Industrial production, health and disease in sub-Saharan Africa

Industrial development in Africa has carried with it significant health costs. These costs are normally defined rather narrowly by those concerned about occupational or industrial health and safety and refer only to the health consequences of worker exposure to specific hazardous processes, materials or environmental conditions associated with the workplace. A more comprehensive measurement of industrial health costs, however, must also include an assessment of the impact which industrial development and the creation of an industrial workforce has on ecological relationships, environmental conditions and patterns of sickness and health in the areas surrounding industrial centers. Traditional definitions of occupational health also tend to focus attention on the immediate causal linkages which exist between the development of particular industrial processes and specific health hazards. Yet any attempt to fully understand the causes of industrial health problems in Africa must look beyond these immediate causal linkages and examine the wider political and economic forces which determine the shape of industrial development and the extent to which the health costs of this development are borne by industrial workers and their families, as well as by people who may not be directly or even indirectly connected to industrial development, but may, nonetheless, be exposed to its health risks. The paper surveys the direct and indirect health costs of mining, large scale agriculture, and manufacturing in Africa and examines the economic and political interests which have determined the distribution of these costs.     

Segmental intestinal muscular thinning: a possible cause of intestinal obstruction in the newborn

Intestinal obstruction proximal to a transition zone without an interposed physical barrier usually indicates Hirschsprung disease. The authors report one case of focal small bowel muscular thinning just distal to a transition zone that produced clinical and radiographic findings that simulated long-segment Hirschsprung disease in a 2-day-old infant.     

Mutations in the retinal guanylate cyclase (RETGC-1) gene in dominant cone-rod dystrophy

The dominant cone-rod dystrophy gene CORD6 has previously been mapped to within an 8 cM interval on chromosome 17p12-p13. The retinal- specific guanylate cyclase gene (RETGC-1), which maps to within this genetic interval and previously was implicated in Leber's congenital amaurosis, was screened for mutations within this family and in a panel of small families and individuals with various cone and cone- rod dystrophy phenotypes. A missense mutation (E837D) was identified in affected members of the CORD6 family, as well as a second missense mutation (R838C) in three other families with dominant cone-rod dystrophy. RETGC-1 is only the fourth gene to be implicated in cone-rod dystrophy and this is the first report of dominant mutations in this gene.      

Immunohistochemical, in situ hybridization, and ultrastructural localization of SARS-associated coronavirus in lung of a fatal case of severe acute respiratory syndrome in Taiwan

This article describes the pathological studies of fatal severe acute respiratory syndrome (SARS) in a 73-year-old man during an outbreak of SARS in Taiwan, 2003. Eight days before onset of symptoms, he visited a municipal hospital that was later identified as the epicenter of a large outbreak of SARS. On admission to National Taiwan University Hospital in Taipei, the patient experienced chest tightness, progressive dyspnea, and low-grade fever. His condition rapidly deteriorated with increasing respiratory difficulty, and he died 7 days after admission. The most prominent histopathologic finding was diffuse alveolar damage of the lung. Immunohistochemical and in situ hybridization assays demonstrated evidence of SARS-associated coronavirus (SARS-CoV) infection in various respiratory epithelial cells, predominantly type II pneumocytes, and in alveolar macrophages in the lung. Electron microscopic examination also revealed coronavirus particles in the pneumocytes, and their identity was confirmed as SARS-CoV by immunogold labeling electron microscopy. This report is the first to describe the cellular localization of SARS-CoV in human lung tissue by using a combination of immunohistochemistry, double-stain immunohistochemistry, in situ hybridization, electron microscopy, and immunogold labeling electron microscopy. These techniques represent valuable laboratory diagnostic modalities and provide insights into the pathogenesis of this emerging infection.     

Methylprednisolone inhibits the alternative and amplification pathways of complement.

Methylprednisolone sodium succinate limited the ability of zymosan or lipopolysaccharide to activate complement in normal serum by the alternative amplification pathways. Methylprednisolone limited B consumption in a reaction mixture which contained purified C3b, D, and B, indicating that soluble steroid directly inhibited the amplification pathway. The ability of soluble steroid to inhibit events in the alternative and amplification pathways of complement may provide a partial explanation for the effectiveness of steroids in treating gram negative septic shock.