36 research outputs found

    Food Price Shocks and the Political Economy of Global Agricultural and Development Policy

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    The recent spikes of global food prices induced a rapid increase in mass media coverage, public policy attention, and donor funding for food security and for agriculture and rural poverty. This has occurred while the shift from low to high food prices has induced a shift in (demographic or social) location of the hunger and poverty effects, but the total number of undernourished and poor people has declined over the same period. We suggest that the observed pattern can be explained by the presence of a global urban bias on agriculture and food policy in developing countries, and we discuss whether this global urban bias may actually benefit poor farmers. We argue that the food price spikes have succeeded where others have failed in the past: to move the problems of poor and hungry farmers to the top of the policy agenda and to induce development and donor strategies to help them

    Agri-food business: Global challenges â Innovative solutions

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    The rise of a western-style middle class in many successful emerging economies like China currently is inducing deep structural changes on agricultural world markets and within the global agri-food business. As a result of both higher incomes and concerns over product safety and quality the global demand for high-quality and safe food products is increasing significantly. In order to meet the new required quality, globally minimum quality standards are rising and private standards emerging. All over the world these developments cause adjustments at the enterprise, chain and market levels. At the same time, the tremendously increasing demand for renewable energy has led to the emergence of a highly promising market for biomass production. This has far-reaching consequences for resource allocation in the agri-food business, for the environment, for the poor in developing countries and for agricultural policy reforms. The challenges increase with ongoing liberalisation, globalisation and standardisation, all of which change trade patterns for agricultural and food commodities, and influence production costs and commodity prices. The objective of the IAMO Forum is to show opportunities as well as risks for all participants of the food economy in the ongoing globalisation process: for small peasants in developing countries, farmers in Europe and globally active food enterprises and retailers. The success of enterprises depends on the ability to find innovative solutions with regard to the organisation of enterprises, chains, and markets, as well as future policy design. Concerning bio-energy strategies has to be identified to combat global warming most efficiently and concurrently attenuate the competition between "tank and table" on farmland. IAMO Forum 2008, as well as this book, would not have been possible without the engagement of many people and institutions. We thank the authors of the papers, as well as the referees. Furthermore we are highly indebted to MARLIES LOHR, NADINE GIEMSA and RONNY RECKE who in an outstanding way contributed to the organisation of the Forum. This is true as well for the IAMO administration, whose work we gratefully acknowledge. Many sponsors has funded the IAMO Forum 2008. We are very grateful to the German Research Foundation (DFG), The Federal Ministry of Food, Agriculture and Consumer Production in Germany, The Ministry of Cultural Affairs of the Federal State Saxony-Anhalt, Germany and last but not least the City of Halle. Further Conference sponsors are the BIONADE Corporation, Gaensefurther Mineral Water, The Wine Growers Association of the Region Saale-Unstrut, Germany, Obsthof am SüÃen See GmbH, Monsanto Company, KWS Saat AG, Sachsen-Anhalt-Tours, Baumkuchen Salzwedel and the Hallesches Brauhaus.Agribusiness, Agricultural and Food Policy, Agricultural Finance, Community/Rural/Urban Development, Industrial Organization, Institutional and Behavioral Economics, International Development, Marketing, Political Economy,

    Lipid degradation promotes prostate cancer cell survival

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    Prostate cancer is the most common male cancer and androgen receptor (AR) is the major driver of the disease. Here we show that Enoyl-CoA delta isomerase 2 (ECI2) is a novel AR-target that promotes prostate cancer cell survival. Increased ECI2 expression predicts mortality in prostate cancer patients (p = 0.0086). ECI2 encodes for an enzyme involved in lipid metabolism, and we use multiple metabolite profiling platforms and RNA-seq to show that inhibition of ECI2 expression leads to decreased glucose utilization, accumulation of fatty acids and down-regulation of cell cycle related genes. In normal cells, decrease in fatty acid degradation is compensated by increased consumption of glucose, and here we demonstrate that prostate cancer cells are not able to respond to decreased fatty acid degradation. Instead, prostate cancer cells activate incomplete autophagy, which is followed by activation of the cell death response. Finally, we identified a clinically approved compound, perhexiline, which inhibits fatty acid degradation, and replicates the major findings for ECI2 knockdown. This work shows that prostate cancer cells require lipid degradation for survival and identifies a small molecule inhibitor with therapeutic potential.</p

    Lipid droplet degradation by autophagy connects mitochondria metabolism to Prox1-driven expression of lymphatic genes and lymphangiogenesis.

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    Autophagy has vasculoprotective roles, but whether and how it regulates lymphatic endothelial cells (LEC) homeostasis and lymphangiogenesis is unknown. Here, we show that genetic deficiency of autophagy in LEC impairs responses to VEGF-C and injury-driven corneal lymphangiogenesis. Autophagy loss in LEC compromises the expression of main effectors of LEC identity, like VEGFR3, affects mitochondrial dynamics and causes an accumulation of lipid droplets (LDs) in vitro and in vivo. When lipophagy is impaired, mitochondrial ATP production, fatty acid oxidation, acetyl-CoA/CoA ratio and expression of lymphangiogenic PROX1 target genes are dwindled. Enforcing mitochondria fusion by silencing dynamin-related-protein 1 (DRP1) in autophagy-deficient LEC fails to restore LDs turnover and lymphatic gene expression, whereas supplementing the fatty acid precursor acetate rescues VEGFR3 levels and signaling, and lymphangiogenesis in LEC-Atg5-/- mice. Our findings reveal that lipophagy in LEC by supporting FAO, preserves a mitochondrial-PROX1 gene expression circuit that safeguards LEC responsiveness to lymphangiogenic mediators and lymphangiogenesis.We thank K. Rillaerts, J. Souffreau, and A. Bouche, for expert technical support and Dr. A. Luttun and Dr. A. Zijsen for sharing tools and advices. P.A. is supported by grants from the Flemish Research Foundation (FWO-Vlaanderen; G076617N, G049817N, G070115N), the EOS MetaNiche consortium N degrees 40007532, Stichting tegen Kanker (FAF-F/2018/1252) and the iBOF/21/053 ATLANTIS consortium with G.B. D.H. is the recipient of an FWO Doctoral Fellowship from the Flemish Research Foundation (FWO-Vlaanderen, 1186019N), Belgium. M.B. is supported by the `Fonds voor Wetenschappelijk Onderzoek' (FWO). K.J. is the recipient of an FWO Postdoctoral Fellowship from the Flemish Research Foundation (FWO-Vlaanderen). P.C. is supported by Methusalem funding by the Flemish government, and by an ERC Advanced Research Grant (EU-ERC269073).S

    Trade and the political economy of food standards

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    This article presents a political economy model of public standards in an open economy. We use the model to derive the political optimum and to analyse different factors that have an influence on this political equilibrium. We analyse the relationship between trade and the political equilibria and compare the political outcome with the social optimum to identify under which cases political considerations lead to standards being set 'too low' or 'too high', and which standards could be labelled as protectionist measures. © 2011 The Agricultural Economics Society.status: publishe
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