4 research outputs found

    Do a threatened native amphibian and its invasive congener differ in response to human alteration of the landscape?

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    Anthropogenic changes to habitat are a global phenomenon and the impact of these changes may act in tandem to cause loss of biodiversity. One major global change is the introduction of invasive species. In order to determine whether other human impacts might correlate with populations of invaders, we examined the habitat correlates of distribution, persistence and reproduction of a global invader, the American bullfrog (Rana catesbeiana). We then compared these correlates with those of a threatened, native congener, the California red-legged frog (Rana draytonii). We found striking differences between the two species in response to habitat fragmentation and degradation. Our work suggests that human alteration of habitat, in particular the hydrology of freshwater sites and through building roads, favors this invasive species across the landscape

    Chronic inflammation enhances NGF-β/TrkA system expression via EGFR/MEK/ERK pathway activation in Sjögren’s syndrome

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    Primary Sjögren's syndrome (pSS) is a chronic autoimmune exocrine disease associated with variable lymphocytic infiltration of the affected organs (primarily salivary and lachrymal glands). To investigate the potential implication of nerve growth factor-β (NGF-β) and its high affinity receptor tyrosine kinase receptor A (TrkA) in the regulation of pSS inflammatory responses, we studied their expression in the human salivary gland epithelial cells (SGEC) cultures from pSS minor salivary glands (MSG) biopsies and their relationship with histopathological disease parameters. Here, we demonstrated an increased expression of the NGF-β/TrkA system in pSS SGEC, correlated with the MSG inflammation grade. The results demonstrate that the pro-inflammatory cytokines TNF-α and IL-6 enhance NGF-β production; on the contrary, NGF-β production was reduced in the presence of both Raf-1 kinase and MEK inhibitors. Furthermore, TNF-α/IL-6 treatment increased ERK1/2 phosphorylation. Inhibition of the EGF/EGFR system also decreased NGF-β release by pSS SGEC, indicating that the chronic inflammatory condition characteristic of pSS enhances NGF-β production via EGFR/Raf-1/MEK/ERK pathway activation. KEY MESSAGE: NGF-β and TrkA expression is elevated in salivary gland epithelial cells of primary Sjögren's syndrome (pSS). Overexpression of NGF-β/TrkA system in pSS occurs via EGFR/Raf-1/MEK/ERK pathway. In pSS, NGF-β overexpression was prevented by EGFR/Raf-1/MEK/ERK pathway inhibition
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