Why are there more species in the tropics than in temperate regions? In recent years, this long-standing question has been addressed primarily by seeking environmental correlates of diversity. But to understand the ultimate causes of diversity patterns, we must also examine the evolutionary and biogeographic processes that directly change species numbers (i.e., speciation, extinction, and dispersal). With this perspective, we dissect the latitudinal diversity gradient in hylid frogs. We reconstruct a phylogeny for 124 hylid species, estimate divergence times and diversification rates for major clades, reconstruct biogeographic changes, and use ecological niche modeling to identify climatic variables that potentially limit dispersal. We find that hylids originated in tropical South America and spread to temperate regions only recently (leaving limited time for speciation). There is a strong relationship between the species richness of each region and when that region was colonized but not between the latitudinal positions of clades and their rates of diversification. Temperature seasonality seemingly limits dispersal of many tropical clades into temperate regions and shows significant phylogenetic conservatism. Overall, our study illustrates how two general principles (niche conservatism and the time-for-speciation effect) may help explain the latitudinal diversity gradient as well as many other diversity patterns across taxa and regions.

A method for building flexible shape models is presented in which a shape is represented by a set of labelled points. The technique determines the statistics of the points over a collection of example shapes. The mean positions of the points give an average shape and a number of modes of variation are determined describing the main ways in which the example shapes tend to deform from the average. In this way allowed variation in shape can be included in the model. The method produces a compact flexible 'Point Distribution Model' with a small number of linearly independent parameters, which can be used during image search. We demonstrate the application of the Point Distribution Model in describing two classes of shapes.

Many phylogeographic studies have revealed strongly diverged lineages within species that are masked by a lack of congruent morphological differentiation. To assess the extent to which the genetic component of diversity affects conservation assessments, we compared spatial patterns of endemism and conservation value for 22 species of Californian amphibians and reptiles with the 75 phylogeographic lineages that they contain. We used bioclimatic distribution modeling with environmental layers to generate 5-km spatial-resolution maps of predicted distribution for each species and lineage. We found concentrations of lineage breaks across the Central Valley, San Francisco Bay, the Sierra Nevada, and the Tehachapi and Trinity ranges. Subdivision of the ranges of species into phylogeographic units revealed novel areas of endemism. Several areas of very high conservation value for lineages were not evident in the species-level analysis. These observations illustrate the importance of considering multiple levels of biodiversity in conservation assessments.

Furazolidone combination therapy appears to be effective. Additional studies with different antimicrobial combinations and duration of therapy are warranted.

The development of a model for axonal injury in the optic nerve of the guinea pig has allowed analysis of early morphological changes within damaged axons. We provide evidence that the initial site of damage after stretch is the nodes of Ranvier, some of which develop 'nodal blebs'. The development of nodel blebs is correlated with the loss of subaxolemmal density, disruption of the neurofilament cytoskeleton and aggregation of membranous profiles of smooth endoplasmic reticulum. Nodal blebs are numerous 15 min after injury but less so at later survivals. The glial-axonal junction is intact at early survivals in damaged nodes. Marked accumulation of membranous organelles occurs in the paranodal and internodal regions adjacent to damaged nodes between two and six hours and is correlated with disruption of the myelin sheath. Axotomy and the formation of degeneration bulbs occurs between 24 and 72 h. The area of axonal injury is invaded by phagocytic cells by 72 h and large numbers of myelin figures occur within the neuropil until 14 days. The results are compared with those of other studies of diffuse axonal injury and other neuropathies. The time course of axonal changes is more rapid than during Wallerian degeneration. Our data from longer surviving animals is exactly comparable with published data. We are confident that the principal site of axonal injury is the node of Ranvier. We suggest that damage at the node results in disruption of axonal transport, which in turn leads to a cascade of events, culminating in axotomy between 24 and 72 h after the initial insult.