Re-modelling clay: ceramic practice and the museum in Britain (1970-2014)

This thesis analyses how the dialogue between ceramic practice and museum practice has contributed to the discourse on ceramics. Taking Mieke Bal’s theory of exposition as a starting point, it explores how ‘gestures of showing’ have been used to frame art‑oriented ceramic practice. Examining the gaps between the statements these gestures have made about and through ceramics, and the objects they seek to expose, it challenges the idea that ceramics as a category of artistic practice has ‘expanded.’ Instead, it forwards the idea that ceramics is an integrative practice, through which practitioners produce works that can be read within a range of artistic (and non-artistic) frameworks. Focusing on activity in British museums between 1970 and 2014, it takes a thematic and broadly chronological approach, interrogating the interrelationship of ceramic practice, museum practice and political and critical shifts at different points in time. Revealing an ambiguity at the core of the category ‘ceramics,’ it outlines numerous instances in which ‘gestures of showing’ have brought the logic of this categorisation into question, only to be returned to the discourse on ‘ceramics’ as a distinct category through acts of institutional recuperation. Suggesting that ceramics practitioners who wish to move beyond this category need to make their vitae as dialogic as their works, it indicates that many of those trying to raise the profile of ‘ceramics’ have also been complicit in separating it from broader artistic practice. Acknowledging that those working within institutions that sustain this distinction are likely to re-make, rather than reconsider ceramics, it leaves the ball in their court.

Effects of lycopene on the induction of foam cell formation by modified LDL.

The effect of lycopene on macrophage foam cell formation induced by modified low-density lipoprotein (LDL) was studied. Human monocyte-derived macrophages (HMDM) were incubated with lycopene in the presence or absence of native LDL (nLDL) or LDL modified by oxidation (oxLDL), aggregation (aggLDL), or acetylation (acLDL). The cholesterol content, lipid synthesis, scavenger receptor activity, and the secretion of inflammatory [interleukin (IL)-1β and tumor necrosis factor (TNF)-α] and anti-inflammatory (IL-10) cytokines was determined. Lycopene was found to decrease the synthesis of cholesterol ester in incubations without LDL or with oxLDL while triacylglycerol synthesis was reduced in the presence of oxLDL and aggLDL. Scavenger receptor activity as assessed by the uptake of acLDL was decreased by ∼30% by lycopene. In addition, lycopene inhibited IL-10 secretion by up to 74% regardless of the presence of nLDL or aggLDL but did not affect IL-1β or TNF-α release. Lycopene also reduced the relative abundance of mRNA transcripts for scavenger receptor A (SR-A) in THP-1 macrophages treated with aggLDL. These findings suggest that lycopene may reduce macrophage foam cell formation induced by modified LDL by decreasing lipid synthesis and downregulating the activity and expression of SR-A. However, these effects are accompanied by impaired secretion of the anti-inflammatory cytokine IL-10, suggesting that lycopene may also exert a concomitant proinflammatory effect.

The induction of macrophages foam cell formation by chylomicron remnants

The accumulation of foam cells in the artery wall causes fatty streaks, the first lesions in atherosclerosis. LDL (low-density lipoprotein) plays a major role in foam cell formation, although prior oxidation of the particles is required. Recent studies, however, have provided considerable evidence to indicate that CMRs (chylomicron remnants), which carry dietary lipids in the blood, induce foam cell formation without oxidation. We have shown that CMRs are taken up by macrophages and induce accumulation of both triacylglycerol and cholesterol, and that the rate of uptake and amount of lipid accumulated is influenced by the type of dietary fat in the particles. Furthermore, oxidation of CMRs, in striking contrast with LDL, inhibits, rather than enhances, their uptake and induction of lipid accumulation. In addition, the lipid accumulated after exposure of macrophages to CMRs is resistant to efflux, and this may be due to its sequestration in lysosomes. These findings demonstrate that CMRs induce pro-atherogenic changes in macrophages, and that their effects may be modulated by dietary factors including oxidized fats, lipophilic antioxidants and the type of fat present.