The Determination of Technology and Commodity Policy in the U.S. Dairy Industry

United States dairy policy includes both predatory and productive components. The milk price support program is designed to transfer income to dairy farmers while research and extension expenditures are designed to increase social welfare. The purpose of this chapter is to provide an empirical example of the theory developed in the previous chapter. It has long been recognized the government research and extension policies have been significant contributors to technological advance in agriculture (Evenson and Kislev 1976, Evenson, Waggoner, and Ruttan 1979). The advent of technological change on agriculture and its policy implications was first noted by Schultz (1945, 1953). Some, like Cochrane (1958) in characterizing his famous technological treadmill thesis, argued for price supports in order to compensate farmers for the adverse effects of research on farmers\u27 welfare. Indeed, commentators like Thurow (1981) and Schlesinger (1984) argue that public good provision in agriculture is one of the few major economic success stories of government intervention in the history of the United States. Nevertheless, one of the most stylized facts in government policy intervention in agriculture is the pervasive level and overwhelming evidence of underinvestment in public research (Ruttan 1982). Concomitant to this notion, economists have alleged that governments \u27overinvest\u27 in commodity policies because of the associated deadweight losses generated

Bringing Agriculture into the GATT: Designing Acceptable Agricultural Policies

Agricultural and Food Policy, International Relations/Trade,

Reply to the letter to the editor: Could the use of bone morphogenetic proteins in fracture healing do more harm than good to our patients?

Surger

Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes

Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion

Use and efficacy of bone morphogenetic proteins in fracture healing

Signal transduction in aging related disease

The role of inflammation in epilepsy.

Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the approximately 30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators-released by brain cells and peripheral immune cells-in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data