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A recent paper suggests that supplementing the diet with large amounts of vitamin A may overcome some inherited blindness. But it also raises some serious questions.
Predicting how proteins fold from their amino acid sequence is largely a matter of guesswork. But the rules may be written into the genetic code (pages 894–901).
The molecular and neural bases for pain have proven elusive, but new studies approach an explanation from different directions (pages 766–773 and pages 774–780).
A mathematical approach to the transmission dynamics of tuberculosis offers a new understanding of past epidemics and suggests future interventions (pages 815–821).
Previous studies that suggested that lens-wearing may affect eye growth are supported now by primate studies, which raises questions about the use of eyeglasses in children (pages 761–765).
Even though diagnosis of prostate cancer can be made earlier than in the past, prognosis is still difficult. The discovery of new metastatic markers should aid in treatment design.
The importahce of preserving biodiversity extends beyond the discovery of new drugs to understanding how other species have dealt with medical problems we currently face.
Technological miniaturization combined with the power of molecular genetics makes the mouse a model animal for understanding human cardiovascular and pulmonary diseases.
Understanding the genetic defects underlying cystic fibrosis is only half the battle. Identifying the specific bacterium infecting CF patients is just as important (pages 661–666).
The gains made in life expectancy and against infant mortality in low-income nations are being accompanied by increases in mental-health-related problems.
The promising description of a potential basis for gene therapy in treating HIV infection does not mean that traditional approaches should be abandoned (pages 667–673).
The recent descriptions of T-cell dynamics in HIV disease have refocused efforts to understand the normal homeostatic processes that maintain T-cell populations (pages 674–680).
Mutations in tumour suppressors often lead to tumorigenesis. But other genetic mechanisms affecting suppressor gene expression can be just as effective (pages 686–692).