Electromagnetic moments of the beta-emitting nucleus 16N.

The nuclear magnetic dipole moment mu and electric quadrupole moment Q of the beta-emitting 16N(Ipi = 2(-), T(1/2) = 7.13 s) nucleus have been determined for the first time by detecting its beta-NMR in a MgO crystal and beta-NQR (nuclear quadrupole resonance) in a TiO (2) crystal to be /mu/ = (1.9859+/-0.0011) mu(N) and /Q/ = (17.9+/-1.7) mb, respectively. Although the prediction of mu given by the Hartree-Fock calculation agrees well with the experiment, an abnormally small effective charge for neutrons is required to account for the experimental Q.

Serum lipid and lipoprotein abnormalities in major clinical entities of renal disease.

More than half of the patients with glomerulonephritis, nephrotic syndrome and renovascular hypertension showed obviously abnormal profiles of serum lipoproteins (Lps). The abnormal profiles returned to normal or near-normal when the disease was ameliorated or corrected surgically. A unique Lp profile (broad midband pattern, BMP) was observed in approximately 89% of uremic patients on hemodialysis therapy. The results of the current investigations indicated that the BMP could probably be formed by the accumulation of catabolic remnants of VLDL.

Studies on a beta-migrating high density lipoprotein.

An unusual serum lipoprotein (Lp) profile was detected in a Japanese family. A double beta-Lp was observed when serum was subjected to polyacrylamide gel electrophoresis. The slower migrating beta-Lp was identified as a subfraction of high density lipoprotein (HDL). It was present in the d 1.063--1.21 fraction, migrated to the position designated as the midband L.1 (sinking pre-beta-lipoprotein) by Mead, M.G. and Dangerfield, W.G. (1974) (Clin. Chim. Acta 51, 173--182) [1], and reacted against human anti-beta-Lp antiserum. This lipoprotein contained greater amounts of triglyceride than the usual beta-lipoprotein and could not be clearly detected by paper electrophoresis. Individuals exhibiting this high density midband lipoprotein appeared to be heterozygous for an autosomal dominant gene. Although other reports have indicated the possibility of a positive association between the occurrence of serum lipoproteins with unusual eletrophoretic mobility and premature ischemic heart disease, no such correlation was demonstrable in these subjects.

Studies on the effects of hemodialysis on plasma lipoproteins.

Plasma Lps of the patients on maintenance hemodialysis and the patients with other specific renal diseases have been studied. The patients on hemodialysis frequently showed gross abnormality in their plasma Lps, which was differentiated from the abnormalities demonstrated in other renal diseases or clinical entities. An exception was type-III hyperlipoproteinemia; i.e. Lp electrophoretograms of the hemodialysis patients resembled those ultracentrifugal fractions had been made had VLDL of beta-migration in paper electrophoresis and another had VLDL or pre-beta-migration. During hemodialysis, intravascular lipolysis, accelerated by heparin infusion, affected all plasma Lps, producing an increase of alpha-Lps and cholestrol ester-rich-beta-Lp. The accelerated triglyceride hydrolysis under circumstances of high glucose availability may stimulate resynthesis of endogenous triglyceriderich Lps, which characterizes the plasma Lp abnormality in more than half of the hemodialysis patients. The abnormality may not be attribuate to the predisposing renal disease but due to an accumlation of the characteristic Lp during the course of maintenace hemodialysis. A possible cause of accelerated atherosclerosis in the hemodialysis patients may be the accumulation of remnants of plasma Lp catabolism and the stimulated synthesis of triglycerdie-rich plasma Lp.