This paper considers the impact of managerialism and the reactions it has engendered in university life. It examines the degree to which institutions of higher education in the UK have in recent years been subjected to what some commentators have seen as a managerial assault, alongside economic pressures to restructure and reform, and explores the reactions of academic and administrative staff in middle and junior levels through a case study of two universities. Consideration is given to attempts to introduce managerial controls, including the setting of targets, appraisals and peer review, as well as to the resistances which followed. It is argued that the notion of resistance to domination and control has been underplayed in the literature of organization and management. In exploring its various manifestations it is shown that managerialism is not fully embedded in university life and that matters are far from settled. It is contended that those engaged in academe in middle and junior levels of the organizational hierarchy are actively seeking to keep alive the craft of scholarship by mediating and moderating the harsher effects of the changes through supportive or transformational styles of working.

In recent years academic commentators have born witness to the emergence of what has been called a New Public Management, or NPM, evident in a number of countries around the world. While the literature has sought to document its appearance and attempt to assess its impact, this article considers an aspect of the NPM which has been little explored: the human cost associated with its introduction. In examining higher education in England, one of the countries where the NPM is thought to have been embraced at least relatively enthusiastically, the article explores research on the experiences and reactions of those working in academe to recent attempts to change working practices through an analysis of the stresses and strains experienced by those subjected to the processes of managerialism. In drawing on published sources and the authors’ own empirical work it is argued that the NPM, not least in intensifying the labour of academics as intellectual workers, has provoked a range of responses which include collusion, resentment and resistance. The consequences of the NPM, it is argued, include blaming of the victim and diverting attention away from processes of control and the action of human agents who initiate stressful conditions of work by implementing the NPM in particularly harsh ways. It is further contended that attempts to encroach on professional autonomy, and operationalize the NPM in English universities in harsh ways, are being mediated by those subjected to the changes who are seeking to preserve elements of collegiality.

Calprotectin, a heterodimer of S100A8 and S100A9, is an abundant neutrophil protein which possesses anti-microbial activity primarily due to its ability to chelate zinc and manganese. In the current study, we showed that neutrophils from calprotectin-deficient S100A9 −/− mice have an impaired ability to inhibit Aspergillus fumigatus hyphal growth in vitro, and in infected corneas in a murine model of fungal keratitis; however, the ability to inhibit hyphal growth was restored in S100A9−/− mice by injecting recombinant calprotectin. Further, using recombinant calprotectin with mutations in either the Zn and Mn binding sites or the Mn binding site alone, we show that both zinc and manganese binding are necessary for calprotectin’s anti-hyphal activity. In contrast to hyphae, we found no role for neutrophil calprotectin in uptake or killing of intracellular A. fumigatus conidia either in vitro, or in a murine model of pulmonary aspergillosis. We also found that an A. fumigatus ΔzafA mutant, which demonstrates deficient zinc transport, exhibits impaired growth in infected corneas and following incubation with neutrophils or calprotectin in vitro as compared to wild-type. Collectively, these studies demonstrate a novel stage - specific susceptibility of A. fumigatus to zinc and manganese chelation by neutrophil-derived calprotectin.

Filamentous fungi are an important cause of pulmonary and systemic morbidity and mortality, and also cause corneal blindness and visual impairment worldwide. Utilizing in vitro neutrophil killing assays and a model of fungal infection of the cornea, we demonstrated that Dectin-1 dependent IL-6 production regulates expression of iron chelators, heme and siderophore binding proteins and hepcidin in infected mice. In addition, we show that human neutrophils synthesize lipocalin-1, which sequesters fungal siderophores, and that topical lipocalin-1 or lactoferrin restricts fungal growth in vivo. Conversely, we show that exogenous iron or the xenosiderophore deferroxamine enhances fungal growth in infected mice. By examining mutant Aspergillus and Fusarium strains, we found that fungal transcriptional responses to low iron levels and extracellular siderophores are essential for fungal growth during infection. Further, we showed that targeting fungal iron acquisition or siderophore biosynthesis by topical application of iron chelators or statins reduces fungal growth in the cornea by 60% and that dual therapy with the iron chelator deferiprone and statins further restricts fungal growth by 75%. Together, these studies identify specific host iron-chelating and fungal iron-acquisition mediators that regulate fungal growth, and demonstrate that therapeutic inhibition of fungal iron acquisition can be utilized to treat topical fungal infections.