 for propionate were reached under relatively mild conditions (20â bar, 100 °C, 0.5â mol % Ru, 40â mol % H2 O vs. HSiEt3 ). Possible mechanisms are discussed.
Subject(s)
Delusions/etiology , Infarction/diagnostic imaging , Mesencephalon/diagnostic imaging , Aged , Cerebellar Ataxia/etiology , Delusions/psychology , Diplopia/etiology , Humans , Infarction/rehabilitation , Magnetic Resonance Imaging , Male , Mobility Limitation , Neuropsychological Tests/statistics & numerical dataABSTRACT
APOBEC3 proteins function as part of innate antiviral immunity and induce G to A hypermutation in retroviruses and hepatitis B virus (HBV) genomes. Whether APOBEC3 proteins affect viruses that replicate without a reverse transcription step is unknown. TT virus (TTV), known to present in serum of healthy individuals and HBV carriers, has a single-stranded circular DNA genome and replicates without reverse transcription. In this study, we examined 67 blood samples obtained from healthy individuals and HBV carriers and observed G to A hypermutation of genomes of TTV in both healthy individuals and HBV carriers. During ALT flare-up in HBV carriers, G to A hypermutation of HBV increased, but TTV genomes significantly decreased in number and hypermutated TTV genomes became undetectable. Our results show that hypermutated TTV exist in healthy individuals and HBV carriers and that TTV genomes were susceptible to immune reaction directed to HBV by interacting with APOBEC3 proteins.