Chemical burns as assault injuries in Jamaica

A three-fold greater incidence of chemical burn injuries in Jamaican hospitals, compared to burn centers in other industrial countries, underscores the problem of the use of common chemicals for assault weapons in this country. With the increased availability of guns for personal use, many Jamaicans learned the value of carrying household chemicals such as sulphuric acid from batteries or sodium hydroxide obtained from cleaning supplies. Chemical carried in a container, such as one might carry mace, afforded a means of defence among the lower socioeconomic groups who could not afford handguns. The use of dangerous chemicals for defensive weapons has extended to the use of chemicals for assault. The pattern of chemical injury differs significantly from most reports in the literature in both prevalence and aetiology. This review was prepared to examine these injuries with a view to planning strategies for prevention. (AU)

Acid ingestion causing pyloric obstruction

A case of gastric outlet obstruction following acid ingestion in a 21/2-year-old child is reported. The characteristic features of this injury are minor injury to the mouth, pharynx and oesophagus, and major injury to the stomach. A small amount of acid can produce considerable damage to the stomach. Therefore all patients require admission to hospital. Early barium meal examination and, if available, flexible endoscopy, will identify the extent of damage so as to avoid early discharge of patients when gastric performation is likely. Emphasis is placed on the need for public education in the prevention of ingestion of corrosive substances by children (AU)

Rhein, a selective inhibitor of the DPNH-flavin step in mitochondrial electron transport

Previous findings in the literature that rhein inhibits DPNH-linked mitochondrial oxidations by acting in the DPNH dehydrogenase region of the respiratory chain have been confirmed and extended. In the micromolar range rhein inhibits DPNH oxidase and DPNH-ferricyanide activities and the energy-linked reduction of DPNH by succinate in membrane preparations from heart, as wellas the DPNH dehydrogenase and transhydrogenase activities of the soluble, purified enzyme. The inhibition of the activities of the soluble enzyme are purely competitive with respect to substrate. These facts localize the primary inhibition site of rhein between substrate and FMN. In heart ETP a second noncompetitive inhibition is also present but is detectable only at very low (<10æM) rhein concentrations. Rhein also inhibits DPNH dehydrogenase in Candida utilis mitochondria and the purified enzyme from liver. On conversion of the heart enzyme to the low molecule weight DPNH-cytochrome reductase the typical effect of rhein disappears and is replaced by a slight stimulation or inhibition, depending on the electron acceptor used, showing that the substrate binding site is modified in this form of the enzyme. In beef liver mitochondria DPNH oxidation may appear insensitive to rhein, probably because of the strong binding of rhein to other proteins. To a lesser extent unspecific binding of rhein and resultant interference with the inhibition of DPNH dehydrogenase is also shown by BSA and by proteins in heart ETP. Rhein also inhibits transhydrogenations in mitochondria and at higher concentrations lactate and malate dehydrogenases but has no effect on sccinate, alcohol (liver nad yeast), and glucose-6-p dehydrogenases or on Neuospora DPN-ase, glucose-6-phosphatase, and amine oxidase. (SUMMARY)