A perfect quick guide for postgraduate researchers in education. Looking at the interdependence of teaching and research, the authors show that a critical and analytical exploration of policies and practices is a necessary part of what we mean by being a 'professional' in education. The book is structured around a range of methods applicable to educational research and appropriate for use by practitioners at all stages of their professional development. BERA/SAGE Research Methods in Education July 2012 • 272 pages Paperback (978-1-4462-0807-6) Price £21.99 Hardback (978-1-4462-0806-9) Price £65.00

The COVID-19 pandemic has confronted school leaders across the four devolved nations of the United Kingdom (UK) with a period of exceptional crisis. This responsive, small-scale, but UK-wide study focuses on headteacher perspectives on leadership and management in the initial stages of this pandemic, contributing to our understanding of this crucial period. The headteacher respondents met the multiple predicaments and situational ambiguities of the pandemic with a resilience which drew heavily upon the strengths of pre-existing structures and teams. They were required to provide effective emotional and moral leadership in uncharted and rapidly shifting territory. They spoke most eloquently of how they developed pragmatic, versatile and personally reassuring approaches to communication with parents, staff, pupils, and a range of external agencies, all of which were also facing extraordinary circumstances with varying degrees of resilience. The paper concludes by conceptualising the key elements of headteachers’ leadership and management, both inside and outside of school, at in the early stages of societal crisis.

In this paper, we argue for a social psychological approach to citizenship which focuses on how social actors define competent and legitimate polity membership, together with the associated rights and responsibilities that this entails. A perspective based on the principles of rhetorical psychology is adopted in order to explore these issues in an analysis of a sample of young people's talk about issues of immigration to the UK. Analysis considers how matters of ‘race’, national identity and culture were oriented to and constructed during the interviews. We then explore how rights and responsibilities concerning cultural expression, interpersonal civility/courtesy and (implicitly acultural) legal frameworks were articulated as practical criteria for judgements about competent and legitimate polity membership. These findings are discussed in relation to existing social psychological work on issues such as racism and national identity, with a view to situating these matters within an overarching concern for the construction of polity membership. We conclude by briefly considering the implications of these findings for contemporary debates concerning citizenship education in the UK. Copyright © 2011 John Wiley & Sons, Ltd.

1 The immunosuppressive and anti-in¯ammatory drug le¯unomide has several sites of action, although its precise mode of action is unknown. 2 Here we show in vitro and in vivo that le¯unomide and/or its active metabolite A771726, inhibit the activity of cyclo-oxygenase (COX) at doses below those that a ect protein expression. 3 In J774.2 macrophages treated with endotoxin for 24 h to induce COX-2 and iNOS, le¯unomide and A771726 inhibited more potently the accumulation of PGE 2 (A771726, IC 50 3.5 mg ml 71 ) than of NO 2 (A771726, IC 50 380 mg ml 71 ). At high concentrations (4300 mg ml 71 ) A771726 also exhibited the expression of COX-2 and iNOS proteins. 4 In A549 cells treated for 24 h with interleukin-1b, to induce COX-2, A771726 potently inhibited PGE 2 synthesis (IC 50 0.13 mg ml 71 ). In the same cells, A771726 was notably less active (IC 50 , 52 mg ml 71 ) at inhibiting the formation of PGE 2 stimulated by exposure to 30 mM arachidonic acid. 5 In a human whole blood assay, measuring the accumulation of TxB 2 in response to calcium ionophore as a measure of COX-1 activity and in response to incubation with bacterial endotoxin as a measure of COX-2 activity, le¯unomide inhibited COX-1 and COX-2 with IC 50 values of 31 and 185 mg ml 71 ; for A771726 the corresponding values were 40 and 69 mg ml 71 . 6 Pre-treatment of rats with le¯unomide or A771726 (10 mg kg 71 , i.p.) inhibited the plasma accumulation of 6-keto-PGF 1a but not NO 2 /NO 3 following infusion of endotoxin. Injection of a bolus of arachidonic acid following 6 h infusion of endotoxin caused a marked acute rise in plasma 6-keto-PGF 1a which was inhibited only by higher doses of A771726 (50 mg kg 71 , i.p.). 7 In conclusion, le¯unomide via A771726 can directly inhibit the activity of COX, an e ect that appears blunted both by increases in substrate supply and possibly by plasma binding. Only at much higher drug levels does le¯unomide and/or A771726 inhibit the induction of COX-2 or iNOS proteins.

1 Endotoxaemia is associated with the expression of the inducible isoform of cyclo-oxygenase, cyclooxygenase-2 (COX-2), and an overproduction of arachidonic acid (AA) metabolites. The role of the AA metabolites generated by COX-2 in the circulatory failure and multiple organ dysfunction caused by endotoxin is unclear. Dexamethasone prevents the expression of COX-2 and exerts bene®cial e ects in animal models of shock. 2 Here we compare the e ects of two inhibitors of COX-2 activity, namely NS-398 (5 mg kg 71 , i.p., n=7) and SC-58635 (3 mg kg 71 , i.p., n=9) with those of dexamethasone (3 mg kg 71 , i.p., n=9) on the circulatory failure and organ dysfunction caused by lipopolysaccharide (LPS, E. coli, 6 mg kg 71 , i.v., n=11) in the rat. 3 Endotoxaemia for 6 h caused hypotension, acute renal dysfunction, hepatocellular injury, pancreatic injury and an increase in the plasma levels of 6-keto-PGF 1a (indicator of the induction of COX-2) and nitrite/nitrate (indicator of the induction of iNOS). 4 Pretreatment of rats with dexamethasone attenuated the hypotension, the renal dysfunction, the hepatocellular and pancreatic injury and the induction of COX-2 and iNOS caused by LPS. In contrast, inhibition of COX-2 activity with SC-58635 or NS-398 neither attenuated the circulatory failure nor the multiple organ failure caused by endotoxin. 5 Thus, the prevention of the circulatory failure and the multiple organ injury/dysfunction caused by dexamethasone in the rat is not due to inhibition of the activity of COX-2. Our results suggest that an enhanced formation of eicosanoids by COX-2 does not contribute to the development of organ injury and/or dysfunction in rats with endotoxaemia.