Designing Regional Systems of Biotechnology Regulation A Transaction Cost Approach to Regulatory Governance

Many developing countries are currently in the process of designing regulatory systems that should make it possible to use the potential of genetically modified organisms (GMOs) for agricultural development, while at the same time managing the risks for food safety and the environment that are potentially associated with these technologies. In view of the considerable costs associated with biotechnology regulation and the scarcity of biosafety specialists, there are processes in various regions of the developing world to establish regional systems of biotechnology regulation. So far, there are major knowledge gaps as to how regional systems of biotechnology regulation can be designed to be effective and efficient and to fulfill principles of good governance, such as transparency, voice and accountability, control of corruption, and avoidance of special interest capture. There is a wide variety of possible regional approaches, which differ with regard to the level of centralization, the scope of a regional system, the types of regional institutions and processes, and the types of financing mechanisms. Based on the literature on environmental and fiscal federalism and transaction costs economics, the paper develops a conceptual framework for the assessment of regional systems of biotechnology regulation. The framework specifies design options and assessment criteria, and identifies major trade-offs as well as the factors affecting these trade-offs. The paper takes West Africa as an example to illustrate this framework and refers to the European Union for comparison. The paper concludes that involving regional experts, stakeholders and policy-makers into debates on the design of a regional regulatory system is an important strategy to fill knowledge gaps and arrive at conclusions regarding the trade-offs involved in regional biotechnology regulation. Key words: regional biotechnology regulation; regulatory federalism; transaction cost economics; West Africa; European Unionregional biotechnology regulation, regulatory federalism, transaction cost economics, European Union, Agricultural and Food Policy, Community/Rural/Urban Development, Consumer/Household Economics, Environmental Economics and Policy, Farm Management, Food Consumption/Nutrition/Food Safety, Food Security and Poverty, International Relations/Trade, Marketing, Production Economics, Research and Development/Tech Change/Emerging Technologies,

Nonlithographic epitaxial Sn_xGe_(1–x) dense nanowire arrays grown on Ge(001)

We have grown 1-µm-thick Sn_xGe_(1–x)/Ge(001) epitaxial films with 0 < x < 0.085 by molecular-beam epitaxy. These films evolve during growth into a dense array of Sn_xGe_(1–x) nanowires oriented along [001], as confirmed by composition contrast observed in scanning transmission electron microscopy in planar view. The Sn-rich regions in these films dominate optical absorption at low energy; phase-separated Sn_xGe_(1–x) alloys have a lower-energy band gap than homogeneous alloys with the same average Sn composition

Immunohistochemistry in Irradiated Skin Tissue

Currently there is no effective treatment for radiation dermatitis that results from clinical or accidental radiation exposures. Radiation exposure can cause severe burns and sloughing of the skin and damage muscle and bone layers underneath the skin. Radiation exposure in cells results in several types of cell death, such as necrosis, apoptosis, or autophagy, or accelerated senescence. Preliminary experiments demonstrated that accelerated senescence is a primary response to radiation in normal skin cells in culture and skin tissue in vivo in mice. We wanted to use immunohistochemistry to identify the skin cells that undergo senescence in tissues obtained from 4 mice over a time course from 1-30 days following exposure to 17.9 Gy (0.6 Gy/min) irradiation. The different stains that are going to be used are hematoxylin and eosin stain which shows the morphology of the whole tissue, K15 which marks adult skin epidermal stem cells, p21/waf1 which is a marker for senescence, DCT which marks melanocyte stem cells, and c-kit which marks melanocytes and basal epithelial cells. The results from these experiments will help us to determine which cells to protect in order to treat severe radiation exposure

The Cure Can Be Worse than the Disease: A Cautionary Tale Regarding Instrumental Variables

In this paper we draw attention to two problems associated with the use of instrumental variables (IV) whose importance for empirical work has not been fully appreciated. First, using potential instruments that explain little of the variation in the: endogenous explanatory variables can lead to large inconsistencies of the IV estimates even If only a weal

Translation inhibition by rocaglates is independent of eIF4E phosphorylation status

Rocaglates are natural products that inhibit protein synthesis in eukaryotes and exhibit antineoplastic activity. In vitro biochemical assays, affinity chromatography experiments coupled with mass spectrometry analysis, and in vivo genetic screens have identified eukaryotic initiation factor (eIF) 4A as a direct molecular target of rocaglates. eIF4A is the RNA helicase subunit of eIF4F, a complex that mediates cap-dependent ribosome recruitment to mRNA templates. The eIF4F complex has been implicated in tumor initiation and maintenance through elevated levels or increased phosphorylation status of its cap-binding subunit, eIF4E, thus furthering the interest toward developing rocaglates as antineoplastic agents. Recent experiments have indicated that rocaglates also interact with prohibitins 1 and 2, proteins implicated in c-Raf-MEK-ERK signaling. Because increased ERK signaling stimulates eIF4E phosphorylation status, rocaglates are also expected to inhibit eIF4E phosphorylation status, a point that has not been thoroughly investigated. It is currently unknown whether the effects on translation observed with rocaglates are solely through eIF4A inhibition or also a feature of blocking eIF4E phosphorylation. Here, we show that rocaglates inhibit translation through an eIF4E phosphorylation-independent mechanism.P50 GM067041 - NIGMS NIH HHS; R01 GM073855 - NIGMS NIH HHS; GM-067041 - NIGMS NIH HHS; MOP-106530 - Canadian Institutes of Health Researc