Labour and the free churches 1918-1939: radicalism, righteousness and religion

It is a commonplace that the labour movement was somehow nurtured within the witness for liberty of the Free Churches. Exploring this at a range of levels - including organisation, rhetoric, policies, electoral politics and people - this book demonstrates the extent to which this remained a reality into the inter-war years. The distinctive religious setting in which it emerged indeed helps to explain the differences between Labour and more Marxist counterparts on the Continent. It is shown here that this setting continued to influence Labour approaches towards welfare, nationalisation and industrial relations between the wars. In the process Labour also adopted some of the righteousness of tone of the Free Churches. This setting was, however, changing. Dropping their traditional suspicion of the State, Nonconformists instead increasingly invested it with religious values, turning it through its growing welfare functions into the provider of practical Christianity. This nationalisation of religion continues to shape British attitudes to the welfare state as well as imposing narrowly utilitarian and material tests of relevance upon the churches and other social institutions. The elevation of the State was not, however, intended as an end in itself. What mattered were the social and individual outcomes. Socialism, for those Free Churchmen and women who helped to shape Labour in the early twentieth century, was about improving society as much as systems.

The Edinburgh Critical Edition of the Selected Writings of Andrew Lang: volume 1

This is the first critical edition of the works of Andrew Lang (1844-1912), the Scottish writer whose enormous output spanned the whole range of late nineteenth century intellectual culture. Neglected since his death, partly because of the diversity of his interests and the volume of his writing, his cultural centrality and the interdisciplinary nature of his work make him a vital figure for contemporary scholars. This volume covers his work in anthropology, including that on fairy tale, folklore, the origins of religion, and psychical research.

Effect of Short-Chain Fatty Acid Acetate on Colon Cancer

Acetate is a short chain fatty acid produced as a result of fermentation of ingested fibers by the gut microbiota. While it has been shown to reduce cell proliferation in some cancer cell lines1,2, more recent studies on liver3 and brain4 tumours suggest that acetate may actually promote tumour growth. Acetate in the cell is normally converted into acetyl-coA by two enzymes and metabolized; mitochondrial (ACSS1) and cytosolic (ACSS2) acetyl-coA synthetase. In the mitochondria acetyl-coA is utilized in the TCA cycle. In the cytosol it is utilized in lipid synthesis. In this study, the effect of acetate treatment on the growth of HT29 colon cancer cell line and its mechanism of action was assessed. HT29 human colorectal adenocarcinoma cells were treated with 10mM NaAc and cell viability, cellular bioenergetics and gene expression were investigated. Cell viability was assessed 24 hours after treatment using an MTT assay (Sigma, UK, n=8). Cellular oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) was measured by XFe Analyzer (Seahorse Bioscience, USA). After a baseline reading cells were treated and OCR and ECAR measurements were observed for 18 hours (n=4). Total mRNA was isolated 24 hours after treatment using RNeasy kit (Qiagen, USA). Quantitative PCR reactions were performed using Taqman gene expression assays and Taqman Universal PCR Master Mix (ThermoFisher Scientific, UK) on Applied Biosystems 7500 Fast Real-Time PCR System (Life Technologies, USA) and analysed using ΔΔCt method (n=3). Acetate treatment led to a significant reduction in cell viability (15.9%, Figure 1). OCR, an indicator of oxidative phosphorylation, was significantly increased (p<0.0001) while ECAR, an indicator of glycolysis, was significantly reduced (p<0.0001, Figure 2). Gene expression of ACSS1 was increased by 1.7 fold of control (p=0.07) and ACSS2 expression was reduced to 0.6 fold of control (p=0.06, Figure 3). In conclusion, in colon cancer cells acetate supplementation induces cell death and increases oxidative capacity. These changes together with the trending decrease in ACSS2 expression suggest suppression of lipid synthesis pathways. We hypothesize that the reduced tumor growth by acetate is a consequence of the suppression of ACSS2 and lipid synthesis, both effects reported previously to reduce tumor growth3–5. These effects clearly warrant further investigation.