1. Apolipoprotein B-48, the transport protein for chylomicrons, is identical with apolipoprotein B-100 for the first 48% of its sequence. No antiserum has yet been reported that can recognize apolipoprotein B-48, but not apolipoprotein B-100. 2. In the present study an antiserum was raised to the C-terminal sequence of apolipoprotein B-48, using specific chemical reactions to ensure that the charged carboxyl group of the C-terminal isoleucine residue was free. In a Western blot the antiserum was shown to bind to a protein band having the characteristics of apolipoprotein B-48, but not to apolipoprotein B-100. 3. In the early evening 11 subjects were given a test meal which contained 40 g of mixed oil and retinyl palmitate. Blood samples were collected over 9 h. Chylomicron-enriched fractions were prepared and analysed for triacylglycerol, retinyl palmitate and apolipoprotein B-48, the latter after separation using SDS/PAGE and visualization by chemiluminescence on a Western blot. Both triacylglycerol and apolipoprotein B-48 showed an early peak at 1 h, which was not seen with retinyl palmitate. All three substances gave a broader peak between 5 and 6 h post-prandially. Retinyl palmitate concentrations declined rapidly during the late (6-9 h) postprandial period, but apolipoprotein B-48 concentrations remained elevated. 4. This study has shown that an antiserum has been produced which is specific for apolipoprotein B-48. This has enabled measurement of postprandial concentrations of the protein that revealed features of chylomicron metabolism which have not been reported previously.

1. Synthetic human parathyroid hormone (hPTH) 1-34 was given by intravenous injection to two healthy men. The time course of its appearance in and disappearance from the plasma was monitored both by cytochemical bioassay and by a specific radioimmunoassay (RIA) system. 2. Immunoreactive N -region parathyroid hormone (iPTH) reached peak concentrations in plasma at 2 min after injection, whereas peak concentrations of biologically active parathyroid hormone (bioPTH) were delayed until 4-6 min. Bioassayable PTH-like activity then disappeared from the plasma (mean transit times 5.8 and 8.6 min), approximately twice as fast as immuno-reactivity. 3. After separate subcutaneous administrations, a calculated 22-37% of administered hPTH 1-34 was subsequently detected in the plasma, by both assay systems. 4. It was not possible to explain fully the non-parallel appearances of bio- and immuno-reactivities in the plasma after intravenous injection nor the non-parallel disappearances after both intravenous and subcutaneous injections on the basis of the present data. It seems likely, however, that in the process of biological degradation the immunoreactive locus is inactivated by a different reaction from that which destroys bioactivity. 5. To investigate these activity dissociations further will require the application of microfractionation procedures in conjunction with both types of assay system.

1. The free deoxycorticosterone pool in the rat was measured by means of a radioimmunoassay in vivo. 2. The free deoxycorticosterone pool in rats with adrenal regeneration with normal or high blood pressure was similar. 3. In rats with adrenal regeneration, the free deoxycorticosterone pool 21 days post-operatively was significantly lower than that in sham-operated control rats and returned to control values at 60 days.

1. Plasma dopamine β-hydroxylase (DβH) amounts were measured by radioimmunoassay in twenty-eight patients, twenty of whom had essential hypertension. There was a positive correlation between resting diastolic blood pressure and plasma DβH concentration. 2. Plasma DβH amounts also correlated significantly with those of plasma noradrenaline (NA) in individual patients. 3. These findings provide further support for the conclusions drawn from studies of plasma catecholamines that the sympathetic nervous system contributes toward the maintenance of the elevated blood pressure in essential hypertension.