New spaces of food justice

‘Food is fundamental to life’ (Sbicca 2012, 456) and this shared need establishes food as a site of potential for connective and convivial practices and relations. Yet, when we realise that more than one billion people are undernourished worldwide (Food Ethics Council 2010), despite the fact that the world produces enough food to feed billions more than the current global population of seven billion (Holt-Gimenez et al. 2012), the social, political, economic and environmental challenges posed by contemporary food systems start to become apparent. Given current global production levels – whether we agree with the social and environmental implications of these or not – it is clear that malnutrition rates worldwide are not simply an indicator of agricultural praxis but demonstrate the continued, broader social and structural issues of access, equity and justice. Recognising that many feel increasingly disenfranchised from formal political representation, marginalised by a hegemonic neoliberal capitalism or disconnected from ‘healthy’ social or environmental relations, food offers an opportunity to re-engage individuals and society with critical questions and practices of justice because, as Allen (2008, 159) notes, ‘no other public issue is as accessible to people in their daily lives as that of food justice. Everyone – regardless of age, gender, ethnicity, or social class – eats. We are all involved and we are all implicated’. The multiplicity of ways in which we can engage with food – including growing, buying, eating, cooking, writing, processing, marketing, selling and watching – enacts its radical potential as a set of dynamic socio-material relations (Alkon 2013; Alkon et al. 2013) that can both conform to and subvert existing practices and understandings, enabling food to ‘speak’ to many different people in a range of different contexts. Although this multiplicity has its dangers (Heynen, Kurtz, and Trauger 2012), it also means that food matters and matters in complex and diverse ways: ‘It rallies people and it often induces unexpected changes in society’ (Van der Ploeg 2013, 999)

Identification of the PS1 Thr147Ile Variant in a Family with Very Early Onset Dementia and Expressive Aphasia

Background: Early onset dementias have variable clinical presentations and are often difficult to diagnose. We established a family pedigree that demonstrated consistent recurrence of very early onset dementia in successive generations. Objective and Method: In order to refine the diagnosis in this family, we sequenced the exomes of two affected family members and relied on discrete filtering to identify disease genes and the corresponding causal variants. Results: Among the 720 nonsynonymous single nucleotide polymorphisms (SNPs) shared by two affected members, we found a C to T transition that gives rise to a Thr147Ile missense substitution in the presenilin 1 (PS1) protein. The presence of this same mutation in a French early-onset Alzheimer’s disease family, other affected members of the family, and the predicted high pathogenicity of the substitution strongly suggest that it is the causal variant. In addition to exceptionally young age of onset, we also observed significant limb spasticity and early loss of speech, concurrent with progression of dementia in affected family members. These findings extend the clinical presentation associated with the Thr147Ile variant. Lastly, one member with the Thr147Ile variant was treated with the PKC epsilon activator, bryostatin, in a compassionate use trial after successful FDA review. Initial improvements with this treatment were unexpectedly clear, including return of some speech, increased attentional focus, ability to swallow, and some apparent decrease in limb spasticity. Conclusions: Our findings confirm the role of the PS1 Thr147Ile substitution in Alzheimer’s disease and expand the clinical phenotype to include expressive aphasia and very early onset of dementia

The celebrification of farmers: celebrity and the new politics of farming

Michelle Phillipov and Michael K. Goodma

Bryostatin enhancement of memory in Hermissenda

Author Posting. © Marine Biological Laboratory, 2006. This article is posted here by permission of Marine Biological Laboratory for personal use, not for redistribution. The definitive version was published in Biological Bulletin 210 (2006): 201-214.Bryostatin, a potent agonist of protein kinase C (PKC), when administered to Hermissenda was found to affect acquisition of an associative learning paradigm. Low bryostatin concentrations (0.1 to 0.5 ng/ml) enhanced memory acquisition, while concentrations higher than 1.0 ng/ml down-regulated the pathway and no recall of the associative training was exhibited. The extent of enhancement depended upon the conditioning regime used and the memory stage normally fostered by that regime. The effects of two training events (TEs) with paired conditioned and unconditioned stimuli, which standardly evoked only short-term memory (STM) lasting 7 min, were—when bryostatin was added concurrently—enhanced to a long-term memory (LTM) that lasted about 20 h. The effects of both 4- and 6-paired TEs (which by themselves did not generate LTM), were also enhanced by bryostatin to induce a consolidated memory (CM) that lasted at least 5 days. The standard positive 9-TE regime typically produced a CM lasting at least 6 days. Low concentrations of bryostatin (<0.5 ng/ml) elicited no demonstrable enhancement of CM from 9-TEs. However, animals exposed to bryostatin concentrations higher than 1.0 ng/ml exhibited no behavioral learning. Sharp-electrode intracellular recordings of type-B photoreceptors in the eyes from animals conditioned in vivo with bryostatin revealed changes in input resistance and an enhanced long-lasting depolarization (LLD) in response to light. Likewise, quantitative immunocytochemical measurements using an antibody specific for the PKC-activated Ca2+/GTP-binding protein calexcitin showed enhanced antibody labeling with bryostatin. Animals exposed to the PKC inhibitor bisindolylmaleimide-XI (Ro-32-0432) administered by immersion prior to 9-TE conditioning showed no training-induced changes with or without bryostatin exposure. However, if animals received bryostatin before Ro-32, the enhanced acquisition and demonstrated recall still occurred. Therefore, pathways responsible for the enhancement effects induced by bryostatin were putatively mediated by PKC. Overall, the data indicated that PKC activation occurred and calexcitin levels were raised during the acquisition phases of associative conditioning and memory initiation, and subsequently returned to baseline levels within 24 and 48 h, respectively. Therefore, the protracted recall measured by the testing regime used was probably due to bryostatin-induced changes during the acquisition and facilitated storage of memory, and not necessarily to enhanced recall of the stored memory when tested many days after training.AMK and HTE acknowledge the support of the Marine Biological Laboratory and Blanchette Rockefeller Neurosciences Institutes for these initial studies

The fables of pity: Rousseau, Mandeville and the animal-fable

Copyright @ 2012 Edinburgh University PressPrompted by Derrida’s work on the animal-fable in eighteenth-century debates about political power, this article examines the role played by the fiction of the animal in thinking of pity as either a natural virtue (in Rousseau’s Second Discourse) or as a natural passion (in Mandeville’s The Fable of the Bees). The war of fables between Rousseau and Mandeville – and their hostile reception by Samuel Johnson and Adam Smith – reinforce that the animal-fable illustrates not so much the proper of man as the possibilities and limitations of a moral philosophy that is unable to address the political realities of the state