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Objective: To test the hypothesis that childhood sexual abuse increases the risk of eating disturbance in children., Method: Data obtained from 20 sexually abused children were compared with data obtained from 20 nonabused control children. All subjects were female and between the ages of 10 and 15 years. Subjects completed a battery of tests assessing eating disorder behaviors, body image concern, and childhood trauma history., Results: Comparison of the 2 groups revealed that the abused children had higher levels of weight dissatisfaction and purging and dieting behavior. Furthermore, abused children reported eating less than control children when they felt emotionally upset. Abused children were less likely than control children to exhibit perfectionistic tendencies, but more likely to desire thinner body types., Conclusions: This is the first controlled study to examine the relationship between childhood sexual abuse and eating disturbance which relied on children as subjects. The results support previous findings with adult subjects which indicate that a history of childhood sexual abuse is associated with weight and body dissatisfaction, along with purging and dietary restriction.

Objectives: Research has linked eating disturbances with behavioral impulsivity. Little is known, however, about whether eating disturbances and aggressive behavior have a tendency to co-occur in the same girls. This article assesses the eating disturbance-aggressive behavior association and then examines the extent to which these factors confer a risk on drug use and attempted suicide., Method: Survey data were gathered from 3,630 girls in grades 6 through 12 in the upper Midwest. Girls responded anonymously to questions regarding binge eating and purging, dietary restriction, aggressive behavior, drug use, and attempted suicide. Logistic regression analysis was used to assess the unique contribution of demographic variables, eating disturbances, and aggression on drug use and attempted suicide., Results: Eating disturbances were significantly associated with aggressive behavior. Girls who endorsed binge eating and purging or dietary restriction had odds of aggressive behavior 2 to 4 times higher than girls who did not endorse these items. Logistic regression revealed that eating disturbances and aggressive behavior were significantly associated with both drug use and attempted suicide., Conclusions: Eating disturbances are significantly associated with aggressive conduct in adolescent girls. The constellation of eating disturbances and aggressive behavior is associated with a greater risk of drug use and attempted suicide.

We have previously shown that changes in glutathione peroxidase-1 (GPX1; H2O2:oxidoreductase, EC 1.11.1.9), plasma thyroid hormone and glutathione-S-transferase were not associated with changes in growth observed in second-generation (F2) severely Se-deficient rats; we also found that liver phospholipid hydroperoxide glutathione peroxidase (GPX4; EC 1.11.1.12) activity falls in first-generation (F1) Se-deficient rats to 41% of levels in Se-adequate rats. The purposes of this study were to determine the effect of F2 Se deficiency on GPX4 and to detect early changes in Se parameters associated with growth after single, small Se injections. Se-deficient male F2 weanling rats were randomly divided into two groups and fed a Se-deficient crystalline amino acid (0.003 microg Se/g diet; -Se) diet or that diet supplemented for 14 d with 0.2 microg Se/g diet (+Se) as Na2SeO3. Growth of -Se rats was 55% of the rate of +Se rats. Liver Se, GPX1 activity, GPX4 activity and testis GPX4 activity in -Se rats at 14 d were 1, 2, 23 and 13%, respectively, of levels in +Se rats. In a series of experiments, additional F2 male weanling rats were fed the -Se diet for 14 d and then were given an intraperitoneal single saline injection of 0, 1 or 5 microg Se/100 g body weight (BW) as Na2SeO3 and killed 1 or 7 d later. Rats injected with 1 or 5 microg Se/100 g BW grew 36 or 48%, respectively, above the rate of saline-injected rats. Liver Se concentration increased 367% and testis GPX4 activity doubled in rats 1 d after injection of 1 microg Se/100 g BW compared with saline-injected rats; these parameters were further elevated with 5 microg Se/100 g BW injections. Increases in liver Se and testis GPX4 activity were the parameters best associated with improved growth after Se injection, but the molecular role for Se in growth remains unclear.

To determine critically the selenium (Se) requirement for weanling female rats, we used glutathione peroxidase (GSH: H2O2 oxidoreductase, EC 1.11.1.9) (GPX) mRNA and a number of other parameters to assess Se status. Rats were fed a basal torulayeast diet (0.007 micrograms Se/g) supplemented with Se as Na2SeO3 in graded levels from 0 to 0.3 micrograms Se/g diet for 32 d (3 rats/group). Selenium supplementation had no effect on growth, showing that the Se requirement for growth is less than 0.007 micrograms Se/g diet, whereas other parameters showed significant increases with Se supplementation. In rats fed the Se-deficient basal diet, liver Se concentration was 4 +/- 0%, plasma GPX activity was 8 +/- 1%, erythrocyte GPX activity was 40 +/- 3%, liver GPX activity was 2 +/- 1%, and liver GPX mRNA levels were 11-17% of the levels in rats fed 0.1 micrograms Se/g diet. Liver Se concentration and GPX activity in plasma, erythrocytes and liver all reached a plateau breakpoint at or near 0.1 micrograms Se/g diet, indicating that the dietary Se requirement for maximal GPX activity in growing female rats is 0.1 micrograms Se/g diet. Liver GPX mRNA levels reached the plateau breakpoint at 0.05 micrograms Se/g diet, showing that the minimum dietary Se requirement for maximal GPX mRNA levels in female rats is half of the Se requirement for maximal GPX activity. This experiment demonstrates that GPX mRNA can be used to determine the dietary Se requirement; the gap between the dietary Se necessary for maximal GPX mRNA and that for maximal GPX activity may represent an evolutionarily derived biological margin of safety.

