Bounds on net survival probabilities for dependent competing risks

Bounds on the marginal survival function based on data from a competing-risks experiment are obtained. These bounds require an investigator to specify a range of possible concordances for the times to occurrences of the competing risks. These bounds are tighter than those of Peterson (1976, Proceedings of the National Academy of Sciences 73, 11-13).     

The major pterin in Tetrahymena pyriformis is 6-(D-threo-1,2,3-trihydroxypropyl)-pterin (D-monapterin) and not 6-(L-threo-1,2-dihydroxypropyl)-pterin (ciliapterin).

The major pterin in Tetrahymena pyriformis, strain W, earlier suggested to be L-threo-biopterin and named ciliapterin [1] is now identified as D-threo-neopterin (D-monapterin). This is the first example of a natural D-monapterin. This compound was characterized by its chromatographic behavior, its fluorescence properties and by its oxidation product with alkaline permanganate. The final identification was obtained by comparison with an authentic material using an exchange ligand chromatography method with D-phenylalanine as chiral modifier and Cu (II) as metal ion. D-monapterin is also present as the major pterin in Tetrahymena pyriformis strains GL and ST, and in Tetrahymena thermophila.     

Mapping of class alpha glutathione S-transferase 2 (GST-2) genes to the vicinity of the d locus on mouse chromosome 9

Recombinant inbred strains of mice were used to localize the genes coding for the class alpha glutathione S-transferase 2 (Gst-2). The genes showed three distinct strain distribution patterns, indicating that they occur in at least three clusters separable by recombination. All three clusters are located in the vicinity of the d locus on mouse chromosome 9, but two of them are closer to d than the third. Linked to Gst-2 on mouse chromosome 9 are two enzyme-encoding loci, Pgm-3 and Mod-1. The human counterparts of Gst-2, Pgm-3, and Mod-1 map to 6p12, 6q12, and 6q12, respectively. Thus, the pericentric region of human chromosome 6 has its homolog in the segment spanning Gst-2, Pgm-3, and Mod-1 on mouse chromosome 9. The fact that the syntenic group extends across the centromere of human chromosome 6 can best be explained by a pericentric inversion postulated to have taken place in the primate lineage leading to Catarhini.     

The influence of feeding,enrichment, and seasonal context on the behavior of Pacific Walruses (Odobenus rosmarus divergens)

Though some research exists concerning general behavior and activity patterns of Walruses in zoos or aquariums, less is known about how these patterns change in response to various environmental and temporal contexts. This study presents two studies assessing behavioral changes in relation to feeding period, object enrichment (OE), and season in a social group of four Pacific Walruses at the New York Aquarium. Study 1 examined behavior in relation to feeding context (nonfeed, prefeed, postfeed); data were collected over a three‐week period, resulting in 47 observation sessions for each feeding context. Study 2 examined behavior in relation to OE and season; data were collected in two phases resulting in 12 enrichment and 9 no‐enrichment (NE) observation sessions (Phase 1), and 21 enrichment and 18 NE observation sessions (Phase 2). Study 1 showed that after feeding, oral behavior increased while social behavior and total swim frequency decreased. In Study 2, both swim frequency and social behavior were found to interact with OE and phase, while oral behavior remained constant across all conditions. As in the wild, both studies found all animals to be swimming the majority of the time. Though every animal spent much of its swim time engaged in an Individual Swimming Pattern (ISP), both studies showed that the proportion of ISP (in relation to total time swimming) remained stable across all contexts, suggesting a potential functional role of the ISPs. These results are discussed in light of the ongoing debate over the role of stereotypies in welfare assessment. Zoo Biol 29:397–404, 2010. © 2009 Wiley‐Liss, Inc.