British medical bulletin
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Recent follow-up studies have provided convincing evidence that the foundations of chronic airflow obstruction (CAO) are laid in utero and early childhood. Men born in Hertfordshire and Derbyshire, England, were more likely to have impaired lung function at 60-70 years of age if they had been lighter at birth and if they had had lower respiratory tract infection (LRTI) in the first 2 years of life. ⋯ These findings suggest that impairment of pulmonary growth in utero and early childhood, as a consequence of undernutrition and LRTI, plays an important part in the development of CAO in late adult life. This may be of particular importance for the future respiratory health of developing nations as the additive effects of smoking take hold.
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The discovery that CED-3, the product of a gene necessary for programmed cell death in the nematode Caenorhabditis elegans, is related to the mammalian cysteine protease interleukin-1 beta converting enzyme (ICE/caspase-1) has led to intense interest in the role of proteases in apoptosis. It is now clear that at least some members of the caspase (ICE/CED-3) family, which at present includes ten homologues of human origin, are essential components of an evolutionarily conserved pathway of apoptosis. These enzymes appear to be involved in both the initial signaling events and the downstream proteolytic cleavages that result in the apoptotic phenotype. Selective macromolecular and peptide-based inhibitors attenuate apoptosis in whole cells, suggesting that one or more of these enzymes will be suitable targets for therapeutic intervention in diseases resulting from inappropriate cell death.