Strongest Evidence Revisited

In response to comments by J. S. Farris (2000, Cladistics 16, 403–410) on the strongest evidence (SE) approach to phylogenetic analysis, I examine the concepts on which it is founded and reevaluate its merits. SE's null model of signal absence in characters is not treated as background knowledge, but as a reference point for evaluating a data set's phylogenetic signal in a tree-specific manner. In simulation tests, the SE methods perform reasonably well; although parsimony is generally more accurate and less biased than SE, SE is distinctly more accurate in some circumstances. Simulations further indicate that jackknifing is often beneficial in both SE and parsimony analyses. Iterative fixation of splits shows promise as an auxiliary procedure for SE and other methods that weight according to apparent homoplasy.     

Automatic preparation, calibration, and simulation of deformable objects

Many simulation environments - particularly those intended for medical simulation - require solid objects to deform at interactive rates, with deformation properties that correspond to real materials. Furthermore, new objects may be created frequently (for example, each time a new patient's data is processed), prohibiting manual intervention in the model preparation process. This paper provides a pipeline for rapid preparation of deformable objects with no manual intervention, specifically focusing on mesh generation (preparing solid meshes from surface models), automated calibration of models to finite element reference analyses (including a novel approach to reducing the complexity of calibrating nonhomogeneous objects), and automated skinning of meshes for interactive simulation.     

Centrosomes and cancer.

The centrosome functions as the major microtubule organizing center (MTOC) of the cell and as such it determines the number, polarity, and organization of interphase and mitotic microtubules. Cytoplasmic organization, cell polarity and the equal partition of chromosomes into daughter cells at the time of cell division are all dependent on the normal function of the centrosome and on its orderly duplication, once and only once, in each cell cycle. Malignant tumor cells show characteristic defects in cell and tissue architecture and in chromosome number that can be attributed to inappropriate centrosome behavior during tumor progression. In this review, we will summarize recent observations linking centrosome defects to disruption of normal cell and tissue organization and to chromosomal instability found in malignant tumors.