Beyond 2000: science/biology education for the future

A number of countries are currently tackling the issue of curriculum reform in school science. In England and Wales, a 5-year moratorium on curriculum reform across the 5-16 age range will end in the year 2000. This article reviews the conclusions of a 2-year project, funded by the Nuffield Foundation, which explored ways in which a new science curriculum might be constructed and what it might look like. Particular attention is paid to the aims of science education, to the relationship between the content of a syllabus and its assessment, and to the suggestion that the science curriculum would be better presented as a relatively small number of explanatory stories rather than as a mass of detail. The proposals outlined here would allow for small but significant changes in the year 2000, and for more substantive changes thereafter, to be introduced only after adequate trialling. Our hope is that school science education in England and Wales can build on some of its current strengths and address certain weaknesses, leading to a more relevant and fulfilling education for future generations.     

Hyperhomocysteinemia, thrombosis and vascular biology.

Epidemiological evidence suggests that hyperhomocysteinemia (HH) is an independent risk factor for arterial thrombotic diseases such as acute myocardial infarction, stroke, peripheral ischemic occlusive disorders as well as venous thromboembolism. This article presents a hypothesis to explain the pathogenesis of increases in plasma homocysteine level and associated increased risk of thrombotic disease. It is based on the data in the literature and results from our laboratory on the impact of folate induced HH in rats. These results include: a) Effects on whole blood coagulation, which is characterized by increased velocity of coagulation, increased firmness of the formed coagulum and prolonged initiation phase of the coagulation; b) Genetic regulation of blood cells, which is characterized by increased platelet activation, impaired fibrinolysis and impaired function of the contact activation pathway of coagulation, and c) Reduced functional activities of single coagulation factors FXII:C, FX:C and FII:C.