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Biology subjects

Hung, E.

Publications and source records attributed to Hung, E..

2 recordsLinked to original sources

Urbanization effects are trait-specific and city-dependent across a widespread spider's global range

Urban environments impose strong selective pressures through biotic and abiotic factors, driving changes in behavior, physiology, and morphology. Yet, responses vary across taxa and cities, and it remains unclear which traits respond consistently and what factors moderate this variation. We addressed these questions using the widespread European garden spider (Araneus diadematus) as a model, measuring size, color, and web-building traits along urban-rural transects in 22 cities across its distribution range. Using a meta-analytic framework, we assessed how city-specific characteristics influenced trait variation. Urbanization consistently reduced relative abdomen surface area, a proxy for body condition. Exploratory meta-regressions suggest that web-building response was predicted by temperature: compared to their non-urban surroundings, urban webs are larger in colder regions and smaller in warmer regions. In contrast, body size and abdomen brightness varied among cities without clear environmental predictors. These findings show that urbanization effects are trait- and context-dependent, likely influenced by local factors such as heat island intensity, microclimate, or prey availability. Linking within- and between-city variation will improve understanding of species phenotypic responses to urban environments.

ecology↗

Systems profiling reveals recurrently dysregulated cytokine signaling responses in ER+ breast cancer patients' blood

Cytokines mediate cell-to-cell communication across the immune system and therefore are critical to immunosurveillance in cancer and other diseases. Several cytokines show dysregulated abundance or signaling responses in breast cancer, associated with the disease and differences in survival and progression. Cytokines operate in a coordinated manner to affect immune surveillance and regulate one another, necessitating a systems approach for a complete picture of this dysregulation. Here, we profiled cytokine signaling responses of peripheral immune cells from breast cancer patients as compared to healthy controls in a multidimensional manner across ligands, cell populations, and responsive pathways. We find alterations in cytokine responsiveness across pathways and cell types that are best defined by integrated signatures across dimensions. Alterations in the abundance of a cytokines cognate receptor do not explain differences in responsiveness. Rather, alterations in baseline signaling and receptor abundance suggesting immune cell reprogramming are associated with altered responses. These integrated features suggest a global reprogramming of immune cell communication in breast cancer. Significance StatementWhile individual cytokine responses have previously been observed to be altered in breast cancer, cytokine signaling responses are tightly interconnected in a way that has not been previously characterized. Here, we profile cytokine signaling responses and find alterations that are shared across both pathways and cell types. The signatures across these measurements better define the alterations and point to a broad immunosuppression response. HighlightsO_LIBaseline and post-stimulation cytokine signaling profiles differ between healthy donors and breast cancer patients. C_LIO_LIChanges in cytokine response are not explained by differences in abundance of the cognate receptor C_LIO_LIFeatures of signaling response and receptor abundance dysregulation are coordinated across patients C_LIO_LIIntegrated patterns of dysregulation in breast cancer patients share features of Th17 like-response as well as regulatory-like B and CD8+ T cells C_LI

cancer biology↗