No large population-based study has addressed the question of how overnutrition is related to subsequent height gain in childhood, timing of puberty, and final height. The present data represent a large Swedish population-based longitudinal growth study. Height gain in childhood, timing of reaching peak height velocity and height gain during adolescence, and final height were regarded as the short-term, interim, and long-term outcomes of childhood nutritional status, i.e. body mass index (BMI) change between 2 and 8 y. Midparental height was adjusted as the genetic influence on linear growth of the child. Childhood BMI gain was related to an increased height gain during the same period, i.e. an increase of 1 BMI unit was associated with an increase in height of 0.23 cm in boys and 0.29 cm in girls. A higher BMI gain in childhood was related to an earlier onset of puberty; the impact on the timing of puberty was 0.6 y in boys and 0.7 y in girls. Each increased unit of BMI gain in childhood also reduced the height gain in adolescence, 0.88 cm for boys and 0.51 cm for girls. No direct correlation was shown between childhood BMI gain and final height. We conclude that overnutrition between 2 and 8 y of age will not be beneficial from a final height point of view, as the temporary increase in height gain in childhood will be compensated by an earlier pubertal maturity and a subnormal height gain in adolescence. Abbreviations: BMI, body mass index PHV, peak height velocity ⌬B8 -2, BMI change between 2 and 8 y of age ⌬HCM8 -2, height gain between 2 and 8 y of age ⌬HCM18 -8, height gain between 8 and 18 y of age It is known that adequate nutrition is needed for normal growth during the pediatric years (1, 2). Some earlier studies of pediatric subjects also seem to support the hypothesis that overnutrition not only produces a normal growth but also accelerates linear growth (3, 4). Earlier studies were based on inpatient or outpatient series, and the number of subjects was relatively small. One study explored the association between obesity and height throughout childhood and adolescence (5); the obese subjects were seen to be taller than average in childhood, whereas during puberty they demonstrated a smaller growth spurt when compared with lean subjects. The series was taken from an obesity clinic, and the follow-up period was relatively short.The objective of this study is to investigate the association between BMI change in childhood, i.e. from 2 to 8 y of age, and gain in height during childhood, the timing of the puberty growth spurt, i.e. the age at PHV during puberty, and final height. The linear growth data were obtained from a population-representative longitudinal growth study of 3650 healthy children born at full-term between 1973 and 1975 in Göteborg, Sweden (6). METHODS Study population.The study subjects were selected from 5111 final grade-school children born in the early 1970s in Göteborg, Sweden, or the surrounding area of the city. The annual birth rate in Göteborg is around 4000 to 5500 newborns in t...

The p38 MAPK mediates transcriptional and posttranscriptional control of cyclooxygenase-2 (COX-2) mRNA following interleukin-1(IL-1)/lipopolysaccharide cellular activation. We explored a positive feedback, prostaglandin E 2 (PGE 2 )-dependent stabilization of COX-2 mRNA mediated by the p38 MAPK cascade in IL-1␤-stimulated human synovial fibroblasts. We observed a rapid (5 min), massive (>30-fold), and sustained (>48 h) increase in COX-2 mRNA, protein, and PGE 2 release following a recombinant human (rh) IL-1␤ signal that was inhibited by NS-398, a COX-2 inhibitor, and SB202190, a selective, cell-permeable p38 MAPK inhibitor. PGE 2 completely reversed NS-398-mediated inhibition but not SB202190-dependent inhibition. The eicosanoid didn't potentiate IL-1␤-induced COX-2 expression nor did it activate COX-2 gene expression in quiescent cells. Transfection experiments with a human COX-2 promoter construct revealed a minor element of p38 MAPK-dependent transcriptional control after IL-1␤ stimulation. p38 MAPK synergized with the cAMP/cAMP-dependent protein kinase cascade to transactivate the COX-2 promoter. When human synovial fibroblasts were activated with rhIL-1␤ for 3-4 h (steady state) followed by washout, the elevated levels of COX-2 mRNA declined rapidly (<2 h) to control levels. If PGE 2 , unlike EP2/3 agonists butaprost and sulprostone, was added to fresh medium, COX-2 mRNA levels remained elevated for up to 16 h. SB202190 or anti-PGE 2 monoclonal antibody compromised the stabilization of COX-2 mRNA by PGE 2 . Deletion analysis using transfected chimeric luciferase-COX-2 mRNA 3-untranslated region reporter constructs revealed that IL-1␤ increased reporter gene mRNA stability and translation via AU-containing distal regions of the untranslated region. This response was mediated entirely by a PGE 2 /p38 MAPK-dependent process. We conclude that the magnitude and duration of the induction of COX-2 mRNA, protein, and PGE 2 release by rhIL-1␤ is primarily the result of PGE 2 -dependent stabilization of COX-2 mRNA and stimulation of translation, a process involving a positive feedback loop mediated by the EP4 receptor and the downstream kinases p38 MAPK and, perhaps, cAMP-dependent protein kinase.

In this mini-review, progress made in the use of ionic liquid catalysts and related systems for cycloaddition reactions of carbon dioxide with epoxides is described with the primary focus on results from the past eight years.