Post-compulsory education and training: transformism and the struggle for change

The paper addresses a number of issues concerning policy and curriculum in post-compulsory education and training (PCET). Firstly, it seeks to locate PCET within its socio-economic context as it is this that frames curricula within the learning and skills sector and serves to legitimate its particular form. Secondly, the paper addresses the manner in which state policy impacts upon the sector and is followed by a discussion of curricula issues. It is argued that the rhetoric of competitiveness is over-stated and that this serves to tie educational processes to economic needs. This is reflected in curricular divisions as well as differentiations between learners. These, rather than challenging existing social relations, serve to conserve these resulting in a 'transformist' politics. The paper concludes with a section that explores the struggle for social justice, arguing that a radical educational politics needs to address inequalities endemic in wider society. Localized educational responses are limited and can only take us so far in the struggle for social justice

Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity

In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively in adipocytes(1). Adipose-specific knockout or overexpression of Glut4 alters systemic insulin sensitivity(2). Here we show, using DNA array analyses, that nicotinamide N-methyltransferase (Nnmt) is the most strongly reciprocally regulated gene when comparing gene expression in white adipose tissue (WAT) from adipose-specific Glut4-knockout or adipose-specific Glut4-overexpressing mice with their respective controls. NNMT methylates nicotinamide (vitamin B3) using S-adenosylmethionine (SAM) as a methyl donor(3,4). Nicotinamide is a precursor of NAD(+), an important cofactor linking cellular redox states with energy metabolism(5). SAM provides propylamine for polyamine biosynthesis and donates a methyl group for histone methylation(6). Polyamine flux including synthesis, catabolism and excretion, is controlled by the rate-limiting enzymes ornithine decarboxylase (ODC) and spermidine–spermine N(1)-acetyltransferase (SSAT; encoded by Sat1) and by polyamine oxidase (PAO), and has a major role in energy metabolism(7,8). We report that NNMT expression is increased in WAT and liver of obese and diabetic mice. Nnmt knockdown in WAT and liver protects against diet-induced obesity by augmenting cellular energy expenditure. NNMT inhibition increases adipose SAM and NAD(+) levels and upregulates ODC and SSAT activity as well as expression, owing to the effects of NNMT on histone H3 lysine 4 methylation in adipose tissue. Direct evidence for increased polyamine flux resulting from NNMT inhibition includes elevated urinary excretion and adipocyte secretion of diacetylspermine, a product of polyamine metabolism. NNMT inhibition in adipocytes increases oxygen consumption in an ODC-, SSAT- and PAO-dependent manner. Thus, NNMT is a novel regulator of histone methylation, polyamine flux and NAD(+)-dependent SIRT1 signalling, and is a unique and attractive target for treating obesity and type 2 diabetes