No abstract

Starch‐gel electrophoresis was used to examine the levels and distribution of genetic diversity in two Adenophora species: the narrow endangered Adenophora lobophylla and its widespread congener, A. potaninii. Based on allozyme variation at 18 putative loci, we measured high levels of genetic variability both in the endangered and the widespread species, with 83.3% of the loci being polymorphic. The mean expected heterozygosity within populations (  Hep  ) and within species (  Hes  ) were 0.234 and 0.244 for A. potaninii and were as high as 0.210 and 0.211 for A. lobophylla. There was higher differentiation among populations in A. potaninii (  FST = 0.155) than in A. lobophylla (  FST = 0.071). The high levels of genetic diversity in the present allozyme survey are consistent with the morphological variation observed in these species and may be attributed to high outcrossing rates in the Adenophora species. In addition, A. lobophylla was identified as a distinct species on the basis of Nei’s genetic distances and thus should be given a high priority for protection. It is noteworthy that the endangered A. lobophylla maintains much higher genetic diversity than most endemic or narrowly distributed plant species in spite of its restricted distribution. We hypothesize that A. lobophylla has become endangered for ecological and stochastic reasons, including habitat destruction or environmental changes, mud slides, and human disturbance such as grazing and mowing. Consequently, habitat protection is of particular importance for conserving this endangered species.

We examined the fate of neutrophils following transmigration through an endothelial monolayer cultured on "Transwell" membrane filters. Treatment of human umbilical vein endothelial cells (HUVEC) with increasing doses of tumor necrosis factor-α increased the efficiency of transmigration and markedly reduced apoptosis among the transmigrated neutrophils in a dosedependent manner. Apoptosis was also inhibited after transmigration of neutrophils through HUVEC stimulated with interleukin (IL)-1β but not so effectively after chemotaxis through unstimulated HUVEC driven by IL-8 added below the filter. Inhibition of β 2 -integrin binding after transmigration or coating the lower chamber with a nonadhesive polymer (polyhydroxyl-ethylmethacrylate) abrogated neutrophil survival. Although integrin engagement during migration itself was not essential to inhibit apoptosis, activation of neutrophils through CXC chemokine receptors was necessary. Quite brief exposure to the HUVEC (30-120 min) was effective in reducing subsequent apoptosis, although if coincubation with the HUVEC were prolonged, neutrophil apoptosis was reduced further. Neutralization of granulocyte macrophage-colony stimulating factor inhibited this additional effect. Thus, a complex interplay between migration-and activation-dependent signals and adhesive interaction in tissue may combine to effectively prolong the survival of neutrophils recruited during inflammation.