With The Birthright Lottery: Citizenship and Global Inequality, Ayelet Shachar is the first major scholar to put the rich theory of property law theory to work in the realm of citizenship. Assessed on its own criteria, the book delivers on its promise to shake up our thinking on this question. Nevertheless, I argue in this paper that her account is not ultimately persuasive. First, Shachar takes for granted that citizenship is a valuable resource. I suggest that today legal residency is (...) more highly valued that citizenship. Also her defense of the state and the social advantages of having stable citizenship regimes does nothing to confront its decline as the central organizing principle of political life. Last but not least, the modalities of a birthright citizenship levy calls into question the underlying analysis. For instance, the current proposal looks undistinguishable from foreign aid and it would demand much more robust institutional organs of global governance that now exist. The second prong of her argument works at the domestic level as it tackles the problem of under- and over-inclusiveness of birthright citizenship. Here too I have reservations highlighted by modes of implementation. (shrink)

Inflammation is activated by diverse triggers that induce the expression of cytokines and adhesion molecules, which permit a succession of molecules and cells to deliver stimuli and functions that help the immune system clear the primary cause of tissue damage, whether this is an infection, a tumor, or a trauma. During inflammation, short-term changes in the expression and secretion of strong mediators of inflammation occur, while long-term changes occur to specific groups of cells. Long-term changes include cellular transdifferentiation for some (...) types of cells that need to regenerate damaged tissue, as well as death for specific immune cells that can be detrimental to tissue integrity if they remain active beyond the boundaries of essential function. The transcriptional regulator NFκB enables some of the fundamental gene expression changes during inflammation, as well as during tissue development. During recurrence of malignant disease, cell stress-induced alterations enable the growth of cancer cell clones that are substantially resistant to therapeutic intervention and to the immune system. A number of those alterations occur due to significant defects in feedback signal cascades that control the activity of NFκB. Specifically, cell stress contributes to feedback defects as it overrides modules that otherwise control inflammation to protect host tissue. NFκB is involved in both the suppression and promotion of cancer, and the key distinctive feature that determines its net effect remains unclear. This paper aims to provide a clear answer to at least one aspect of this question, namely the mechanism that enables a divergent response of cancer cells to critical inflammatory stimuli and to cell stress in general. (shrink)