Realism and national identity in 'Y Tu Mamá También': an audience perspective

When referring to cinema and its emancipatory potential, realism, like Plato’s pharmakon, has signified both illness and cure, poison and medicine. On the one hand, realism is regarded as the main feature of so-called classical cinema, inherently conservative and thoroughly ideological, its main raison d’être being to reify and make a particular version of the status quo believable and to pass it out as ‘reality’ (Burch, 1990; MacCabe, 1974). On the other, realism has also been interpreted as a quest for truth and social justice, as in the positivist ethos that informs documentary (Zavattini, 1953). Even in the latter sense, however, the extent to which realism has served colonizing ends when used to investigate the ‘truth’ of the Other has also been noted, rendering the form profoundly suspicious (Chow, 2007, p. 150). For realism has been a Western form of representation, one that can be traced back to the invention of perspective in painting and that peaked with the secular worldview brought about by the Enlightenment. And like realism, the nation state too is a product of the Enlightenment, nationalism being, as it were, a secular replacement for the religious - that is enchanted or fantastic - worldview. In this way, realism, cinema and nation are inextricably linked, and equally strained under the current decline of the Enlightenment paradigm. This chapter looks at Y tu Mamá También by Alfonso Cuarón (2001), a highly successful road movie with documentary features, to explore the ways in which realism, cinema and nation interact with each other in the present conditions of ‘globalization’ as experienced in Mexico. The chapter compares and contrasts various interpretations of the role of realism in this film put forward by critics and scholars and other discourses about it circulating in the media with actual ways of audience engagement with it.

Steroid induced neuroprotection of damaged photoreceptor cells

Retinitis Pigmentosa (RP) is the name given to a group of hereditary diseases causing progressive and degenerative blindness. RP affects over 1 in 4000 individuals, making it the most prevalent inherited retinal disease worldwide, yet currently there is no cure. In 2011, our group released a paper detailing the protective effects of the synthetic progestin ‘Norgestrel’. A common component of the female oral contraceptive pill, Norgestrel was shown to protect against retinal cell death in two distinct mouse models of retinal degeneration: in the Balb/c light damage model and the Pde6brd10 (rd10) model. Little was known of the molecular workings of this compound however and thus this study aimed to elucidate the protective manner in which Norgestrel worked. To this aim, the 661W cone photoreceptor-like cell line and ex vivo retinal explanting was utilised. We found that Norgestrel induces a increase in neuroprotective basic fibroblast growth factor (bFGF) with subsequent downstream actions on the inhibition of glycogen synthase kinase 3β. Progesterone receptor expression was subsequently characterised in the C57 and rd10 retinas and in the 661W cell line. Norgestrel caused nuclear trafficking of progesterone receptor membrane complex one (PGRMC1) in 661W cells and thus Norgestrel was hypothesised to work primarily through the actions of PGRMC1. This trafficking was shown to be responsible for the critical upregulation of bFGF and PGRMC1- Norgestrel binding was proven to cause a neuroprotective bFGF-mediated increase in intracellular calcium. The protective properties of Norgestrel were further studied in the rd10 mouse model of retinitis pigmentosa. Using non-invasive diet supplementation (80mg/kg), we showed that Norgestrel gave significant retinal protection out to postnatal day 40 (P40). Overactive microglia have previously been shown to potentiate photoreceptor cell loss in the degenerating rd10 retina and thus we focussed on Norgestrel-mediated changes in photoreceptor-microglial crosstalk. Norgestrel acted to dampen pro-inflammatory microglial cell reactivity, decreasing chemokine (MCP1, MCP3, MIP-1α, MIP-1β) and subsequent damaging cytokine (TNFα, Il-1β) production. Critically, Norgestrel up-regulated photoreceptor-microglial, fractalkine-CX3CR1 signalling 1000-fold in the P20 rd10 mouse. Known to prevent microglial activation, we hypothesise that Norgestrel acts as a vital anti-inflammatory in the diseased retina, driving fractalkine-CX3CR1 signalling to delay retinal degeneration. This study stands to highlight some of the neuroprotective mechanisms utilised by Norgestrel in the prevention of photoreceptor cell death. We identify for the first time, not only a pro-survival pathway activated directly in photoreceptor cells, but also a Norgestreldriven mediation of an otherwise damaging microglial cell response. All taken, these results form the beginning of a case to bring Norgestrel to clinical trials, as a potential therapeutic for the treatment of RP.