I still remember as a green 16-year-old being completely seduced by Newman's portrait of a university – the ideal of a liberal education. I was completely charmed not only by Newman's seductive prose – but by the humanising ideals of the effects of an excellent education. The picture was compelling and inspirational to the daughter of a small farmer whose parents were forced to leave school at 12 years of age to go and earn a living. I was sitting in the “lap of luxury” in a boarding school for girls, whose excellent principal generated a huge respect for, and absolute belief in, the right to and the ability to gain from a rigorous and serious education – which for me at that time in the 1970s extended at least to the end of secondary schooling – a luxury no one in my family had access to in the previous generation. What are universities for? Many authors have considered this issue since Newman's time – in recent times for example Boyd (1979), Graham (2005), Collini (2012). They all, in different ways suggests the need not only to respond to societal / economic needs, but also the need for a more balanced, holistic conception of university activity. Leaders of universities in the 21st century must try to articulate this, seek greater understanding of it. We must lobby government for greater recognition, understanding and support for the university's role not only for the present but also for the future. Contingency, vulnerability, adaptability, recognising the provisional nature of knowledge (and control); the caring versus the careless – all of this implies the need for diversity of disciplines, gender and experiences among university leadership in both the national and the international arena.
Intervertebral disc (IVD) degeneration is a major cause of low back pain (LBP). Degenerate discs are associated with accelerated cellular senescence. Cell senescence is associated with a secretory phenotype characterised by increased production of catabolic enzymes and cytokines. However, to date, the mechanism of cell senescence within disc degeneration is unclear. Senescence can be induced by increased replication or induced by stress such as reactive oxygen species or cytokines. This study investigated the association of cellular senescence with markers of DNA damage and presence of cytoplasmic DNA (which in cancer cells has been shown to be a key regulator of the secretory phenotype), to determine mechanisms of senescence in disc degeneration. Immunohistochemistry for the senescence marker: p16INK4A was firstly utilised to screen human intervertebral discs for discs displaying at least 30% immunopostivity. These discs were then subsequently analysed for immunopostivity for DNA damage markers γH2AX and cGAS and the presence of cytoplasmic DNA. The number of immunopositive cells for p16 INK4A positively correlated with the expression of γH2AX and cGAS. Senescent cells were also associated with the presence of cytoplasmic DNA. These new findings elucidated a role of cGAS and γH2AX as a link from genotoxic stress to cytokine expression which is associated with senescent cells. The findings indicate that cellular senescence
