Logics, rhetoric and 'the blob': populist logic in the Conservative reforms to English schooling

A lot has been written about the lasting implications of the Conservative reforms to English schooling, particularly changes made by Michael Gove as Education Secretary (2010–2014). There is a lot less work, however, on studying the role that language, strategy and the broader political framework played in the process of instituting and winning consent for these reforms. Studying these factors is important for ensuring that any changes to education and schooling are not read in isolation from their political context. Speeches particularly capture moments where intellectual and strategic political traditions meet, helping us to form a richer understanding of the motives behind specific reform goals and where they fit into a political landscape. This article analyses speeches and policy documents from prominent politicians who led the Conservative education agenda between 2010–2014 to illustrate how politicians mobilised a deliberate populist strategy and argumentation to achieve specific educational goals, but which have had broader social and political implications. Concepts from interpretive political studies are used to develop a case analysis of changes to teacher training provision and curriculum reform, illustrating how politicians constructed a frontier between ‘the people’ (commonly teachers or parents) and an illegitimate ‘elite’ (an educational establishment) that opposed change. This anti‐elite populist rhetoric, arguably first tested in the Department for Education, has now become instituted more widely in our current British politics

Ocean Seismic Network Pilot Experiment

Author Posting. © American Geophysical Union, 2003. It is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geochemistry Geophysics Geosystems 4 (2003): 1092, doi:10.1029/2002GC000485.The primary goal of the Ocean Seismic Network Pilot Experiment (OSNPE) was to learn how to make high quality broadband seismic measurements on the ocean bottom in preparation for a permanent ocean seismic network. The experiment also had implications for the development of a capability for temporary (e.g., 1 year duration) seismic experiments on the ocean floor. Equipment for installing, operating and monitoring borehole observatories in the deep sea was also tested including a lead-in package, a logging probe, a wire line packer and a control vehicle. The control vehicle was used in three modes during the experiment: for observation of seafloor features and equipment, for equipment launch and recovery, and for power supply and telemetry between ocean bottom units and the ship. The OSNPE which was completed in June 1998 acquired almost four months of continuous data and it demonstrated clearly that a combination of shallow buried and borehole broadband sensors could provide comparable quality data to broadband seismic installations on islands and continents. Burial in soft mud appears to be adequate at frequencies below the microseism peak. Although the borehole sensor was subject to installation noise at low frequencies (0.6 to 50 mHz), analysis of the OSNPE data provides new insights into our understanding of ocean bottom ambient noise. The OSNPE results clearly demonstrate the importance of sediment borne shear modes in ocean bottom ambient noise behavior. Ambient noise drops significantly at high frequencies for a sensor placed just at the sediment basalt interface. At frequencies above the microseism peak, there are two reasons that ocean bottom stations have been generally regarded as noisier than island or land stations: ocean bottom stations are closer to the noise source (the surface gravity waves) and most ocean bottom stations to date have been installed on low rigidity sediments where they are subject to the effects of shear wave resonances. When sensors are placed in boreholes in basement the performance of ocean bottom seismic stations approaches that of continental and island stations. A broadband borehole seismic station should be included in any real-time ocean bottom observatory.This work was sponsored by the National Science Foundation (NSF Grant Numbers: OCE-9522114, OCE-9523541 and OCE-9819439) with additional support from Incorporated Research Institutions for Seismology (IRIS), Joint Oceanographic Institutions, Inc. (JOI Contract No: 12-94), Scripps Institution of Oceanography, a Mellon Grant from Woods Hole Oceanographic Institution, and the Earthquake Research Institute at the University of Tokyo (Visiting Professorship for RAS)

Mutations in DCHS1 Cause Mitral Valve Prolapse

SUMMARY Mitral valve prolapse (MVP) is a common cardiac valve disease that affects nearly 1 in 40 individuals1–3. It can manifest as mitral regurgitation and is the leading indication for mitral valve surgery4,5. Despite a clear heritable component, the genetic etiology leading to non-syndromic MVP has remained elusive. Four affected individuals from a large multigenerational family segregating non-syndromic MVP underwent capture sequencing of the linked interval on chromosome 11. We report a missense mutation in the DCHS1 gene, the human homologue of the Drosophila cell polarity gene dachsous (ds) that segregates with MVP in the family. Morpholino knockdown of the zebrafish homolog dachsous1b resulted in a cardiac atrioventricular canal defect that could be rescued by wild-type human DCHS1, but not by DCHS1 mRNA with the familial mutation. Further genetic studies identified two additional families in which a second deleterious DCHS1 mutation segregates with MVP. Both DCHS1 mutations reduce protein stability as demonstrated in zebrafish, cultured cells, and, notably, in mitral valve interstitial cells (MVICs) obtained during mitral valve repair surgery of a proband. Dchs1+/− mice had prolapse of thickened mitral leaflets, which could be traced back to developmental errors in valve morphogenesis. DCHS1 deficiency in MVP patient MVICs as well as in Dchs1+/− mouse MVICs result in altered migration and cellular patterning, supporting these processes as etiological underpinnings for the disease. Understanding the role of DCHS1 in mitral valve development and MVP pathogenesis holds potential for therapeutic insights for this very common disease