Gendered struggles over land: shifting inheritance practices among the Serer in rural Senegal

Although women's land rights are often affirmed unequivocally in constitutions and international human rights conventions in many African countries, customary practices usually prevail on the ground and often deny women's land inheritance. Yet land inheritance often goes unnoticed in wider policy and development initiatives to promote women's equal access to land. This paper draws on feminist ethnographic research among the Serer ethnic group in two contrasting rural communities in Senegal. Through analysis of land governance, power relations and 'technologies of the self', this article shows how land inheritance rights are contingent on the specific effects of intersectionality in particular places. The contradictions of legal pluralism, greater adherence to Islam and decentralisation led to greater application of patrilineal inheritance practices. Gender, religion and ethnicity intersected with individuals' marital position, status, generation and socio-ecological change to constrain land inheritance rights for women, particularly daughters, and widows who had been in polygamous unions and who remarried. Although some women were aware that they were legally entitled to inherit a share of the land, they tended not to 'demand their rights'. In participatory workshops, micro-scale shifts in women's and men's positionings reveal a recognition of the gender discriminatory nature of customary and Islamic law and a desire to 'change with the times'. While the effects of 'reverse' discourses are ambiguous and potentially reinforce prevailing patriarchal power regimes, 'counter' discourses, which emerged in participatory spaces, may challenge customary practices and move closer to a rights-based approach to gender equality and women's land inheritance.

Regulation of bcl-2 family proteins during development and in response to oxidative stress in cardiac myocytes: association with changes in mitochondrial membrane potential.

Cardiac myocyte apoptosis is potentially important in many cardiac disorders. In other cells, Bcl-2 family proteins and mitochondrial dysfunction are probably key regulators of the apoptotic response. In the present study, we characterized the regulation of antiapoptotic (Bcl-2, Bcl-xL) and proapoptotic (Bad, Bax) Bcl-2 family proteins in the rat heart during development and in oxidative stress-induced apoptosis. Bcl-2 and Bcl-xL were expressed at high levels in the neonate, and their expression was sustained during development. In contrast, although Bad and Bax were present at high levels in neonatal hearts, they were barely detectable in adult hearts. We confirmed that H(2)O(2) induced cardiac myocyte cell death, stimulating poly(ADP-ribose) polymerase proteolysis (from 2 hours), caspase-3 proteolysis (from 2 hours), and DNA fragmentation (from 8 hours). In unstimulated neonatal cardiac myocytes, Bcl-2 and Bcl-xL were associated with the mitochondria, but Bad and Bax were predominantly present in a crude cytosolic fraction. Exposure of myocytes to H(2)O(2) stimulated rapid translocation of Bad (<5 minutes) to the mitochondria. This was followed by the subsequent degradation of Bad and Bcl-2 (from approximately 30 minutes). The levels of the mitochondrial membrane marker cytochrome oxidase remained unchanged. H(2)O(2) also induced translocation of cytochrome c from the mitochondria to the cytosol within 15 to 30 minutes, which was indicative of mitochondrial dysfunction. Myocytes exposed to H(2)O(2) showed an early loss of mitochondrial membrane potential (assessed by fluorescence-activated cell sorter analysis) from 15 to 30 minutes, which was partially restored by approximately 1 hour. However, a subsequent irreversible loss of mitochondrial membrane potential occurred that correlated with cell death. These data suggest that the regulation of Bcl-2 and mitochondrial function are important factors in oxidative stress-induced cardiac myocyte apoptosis.