Pleistocene and Holocene rhinocerotids (Mammalia,Perissodactyla) from the Indochinese Peninsula

Rhinocerotids were abundant and diverse in southern Asia during the Pleistocene and the Holocene epochs, as shown by palaeontological and archaeological discoveries published throughout the last century, whereas the only living rhinoceros in the Indochinese Peninsula is Rhinoceros sondaicus (Cat Loc Reserve, Vietnam). The Pleistocene-Holocene Indochinese rhinocerotid record consists of the extinct species Dicerorhinus gwebinensis (Early Pleistocene, Myanmar) and representatives of the Recent Asian Species Rhinoceros unicornis (Middle-Late Pleistocene), R. sondaicus (Middle Pleistocene-Recent), and Dicerorhinus sumatrensis (Middle Pleistocene-Holocene). This fossil record is synthesized, mapped for Early/Middle/Late Pleistocene and Holocene/Recent times, and then compared with coeval rhinocerotid assemblages from the adjacent areas (South China), subregions (Indian, Sundaic, Philippine, and Wallacean), and region (Palearctic), from a biochronological and biogeographical perspective.     

Interferons mediate terminal differentiation of human cortical thymic epithelial cells

In the thymus, epithelial cells comprise a heterogeneous population required for the generation of functional T lymphocytes, suggesting that thymic epithelium disruption by viruses may compromise T-cell lymphopoiesis in this organ. In a previous report, we demonstrated that in vitro, measles virus induced differentiation of cortical thymic epithelial cells as characterized by (i) cell growth arrest, (ii) morphological and phenotypic changes, and (iii) apoptotis as a final step of this process. In the present report, we have analyzed the mechanisms involved. First, measles virus-induced differentiation of thymic epithelial cells is shown to be strictly dependent on beta interferon (IFN-beta) secretion. In addition, transfection with double-stranded RNA, a common intermediate of replication for a broad spectrum of viruses, is reported to similarly mediate thymic epithelial cell differentiation through IFN-beta induction. Finally, we demonstrated that recombinant IFN-alpha, IFN-beta, or IFN-gamma was sufficient to induce differentiation and apoptosis of uninfected thymic epithelial cells. These observations suggested that interferon secretion by either infected cells or activated leukocytes, such as plasmacytoid dendritic cells or lymphocytes, may induce thymic epithelium disruption in a pathological context. Thus, we have identified a new mechanism that may contribute to thymic atrophy and altered T-cell lymphopoiesis associated with many infections.     

Evolutionary syndromes linking dispersal and mating system: the effect of autocorrelation in pollination conditions

Self-fertilization is classically thought to be associated with propagule dispersal because self-fertilization is a boon to colonizers entering environments devoid of pollinators or potential mates. Yet, it has been theoretically shown that random fluctuations in pollination conditions select for the opposite association of traits. In nature, however, various ecological factors may deviate from random variations, and thus create temporal correlation in pollination conditions. Here, we develop a model to assess the effects of pollination condition autocorrelation on the joint evolution of dispersal and self-fertilization. Basically, two syndromes are found: dispersing outcrossers and nondispersing (partial) selfers. Importantly, (1) selfers are never associated with dispersal, whereas complete outcrossers are, and (2) the disperser/outcrosser syndrome is favored (resp. disfavored) by negative (resp. positive) autocorrelation in pollination conditions. Our results suggest that observed dispersal/mating system syndromes may depend heavily on the regime of pollination condition fluctuations. We also point out potential negative evolutionary effects of anthropic management of the environment on outcrossing species.     

Double-label expression studies of prostacyclin synthase, thromboxane synthase and COX isoforms in normal aortic endothelium

We have performed double-label immunofluorescence microscopy studies to evaluate the extent of co-localization of prostacyclin synthase (PGIS) and thromboxane synthase (TXS) with cyclooxygenase (COX)-1 and COX-2 in normal aortic endothelium. In dogs, COX-2 expression was found to be restricted to small foci of endothelial cells while COX-1, PGIS and TXS were widely distributed throughout the endothelium. Quantification of the total cross-sectioned aortic endothelium revealed a 6- to 7-fold greater expression of COX-1 relative to COX-2 (55 vs. 8%) and greater co-distribution of PGIS with COX-1 compared to COX-2 (19 vs. 3%). These results are in contrast to the extensive co-localization of PGIS and COX-2 in bronchiolar epithelium. In rat and human aortas, immunofluorescence studies also showed significant COX-1 and PGIS co-localization in the endothelium. Only minor focal COX-2 expression was detected in rat endothelium, similar to the dog, while COX-2 was not detected in human specimens. Inhibition studies in rats showed that selective COX-1 inhibition caused a marked reduction of 6-keto-PGF(1alpha) and TXB(2) aortic tissue levels, while COX-2 inhibition had no significant effect, providing further evidence for a functionally larger contribution of COX-1 to the synthesis of prostacyclin and thromboxane in aortic tissue. The data suggest a major role for COX-1 in the production of both prostacyclin and thromboxane in normal aortic tissue. The extensive co-localization of PGIS and COX-2 in the lung also indicates significant tissue differences in the co-expression patterns of these two enzymes.     

Environment-dependent inbreeding depression: its ecological and evolutionary significance

Inbreeding depression is a major evolutionary and ecological force that influences population dynamics and the evolution of inbreeding-avoidance traits such as mating systems and dispersal. There is now compelling evidence that inbreeding depression is environment-dependent. Here, we discuss ecological and evolutionary consequences of environment-dependent inbreeding depression. The environmental dependence of inbreeding depression may be caused by environment-dependent phenotypic expression, environment-dependent dominance, and environment-dependent natural selection. The existence of environment-dependent inbreeding depression challenges classical models of inbreeding as caused by unconditionally deleterious alleles, and suggests that balancing selection may shape inbreeding depression in natural populations; loci associated with inbreeding depression in some environments may even contribute to adaptation to others. Environment-dependent inbreeding depression also has important, often neglected, ecological and evolutionary consequences: it can influence the demography of marginal or colonizing populations and alter adaptive optima of mating systems, dispersal, and their associated traits. Incorporating the environmental dependence of inbreeding depression into theoretical models and empirical studies is necessary for understanding the genetic and ecological basis of inbreeding depression and its consequences in natural populations.     

Global-scale atmospheric modeling of aerosols to assess metal source-receptor relationships for life cycle assessment

The International Journal of Life Cycle Assessment - Metals have often been identified as the main contributors to (eco)toxicological impacts in life cycle assessment (LCA) studies. Indeed,...