Phospholipid hydroperoxide glutathione peroxidase (PHGPX) and classical glutathione peroxidase (GPX1) are encoded by separate genes with only about 40% amino acid and nucleic acid sequence identity. To determine the response of tissue PHGPX expression to dietary Se level and to compare these responses with those for GPX1, weanling male rats were fed amino acid diets containing from 2 (-Se) to 130 (+Se) microgram Se/kg diet or a torula diet containing 5 and 190 micrograms Se/kg diet as Na2SeO3 for 28 d. Tissues were analyzed for PHGPX and GPX1 activity and mRNA. There was no effect of Se on growth. In -Se rats, GPX1 activity was reduced to 1% in liver and 4-9% in heart, kidney and lung compared with +Se rats; PHGPX activity was reduced only to 25-50% in these four tissues. The Se response curves indicated that the dietary Se requirement to reach plateau liver PHGPX activity was half that required for plateau GPX activity. In -Se rats, liver and heart GPX1 mRNA levels were reduced to 6 and 12%, respectively, whereas PHGPX mRNA was not significantly affected by Se deficiency. Notably, 65 micrograms Se/kg diet resulted in plateau liver GPX1 mRNA levels but not plateau GPX activity. Testis had the lowest GPX activity and GPX1 mRNA of all tissues examined, but had 15-fold higher PHGPX activity and 45-fold higher PHGPX mRNA levels when compared with liver. There was no significant effect of dietary Se on testis GPX1 and PHGPX mRNA levels. This study demonstrates that these two selenoperoxidases are differentially regulated by dietary Se.(ABSTRACT TRUNCATED AT 250 WORDS)

Classical glutathione peroxidase (GPX) is a useful Se-dependent parameter for determining Se status, but loss of GPX activity alone cannot explain the full effects of Se deficiency. The recent identification of type I thyroxine 5'-deiodinase as a Se-dependent enzyme provides a new potentially critical role for Se. To develop a model of impaired growth due to Se deficiency, second generation deficient weanling rats were fed a Se-deficient amino acid diet with adequate vitamin E and methionine. Initial growth rates of deficient males and females were 53 and 63%, respectively, of rats fed 0.1 micrograms Se/g diet. In short-term experiments with deficient males, liver Se and GPX activity were reduced 99%, liver glutathione-s-transferase activity was increased 114%, plasma thyroxine concentrations were increased 67%, plasma triiodothyronine was decreased 23% and the plasma triiodothyronine:thyroxine ratio was decreased 55%, compared with rats fed 0.2 micrograms Se/g diet. When deficient rats were injected on d 14 with 0, 1, 5 or 10 micrograms Se/100 g, rats grew 4.45, 7.62, 7.17 and 9.05 g/d, respectively, over the next 7 d. Injection with 10 micrograms Se/100 g restored plasma thyroxine and triiodothyronine concentrations 7 d later. Rats injected with 1 microgram Se/100 g rat had significantly altered plasma thyroxine and triiodothyronine concentrations 1 but not 7 d after injection. Infusion of Se-deficient rats with 438 ng triiodothyronine/d for 7 d restored plasma triiodothyronine concentrations but did not increase growth rate compared with rats infused with saline. This model produced a significant growth depression that was significantly reversed by as little as 1 microgram Se/100 g rat, but not by triiodothyronine infusion, suggesting that other Se-dependent roles in addition to 5'-deiodinase and GPX are necessary for adequate growth.

The mouse myeloma X63-Ag8.653 was fused to peripheral blood lymphocytes (PBL) from apparently healthy individuals, autoimmune patients and volunteers immunised with Rhesus (D) positive erythrocytes. Fusions were performed with or without prior transformation of PBL with Epstein-Barr virus (EBV). Using untransformed PBL, under the best conditions a mean fusion frequency of 8.4 X 10(-6) was obtained, with 22% of the resulting hybridomas secreting human immunoglobulin. Fusions with EBV-transformed cells gave fusion frequencies of 1.0 X 10(-4), with 85-90% of hybridomas secreting human immunoglobulin. The heterohybridomas formed in both cases cloned efficiently and had doubling times of 24-30 h. The heterohybridomas secreted human IgM, IgG and IgA of both kappa and lambda isotypes and culture supernatants contained up to 50 micrograms ml-1 of human immunoglobulin. Mouse immunoglobulin was not detected in the culture supernatants. 28 hybrids were selected for vigorous growth and antibody production by repeated cloning. Immunoglobulin synthesis was stabilised in 26 of these hybridomas after two or three cloning steps. The heterohybridomas have been successfully grown in large volumes for periods up to 15 months. It is concluded that the mouse myeloma X63-Ag8.653 is a suitable fusion partner with EBV-transformed B cells in the efficient production of human monoclonal antibodies.

Stable cell lines producing monoclonal human antibodies can be derived by fusion of Epstein-Barr virus-transformed peripheral blood B lymphocytes (LCL) with the mouse myeloma line X63-Ag8.653. One major limitation to this approach is the establishment of LCL cultures with sufficient cells secreting the specific antibody. In this study on the production of anti-D(Rh) antibodies, the kinetics of the appearance of specific EBV-transformable precursors in the circulation was followed after secondary immunization, and the optimum time for obtaining B cells for the establishment of suitable LCLs was found to be during the period 2-4 weeks post boost. During this period the probability of obtaining LCLs suitable for fusion is significantly higher than from blood samples collected randomly. From these high-titre LCLs the success rate for the fusion process was high. The specific EBV target cells are presumably memory cells produced after the peak of the antibody response and having only a transient appearance in the circulation.