Cyclic olefin copolymer based microfluidic devices for biochip applications: Ultraviolet surface grafting using 2-methacryloyloxyethyl phosphorylcholine

This report studies the surface modification of cyclic olefin copolymer (COC) by 2-methacryloyloxyethyl phosphorylcholine (MPC) monomer using photografting technique for the purpose of biointerface applications, which demonstrate resistance to both protein adsorption and cell adhesion in COC-based microfluidic devices. This is essential because the hydrophobic nature of COC can lead to adsorption of specific compounds from biological fluids in the microchannel, which can affect the results during fluidic analysis and cause clogging inside the microchannel. A correlation was found between the irradiation time and hydrophobicity of the modified substrate. Static water contact angle results show that the hydrophilicity property of the MPC-grafted substrate improves with increasing irradiation time. The contact angle of the modified surface decreased to 20 ± 5° from 88 ± 3° for the untreated substrate. The surface characterization of the modified surface was evaluated using x-ray photoelectron spectroscopy (XPS) and Fourier transform infrared spectroscopy (FTIR spectroscopy). Attenuated total reflection-FTIR and XPS results show the presence of the phosphate group (P-O) on modified COC substrates, indicating that the hydrophilic MPC monomer has successfully grafted on COC. Finally, it was demonstrated that cell adhesion and protein adsorption on the MPC modified COC specimen has reduced significantly.     

Genes, environment, and dyslexia the 2005 Norman Geschwind memorial lecture

This article presents an overview of some methods and results from our continuing studies of genetic and environmental influences on dyslexia, and on individual differences across the normal range that have been conducted over the past 25 years in the Colorado Learning Disabilities Research Center (CLDRC) and in related projects. CLDRC investigators compare the similarities of identical twin pairs who share all their genes and fraternal twins who share half their segregating genes to assess the balance of genetic, shared family environment, and nonshared environment influences on dyslexia and on individual differences across the normal range. We have learned that among the children we have studied in Colorado, group deficits in reading (dyslexia) and individual differences in reading across the normal range are primarily due to genetic influences, and these genetic influences are often shared with some of the same genetic influences on deficits and individual differences in language and ADHD. We have also learned from our molecular-genetic linkage studies that there are regions on several chromosomes likely to contain genes that influence dyslexia. Several specific genes within these regions have been tentatively identified through molecular-genetic association analyses, but much more research is needed to understand the pathways among specific genes, regions of noncoding DNA that regulate the activity of those genes, the brain, and dyslexia. I conclude with a discussion of our research on individual differences in early reading development, on the role of early learning constraints in dyslexia, and on how genetic influences are expressed through their interaction and correlation with the environment.     

Erroneous concerns about child sexual abuse

AIM: To assess the incidence and nature of concerns about sexual abuse, with particular reference to erroneous concerns of sexual abuse made by children. METHODS: A review of case notes of all child sexual abuse reports to the Denver Department of Social Services over 12 months. Cases were put into four groups: substantiated, not sexual abuse, inconclusive and erroneous accounts by children. RESULTS: 551 cases were reviewed. Forty-three percent were substantiated, 21% were inconclusive and 34% were not considered to be abuse cases. There were 14 (2.5%) erroneous concerns emanating from children. They comprised three cases of allegations made in collusion with a parent, three cases where an innocent event was misinterpreted as sexual abuse and eight cases (1.5%) of false allegations of sexual abuse.CONCLUSION: Erroneous concern of sexual abuse from children are uncommon. The four categories of concern in this study, in contrast to the simple classification of substantiated and unsubstantiated, provide a means of encouraging open minded assessments of the typical concerns which a child protection agency receives.     

Measuring poly-victimization using the Juvenile Victimization Questionnaire

OBJECTIVE: Children who experience multiple victimizations (referred to in this paper as poly-victims) need to be identified because they are at particularly high risk of additional victimization and traumatic psychological effects. This paper compares alternative ways of identifying such children using questions from the Juvenile Victimization Questionnaire (JVQ). METHODS: The JVQ was administered in a national random digit dial telephone survey about the experiences of 2,030 children. The victimizations of children 10-17 years old were assessed through youth self-report on the JVQ and the victimizations of children 2-9 assessed through JVQ caregiver proxy report. RESULTS: Twenty-two percent of the children in this sample had experienced four or more different kinds of victimizations in separate incidents (what we term poly-victimization) within the previous year. Such poly-victimization was highly associated with traumatic symptomatology. Several ways of identifying poly-victims with the JVQ produced roughly equivalent results: a simple count using the 34 victimizations screeners, a count using a reduced set of only 12 screeners, and the original poly-victimization measure using follow-up questions to identify victimizations occurring during different episodes. CONCLUSION: Researchers and clinicians should be taking steps to identify poly-victims within the populations with which they work and have several alternative ways of doing so.     

Differential genetic etiology of reading disability as a function of IQ

To test the hypothesis that the genetic etiology of reading disability differs as a function of IQ, composite reading performance data from 223 pairs of identical twins and 169 pairs of same-gender fraternal twins in which at least one member of each pair was classified with reading disability were subjected to multiple regression analysis (DeFries & Fulker, 1985, 1988). In the total sample, heritability of the group deficit in reading performance (h(g)2) was .58 (+/- .08). However, when the basic regression model was fitted separately to data from twin pairs with average Wechsler (1974, 1981) full scale IQ scores below 100 or 100 and above, resulting estimates of h(g)2 were .43 and .72, respectively, a significant difference (p < or = .03, one-tailed). The results of fitting extended regression models to reading performance and continuous IQ data provide evidence that the genetic etiology of reading disability differs as a linear function of IQ (p < or = .007, one-tailed). These results suggest that IQ is relevant for the diagnosis of reading disability and that environmental influences may be more salient as a cause of reading difficulties in children with lower IQ scores.     

Reading disability and chromosome 6p21.3: evaluation of MOG as a candidate gene

Linkage analysis has localized a gene influencing specific reading disability (dyslexia) to 6p21.3. The myelin oligodendrocyte glycoprotein (MOG) gene, which maps to this region, was selected as a candidate. Myelin oligodendrocyte glycoprotein is a membrane protein, a member of the immunoglobin superfamily, that is found on the outermost lamellae of mature myelin. Although the exact function of this protein is unknown, its presence in the central nervous system and the hypothesized relationship between dyslexia and temporal processing rate as well as a suggested relationship with intelligence made this gene a candidate for dyslexia. Analysis of the coding exons and adjacent splice sites in a subset of 22 children with dyslexia from 10 sibships found a missense mutation in exon 4 in 2 of the sibships. This change from the published sequence also occurred in 86 of 96 random controls, making it considerably less frequent in this small sample of individuals with dyslexia. Subsequent typing of this single nucleotide polymorphism (SNP) in 74 nuclear families in which at least one child had reading disability showed no significant difference in frequency from the controls, however. Sib-pair linkage analysis with these families did not show significant linkage with the SNP nor with a separate polymorphic dinucleotide repeat marker in the MOG gene (MOG31/32), but association analysis identified two alleles of MOG31/32 that were associated with reading disability phenotypes with a low level of significance. Thus, although alleles in the MOG gene may be in linkage disequilibrium with a locus that contributes to reading disability, it is unlikely that the MOG gene itself is involved.