Objective: To investigate whether exothermic sodium acetate mattresses were associated with an improvement in the thermal care of babies <30 weeks gestation between birth and admission to a neonatal unit.Study Design: Analysis of a three case series of babies: the first with traditional thermal care of drying and wrapping in a towel, the second with wrapping in food standard polythene bags and the third with wrapping in polythene bags and nursing on an activated exothermic mattress. The main outcome measure was the temperature on admission to the neonatal unit.Result: There were no significant differences between the groups for gestation and birth weight. Hypothermia was less frequent in the 'bag and mattress' group compared with the 'bag only' and traditional care groups (26 vs 69 vs 84%, respectively) even though the median time to admission was longest in the 'bag and mattress' group (23 min). The proportions of babies admitted with temperatures in the target range of 36.5 to 37.5 1C were 46, 27 and 16%, respectively. Multiple regression analysis showed that use of the mattress raised admission temperatures by 1.04 1C. The median temperature of babies in the 'bag and mattress' group was higher compared with the other groups (36.9 vs 36.0 vs 35.8 1C), but significantly more were hyperthermic (28 vs 4 and 0.4%, respectively).Conclusion: Use of exothermic mattresses for babies <30 weeks gestation was associated with a significantly greater proportion of babies being admitted to the neonatal unit with a temperature in the euthermic range, but there was also an increased risk of hyperthermia.

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Within a set of five separable molecular forms of acetylcholinesterase found in the nematode Caenorhabditis elegans, previously reported differences in kinetic properties identify two classes, A and B, likely to be under separate genetic control. Using differences between these classes in sensitivity to inactivation by sodium deoxycholate, a screening procedure was devised to search for mutants affected only in class A forms. Among 171 previously isolated behavioral and morphological mutant strains examined by this procedure, one (PR946) proved to be of the expected type, exhibiting a selective deficiency of class A acetylcholinesterase forms. Although originally isolated because of its uncoordinated behavior, this strain was subsequently shown to harbor mutations in two genes; one in the previously identified gene unc-3, accounting for its behavior, and one in a newly identified gene, ace-1, accounting for its selective acetylcholinesterase deficiency. Derivatives homozygous only for the ace-1 mutation also lacked class A acetylcholinesterase forms, but were behaviorally and developmentally indistinguishable from wild type. The gene ace-1 has been mapped near the right end of the X chromosome. Gene dosage experiments suggest that it may be a structural gene for a component of class A acetylcholinesterase forms.