The art world is getting wider and more subjective. As for the link with advertising, since its inception in the first half of the twentieth century, these have evolved hand in hand. It has not been until relatively recently when this link appeared as connected to marketing via creativity. Through multiple strategies, marketing manages to give a current approach to advertising through new associations between ideas and concepts. In this research the evolution of the three disciplines is set from definition. With a content analysis of several advertising pieces awarded with industry recognition and with a description of the creative attributes that make an advertising piece a work of art. The results of this research allow us to determine what are the creative attributes of branded content that have remained almost unchanged in recent years; from this, a model can be proposed that defines the most representative creative pattern of these tactics, since they offer entertaining content with varying degrees of emotional appeal based on experiential and functionally promoted media.
Pleiotrophin (PTN) is a neurotrophic factor that regulates glial responses in animal models of different types of central nervous system (CNS) injuries. PTN is upregulated in the brain in different pathologies characterized by exacerbated neuroinflammation, including Parkinson’s disease. PTN is an endogenous inhibitor of Receptor Protein Tyrosine Phosphatase (RPTP) β/ζ, which is abundantly expressed in the CNS. Using a specific inhibitor of RPTPβ/ζ (MY10), we aimed to assess whether the PTN/RPTPβ/ζ axis is involved in neuronal and glial injury induced by the toxin MPP+. Treatment with the RPTPβ/ζ inhibitor MY10 alone decreased the viability of both SH-SY5Y neuroblastoma cells and BV2 microglial cultures, suggesting that normal RPTPβ/ζ function is involved in neuronal and microglial viability. We observed that PTN partially decreased the cytotoxicity induced by MPP+ in SH-SY5Y cells underpinning the neuroprotective function of PTN. However, MY10 did not seem to modulate the SH-SY5Y cell loss induced by MPP+. Interestingly, we observed that media from SH-SY5Y cells treated with MPP+ and MY10 decreases microglial viability but may elicit a neuroprotective response of microglia by upregulating Ptn expression. The data suggest a neurotrophic role of microglia in response to neuronal injury through upregulation of Ptn levels.
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