Maternal well-being and its association to risk of developmental problems in children at school entry

<p>Abstract</p> <p>Background</p> <p>Children at highest risk of developmental problems benefit from early identification and intervention. Investigating factors affecting child development at the time of transition to school may reveal opportunities to tailor early intervention programs for the greatest effectiveness, social benefit and economic gain. The primary objective of this study was to identify child and maternal factors associated with children who screened at risk of developmental problems at school entry.</p> <p>Methods</p> <p>An existing cohort of 791 mothers who had been followed since early pregnancy was mailed a questionnaire when the children were aged four to six years. The questionnaire included a screening tool for developmental problems, an assessment of the child's social competence, health care utilization and referrals, and maternal factors, including physical health, mental health, social support, parenting morale and sense of competence, and parenting support/resources.</p> <p>Results</p> <p>Of the 491 mothers (62%) who responded, 15% had children who were screened at high risk of developmental problems. Based on a logistic regression model, independent predictors of screening at high risk for developmental problems at age 5 were male gender (OR: 2.3; 95% CI: 1.3, 4.1), maternal history of abuse at pregnancy (OR: 2.4; 95% CI: 1.3, 4.4), and poor parenting morale when the child was 3 years old (OR: 3.9; 95% CI: 2.1, 7.3). A child with all of these risk factors had a 35% predicted probability of screening at high risk of developmental problems, which was reduced to 13% if maternal factors were favourable.</p> <p>Conclusions</p> <p>Risk factors for developmental problems at school entry are related to maternal well being and history of abuse, which can be identified in the prenatal period or when children are preschool age.</p

Maternal mental health predicts risk of developmental problems at 3 years of age: follow up of a community based trial

<p>Abstract</p> <p>Background</p> <p>Undetected and untreated developmental problems can have a significant economic and social impact on society. Intervention to ameliorate potential developmental problems requires early identification of children at risk of future learning and behaviour difficulties. The objective of this study was to estimate the prevalence of risk for developmental problems among preschool children born to medically low risk women and identify factors that influence outcomes.</p> <p>Methods</p> <p>Mothers who had participated in a prenatal trial were followed up three years post partum to answer a telephone questionnaire. Questions were related to child health and development, child care, medical care, mother's lifestyle, well-being, and parenting style. The main outcome measure was risk for developmental problems using the Parents' Evaluation of Developmental Status (PEDS).</p> <p>Results</p> <p>Of 791 children, 11% were screened by the PEDS to be at high risk for developmental problems at age three. Of these, 43% had previously been referred for assessment. Children most likely to have been referred were those born preterm. Risk factors for delay included: male gender, history of ear infections, a low income environment, and a mother with poor emotional health and a history of abuse. A child with these risk factors was predicted to have a 53% chance of screening at high risk for developmental problems. This predicted probability was reduced to 19% if the child had a mother with good emotional health and no history of abuse.</p> <p>Conclusion</p> <p>Over 10% of children were identified as high risk for developmental problems by the screening, and more than half of those had not received a specialist referral. Risk factors for problems included prenatal and perinatal maternal and child factors. Assessment of maternal health and effective screening of child development may increase detection of children at high risk who would benefit from early intervention.</p> <p>Trial registration</p> <p>Current Controlled Trials ISRCTN64070727</p

CDH1 promoter hypermethylation and E-cadherin protein expression in infiltrating breast cancer

BACKGROUND: The E-cadherin gene (CDH1) maps, at chromosome 16q22.1, a region often associated with loss of heterozygosity (LOH) in human breast cancer. LOH at this site is thought to lead to loss of function of this tumor suppressor gene and was correlated with decreased disease-free survival, poor prognosis, and metastasis. Differential CpG island methylation in the promoter region of the CDH1 gene might be an alternative way for the loss of expression and function of E-cadherin, leading to loss of tissue integrity, an essential step in tumor progression. METHODS: The aim of our study was to assess, by Methylation-Specific Polymerase Chain Reaction (MSP), the methylation pattern of the CDH1 gene and its possible correlation with the expression of E-cadherin and other standard immunohistochemical parameters (Her-2, ER, PgR, p53, and K-67) in a series of 79 primary breast cancers (71 infiltrating ductal, 5 infiltrating lobular, 1 metaplastic, 1 apocrine, and 1 papillary carcinoma). RESULTS: CDH1 hypermethylation was observed in 72% of the cases including 52/71 ductal, 4/5 lobular carcinomas and 1 apocrine carcinoma. Reduced levels of E-cadherin protein were observed in 85% of our samples. Although not statistically significant, the levels of E-cadherin expression tended to diminish with the CDH1 promoter region methylation. In the group of 71 ductal cancinomas, most of the cases of showing CDH1 hypermethylation also presented reduced levels of expression of ER and PgR proteins, and a possible association was observed between CDH1 methylation and ER expression (p = 0.0301, Fisher's exact test). However, this finding was not considered significant after Bonferroni correction of p-value. CONCLUSION: Our preliminary findings suggested that abnormal CDH1 methylation occurs in high frequencies in infiltrating breast cancers associated with a decrease in E-cadherin expression in a subgroup of cases characterized by loss of expression of other important genes to the mammary carcinogenesis process, probably due to the disruption of the mechanism of maintenance of DNA methylation in tumoral cells

