Montreal Children's Hospital

About: Montreal Children's Hospital is a healthcare organization based out in Montreal, Quebec, Canada. It is known for research contribution in the topics: Population & Poison control. The organization has 3842 authors who have published 4816 publications receiving 200198 citations.

Prevalence of low bone mass and deficiencies of vitamins D and K in pediatric patients with cystic fibrosis from 3 Canadian centers.

Abstract: Objective In this cross-sectional observational study, we assessed both vitamins D and K status and bone health in pancreatic insufficient pediatric patients with cystic fibrosis from 3 Canadian cystic fibrosis centers. Methods Eighty-one patients who had cystic fibrosis and were clinically stable for at least 3 months were enrolled. At the time of the clinic visit, anthropometric variables, lung function, pubertal status, intake of calcium and vitamins D and K, and physical activity were assessed. Blood was taken for analysis of biochemical biomarkers of bone turnover and status of vitamins D and K, and a urine sample was obtained for calcium, creatinine, sodium, and deoxypyridoline analyses. Whole-body bone mineral content and lumbar spine (L1-L4) bone mineral density were measured. Results The children were relatively well nourished and had moderate to mild lung disease. Low bone mineral mass defined as a z score between -1.0 and -2.0, for gender and age was detected in 38% of the children for whole body and in 28% for lumbar spine. z score less than -2.0 was observed in 7 children for both bone measures. Suboptimal vitamin D status occurred in 95% of patients; suboptimal vitamin K status occurred in 82% of patients. Measures of plasma osteocalcin and carboxy-terminal propeptide type 1 procollagen and urinary deoxypyridoline compared with reference values for age, gender, and pubertal status reflected a state of suppressed bone formation and elevated bone resorption in a large proportion of the patients. Conclusions Bone mass of the whole body and spine was lower than expected for chronological age in approximately one third of pediatric patients with cystic fibrosis irrespective of gender or age. This may be explained by the observation of low bone turnover for developmental stage as indicated by bone biomarkers. Suboptimal status of vitamins D and K may be key causative factors of the low bone status for age.

High intake of folic acid disrupts embryonic development in mice.

Abstract: BACKGROUND Folic acid fortification and supplementation has increased folate intake and blood folate concentrations and successfully reduced the incidence of neural tube defects. However, the developmental consequences of high folate intake are unknown. This study investigated the impact of high folate intake, alone or with methylenetetrahydrofolate reductase (MTHFR) deficiency, on embryonic and placental development in mice. METHODS Mthfr +/+ or +/− pregnant mice on a control diet (CD; recommended intake of folic acid for rodents) or folic acid-supplemented diet (FASD; 20-fold higher than the recommended intake) were examined for embryonic loss, delay, and defects at 10.5 and 14.5 days post coitum (dpc); 10.5-dpc placenta, and 14.5-dpc embryo hearts were studied histologically. RESULTS Total plasma folate was 10-fold higher in FASD compared to CD mice; plasma homocysteine levels were not affected by diet. At 10.5 dpc, the FASD was associated with embryonic delay and growth retardation, and may confer susceptibility to embryonic defects. The FASD did not adversely affect 10.5-dpc placental development. At 14.5 dpc, embryos from the FASD Mthfr +/+ group were delayed and the FASD was associated with thinner ventricular walls in embryonic hearts. There was a significant interaction between maternal MTHFR deficiency and a high folate diet for several developmental outcomes. CONCLUSIONS Our study suggests that high folate intake may have adverse effects on fetal mouse development and that maternal MTHFR deficiency may improve or rescue some of the adverse outcomes. These findings underscore the need for additional studies on the potential negative impact of high folate intake during pregnancy. Birth Defects Research (Part A), 2011. © 2010 Wiley-Liss, Inc.

The strengths and difficulties questionnaire: validation study in French school-aged children and cross-cultural comparisons

Abstract: To examine the psychometric properties of the French version of the strengths and difficulties questionnaire (SDQ), compare estimates of child mental health problems and SDQ scores across France, US and UK. The French version of the parent-reported SDQ was administered to the parents of a representative sample of 1,348 French children aged 6–11 years old. The response rate was 57.6%. We performed three scoring methods and examined their association with socio-demographic data. French SDQ scores were compared with SDQ scores from US and UK national surveys. The French cut-off points for the scoring bands were similar to those of the UK and US, with a few exceptions (peer relationship problems, prosocial behaviour). The internal consistency of the SDQ subscales was acceptable with Cronbach α coefficients ranging from 0.46 for peer relationship problems to 0.74 for hyperactivity/inattention. Known socio-demographic risk factors were associated with SDQ scoring method. For most SDQ scores, differences between France and the UK were smaller (5%) than those between France and the US. The study provided good support for the validity of the parent-reported SDQ in France as well as evidence for the usefulness of the SDQ as a promising screening instrument for epidemiological research and clinical purposes.

Coordinate regulation of DNA methyltransferase expression during oogenesis

Abstract: Background Normal mammalian development requires the action of DNA methyltransferases (DNMTs) for the establishment and maintenance of DNA methylation within repeat elements and imprinted genes. Here we report the expression dynamics of Dnmt3a and Dnmt3b, as well as a regulator of DNA methylation, Dnmt3L, in isolated female germ cells.