Co-Creation as an agonistic practice in the favela of Santa Marta, Rio de Janeiro

This paper explores the potential of ‘Co-Creation’ to develop new understandings of neighbourhood disadvantage in collaboration with civil society partners. It argues that there is a growing need for collaborative knowledge production with communities carrying vernacular knowledges previously invalidated by dominant epistemologies. The first part of the paper undertakes a reconceptualization of ‘co-creation’, a term usually associated with citizen involvement in neoliberal contexts, redeveloping it as a ‘critical artistic practice’ (Chantal Mouffe, 2013) in which new ways of imagining the city can be articulated. The second part of the paper examines the practice of Co-Creation as a participatory methodology involving artists, researchers and stakeholders in developing ‘agonistic spaces’ by scrutinizing a five-day workshop conducted in the Rio de Janeiro favela of Santa Marta to explore multiple understandings and meanings of this neighbourhood. Through an analysis of creative workshop activities such as photovoice and mapping exercises, the authors explore the potential of the Co-Creation approach to construct new subjectivities that can help subvert existing configurations of power. The conclusion formulates some recommendations about future strategies to maximise Co-Creation’s potential to engage communities in collaborative knowledge production about their neighbourhoods and bring about positive change.

Age-dependent molecular alterations in the autophagy pathway in HIVE patients and in a gp120 tg mouse model: reversal with beclin-1 gene transfer.

Aged (>50 years old) human immunodeficiency virus (HIV) patients are the fastest-growing segment of the HIV-infected population in the USA and despite antiretroviral therapy, HIV-associated neurocognitive disorder (HAND) prevalence has increased or remained the same among this group. Autophagy is an intracellular clearance pathway for aggregated proteins and aged organelles; dysregulation of autophagy is implicated in the pathogenesis of Parkinson's disease, Alzheimer's disease, and HAND. Here, we hypothesized that dysregulated autophagy may contribute to aging-related neuropathology in HIV-infected individuals. To explore this possibility, we surveyed autophagy marker levels in postmortem brain samples from a cohort of well-characterized <50 years old (young) and >50 years old (aged) HIV+ and HIV encephalitis (HIVE) patients. Detailed clinical and neuropathological data showed the young and aged HIVE patients had higher viral load, increased neuroinflammation and elevated neurodegeneration; however, aged HIVE postmortem brain tissues showed the most severe neurodegenerative pathology. Interestingly, young HIVE patients displayed an increase in beclin-1, cathepsin-D and light chain (LC)3, but these autophagy markers were reduced in aged HIVE cases compared to age-matched HIV+ donors. Similar alterations in autophagy markers were observed in aged gp120 transgenic (tg) mice; beclin-1 and LC3 were decreased in aged gp120 tg mice while mTor levels were increased. Lentivirus-mediated beclin-1 gene transfer, that is known to activate autophagy pathways, increased beclin-1, LC3, and microtubule-associated protein 2 expression while reducing glial fibrillary acidic protein and Iba1 expression in aged gp120 tg mice. These data indicate differential alterations in the autophagy pathway in young versus aged HIVE patients and that autophagy reactivation may ameliorate the neurodegenerative phenotype in these patients

Hippocampal neuronal cells that accumulate α-synuclein fragments are more vulnerable to Aβ oligomer toxicity via mGluR5--implications for dementia with Lewy bodies.

BackgroundIn dementia with Lewy bodies (DLB) abnormal interactions between α-synuclein (α-syn) and beta amyloid (Aβ) result in selective degeneration of neurons in the neocortex, limbic system and striatum. However, factors rendering these neurons selectively vulnerable have not been fully investigated. The metabotropic glutamate receptor 5 (mGluR5) has been shown to be up regulated in DLB and might play a role as a mediator of the neurotoxic effects of Aβ and α-syn in vulnerable neuronal populations. In this context, the main objective of the present study was to investigate the role of mGluR5 as a mediator of the neurotoxic effects of α-syn and Aβ in the hippocampus.ResultsWe generated double transgenic mice over-expressing amyloid precursor protein (APP) and α-syn under the mThy1 cassette and investigated the relationship between α-syn cleavage, Aβ, mGluR5 and neurodegeneration in the hippocampus. We found that compared to the single tg mice, the α-syn/APP tg mice displayed greater accumulation of α-syn and mGluR5 in the CA3 region of the hippocampus compared to the CA1 and other regions. This was accompanied by loss of CA3 (but not CA1) neurons in the single and α-syn/APP tg mice and greater loss of MAP 2 and synaptophysin in the CA3 in the α-syn/APP tg. mGluR5 gene transfer using a lentiviral vector into the hippocampus CA1 region resulted in greater α-syn accumulation and neurodegeneration in the single and α-syn/APP tg mice. In contrast, silencing mGluR5 with a lenti-shRNA protected neurons in the CA3 region of tg mice. In vitro, greater toxicity was observed in primary hippocampal neuronal cultures treated with Aβ oligomers and over-expressing α-syn; this effect was attenuated by down-regulating mGluR5 with an shRNA lentiviral vector. In α-syn-expressing neuronal cells lines, Aβ oligomers promoted increased intracellular calcium levels, calpain activation and α-syn cleavage resulting in caspase-3-dependent cell death. Treatment with pharmacological mGluR5 inhibitors such as 2-Methyl-6-(phenylethynyl)pyridine (MPEP) and 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine (MTEP) attenuated the toxic effects of Aβ in α-syn-expressing neuronal cells.ConclusionsTogether, these results support the possibility that vulnerability of hippocampal neurons to α-syn and Aβ might be mediated via mGluR5. Moreover, therapeutical interventions targeting mGluR5 might have a role in DLB

