'In the Service of the Honourable East India Company': Politics and Identity in Dean Mahomet's Travels (1794)

The successful career of Dean Mahomet (1759-1851) as a migrant from India to Ireland (and later, England) has led to scholarly and popular interest in his work. His Travels through several parts of India in the Service of the Honourable East India Company (1794) published by subscription in Cork is reputedly the first English book by an Indian, and has been seen to counterbalance the many accounts of India by western travellers, and to assert, in autobiographical form, his identity as an Indian in 1790s Ireland. My paper analyses this text in relation to moral and economic criticisms of the East India Company in the eighteenth century, and in particular to legislation of 1793 which defined the role of the Company in Ireland’s trade with the east. These aspects of colonial politics involving Ireland and India as subject nations of Britain are shown to shape Mahomet’s discursive strategies and the complex identity produced in his text.

Combined inhibition of FLIP and XIAP induces Bax-independent apoptosis in type II colorectal cancer cells.

Death receptors can directly (type I cells) or indirectly induce apoptosis by activating mitochondrial-regulated apoptosis (type II cells). The level of caspase 8 activation is thought to determine whether a cell is type I or II, with type II cells less efficient at activating this caspase following death receptor activation. FLICE-inhibitory protein (FLIP) blocks death receptor-mediated apoptosis by inhibiting caspase 8 activation; therefore, we assessed whether silencing FLIP could convert type II cells into type I. FLIP silencing-induced caspase 8 activation in Bax wild-type and null HCT116 colorectal cancer cells; however, complete caspase 3 processing and apoptosis were only observed in Bax wild-type cells. Bax-null cells were also more resistant to chemotherapy and tumor necrosis factor-related apoptosis inducing ligand and, unlike the Bax wild-type cells, were not sensitized to these agents by FLIP silencing. Further analyses indicated that release of second mitochondrial activator of caspases from mitochondria and subsequent inhibition of X-linked inhibitor of apoptosis protein (XIAP) was required to induce full caspase 3 processing and apoptosis following FLIP silencing. These results indicate that silencing FLIP does not necessarily bypass the requirement for mitochondrial involvement in type II cells. Furthermore, targeting FLIP and XIAP may represent a therapeutic strategy for the treatment of colorectal tumors with defects in mitochondrial-regulated apoptosis.