Organisms are expected to balance energy allocation in such a way that fitness is maximized. While much research has focussed on allocation strategies of reproducing parents, in particular birds, relatively little attention has been paid to how nestlings allocate energy while in the nest. Nestling birds are faced with a trade-off between devoting energy to growth or to thermoregulation, and in altricial species it is likely that the thermal environment of the nest site influences the nature of this trade-off. Here, we experimentally investigate how altering the microclimate of nests affects the growth, size and survival, as well as cell-mediated immune (CMI) response, of nestling tree swallows (Tachycineta bicolor) in a temperate environment. We place air-activated heating pads in nests of swallows when young were between 4 days and 16 days of age, and compared performance of offspring to control nests. Our manipulation raised temperatures of heated nests by approximately 5 degrees C compared to control nests. Offspring in heated nests had enhanced survival while in the nest, and we also found that they were heavier and had longer ninth primary feathers at 16 days of age. In addition, heating nest boxes resulted in significantly faster growth of primaries, and there was a trend for growth rates of mass to also be higher in heated nests. There were no significant differences between heated and control nests in growth rate or size of tarsus at age 16 days, and we speculate that this lack of response to elevated nest temperatures may be due to growth of skeletal structures being limited by other factors such as calcium availability. We also found no difference between heated and control nests in CMI response. Nonetheless, our results show overall that increasing temperatures of nests has significant benefits that enhance the fitness of offspring. As provisioning rates to offspring did not differ between heated and control nests, we suspect that the beneficial effects of heating were not the consequence of changes in parental behaviour. Our results provide insight into factors, other than food supply, that have important consequences in determining reproductive success of birds breeding in temperate environments.

We compared haematocrits and blood haemoglobin concentrations of nestling House Wrens Troglodytes aedon in nests with relatively large numbers of haematophagous larvae of the blow fly Protocalliphora parorum (>6.4 large larvae/nestling) and nests in which exposure to larvae was severely reduced or eliminated (0–2.0 larvae/nestling). Heavily parasitized nestlings showed no reduction in haematocrit levels but a significant 28% reduction in haemoglobin levels. Previous research on avian response to chronic blood loss suggests that parasitized nestlings may show normal volumes of red blood cells as a result of a rapid production of new cells in response to blood loss and, additionally, as a result of swelling of individual cells left in the bloodstream after parasite feeding. Rapid erythropoiesis places high numbers of haemoglobin‐poor, immature cells into the bloodstream which would explain the reduced haemoglobin levels of parasitized nestlings. Our results refute the conclusion that larval feeding has “little direct effect” on nestling wrens in this parasite–host system, drawn earlier by Johnson and Albrecht (1993) based on examination of haematocrits alone. Our results also strongly suggest that researchers wanting to measure effects of blood‐feeding parasites on birds measure haemoglobin levels, not haematocrits.

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Twenty-four novel 2,5-diaryl-1,3,4-oxadiazoline analogs of combretastatin A-4 (CA-4, 1) were designed, synthesized and evaluated for biological activities. The compounds represent two structural classes; the Type I class has three methoxy groups on the A ring and the Type II class has a single methoxy group on the A ring. Biological evaluations demonstrate that multiple structural features control the biological potency. Four of the compounds, 2-(3'-bromophenyl)-5-(3",4",5"-trimethoxyphenyl)-2-acetyl-2,3-dihydro-1,3,4-oxadiazoline (9l), 2-(2',5'-dimethoxyphenyl)-5-(3"-methoxyphenyl)-2-acetyl-2,3-dihydro-1,3,4-oxadiazoline (10h), 2-(3',4',5'-trimethoxyphenyl)-5-(3"-methoxyphenyl)-2-acetyl-2,3-dihydro-1,3,4-oxadiazoline (10i) and 2-(3',5'-dimethoxyphenyl)-5-(3"-methoxyphenyl)-2-acetyl-2,3-dihydro-1,3,4-oxadiazoline (10j), have potent antiproliferative activities against multiple cancer cell lines. Mechanistic studies indicate that they retain the microtubule disrupting effects of compound 1 including microtubule loss, the formation of aberrant mitotic spindles, and mitotic arrest. Compound 10i inhibits purified tubulin polymerization and circumvents drug resistance mediated by P-glycoprotein and βIII tubulin expression. The oxadiazoline analog 10i is a promising lead candidate worthy of further investigation.