Measurement of the Bs Lifetime in Fully and Partially Reconstructed Bs -> Ds- (phi pi-)X Decays in pbar-p Collisions at sqrt(s) = 1.96 TeV

We present a measurement of the Bs lifetime in fully and partially reconstructed Bs -> Ds(phi pi)X decays in 1.3 fb-1 of pbar-p collisions at sqrt(s) = 1.96 TeV collected by the CDF II detector at the Fermilab Tevatron. We measure tau(Bs) = 1.518 +/- 0.041 (stat.) +/- 0.027 (syst.) ps. The ratio of this result and the world average B0 lifetime yields tau(Bs)/tau(B0) = 0.99 +/-0.03, which is in agreement with recent theoretical predictions.Comment: submitted to Phys. Rev. Let

Observation of the Y(4140)Y(4140) structure in the J/ψ ϕJ/\psi\,\phi Mass Spectrum in B±→J/ψ ϕKB^\pm\to J/\psi\,\phi K cays

The observation of the $Y(4140)$ structure in $B^\pm\rightarrow J/\psi\,\phi K^\pm$ decays produced in $\bar{p} p$ collisions at \sqrt{s}=1.96~\TeV is reported with a statistical significance greater than 5 standard deviations. A fit to the $J/\psi\,\phi$ mass spectrum is performed assuming the presence of a Breit-Wigner resonance. The fit yields a signal of $19^{+6}_{-5}$ resonance events, and resonance mass and width of 4143.4^{+2.9}_{-3.0}(\mathrm{stat})\pm0.6(\mathrm{syst})~\MeVcc and 15.3^{+10.4}_{-6.1}(\mathrm{stat})\pm2.5(\mathrm{syst})~\MeVcc respectively. The parameters of this resonance-like structure are consistent with values reported from an earlier CDF analysis.Comment: 7 pages, 2 figures, submited to Phys. Rev. Let

Regulatory Burden for Builders: Government's Effect on Housing Supply and Prices

Having an affordable place to live is a key ingredient for a prosperous and healthy life. Unfortunately for many people, housing is becoming harder and harder to afford, with some markets in Canada priced out of reach for entire generations of middle-income citizens. Affordable rental housing is also very difficult to come by, especially for people towards the bottom of the income distribution. Canada's rental stock of housing is old and deteriorated, with very little development or maintenance of this class of housing over the past 30 years. Governments at all levels affect housing in a variety of ways, and governments and citizens alike should be concerned about the extra cost added to housing through regulatory burden as well as other policies that limit new housing supply. Municipal governments add to the cost of housing through fees and levies and limit supply through zoning laws. This creates a fiscal externality on upper levels of government, since housing becomes less affordable and social spending requirements increase for provincial and federal governments. Provincial governments also interfere with the housing market. Land transfer taxes make land more expensive, and rent controls discourage investment in new rental housing developments. Vacancy and foreign buyer taxes are implemented in order to try to add supply to the rental market and limit speculative demand. Carbon taxes make building supplies—especially the key building ingredient of concrete—more expensive

Pegfilgrastim in pediatric cancer patients

Chemotherapy-induced neutropenia is a major dose-limiting side effect of intensive chemotherapy in cancer patients. Recently, pegfilgrastim (a product with a long half-life, resulting in once-per-cycle dosage) was introduced to prevent neutropenia in adults. The authors report 32 episodes of pegfilgrastim use in seven pediatric cancer patients to diminish chemotherapy-induced neutropenia. Feasibility was assessed by adherence to treatment protocol and safety was assessed by adverse effects. There were only two treatment delays (6%) due to neutropenia. No short-term adverse effects were recorded. The use of pegfilgrastim is feasible in pediatric cancer patients, without short-term adverse effects or major treatment delay due to neutropenia