Confronting the Naturalness of Disaster in the Pacific

ABSTRACT

This introduction sets out some of the key themes addressed by the papers in the special issue on ‘Confronting the Naturalness of Disaster in the Pacific’. Disasters are now widely understood not as ‘natural’ phenomena but as events or processes that unfold at the intersection between natural or artificial hazards and human populations. We review some of the effects of the naturalisation of disaster before turning to the ways in which Pacific disasters are defined through government, media and public discourses. These discourses feature their own distinctive accounts of possible forms of agency in the context of disaster, and draw on markedly different frames of reference in attributing cause and blame. Similarly, contrasting temporalities and spatialities are invoked in addressing disasters as bounded phenomena. We conclude with reflections on the nature of responses to disaster in the Pacific in the context of increasingly unstable cultural, economic and environmental grounds for action induced by global climate change     

Phosphopyruvate carboxylase induction by l-tryptophan. Effects on synthesis and degradation of the enzyme

1. The administration of l-tryptophan to fed rats produces a twofold increase in hepatic phosphopyruvate carboxylase activity that represents a comparable increase in enzyme protein. With specific antibody against the enzyme we have shown that the increase in phosphopyruvate carboxylase is partially mediated via an actinomycin D-sensitive increase in enzyme synthesis. 2. In starved animals tryptophan increases the enzyme activity without any change in the relative rate of phosphopyruvate carboxylase synthesis. In this condition degradation of the enzyme is retarded by tryptophan by a mechanism that is not prevented by cycloheximide.     

Meclofenamate does not affect lung development in fetal sheep

Prostaglandins may be involved in some aspects of fetal lung development, including surfactant metabolism, tracheal fluid production, and possibly lung growth. In the fetus, during the days before delivery, plasma PGE2 concentration increases and concurrently, tracheal fluid production decreases and surfactant production increases. To determine whether the increase in PGE2, specifically plasma PGE2 concentration, is responsible for these changes, we continuously infused the prostaglandin synthetase inhibitor, meclofenamate (0.7 mg/h per kg), into 8 fetal sheep for 5-13 days before delivery; 5 control fetuses received a continuous infusion of solvent for 5-11 days before delivery. Meclofenamate infusion significantly decreased plasma PGE2 concentrations until the day of delivery. However, meclofenamate did not affect tracheal fluid production or its decrease before delivery, fetal plasma cortisol concentration, surfactant content of tracheal fluid and lung tissue, organ weights, lung weights, or lung DNA and protein content. We conclude that the changes in lung development during the days before delivery are not dependent on the usual high fetal plasma concentration of PGE2 or its increase before delivery.