Early Post-Fire Recovery on a Heavily Visited Mojave Desert Burn: Red Rock Canyon near Las Vegas, Nevada

Wildfire has become widespread in southwestern USA deserts. In a record 2005 fire season in the Mojave Desert, for example, more than 385,000 hectares burned (Brooks and Matchett 2006). This burned area is approximately 3% of the entire Mojave Desert. Fueled in large part by exotic annual grasses, these fires burned desert ecosystems thought to have only burned infrequently historically. Burns now occupy significant portions of desert landscapes, posing prominent management challenges. Improving our understanding of plant recovery on desert burns is important for evaluating future fire hazard, whether natural revegetation will meet management objectives, and for planning active revegetation if this becomes a management goal. Desert burns may afford an opportunity for intervention in the grass-fire cycle immediately following a burn if exotic grass competition is temporarily reduced while available nutrients liberated by the fire increase. However, post-fire recovery of plant communities is not a well understood process in desert ecosystems

Early post-fire plant establishment on a Mojave Desert burn

Fire has become more extensive in recent decades in southwestern United States arid lands. Burned areas pose management challenges and opportunities, and increasing our understanding of post-fire plant colonization may assist management decision-making. We examined plant communities, soils, and soil seed banks two years after the 2005 Loop Fire, located in a creosote-blackbrush community in Red Rock Canyon National Conservation Area in southern Nevada’s Mojave Desert. Based on a spring sampling of 20, 0.01-ha plots, live + dead cover of the exotic annual Bromus rubens averaged nine times lower on the burn than on a paired unburned area. Perennial species composition shifted from dominance by late-successional native shrubs (e.g., Coleogyne ramosissima) on the unburned area, to dominance by native perennial forbs (e.g., Sphaeralcea ambigua, Baileya multiradiata) on the burn. Species richness of live plants averaged 26% (100 m2 scale) and 239% (1 m2 scale) greater on the burn compared to the unburned area. Only 5% of Larrea tridentata individuals resprouted, compared to 64% of Yucca schidigera and baccata. Fire and microsite (interspace, below L. tridentata, or below Yucca) interacted to affect several 0–5 cm soil properties, with higher pH, conductivity, and total P and K on burned Yucca microsites. Bromus rubens density in 0–5 cm soil seed banks was four times lower on the burn, and its distribution among microsites reversed. Below-shrub microsites contained the most B. rubens seeds on the unburned area, but the least on the burned area. Intense fire below shrubs may have increased seed mortality, an idea supported by .3-fold decreases we found in emergence density after heating seed bank samples to 100uC. Our study occurred after a post-fire period of below-average precipitation, underscoring a need for longer term monitoring that characterizes moister years

Design and Construction of a Chemical Engineering (ChemE) Car Using Thermoelectrics

Six chemical engineering undergraduates at the University of South Carolina formed a team to compete in the 2014 AIChE Chem-E-Car competition at the Southern Regional Student Conference in San Juan, Puerto Rico, in March. In the Chem-E-Car competition, students must design and build a vehicle powered by an unconventional form of chemical energy to carry a specified weight over a given distance (1). The group used knowledge gained through undergraduate study to construct a small-scale vehicle that is powered by a set of thermoelectric generators utilizing a heat gradient between boiling water and an ethanol-dry ice mixture (2). An iodine clock reaction is used in conjunction with photoresistors and an Arduino microcontroller to stop the car after the reaction goes to completion. The group had a successful run at the regional competition in Puerto Rico, earning first place in the research poster competition and fourth place in the performance competition. The group was selected as one of five teams to advance to the national competition held at the AIChE Annual Meeting in November 2014 in Atlanta, Georgia

Cytosolic Phospholipase A2α and Eicosanoids Regulate Expression of Genes in Macrophages Involved in Host Defense and Inflammation

Acknowledgments: We thank Dr. Robert Barkley and Charis Uhlson for mass spectrometry analysis. Funding: This work was supported by grants from the National Institutes of Health HL34303 (to C.C.L., R.C.M. and D.L.B), DK54741 (to J.V.B.), GM5322 (to D.L.W.) and the Wellcome Trust (to N.A.R.G. and G.D.B.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

Master Recital

Program listing performers and works performe