RESUMO
Inducing positive nitrogen balance and weight gain in patients fed exclusively parenterally was documented first by Dudrick et al. in 1968. Since that time, total parenteral nutrition (TPN) has become commonplace both in acutely ill patients and in those with severe chronic gastrointestinal disease. Clear nutritional benefits accrue, but certain complications associated with TPN have become apparent. In the following discussion we review clinical, biochemical, and pathophysiologic abnormalities of the hepatobiliary system associated with TPN, particularly hepatic dysfunction and gallbladder disease and their management.
Assuntos
Doenças Biliares/etiologia , Hepatopatias/etiologia , Nutrição Parenteral Total/efeitos adversos , Animais , Doenças Biliares/terapia , Colelitíase/etiologia , Colestase Intra-Hepática/etiologia , Humanos , Hepatopatias/patologia , Hepatopatias/fisiopatologia , Hepatopatias/terapiaRESUMO
Kinetoplast DNA, the mitochondrial DNA in trypanosomatids, is a network of thousands of interlocked circles. Most of these circles are minicircles and a few are maxicircles. Minicircles replicate, after decatenation from the network, by a Cairns-type mechanism. The minicircle progeny then reattach to the network (Englund, P. T. (1979) J. Biol. Chem. 254, 4895-4900). We have now discovered a novel intermediate in Crithidia fasciculata minicircle replication. It is a highly gapped 2.5-kilobase free minicircle with nascent fragments of only 20 to 110 nucleotides. These fragments are nonligasable, and some remain nonligasable even after gap filling with DNA polymerase. Solution hybridization studies show that the nascent fragments are predominantly, if not exclusively, heavy strand.
