The total folic acid activity of the serum in health and in various diseases of man has been extensively discussed in the medical literature. These reports have almost completely neglected the possibility of folic acid activity being bound to the serum proteins. However, Toennies, Usdin, and Phillips (1956) found in their studies that the plasma factor was present in the Cohn fractions IV + V of the plasma. It was also present in the glycoproteins, lipoproteins, mucoproteins, and other special proteins. Attention was also focused on the part played by subfraction I V-4. Condit and Grob (1958) found that the electrophoretic mobility of folic acid activity was greater than that of albumin. The same result was reported later by Elsborg (1972). Johns, Sperti, and Burgen (1961) considered there was little or no free folic acid activity in the fasting plasma. Injected tritiumlabelled folic acid activity in plasma was 64 % protein-bound. Neal and Williams (1965) added tritiated folic acid to rat serum and studied its behaviour in electrophoresis. Folic acid activity migrated towards the anode faster than albumin and only small amounts of radioactivity were found in the protein fractions. Unbound folic acid activity was found to run in advance of the albumin, occupying a similar zone to that of natural folate. Traces of

α₂-Macroglobulin, a carrier of folic acid activity (FAA), was isolated from fresh human serum by DEAE Sephadex A-50 gel chroma-, tography. The FAA content of the maximum with α₂-macroglobulin was 136 pg/mg protein and constituted 42% of the FAA eluated with the totalproteins from the chromatography column. Theresults was corroborated by controlled retesting.

1 The efficacy and safety of doxazosin and atenolol were compared following once-daily administration for up to 1 year, with a minimum of 20 weeks' active treatment. 2 According to response, patients received doxazosin 1-16 mg day-I or atenolol 50-100 mg day-1. Mean daily doses at the final efficacy assessment (between 20 weeks and 1 year) were doxazosin 11.8 mg and atenolol 94.2 mg. 3 Atenolol produced somewhat greater falls in blood pressure than doxazosin. The differences were statistically significant in the supine but not in the standing position. A small mean reduction in heart rate was produced by doxazosin whereas atenolol produced a marked bradycardia. Analysis of the same patient group at 20 weeks revealed similar overall profiles of activity except that atenolol produced greater falls in blood pressure than in the longer term analysis. 4 Serum concentrations of HDL/total cholesterol ratio were raised in the doxazosin treatment group and lowered in the atenolol group. Triglyceride concentrations fell in the doxazosin group and rose in the atenolol group. Significant differences (P < 0.001) were observed between treatment groups for these parameters, all differences being in favour of doxazosin. 5 Pharmacokinetics of doxazosin, measured at steady state in 36 patients, showed dose-related plasma concentrations, a mean half-life of about 12 h and relatively low intersubject variation. 6 The incidence of side-effects was slightly greater for patients in the doxazosin group. Drugrelated side-effects were mostly mild to moderate in severity with no serious drug-related occurrences in either treatment group. 7 No serious drug-related abnormalities in laboratory biochemistry and haematology tests were observed in either treatment group.

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Serum proteins were divided into protein groups by DEAE-Sephadex A-50 chromatography. One of the proteins to be identified had gone towardthe cathode and contained no folic acid activity. Theother went in the electrical field toward the anode and contained all the folic acid activity applied. This proteinproved to be transferrin.