1. Oligosaccharides linked to protein (glycoprotein) or lipid (glycolipid) are the major components at the outer surface of mammalian cells. Studies using antibodies and lectins have shown in the past that the oligosaccharides they recognize exhibit tumour-associated changes, i.e. they are carbohydrate tumour-associated antigens. 2. The oligosaccharides have been further characterized in recent years by structural analysis using high-resolution chromatographic techniques, MS and NMR. NMR gives an oligosaccharide fingerprint that is characteristic of monosaccharide type and linkage and which can be correlated with magnetic resonance spectroscopic data on fine-needle tissue aspirates. 3. Also of relevance is the new understanding of the molecular biology of MUC genes, which code for mucin protein backbones, and of the glycosyltransferase genes, which determine oligosaccharide structure and immunological recognition. 4. For these reasons, we believe that tumour-associated oligosaccharide changes should be revisited in the context of what we now know about structure and expression. This review synopsizes the past data using the detection of carbohydrate tumour-associated antigens by binding of lectins and antibodies, and puts it into the context of NMR fingerprints or signatures.

1. A new method has been developed for measuring the total antioxidant capacity of body fluids and drug solutions, based on the absorbance of the ABTS*+ radical cation. 2. An automated method for use on a centrifugal analyser, as well as a manual method, is described. 3. The procedure has been applied to physiological antioxidant compounds and radical-scavenging drugs, and an antioxidant ranking was established based on their reactivity relative to a 1.0 mmol/l Trolox standard. 4. The Trolox equivalent antioxidant capacity of plasma from an adult reference population has been measured, and the method optimized and validated. 5. The method has been applied to investigate the total plasma antioxidant capacity of neonates and how this may be compromised in prematurity.

1. Plasma histamine and serum neutrophil chemotactic activity (S-NCA) were measured in ten atopic asthmatic patients on four separate occasions after allergen bronchial provocation testing (BPT). 2. Single doses of inhaled sodium cromoglycate (SCG; 20 mg), clemastine (0.5 mg), ketotifen (0.5 mg) and isotonic saline (0.9% NaCl) placebo were administered 30 min before bronchial provocation testing in random order and double-blind. 3. The airflow obstruction after BPT was monitored by measurement of forced expiratory volume in 1s (FEV 1 ). Plasma histamine was measured by the double-isotope radioenzymatic assay and S-NCA by a modified Boyden chamber technique. 4. A highly significant decrease in FEV 1 after BPT occurred on the placebo pre-treatment visit ( P < 0.001). Prior administration of inhaled SCG, clemastine and ketotifen significantly reduced the decrease in airflow obstruction seen after BPT when compared with placebo treatment ( P < 0.01, P < 0.02, P < 0.05 respectively). 5. No significant alteration in plasma histamine was detected during allergen-induced airflow obstruction. 6. Levels of S-NCA were significantly higher 5, 10 and 15 min after BPT when compared with the pre-challenge level ( P < 0.01, P < 0.01, P < 0.001 respectively). These levels were not significantly decreased when airflow obstruction was inhibited by the prior inhalation of SCG, clemastine or ketotifen.

1. Serum creatine kinase and oral temperature were measured in 20 patients with primary hypothyroidism before and after 48 h bed rest. Fifteen of these patients were heated during the 48 h period. The remaining five acted as control subjects. In addition, creatine kinase and oral temperature were measured in five control subjects after a 30 min period of exercise and again after a 30 min period of resting. 2. The oral temperature rose and the serum creatine kinase levels fell only in those patients who were actively warmed. In the control subjects the period of exercise followed by resting caused no significant change in creatine kinase levels. 3. A subnormal body temperature appears to be an important determinant of the raised serum creatine kinase levels seen in patients with primary hypothyroidism.

1. The action of insulin on plasma cyclic nucleotide concentrations in normal human subjects has been studied after intravenous injection, alone and in combination with glucagon. 2. After injection of insulin alone there was an initial small, though not significant, decrease in plasma cyclic AMP at 15 min followed by an increase to more than twice the initial concentration at 30 min. The increase was absent when hypoglycaemia was lessened by infusion of glucose after insulin injection. 3. Injection of insulin caused no significant change in plasma cyclic GMP concentration, whether or not glucose was infused after the hormone. 4. Glucagon (3–300 nmol, 10–1000 μg), caused a dose-dependent increase in plasma cyclic AMP concentration. The rise in plasma cyclic AMP produced by 3 or 30 nmol of glucagon was not significantly modified by simultaneous injection of insulin (44 nmol; 6 units).

1. The rebreathing and steady-state methods for assessing the response to inhaled carbon dioxide were compared in six normal subjects under control conditions and during metabolic acidosis and alkalosis. 2. The slopes of the CO 2 response lines obtained with the two methods under control conditions were not significantly different. 3. Metabolic acidosis and alkalosis produced a significant change in the intercept of the response line when this was assessed with the steady-state technique. The slope of the response lines did not change significantly in alkalosis but there was probably a small increase during acidosis. 4. Using the rebreathing technique there was no significant change in intercept in acidosis and alkalosis, but the slope varied significantly from control values. 5. It is concluded that the two methods of assessing the respiratory response to inhaled CO 2 are comparable under normal acid-base conditions. This similarity does not hold in metabolic changes of the acid-base state.