Higher-Order Homoplasy Tests

The Le Quesne test of character compatibility uses pairwise comparisons of characters to detect homoplasy in phylogenetic character data. If a pair of characters fails this test we can conclude that a minimum of a single extra step is required by the pair of characters. The rationale of the Le Quesne test is extended to comparisons of triplets of characters. The triplet homoplasy test can reveal that that there is a minimum of four extra steps across a triplet of characters and thus that there are at least two extra steps associated with one of the characters. The triplet homoplasy test can thus detect higher orders of homoplasy than can be detected by the pairwise Le Quesne test. The possibility of quartet and other higher-order homoplasy tests is discussed. The utility of higher-order homoplasy tests is discussed. It is suggested higher-order homoplasy tests have potential uses analogous to the uses of the Le Quesne test, particularly with respect to data exploration.     

Identification and functional analysis of NOL7 nuclear and nucleolar localization signals

Background  

NOL7 is a candidate tumor suppressor that localizes to a chromosomal region 6p23. This locus is frequently lost in a number of malignancies, and consistent loss of NOL7 through loss of heterozygosity and decreased mRNA and protein expression has been observed in tumors and cell lines. Reintroduction of NOL7 into cells resulted in significant suppression of in vivo tumor growth and modulation of the angiogenic phenotype. Further, NOL7 was observed to localize to the nucleus and nucleolus of cells. However, the mechanisms regulating its subcellular localization have not been elucidated.     

Role of different lymphoid tissues in the initiation and maintenance of DNA-raised antibody responses to the influenza virus H1 glycoprotein.

Antibody responses in mice immunized by a single gene gun inoculation of plasmid expressing the influenza virus H1 hemagglutinin and in mice immunized by a sublethal H1 influenza virus infection have been compared. Both immunizations raised long-lived serum responses that were associated with the localization of antibody-secreting cells (ASC) to the bone marrow. However, the kinetics of these responses were 4 to 8 weeks slower in the DNA-immunized than in the infection-primed mice. Following a gene gun booster, the presence of ASC in the inguinal lymph nodes, but not in other lymph nodes, revealed gene gun responses being initiated in the nodes that drain the skin target site. Both pre- and postchallenge, the DNA-immunized mice had 5- to 10-times-lower levels of antibody and ASC than the infection-primed mice.