Silver sulfadiazine cream (SSD) has been used successfully in the management of burn wound sepsis. Silver deposition has been found in the skin, gingiva, cornea, liver, and kidney of patients treated with this cream, causing argyria, ocular injury, leukopenia, and toxicity in kidney, liver, and neurologic tissues. Monitoring concentrations of silver in blood and urine of patients receiving this treatment has become necessary, but sensitive and suitable methods adaptable to a clinical laboratory are still needed. We have developed a flameless thermal atomic absorption spectrophotometric method to measure silver concentrations in blood, urine, and other tissues. The detection limit is 0.4 microgram/L; the within-run precisions (CV) are 5.16%, 3.83%, and 2.79% for concentrations of 5, 13.5, and 42 micrograms/L, respectively; and the between-run precisions are 4.3% and 3.2% for concentrations of 13.5 and 42 micrograms/L. The concentrations of silver in blood, urine, liver, and kidney of subjects without industrial or medicinal exposure are less than 2.3 micrograms/L, 2 micrograms/day, 0.05 microgram/g wet tissue, and 0.05 microgram/g wet tissue, respectively. In SSD cream-treated burn patients, plasma concentrations may be as great as 50 micrograms/L within 6 h of treatment and can reach a maximum of 310 micrograms/L. Silver in urine is detectable after one day of treatment and may reach a maximum of 400 micrograms/day. After absorption, silver was found to be deposited in various tissues. Tissue silver concentrations in one burn patient who died of renal failure after eight days of treatment were 970, 14, and 0.2 micrograms/g wet tissue in cornea, liver, and kidney, respectively.

Summary, The effect of ketone bodies on ihe growth, in culture, of transformed lymphoblasts (Raji cells) was investigated. Cell growth was inhibited and this efTect was reversible, non-toxic, and proportional to the concentmtion of D-j^-hydroxybutyrate up to 20mM. The total glucose utilisation and the total lactate production were reduced in proportion to the inhibition of cell proliferaiion. D-^-hydroxybutyrate was not metabolised by the eells. Other glycolytic inhibitors and chemical analogues of f5-^-hydroxybutyrate either did not inhibit or proved to be too toxic for cell growth. D-/?-hydroxybutyrate also inhibited the growth of rabbit kidney (RK13), HeLa, mouse melanoma (BIft), fibroblast and trypsin-dispersed human ihyroid and beef tcstis cells. Moreover, in vivo dietary-induced ketosis redticed the number of B16 melanoma deposits in the lungs of C57BL/6 mice by two-thirds. The sinnificunce of these results in the clinical management of cancer cachexia is discussed.

A group of 18 male high performance track endurance and sprint cyclists were assessed to provide a descriptive training season specific physiological profile, to examine the relationship between selected physiological and anthropometric variables and cycling performance in a 4000-m individual pursuit (IP4000) and to propose a functional model for predicting success in the IP4000. Anthropometric characteristics, absolute and relative measurements of maximal oxygen uptake (VO2max), blood lactate transition thresholds (Thla- and Th(an),i), VO2 kinetics, cycling economy and maximal accumulated oxygen deficit (MAOD) were assessed, with cyclists also performing a IP4000 under competition conditions. Peak post-competition blood lactate concentrations and acid-base values were measured. Although all corresponding indices of Thla- and Th(an),i occurred at significantly different intensities there were high intercorrelations between them (0.51-0.85). There was no significant difference in MAOD when assessed using a 2 or 5 min protocol (61.4 vs 60.2 ml.kg-1, respectively). The highest significant correlations were found among IP4000 and the following: VO2max (ml.kg-2/3.min-1; r = -0.79), power output at lactate threshold (Wthla) (W; r = -0.86), half time of VO2 response whilst cycling at 115% VO2max (s; r = 0.48) and MAOD when assessed using the 5 min protocol (ml.kg-1; r = -0.50). A stepwise multiple regression yielded the following equation, which had an r of 0.86 and a standard error of estimate of 5.7 s: IP4000 (s) = 462.9 - 0.366 x (Wthla) - 0.306 x (MAOD) - 0.438 x (VO2max) where Wthla is in W, MAOD is in ml.kg-1 and VO2max is in ml.kg-1 x min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

First, pharmacological treatment of SV during harvesting, especially with GV solution, allows the use of a lower distension pressure and reduces the breakdown of high-energy phosphates in the vein wall. Second, topical and intraluminal use of GV solution during vein harvesting improves endothelial coverage compared with the topical use of Pap or no pharmacological treatment.

Ketohexokinase (EC 2.7.1.3) was purified to homogeneity from human liver, and fructose-bisphosphate aldolase (EC 4.1.2.13) was partially purified from the same source. Ketohexokinase was shown, by column chromatography and polyacrylamide-gel electrophoresis, to be a dimer of Mr 75000. Inhibition studies with p-chloromercuribenzoate and N-ethylmaleimide indicate that ketohexokinase contains thiol groups, which are required for full activity. With D-xylulose as substrate, ketohexokinase and aldolase can catalyse a reaction sequence which forms glycolaldehyde, a known precursor of oxalate. The distribution of both enzymes in human tissues indicates that this reaction sequence occurs mainly in the liver, to a lesser extent in the kidney, and very little in heart, brain and muscle. The kinetic properties of ketohexokinase show that this enzyme can phosphorylate D-xylulose as readily as D-fructose, except that higher concentrations of D-xylulose are required. The kinetic properties of aldolase show that the enzyme has a higher affinity for D-xylulose 1-phosphate than for D-fructose 1-phosphate. These findings support a role for ketohexokinase and aldolase in the formation of glycolaldehyde. The effect of various metabolites on the activity of the two enzymes was tested to determine the conditions that favour the formation of glycolaldehyde from xylitol. The results indicate that few of these metabolites affect the activity of ketohexokinase, but that aldolase can be inhibited by several phosphorylated compounds. This work suggests that, although the formation of oxalate from xylitol is normally a minor pathway, under certain conditions of increased xylitol metabolism oxalate production can become significant and may result in oxalosis.