The Correlation between Children's Intelligence Quotient and Their Behavior in Dental Setting: A Cross-Sectional Study.

Children with high intelligence quotient (IQ) are more capable of managing adverse situations. These children may show more cooperation to receive dental treatments. This study assessed the effect of intelligence quotient (IQ) of 5-10-year-old children on their cooperation during dental treatments. Eighty children without previous dental history and in need of pulpotomy and stainless steel crowns in one tooth were selected. A written consent was obtained from the parents, and after the children's IQ was measured by Raven intelligence test, the treatments were performed and their cooperation level was determined using Frankl's behavior rating scale with rating 1 to rating 4 (definitely negative, negative, positive, and definitely positive). In this cross-sectional study, the relationship between IQ and cooperation level was analyzed by one-way ANOVA test while the effect of age and gender on IQ and cooperation level was studied by ordinal regression test. Out of the total samples, 5% had definitely negative, 16.2% had negative, 56.3% had positive, and 22.5% had definitely positive level of cooperation according to Frankl criteria. There was a significant and positive correlation between IQ and level of cooperation (r = 0.87, p < 0.001). According to the results of the linear regression analysis, to examine the effect of age, sex, and IQ variables on cooperation, children's age (p value = 0.003) had a positive effect on their cooperation, but gender had no effect on predicting IQ and cooperation level (p value = 0.557). Regarding significant relationship between IQ scores and cooperation level, dentists can predict cooperation in pediatric patients to deliver better treatments and increase patients' satisfaction.

Species-specific glucocorticoid and 1,25-dihydroxyvitamin D responsiveness in mouse MC3T3-E1 osteoblasts: dexamethasone inhibits osteoblast differentiation and vitamin D down-regulates osteocalcin gene expression.

The mouse MC3T3-E1 cell line is nontumorigenic and undergoes a typical program of osteoblast differentiation in vitro, producing a bone-like mineralized extracellular matrix. We report responses of these cells to dexamethasone (Dex) and 1,25-(OH)2D3 that are in contrast to findings from other osteoblast culture systems. First, chronic exposure of both early- and late-passaged MC3T3-E1 cells to 10(-7) M Dex, initiated during the proliferation period, blocked osteoblast differentiation, in contrast to the enhanced differentiation observed in cultures of fetal rat calvarial-derived cells. Secondly, 1,25-(OH)2D3 did not up-regulate expression (messenger RNA or protein synthesis) of the endogenous mouse osteocalcin (OC) gene. Several lines of evidence are presented that suggest this response is caused by sequence specific properties of the mouse OC vitamin D response element. We also observed both qualitative and quantitative differences in expression of cell growth (histone H2B) and phenotype-related genes (collagen, OC, osteopontin, glucocorticoid receptor, and 1, 25-(OH)2D3 receptor), between pre- and postmineralization stage osteoblasts, in response to 24 h steroid hormone treatment. Our findings in MC3T3-E1 cells are consistent with current concepts of selective influences of 1,25-(OH)2D3 and glucocorticoids as a function of osteoblast maturation. However, the inhibition of osteoblast differentiation by chronic Dex at 10(-7) M and the down-regulation of OC by 1,25-(OH)2D3 are novel observations relevant to species-specific responsiveness of mouse bone-expressed genes to steroid hormones during osteoblast differentiation.

Effects of neuroleptics on glutaminase from rat synaptosomes.

Phosphate-activated glutaminase was isolated from synaptosomes from three areas of rat brain. Glutamine utilization phosphate activation and inhibition by glutamate or ammonia were assessed in the absence or presence of haloperidol, chlorpromazine, or clozapine. All three drugs (at 1 micromolar concentration) elevated the Km for glutamine using preparations from the amygdala, hippocampus, or striatum. They interfered with phosphate activation only in the amygdala preparation. No drug affected end-product inhibition. The data suggest that neuroleptics may depress the release of glutamic acid from synaptosomes by interfering with the activation of glutaminase by phosphate.