Knowledge, the curriculum, and democratic education: the curious case of school English

Debate over subject curricula is apt to descend into internecine squabbles over which (whose?) curriculum is best. Especially so with school English, because its domain(s) of knowledge have commonly been misunderstood, or, perhaps, misrepresented in the government’s programmes of study. After brief consideration of democratic education (problems of its form and meaning), I turn to issues of knowledge and disciplinarity, outlining two conceptions of knowledge – the one constitutive and phenomenological, the other stipulative and social-realist. Drawing on Michael Young and Johan Muller, I argue that, by social-realist standards of objectivity, school English in England -- as currently framed in national curriculum documents -- falls short of the standards of ‘powerful knowledge’ and of a democratic education conceived as social justice. Having considered knowledge and disciplinarity in broad terms, I consider the curricular case of school English, for it seems to me that the curious position of English in our national curriculum has resulted in a model that is either weakly, perhaps even un-, rooted in the network of academic disciplines that make up English studies

Noncanonical NF-kappa B signaling in microvessels of atherosclerotic lesions is associated with inflammation, atheromatous plaque morphology and myocardial infarction

Neovascularization is associated with atherosclerotic plaque instability and increased chance of myocardial infarction (MI). Patients with chronic inflammatory diseases (CID) have increased risk of atherosclerosis, and evidence demonstrates that NF-κB inducing kinase (NIK)-mediated noncanonical NF-κB signaling in endothelial cells (EC) is linked to inflammation and angiogenesis. Here, we hypothesized NIK may also be activated in EC of atherosclerotic lesion microvessels. Using cohorts of atherosclerotic lesions from coronary and carotid arteries, we quantified NIK expression in plaque microvessels and compared it to pathological markers, including inflammatory cell content, plaque characteristics and MI. Differences in gene transcripts were evaluated between stable and ruptured lesions. NIK+EC were present in both coronary and carotid lesions. In CID patients, plaques with stenosis >40% had an increased number of NIK+EC and higher content of immune cells (p  < .05) as compared to controls. Immune cells per NIK+EC were also greater in CID patients (p  < .05), with pronounced differences as stenosis increased. In unstable lesions, NIK+EC were elevated as were EC expressing CXCL12 (p  < .05). NIK+EC were increased in lesions with lipid content >40% (p  < .05) and more abundant in coronary artery lesions implicated in MI (p  < .05). These vessels also associated with atheromatous rather than fibrous plaque morphology (p  < .05). Transcriptomic profiling demonstrated components of noncanonical NF-κB pathway were also upregulated in ruptured plaques (p  < .05). NIK+EC associate with chronic inflammation in advanced lesions and are linked to markers of local inflammation, lipid content, unstable plaque phenotype and development of MI. Therefore, targeting noncanonical NF-κB signaling may hold therapeutic potential for patients with atherosclerosis and cardiovascular diseas