Within-Colony Variation in the Immunocompetency of Managed and Feral Honey Bees (Apis mellifera L.) in Different Urban Landscapes

Urbanization has the potential to dramatically affect insect populations worldwide, although its effects on pollinator populations are just beginning to be understood. We compared the immunocompetency of honey bees sampled from feral (wild-living) and managed (beekeeper-owned) honey bee colonies. We sampled foragers from feral and managed colonies in rural, suburban, and urban landscapes in and around Raleigh, NC, USA. We then analyzed adult workers using two standard bioassays for insect immune function (encapsulation response and phenoloxidase activity). We found that there was far more variation within colonies for encapsulation response or phenoloxidase activity than among rural to urban landscapes, and we did not observe any significant difference in immune response between feral and managed bees. These findings suggest that social pollinators, like honey bees, may be sufficiently robust or variable in their immune responses to obscure any subtle effects of urbanization. Additional studies of immune physiology and disease ecology of social and solitary bees in urban, suburban, and natural ecosystems will provide insights into the relative effects of changing urban environments on several important factors that influence pollinator productivity and health

Ischemic Preconditioning Phosphorylates Mitogen-activated Kinases and Heat Shock Protein 27 in the Diabetic Rat Heart

Diabetes mellitus blocks protection by ischernic preconditioning (IPC), but the mechanism is not known. We investigated the effect of ischemic preconditioning on mitogen-activated protein kinases (extracellular signal-regulated kinases I and 2, C-Jun N-terminal kinases, p38 mitogen-activated kinase) and heat shock protein 27 phosphorylation in diabetic and nondiabetic rat hearts in vivo. Two groups of anaesthetized nondiabetic and diabetic rats underwent a preconditioning protocol (3 cycles of 3 min coronary artery occlusion and 5 min of reperfusion). Two further groups served as untreated controls. Hearts were excised for protein measurements by Western blot. Four additional groups underwent 25 min of coronary occlusion followed by 2h of reperfusion to induce myocardial infarction. In these animals, infarct size was measured. IPC reduced infarct size in the nondiabetic rats but not in the diabetic animals. In diabetic rats, IPC induced phosphorylation of the mitogen-activated protein kinases and of heat shock protein 27. We conclude that protection by IPC is blocked by diabetes mellitus in the rat heart in vivo without affecting phosphorylation of mitogen-activated protein kinases or heat shock protein 27. Therefore, the blockade mechanism of diabetes mellitus is downstream of mitogen-activated kinases and heat shock protein 2

Survival plot of control and paraquat treated bees.

<p>Red crosses indicate censored individuals. (Cox model for control bees: <i>p <</i> 0.01; Cox model for paraquat bees: <i>p <</i> 0.05). Although urbanization was analyzed as a continuous variable (percent impervious surface) in the Cox model, it is represented here as two categories for visual clarity; the categories represent sites above and below the median level of urbanization.</p