Extrahepatic biliary atresia is a devastating disease occurring in 1 in 10,000 to 14,000 infants annually in the United States. We have recently described preliminary data suggesting an association of group C rotavirus with biliary atresia in two infants. However, a group C rotavirus animal model of biliary atresia is not presently available. On the other hand, some strains of the better-characterized and much more common group A rotaviruses produce hepatobiliary disease in infant mice. This disease shares many characteristics of the human infection. The present report describes extrahepatic biliary obstruction in immunocompetent BALB/c infant mice infected with a human or animal strain of group A rotavirus. Two-d-old BALB/c mice orally inoculated with hepatobiliary tropic rotavirus were shown to have active virus replication in the biliary tract and liver as early as 48 h postinoculation. At approximately 7 d postinoculation, between one fourth and one half of infant mice, depending on the virus strain, showed signs of inflammation and swelling in the bile ducts. The obstruction was complete in about one half of symptomatic animals. Although there was no obvious atresia as described in human infants, the obstruction was irreversible about 50% of the time, and the resulting fibrosis and bile ductular proliferation in the liver were strikingly similar to those seen in the liver of the human infant with biliary atresia.

Nickel(II) heterocyclic carbene complexes of the formula NiI2(carbene)2 (carbene = 3-methyl-1-propylimidazolin-2-ylidene (1), 1-butyl-3-methylimidazolin-2-ylidene (2), 1-isopropyl-3-methylimidazolin-2-ylidene (3), 1,3-diisopropylimidazolin-2-ylidene (4)) have been prepared and fully characterized by both spectroscopic methods and single-crystal X-ray structure analysis. All complexes have “square-planar” nickel environments, with the donor atoms pairwise trans, all obligate, except for one of the two independent molecular types found in 2, in which, with different substituents at the nitrogen atoms, the two rotamers are observed as independent molecules in the one crystal. Complexes 1−4 were tested as catalysts for propene and 1-butene dimerization in both toluene and an imidazolium−chloroaluminate ionic liquid. While the complexes are inactive to sparingly active in toluene, highly active catalysts are produced in the ionic liquid. In all cases the complexes are more active toward 1-butene dimerization than is NiCl2(PCy3)2 in the ionic liquid. The results are interpreted in terms of catalyst stabilization by the imidazolium-based ionic liquid. In toluene the complexes decompose rapidly via reductive elimination of imidazolium cations, while in the ionic liquid no decomposition is observed. While reductive elimination of imidazolium is possible in the ionic liquid, a rapid reoxidation via addition of the solvent imidazolium cation seems possible and may prevent the formation of Ni0 deposits associated with catalyst deactivation.

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