Energy relations of winter roost-site utilization by American goldfinches ( Carduelis tristis )

American goldfinches ( Carduelis tristis ) were observed roosting in Colorado blue spruce ( Picea pungens ), which comprised part of a mixed stand of conifers. Their winter roost-sites were distally situated among the most densely-needled branches on the leeward sides of these trees. Heated and unheated taxidermic goldfinch mounts were placed within these sites and at the same height in an adjacent clearing. The radiative and convective characteristics of these locations were monitored simultaneously and compared to predicted power requirements of live goldfinches (based on laboratory calibration of heated mounts) and operative temperatures ( T e ; based on body temperatures of unheated mounts). The winter roost-sites significantly reduced radiative and convective heat exchanges between goldfinches and the environment. Based on body composition data for winter goldfinches, all but two birds sampled could endure a 15-h roost period at average overnight T e 's as low as-40°C. In contrast, if these birds were prevented from feeding the following day, only 30% could survive the imposition of a 39-h fast at average T e 's of-2°C. Winter roost-site selection may be more constrained by thermoregulatory considerations in small birds than in larger species.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47760/1/442_2004_Article_BF00379484.pd

HER-2 overexpression differentially alters transforming growth factor-β responses in luminal versus mesenchymal human breast cancer cells

INTRODUCTION: Amplification of the HER-2 receptor tyrosine kinase has been implicated in the pathogenesis and aggressive behavior of approximately 25% of invasive human breast cancers. Clinical and experimental evidence suggest that aberrant HER-2 signaling contributes to tumor initiation and disease progression. Transforming growth factor beta (TGF-β) is the dominant factor opposing growth stimulatory factors and early oncogene activation in many tissues, including the mammary gland. Thus, to better understand the mechanisms by which HER-2 overexpression promotes the early stages of breast cancer, we directly assayed the cellular and molecular effects of TGF-β1 on breast cancer cells in the presence or absence of overexpressed HER-2. METHODS: Cell proliferation assays were used to determine the effect of TGF-β on the growth of breast cancer cells with normal or high level expression of HER-2. Affymetrix microarrays combined with Northern and western blot analysis were used to monitor the transcriptional responses to exogenous TGF-β1 in luminal and mesenchymal-like breast cancer cells. The activity of the core TGF-β signaling pathway was assessed using TGF-β1 binding assays, phospho-specific Smad antibodies, immunofluorescent staining of Smad and Smad DNA binding assays. RESULTS: We demonstrate that cells engineered to over-express HER-2 are resistant to the anti-proliferative effect of TGF-β1. HER-2 overexpression profoundly diminishes the transcriptional responses induced by TGF-β in the luminal MCF-7 breast cancer cell line and prevents target gene induction by a novel mechanism that does not involve the abrogation of Smad nuclear accumulation, DNA binding or changes in c-myc repression. Conversely, HER-2 overexpression in the context of the mesenchymal MDA-MB-231 breast cell line potentiated the TGF-β induced pro-invasive and pro-metastatic gene signature. CONCLUSION: HER-2 overexpression promotes the growth and malignancy of mammary epithelial cells, in part, by conferring resistance to the growth inhibitory effects of TGF-β. In contrast, HER-2 and TGF-β signaling pathways can cooperate to promote especially aggressive disease behavior in the context of a highly invasive breast tumor model