Famine and land in Ireland and India 1845-1880: James Caird and the political economy of hunger

The perception of Ireland and India as ‘zones of famine’ led many nineteenth-century observers to draw analogies between these two troublesome parts of the British empire. This article investigates this parallel through the career of James Caird (1816–92), and specifically his interventions in the latter stages of both the Great Irish Famine of 1845–50, and the Indian famines of 1876–9. Caird is best remembered as the joint author of the controversial dissenting minute in the Indian famine commission report of 1880; this article locates the roots of his stance in his previous engagements with Irish policy. Caird's interventions are used to track the trajectory of an evolving ‘Peelite’ position on famine relief, agricultural reconstruction, and land reform between the 1840s and 1880s. Despite some divergences, strong continuities exist between the two interventions – not least concern for the promotion of agricultural entrepreneurship, for actively assisting economic development in ‘backward’ economies, and an acknowledgement of state responsibility for preserving life as an end in itself. Above all in both cases it involved a critique of a laissez-faire dogmatism – whether manifest in the ‘Trevelyanism’ of 1846–50 or the Lytton–Temple system of 1876–9.

BRCA1 and c-Myc Associate to Transcriptionally Repress Psoriasin, a DNA Damage-Inducible Gene

Evidence is accumulating to suggest that some of the diverse functions associated with BRCA1 may relate to its ability to transcriptionally regulate key downstream target genes. Here, we identify S100A7 (psoriasin), S100A8, and S100A9, members of the S100A family of calcium-binding proteins, as novel BRCA1-repressed targets. We show that functional BRCA1 is required for repression of these family members and that a BRCA1 disease–associated mutation abrogates BRCA1-mediated repression of psoriasin. Furthermore, we show that BRCA1 and c-Myc form a complex on the psoriasin promoter and that BRCA1-mediated repression of psoriasin is dependent on functional c-Myc. Finally, we show that psoriasin expression is induced by the topoisomerase IIA poison, etoposide, in the absence of functional BRCA1 and increased psoriasin expression enhances cellular sensitivity to this chemotherapeutic agent. Therefore, we identified a novel transcriptional mechanism that is likely to contribute to BRCA1-mediated resistance to etoposide.