Parental influences on young girls’ fruit and vegetable, micronutrient, and fat intakes

Objective To evaluate parents’ fruit and vegetable intake and their use of pressure to eat in child feeding as predictors of their 5-year-old daughters’ fruit and vegetable, micronutrient, and fat intakes.Subjects Data were obtained from 191 non-Hispanic white families with 5-year-old girls.Design Parent data included reports of pressure in child feeding and their own fruit and vegetable intake. Girls’ intakes of fruits and vegetables, selected micronutrients, and fat were the main outcomes of interest.Statistical analysis Structural equation modeling was used to test a model describing relationships among parents’ fruit and vegetable intake, parents’ use of pressure in child feeding, and daughters’ fruit and vegetable, micronutrient, and fat intakes.Results The model provided a good fit to the data, revealing that girls’ fruit and vegetable intake was positively related to their parents’ reported fruit and vegetable intake. Parents who consumed fewer fruits and vegetables tended to report greater pressure in child feeding and had daughters who consumed fewer fruits and vegetables. Girls’ reported fruit and vegetable intakes were positively related to their micronutrient intakes and negatively associated with fat intake.Applications/conclusions This research demonstrates that parents’ own fruit and vegetable intake may encourage fruit and vegetable intake in their daughters, leading to higher micronutrient intakes and lower dietary fat intakes. Conversely, pressure to eat may discourage fruit and vegetable intake among young girls. J Am Diet Assoc. 2002;102:58–64.     

A randomized, placebo-controlled trial of calcium supplementation for decreased bone density in corticosteroid-using patients with inflammatory bowel disease: a pilot study

Background: Patients with inflammatory bowel disease (IBD) have a high prevalence of osteoporosis. A number of studies have found that corticosteroid use is associated with the development of osteoporosis in these patients. Calcium supplementation may be of benefit in corticosteroid-induced osteoporosis and calcium may be a nutrient that patients with IBD lack. Aim: To test the benefit of calcium supplementation on bone density in a pilot study over a 1-year period, in a group of corticosteroid-using patients with IBD, in a randomized, double-blind, placebo-controlled treatment study. Methods: Corticosteroid-using patients with IBD including males over the age of 18 years and premenopausal females, were randomized to receive either calcium carbonate 1000 mg plus vitamin D 250 IU (Oscal) or an identically matched placebo. Dual energy X-ray absorptiometry measurements of bone density were obtained at entry and at 1 year. At entry, and every 3 months thereafter, serum was collected for the measurement of haemoglobin, biochemistry and bone hormones. Simultaneously a 24-h urine collection was analysed for calcium excretion and creatinine clearance, and a 4-day food record was collected to document dietary calcium and vitamin D ingestion. Results: We found a high prevalence of moderately severe decreased bone density in corticosteroid-using patients with IBD. The dose of prednisone in the year prior to study entry was inversely correlated with bone density at the hip (R=-0.67, P=0.004). At study entry serum osteocalcin was inversely correlated with corticosteroid dose in the year prior to the study (R=-0.64, P=0.02) and at study end, directly correlated with the percentage change in spine bone density (R=0.59, P=0.01). The dietary calcium intake of these patients was close to the current RDA (recommended daily intake) for premenopausal, post-adolescent adults. Calcium supplementation with small extra doses of vitamin D conferred no obvious benefit to bone density at the end of 1 year. There was no correlation between oral calcium ingestion and bone mass measurements. Both the treatment and placebo groups' bone density remained relatively stable at 1 year, suggesting that bone loss in corticosteroid-using patients may peak early into the use of the corticosteroids. Conclusions: Calcium supplementation (1000 mg/day) conferred no significant benefit to bone density at 1 year in patients with corticosteroid-using IBD patients with osteoporosis. Future investigations should explore other therapeutic avenues that may have greater effects on increasing bone density in patients who already have considerable osteoporosis.     

