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Recent reports on patterns and occurrence of torpor and other natural hypothermic states in birds have prompted a revision of many longstanding opinions. For instance, a larger assortment of birds covering a wider range of body mass than previously recognized uses energy-conserving mechanisms in the face of abundant food supplies. Thus, although acute energetic stress triggers the occurrence of hypometabolic states in many birds, energy deficits can no longer be regarded as the sole stimulus for avian torpor. Additionally, the phenology of this phenomenon (phases, duration, depth) shows more interspecific variation than previously appreciated, and traditional concepts of the phases of torpor are not always adequate. Hence, inclusive definitions of torpor based on physiological and/or behavioral criteria have become more difficult to formulate. However, average nighttime body temperature, which is highly consistent throughout the class Aves (38.54 degrees +/- 0.96 degrees C, n = 202), provides a convenient reference for detecting natural hypothermic states. Of the putative ecological factors associated with avian torpor, food specialization seems a prime candidate as an ultimate factor in the occurrence of this state in birds. With few exceptions, all of these animals capable of torpor are either frugivorous, nectarivorous, or insectivorous, suggesting a correlation between thermoregulatory pattern and predictability of food supply. To date, no clear answer exists as to whether the variety of thermoregulatory patterns evident in birds involves discrete mechanisms or merely steps in a physiological continuum. However, I suggest that the occurrence of differences in torpor patterns among closely related species (e.g., within families) favors the latter interpretation.

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Chronic ethanol abuse is known to increase susceptibility to infections after injury, in part, by modification of macrophage function. Several intracellular signalling mechanisms are involved in the initiation of inflammatory responses, including the nuclear factor-κB (NF-κB) pathway. In this study, we investigated the systemic and hepatic effect of chronic ethanol feeding on in vivo activation of NF-κB in NF-κBEGFP reporter gene mice. Specifically, the study focused on Kupffer cell proinflammatory cytokines IL-6 and TNF-α and activation of NF-κB after chronic ethanol feeding followed by in vitro stimulation with lipopolysaccharide (LPS). We found that chronic ethanol upregulated NF-κB activation and increased hepatic and systemic proinflammatory cytokine levels. Similarly, LPS-stimulated IL-1β release from whole blood was significantly enhanced in ethanol-fed mice. However, LPS significantly increased IL-6 and TNF-α levels. These results demonstrate that chronic ethanol feeding can improve the responsiveness of macrophage LPS-stimulated IL-6 and TNF-α production and indicate that this effect may result from ethanol-induced alterations in intracellular signalling through NF-κB. Furthermore, LPS and TNF-α stimulated the gene expression of different inflammatory mediators, in part, in a NF-κB-dependent manner.