Countergradient variation in embryonic growth and development: do embryonic and juvenile performances trade off? Funct

Summary 1. Countergradient variation in growth rate requires that rapid growth rate trades off with other performances, such that submaximal growth evolves in certain environments. Negative effects of rapid growth on other traits within a single ontogenetic stage are conspicuous candidates for such trade-offs, but trade-offs spanning ontogenetic stages have received much less attention. 2. We tested whether rapid growth and development of embryonic lizards was associated with poor juvenile performance, as estimated by growth rate and sprint speed after hatching. To do so, we raised lizards from three populations that differ in their environmental temperature and measured their performances during embryonic and hatchling stages. 3. Under the same environmental conditions, embryos from two cold environments grew and developed more rapidly than did the embryos from a warm environment. Among populations, rapid growth and development was associated with slow growth after hatching. But surprisingly, the opposite pattern was observed within populations. 4. Our results highlight the need to consider trade-offs mediated by ecological factors (e.g. competition and predation), which calls for similar experiments in natural environments

Bergmann\u27s Clines in Ectotherms: Illustrating a Life-History Perspective with Sceloporine Lizards

The generality and causes of Bergmann\u27s rule have been debated vigorously in the last few years, but Bergmann\u27s clines are rarely explained in the context of life-history theory. We used both traditional and phylogenetic comparative analyses to explore the causes of latitudinal and thermal clines in the body size of the eastern fence lizard (Sceloporus undulatus). The proximate mechanism for larger body sizes in colder environments is delayed maturation, which results in a greater fecundity but a lower survival to maturity. Life-history theory predicts that a higher survivorship of juveniles in colder environments can favor the evolution of a Bergmann\u27s cline. Consistent with this theory, lizards in colder environments survive better as juveniles and delay maturation until reaching a larger body size than that of lizards in warmer environments. We expect similar relationships among temperature, survivorship, and age/size at maturity exist in other ectotherms that exhibit Bergmann\u27s clines. However, life-history traits of S. undulatus were more strongly related to latitude than they were to temperature, indicating that both abiotic and biotic factors should be considered as causes of Bergmann\u27s clines. Nonetheless, analyses of the costs and benefits of particular body sizes in different thermal environments will enhance our understanding of geographic variation

Immunohistochemical localization of fibronectin as a tool for the age determination of human skin wounds

We analyzed the distribution of fibronectin in routinely embedded tissue specimens from 53 skin wounds and 6 postmortem wounds. In postmortem wounds a faint but focal positive staining was exclusively found at the margin of the specimens which dit not extend into the adjacent stroma. Vital wounds were classified into 3 groups. The first comprising lesions with wound ages ranging from a few seconds to 30 min, the second comprising those with wound ages upt to 3 weeks, and the third group with lesions more than 3 weeks old. Ten out of 17 lesions with a wound age up to 30 min showed a clear positive reaction within the wound area. Three specimens in this group were completely negative, while in 4 additional cases the result was not significantly different from postmortem lesions. These 7 cases were characterized by acute death with extremely short survival times (only seconds). In wounds up to 3 weeks old fibronectin formed a distinct network containing an increasing number of inflammatory cells corresponding to the wound age. In 2 cases with a survival time of 17 days and in all wounds older than 3 weeks fibronectin was restricted to the surface of fibroblasts and to parallel arranged fibers in the granulation tissue without any network structures. We present evidence that fibronectin is a useful marker for vital wounds with a survival time of more than a few minutes. Fibronectin appears before neutrophilic granulocytes migrate into the wound area. Since a faint positive fibronectin staining is seen in postmortem lesions and bleedings, we propose that only those wounds which show strong positive fibronectin staining also extending into the adjacent stroma should be regarded as vital

Bergmann’s clines in ectotherms: illustrating a life-history perspective with Sceloporine lizards. American Naturalist 164

abstract: The generality and causes of Bergmann's rule have been debated vigorously in the last few years, but Bergmann's clines are rarely explained in the context of life-history theory. We used both traditional and phylogenetic comparative analyses to explore the causes of latitudinal and thermal clines in the body size of the eastern fence lizard (Sceloporus undulatus). The proximate mechanism for larger body sizes in colder environments is delayed maturation, which results in a greater fecundity but a lower survival to maturity. Lifehistory theory predicts that a higher survivorship of juveniles in colder environments can favor the evolution of a Bergmann's cline. Consistent with this theory, lizards in colder environments survive better as juveniles and delay maturation until reaching a larger body size than that of lizards in warmer environments. We expect similar relationships among temperature, survivorship, and age/size at maturity exist in other ectotherms that exhibit Bergmann's clines. However, life-history traits of S. undulatus were more strongly related to latitude than they were to temperature, indicating that both abiotic and biotic factors should be considered as causes of Bergmann's clines. Nonetheless, analyses of the costs and benefits of particular * E-mail: [email protected]. † E-mail: [email protected]. ‡ E-mail: [email protected]. § E-mail: [email protected]. body sizes in different thermal environments will enhance our understanding of geographic variation

Aprotinin inhibits the contact, neutrophil, and platelet activation systems during simulated extracorporeal perfusion

Aprotinin reduces blood loss after cardiac operations and decreases the bleeding time. The mechanism of action of aprotinin that produces these effects is not clear. During simulated extracorporeal circulation the contact and complement systems, platelets, and neutrophils are activated. We investigated the effect of aprotinin on kallikrein-C1̄-inhibitor complex and C1̄-C1̄-inhibitor complex formation, neutrophil degranulation, and platelet release and aggregation during simulated extracorporeal circulation. Fresh heparinized human blood was recirculated at 37° C for 2 hours in a spiral coil membrane oxygenator-roller pump perfusion circuit. Changes in platelet count, leukocyte count, platelet response to adenosine diphosphate, and plasma levels of β-thromboglobulin, kallikrein-C1̄-inhibitor complexes, C1̄-C1̄-inhibitor complexes, and neutrophil elastase were measured before and at 5, 30, 60, and 120 minutes of recirculation at 0, 0.015, 0.03, 0.06, and 0.12 mg/ml doses of aprotinin. Platelet counts decreased to 36% ± 12% of control values at 5 minutes and increased to 56% ± 13% at 120 minutes without aprotinin. Aprotinin did not affect platelet counts, but it did prevent the decrease in sensitivity of platelets to adenosine diphosphate and it attenuated β-thromboglobulin release. In the absence of aprotinin, kallikrein-C1̄-inhibitor and C1̄-C1̄-inhibitor complexes increased progressively to 0.53 ± 0.14 U/ml and 2.38 ± 0.33 U/ml, respectively, at 120 minutes. Kallikrein-C1̄-inhibitor complexes were completely inhibited and C1̄-C1β-inhibitor complexes were partially inhibited at aprotinin concentrations of 0.03 mg/ml or greater. Release of neutrophil elastase was partially but not completely inhibited at the highest dose of aprotinin and was 50% inhibited at a dose of 0.03 mg/ml. Because activation of the fibrinolytic system does not occur in this system, the changes were independent of the inhibition of plasmin. We conclude that aprotinin in high doses completely inhibited kallikrein-induced activation of neutrophils and partially inhibited complement-induced activation. Aprotinin did not directly affect platelet adhesion or aggregation, but it indirectly preserved platelet sensitivity to agonists and also attenuated release of α-granule contents. The data indicate that in the presence of aprotinin platelet function was partially preserved, kallikrein production was totally inhibited, complement activation was partially inhibited, and neutrophil release was partially inhibited, thus attenuating the 'whole body inflammatory response' associated with cardiopulmonary bypass