No abstract

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. Women's Health and Action Research Centre (WHARC) is collaborating with JSTOR to digitize, preserve and extend access to African Journal of Reproductive Health / La Revue Africaine de la Santé Reproductive.When the Safe Motherhood Initiative was launched in 1987, like the rest of Africa, Nigeria got deeply involved. Nobody expected miracles overnight, nor did anyone expect disasters of such immensity. Sadly, there is hard evidence to demonstrate that much of the good ideas, the good intentions, and the good work done then have failed to come to fruition. Not least is the fact that maternal mortality in sub-Saharan Africa is rising rather than falling, as it has done in all other regions of the Third World. In urban areas in Nigeria, instances abound where women are dying in the hands of good doctors just because they do not have the money to pay. In rural areas, the disaster is expanding more quickly for want of basic necessities of modern life: piped water, electric power supply, road communication, and schools for children.High maternal mortality in Nigeria, estimated to be 1,000 per 100,000 births, will not go away as long as three fundamental issues prevail: mass poverty with gross inequalities, unbooked emergencies, and illiteracy, which bestrides and underlies both. Here, the focus is on the first two factors, as well as on structural adjustment programmes (SAPs) which, together with rampant corruption, constitute a major aggravator of poverty.

We describe the first case of a baby with maternal uniparental disomy of chromosome 2. Growth failure, hypothyroidism, and hyaline membrane disease were present at birth, and the first year of life was complicated by bronchopulmonary dysplasia. At age 14 months, motor and intellectual development were normal, but growth remained below the 10th centile. The baby was investigated for uniparental disomy because trisomy 2 mosaicism had been detected in a second trimester amniocentesis. This is the first reported case in which amniotic fluid chromosome mosaicism has been associated with uniparental disomy. Implications for prenatal diagnosis are considered.

Preferential paternal X-chromosome inactivation occurs in the cell lineages that differentiate first within the female rodent blastula (trophectoderm and extraembryonic endoderm). The present studies were designed to test the nature of X-chromosome inactivation (XCI) in the earliest differentiating cell lineage of the human placenta, the cytotrophoblast. Using glucose-6-phosphate-dehydrogenase (G6PD) polymorphisms as a marker system, term placentae were obtained from 13 female heterozygotes where parental allelic contributions could be determined. Chorionic villi were enzymatically digested and centrifuged in a Percoll density gradient to isolate a pure population of cytotrophoblasts, which was ascertained by cell culture, differentiation to syncytiotrophoblasts. and histochemical staining for α-human chorionic gonadotrophin (α-HCG). On electrophoresis, all 13 samples exhibited exclusive or near exclusive expression of the maternally derived X-linked enzyme variant, regardless of whether it was G6PD A or G6PD B. No intermediate bands were seen, indicating a single active G6PD locus per cell. The stromal cells of the villi, which derive from the mesoderm and differentiate later than the cytotrophoblast, exhibit random XCI. These findings establish preferential paternal XCI in the cytotrophoblast, the cell type first to differentiate within the human blastula.