Influence of Viral Infections on Body Weight, Survival, and Tumor Prevalence of B6C3F1 (C57BL/6N ? C3H/HeN) Mice in Carcinogenicity Studies

Sendai virus (SV), mouse hepatitis virus (MHV), and pneumoniavirus of mice (PVM) are common viral infections of mice. Influenceof these viral infections on the prevalence of liver tumors,lung tumors, and lymphoma is of concern in chemical carcinogenicitystudies. Body weight, survival, and tumor prevalence of B6C3F1mice with and without viral infections in 33 male and 34 femaleuntreated control groups and 32 male and 32 female low- andhigh-dose groups of 2-year chemical carcinogenicity studieswere evaluated. In male mice, the SV infection was associatedwith significantly (p < 0.05) higher survival of control,low-dose, and high-dose groups, and higher prevalence of livertumors and lymphoma. The increases in tumor prevalence are possiblydue to an increase in the survival of male mice that had SVinfection. However, when interlaboratory variability and time-relatedeffects were taken into account, the number of significant effectswas consistent with the expected false-positive rate inherentto the statistical procedures. The MHV and PVM infections didnot cause consistent changes in body weight, survival, and tumorprevalences in the control and chemical treatment groups ofmale mice. Viral infections did not cause consistent increasesor decreases in body weight, survival, or tumor prevalence inthe control and chemical treatment groups of female B6C3F1 mice.     

Detection of Antibodies in Human Sera to Streptococcal Groups A and C Carbohydrates by a Radioimmunoassay

The human lymphokine, leucocyte migration-inhibitory factor (LIF), appears to be a serine esterase and protease by virtue of its susceptibility to the irreversible enzyme inhibitor, phenylmethylsulfonyl fluoride (PMSF), and by the ability of arginine esters and amides to protect LIF against PMSF-induced inactivation. In this paper, three methods are described by which putative substrates for LIF may be investigated. Thus, molecules satisfying the substrate specificities of this lymphokine should (1) protect LIF against inactivation by PMSF, (2) reduce LIF activity in vitro on polymorphonuclear leucocytes, and (3) reduce the esterolytic activity of purified LIF-rich supernatants. The first two reactions were tested by means of the leucocyte migration agarose technique; the third reaction was tested by a sensitive enzyme assay using tritiated tosyl arginine methyl ester as substrate. Guanosine 3',5'-cyclic monophosphoric acid, which is capable of protecting LIF against PMSF-induced inhibition, also inhibited the esterolytic activity of the purified LIF preparation. Four synthetic oligopeptide substrates for trypsin, thombin and plasmin were investigated. Only one, the thrombin- and trypsin-specific benzoyl-phenylalanyl-valyl-agarine-p-nitroanilide, possessed high affinity for the LIF molecule and may therefore prove to be a potent substrate for this lymphokine.     

Linkage relationships between the three phosphoglucomutase loci PGM1, PGM2 and PGM3

1. Phosphoglucomutase phenotypes have been studied in several generations of the family of an individual heterozygous at each of the three loci, PGM₁, PGM₂, and PGM₃. 2. PGM₁ and PGM₂ phenotypes were determined using red cells. Fibroblasts grown in tissue culture were used for PGM₃ phenotyping. 3. The family results support the genetical hypothesis based on the analysis of dizygotic twin pairs that the PGM₃ isozyme patterns found in the placenta are determined by two alleles, PGM¹₃ and PGM²₃. 4. Locus PGM₃ is not closely linked to locus PGM₂ 5. The data also support the previous findings that locus PGM₁ is not closely linked to PGM₂ or PGM₃.     

THE EFFECT OF NICOTINIC ACID ON THE DEPRESSANT ACTION OF ETHANOL AND PENTOBARBITAL

The effect of nicotinic acid (NA) on sleeping time induced bya single dose of ethanol or pentobarbital was studied in rats.It was found that sleeping time was markedly reduced by NA ina dose-dependent manner. The effect was observed when NA wasadministered 10 min before or after ethanol or pentobarbital,but not when given 60 min in advance. NA did not affect therate of ethanol elimination measured up to 5 hr after ethanoladministration. Rats pretreated with NA 60 min before ethanolslept longer than controls. This latter effect was not observedwith pentobarbital. These observations, together with the knownlack of effect of high liver NAD⁺ levels on ethanol metabolismand the rather stable NAD⁺ concentration in brain cells, suggestthat the effect of NA on sleeping time is not mediated by anincrease in ethanol metabolism in liver or by NAD⁺ or NAD⁺-dependentreactions in brain. Our results are consistent with a directaction of NA, or some rapidly formed derivative, on a structureor process associated with brain cell functions or membranes.