Effects of zinc and vitamin A deficient diets on the hepatic mobilization and urinary excretion of vitamin A in rats

Weanling rats were fed diets deficient in zinc (ZD), vitamin A (AD), or both (ZAD) for 3 weeks. Each then received 20 mug of 11,12-3H-retinyl acetate. Plasma retinol was monitored for radioactivity for 5 hours and urine for 6 days. Rats were killed and measurements made of plasma and liver vitamin A and plasma zinc. Plasma vitamin A was depressed but growth was not affected in AD rats compared to pair-fed controls. Radioactivity appeared most rapidly in the plasma retinol fractions of the two vitamin A-depleted groups (AD and ZAD) and was excreted most rapidly in the urine of these same groups. Zinc-deficient diets (ZD and ZAD) caused depressed plasma levels of zinc and vitamin A and growth retardation greater than in pair-fed controls. However zinc deficiency had no effect on mobilization of newly-ingested vitamin A or urinary excretion of labeled metabolites. Liver stores of vitamin A were lower for ZD rats than for controls. The data indicate that zinc deficiency is not a limiting factor in hepatic vitamin A release except as it influences growth and body demand for the vitamin. The data also suggest that newly-absorbed vitamin A is mobilized and utilized in preference to that previously stored in the liver.     

Fibrous myopathy. A rheumatic complication of drug abuse

A progressive fibrous myopathy may result from chronic intramuscular drug abuse. This complication may mimic other rheumatic disorders and early recognition may prevent disability. The patient described here presented with fixed flexion and extension contracture of hips and knees, respectively, after abusing meperidine and other agents for 3 years. Soft tissues of thighs and buttocks were "wood hard," EMG showed absence of action potentials in affected muscles, and biopsy revealed extensive replacement of muscle with dense, acellular fibrous tissue. Possible mechanisms are discussed.     

Long-term results in the treatment of femoral-shaft fractures in young children by immediate spica immobilization

Manual traction reduction without anesthesia and immediate immobilization in a spica cast were used to treat eighty-five children ranging in age from birth to ten years old who had closed femoral-shaft fractures and no associated injuries. Up to two centimeters of overriding, 30 degrees of anterior angulation, and 15 degrees of medial angulation were accepted. Any angulation in excess of these amounts, or lateral or posterior angulation, was corrected by wedging the cast at the fracture site. Further telescoping of the fracture fragments in the case was attributed to the child pressing the foot against the bottom of the cast and was prevented by removing the sole of the cast. Of the seventy-five children examined two to eighteen years after fracture, none had any residual skeletal deformity or joint stiffness. The length discrepancies of the fractured limbs ranged from 1.7 centimeters of shortening to 0.9 centimeter of overgrowth.     

Absorbability of Calcium From Common Beans

Absorption of calcium from white, red, and pinto beans, labeled with ⁴⁵Ca, was measured in 24 women in a three-way randomized design using a calcium load of 72 mg and milk as the referent. Fractional absorption for the three beans averaged 0.219 ± 0.047 and did not differ by type. Milk calcium absorption at the same load was more than two times higher, 0.451 ± 0.088 (P < 0.001). Oxalate content averaged 0.34%, and phytate averaged 1.7%, a stoichiometric excess relative to calcium. To evaluate the relation of phytate to reduced absorbability, labeled pinto beans were pre-treated with phytase and fed to 10 subjects. Fractional absorption rose, averaging 0.318 ± 0.071, (P <0.01 vs. untreated beans), but was significantly below that of milk. The difference was partly accounted for by phytate, with the remainder probably due to relatively high oxalate.     

Luteinizing hormone releasing hormone (LHRH) neurons maintained in nasal explants decrease LHRH messenger ribonucleic acid levels after activation of GABA(A) receptors

Inhibition of the LHRH system appears to play an important role in preventing precocious activation of the hypothalamic-pituitary-gonadal axis. Evidence points to gamma-aminobutyric acid (GABA) as the major negative regulator of postnatal LHRH neuronal activity. Changes in LHRH messenger RNA (mRNA) levels after alterations of GABAergic activity have been reported in vivo. However, the extent to which GABA acts directly on LHRH neurons to effect LHRH mRNA levels has been difficult to ascertain. The present work evaluates the effect of GABAergic activity, via GABA(A) receptors, on LHRH neuropeptide gene expression in LHRH neurons maintained in olfactory explants generated from E11.5 mouse embryos. These explants maintain large numbers of primary LHRH neurons that migrate from bilateral olfactory pits in a directed manner. Using in situ hybridization histochemistry and single cell analysis, we report dramatic alterations in LHRH mRNA levels. Inhibition of spontaneous synaptic activity by GABA(A) antagonists, bicuculline (10(-5) M) or picrotoxin (10(-4) M), or of electrical activity by tetrodotoxin (TTX, 10(-6) M) significantly increased LHRH mRNA levels. In contrast, LHRH mRNA levels decreased in explants cultured with the GABA(A) receptor agonist, muscimol (10(-4) M), or KCl (50 mM). The observed responses suggest that LHRH neurons possess functional pathways linking GABA(A) receptors to repression of neuropeptide gene expression and indicate that gene expression in embryonic LHRH neurons, outside the CNS, is highly responsive to alterations in neuronal activity.