While policymakers constructed an image of ‘the citizen-consumer’ who would take responsibility for heart health through exercising the choice to purchase a drug that was effectively rationed on the NHS and medical professionals
raised concerns about ‘a flawed consumer’ who was likely to misuse the product, both these groups assumed that there would be a market for the drug. By contrast, those who bought the product or potentially fell within its target market might appear as ‘health consumers’, seeking out and paying for different food and lifestyle products and services, including those targeting high cholesterol. However, they were reluctant ‘pharmaceutical consumers’ who either preferred to
take medication on the advice of a doctor, or sought to minimize medicine use. In comparison to previous studies, our analysis builds understanding of individual consumers PF-04929113 supplier in a market, rather than collective action for access to drugs (or, less commonly, compensation for adverse effects). Where some theories of pharmaceuticalisation have presented consumers as creating pressure for expanding markets, our data suggests that sociologists should be cautious about assuming there will be demand for new pharmaceutical products, especially those aimed at prevention or asymptomatic conditions, even in burgeoning health markets. (C) 2014 Elsevier Ltd. All rights reserved.”
“Transforming growth factor-beta (TGF-beta) signaling exerts a wide spectrum of biological functions. To investigate TGF-beta signaling MEK inhibition in amelogenesis, we initially Selleckchem Rigosertib assessed the expression of TGF-beta1 and TGF-beta receptor 1 (TGFBR1) in developing teeth by immunohistochemistry. Both TGF-beta1 and TGFBR1 were strongly expressed in secreting ameloblasts. Next, we studied the effects of TGF-beta signaling on the expression of MMP20 and YLK4 mRNA using ameloblast-lineage cells (ALC) in vitro. Our RT-PCR study showed that TGF-beta1, TGFBR1, and enamel matrix proteases
(MMP20 and KLK4) were expressed in ALC. Following TGF-beta1 treatment, the expression of MMP20 mRNA, but not KLK4 mRNA, was significantly upregulated. To further confirm the TGF-beta signaling involvement in the MMP20 expression, we constructed the activated TGFBR1 vector and transfected the construct into ALC. The activated TGFBR1 notably promoted MMP20 expression, but had no obvious effects on the KLK4 mRNA expression. Our studies strongly suggest that TGF-beta signaling involved in amelogenesis is partially mediated by regulating the expression of MMP20 mRNA. Anat Rec, 292:885-890, 2009. (C) 2009 Wiley-Liss, Inc.”
“Developmental modifications in cell shape depend on dynamic interactions between the extracellular matrix and cytoskeleton.