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.

Time-dependent changes in positively biased self-perceptions of children with attention-deficit/hyperactivity disorder: a developmental psychopathology perspective.

Abstract: This study examined changes in the degree of positive bias in self-perceptions of previously diagnosed 8- to 13-year-old children with attention-deficit/hyperactivity disorder (ADHD; n = 513) and comparison peers (n = 284) over a 6-year period. The dynamic association between biased self-perceptions and dimensional indices of depressive symptoms and aggression also were considered. Across the 6-year time span, comparison children exhibited less bias than children with ADHD, although a normative bolstering of social self-views during early adolescence was observed. Decreases in positive biases regarding social and behavioral competence were associated with increases in depressive symptoms over time, whereas increases in levels of positively biased self-perceptions in the behavioral (but not social) domain were predictive of greater aggression over time. ADHD status moderated the dynamic association between biases and adjustment. Finally, evidence indicated that there was a bidirectional relationship between biases and aggression, whereas depressive symptoms appeared to inversely predict later bias.

Studies of methionine cycle intermediates (SAM, SAH), DNA methylation and the impact of folate deficiency on tumor numbers in Min mice.

Abstract: Several epidemiological studies have suggested a modulatory effect of dietary folate intake on the risk of colorectal cancer. The molecular basis for this inverse association is not clearly understood, but may involve alterations in DNA methylation. In this study, we examined the levels of methylation intermediates [S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH)] and of global DNA methylation in the pre-neoplastic small intestine of Min (multiple intestinal neoplasia) mice. We also studied the effect of folate/choline deficiency on these parameters and on tumor multiplicity in this animal model. In folate-adequate Min mice, we identified positive linear correlations between SAM or SAH and tumor numbers (R(2) = 0.38, P < 0.005; R(2) = 0.26, P = 0.025, respectively). A positive correlation between global DNA hypomethylation and tumor multiplicity was also observed (R(2) = 0.29, P = 0.014). These three biochemical determinants (SAM, SAH and DNA hypomethylation) may, therefore, serve as early markers of cell transformation. Folate/choline deficiency, however, did not produce a consistent effect on tumor numbers in three separate experiments. As an increase in tumor numbers was observed only in folate- and choline-deficient mice with low levels of SAM and DNA hypomethylation, the modulatory role of folate may be dependent on the transformation state of the cell.

Recursive Partition: A Versatile Method for Exploratory-Data Analysis in Biostatistics

Abstract: In clinical and epidemiological studies, interactions among covariates are of primary importance. In the absence of clearly stated a priori hypotheses, it is usual to build predictive models by means of stepwise logistic or Cox regression, a practice that tends to emphasize main effects and overlook possible interactions.

Familial neurofibromatosis 1 microdeletions: cosegregation with distinct facial phenotype and early onset of cutaneous neurofibromata.

Abstract: A notable subset of the recent literature on the disorder neurofibromatosis type 1 (NF1) describes patients with NF1, facial anomalies, and other unusual findings. We describe a molecular re-evaluation of two such families reported previously by Kaplan and Rosenblatt [1985], who suggested that their NF1 manifestations, facial phenotype, and other findings could result from a disorder distinct from NF1. Submicroscopic deletions involving the NF1 gene were identified in both families by fluorescent in situ hybridization and analysis of somatic cell hybrids. Affected subjects of the first family were heterozygous for a microdeletion of approximately 2 Mb, which included the entire NF1 gene and flanking contiguous sequences. The family was remarkable for cosegregation of the NF1 microdeletion with facial abnormalities and a pattern of early onset of cutaneous neurofibromata upon transmission from an affected mother to her three affected children. The propositus of the second family carried a deletion that at the least involved NF1 exon 2 through intron 27, which is ≥ 200 kilobases in length. Because all persons in the family were deceased, the size of the deletion could not be determined precisely. Facial anomalies were observed in the propositus and his NF1-affected mother and sister. The data from these families support our hypothesis, which was initially based solely on sporadic deletion cases, that deletion of the entire NF1 gene, or in conjunction with deletion of unknown contiguous genes, causes the facial anomalies and early onset of neurofibromata observed in this subset of NF1 patients. In addition, other features observed in the persons in these families suggest that some NF1 microdeletion patients may be at increased risk for connective tissue abnormalities and/or neoplasms. Am. J. Med. Genet. 73:197–204, 1997. © 1997 Wiley-Liss, Inc.