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D L Swiderski

Publications and source records attributed to D L Swiderski.

3 recordsLinked to original sources

Why morphometrics is not special: coding quantitative data for phylogenetic analysis.

Thorpe (1984) and Chappill (1989) argued that selection of a coding method should be [figure: see text] based on the purpose of coding. In our view, the purpose of coding is dictated by the principles of phylogenetic systematics. The foundation of phylogenetic systematics is the observation that monophyletic groups can be recognized if homologous character states, shared evolutionary novelties, can be identified (Hennig, 1966). Unfortunately, characters do not have labels indicating their homology. Instead, a systematist must propose a hypothesis of homology and evaluate its congruence with independent hypotheses based on other traits. In this context, the purpose of coding is to represent those hypotheses. The major obstacle to coding is that the a priori groups under analysis (i.e., taxa) often have ranges of variation that overlap to some degree. This is true whether traits are described qualitatively or quantitatively. One advantage of quantitative description is that it permits a more detailed analysis of how much the ranges of variation overlap. It may seem appropriate to use statistical methods to summarize the amount of overlap and even to decide objectively (on a priori grounds) whether taxa are similar or different. Above, we demonstrated some of the problems resulting from these uses of statistical analysis. In our view, the most important problem is the implication that similarity of the feature across taxa is the basis for inferring homology. The similarity that is relevant to phylogenetic analysis is not proximity in morphospace, but shared novelty. Statistical methods can describe proximity, but they cannot recognize novelty. The method of coding we recommend uses graphical displays of individual values. Coding decisions are based on all of the individuals in each taxon, not on summaries derived from models of expected distributions. Then, the evidence for inferring divergence is independently evaluated for each pair of overlapping taxa. Coding decisions are not based on a priori rules that have no bearing on recognition of evolutionary novelty. This is the same approach that is used to code qualitatively described traits.

Animals↗

The bimodal expression of tumor necrosis factor-alpha in association with rat lung reimplantation and allograft rejection.

Lung transplantation has become a therapeutic option for a number of end-stage pulmonary disorders. Lung transplant recipients experience more complications due to acute and chronic allograft rejection as compared to recipients of other solid organs. We postulated that the generation of TNF-alpha plays a significant role in the pathogenesis of acute lung allograft rejection. To test our hypothesis, we used a RT1-incompatible rat lung allograft model and demonstrated the time course, cellular source(s), and major compartment(s) of TNF production during the course of lung allograft rejection. This model allowed for immunogenetic standardization and reproducibility of lung allograft rejection across disparate major histocompatibility barriers. TNF production was characterized at the whole animal, organ, cellular, and molecular levels, and was found to be compartmentalized and expressed in a bimodal fashion from the lung allograft during lung allograft reimplantation and maximal rejection. Lung allograft rejection was significantly attenuated in animals pretreated with neutralizing TNF antisera as compared to animals receiving control sera. These findings may provide interesting insight into the use of novel and specific therapeutic intervention(s) during periods of acute lung allograft rejection.

Animals↗

Expression of interleukin-6 in association with rat lung reimplantation and allograft rejection.

Organ transplantation has become a therapeutic option for the replacement of malfunctioning tissues and organs. Since the advent of the first combined heart-lung transplant in 1981, there has been a rapid growth in the popularity of lung transplantation for a number of end-stage pulmonary disorders. Interestingly, these lung transplant patients experience more complications of acute and chronic allograft rejection compared with recipients of other solid organs. These episodes of rejection are related to a complex series of events that depend on the interaction of many cells and soluble mediators leading to cellular and tissue injury. The histopathology of lung allograft rejection has been actively studied and is associated with the sequestration of activated mononuclear phagocytes, T and B lymphocytes. These cells secrete a number of soluble mediators, that is, cytokines, that participate in the evolution of the immune response via autocrine, paracrine, or endocrine mechanisms. The interaction of cytokines with their targets leads to cellular activation, proliferation, and differentiation. In this study, we postulated that interleukin-6 (IL-6) may have a central role in the pathogenesis of acute lung allograft rejection. To test this hypothesis, we employed an unmodified RT1-incompatible rat lung allograft model and assessed the time course and major tissue compartment(s) of IL-6 production during the evolution of lung allograft rejection. The expression and production of IL-6 during the pathogenesis of lung allograft rejection was measured at the whole-animal, organ, cellular, and molecular levels. The expression of IL-6 was found to be bimodal in character, initially related to the reimplantation response and finally to the maximal allograft rejection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