An Analysis of the Hiskey Nebraska Test of Learning Aptitute for Navajo Children with Suspected Learning Difficulties

The purpose of the study was to evaluate the appropriateness of the Hiskey Nebraska Test of Learning Aptitude as a measure of ability for Navajo students with suspected learning difficulties. Item analytic procedures were employed for the 61 students in the younger group (ages 5-10) and for the 57 students in the older group (ages 11-17). Using Hoyt\u27s analysis of variance routine, reliability estimates of .87 (younger group) and .81 (older group) were obtained. The majority of the items discriminated in the appropriate direction for both subtest and total test scores. It was concluded that the Hiskey Nebraska Test of Learning Aptitude would give acceptably reliable and consistent results for Navajo children with suspected learning difficulties. Further research to demonstrate validity of the instrument for this population was discussed

Electronic media use and academic performance in late childhood: A longitudinal study

Introduction The effects of electronic media use on health has received much attention but less is known about links with academic performance. This study prospectively examines the effect of media use on academic performance in late childhood. Materials and methods 1239 8- to 9-year-olds and their parents were recruited to take part in a prospective, longitudinal study. Academic performance was measured on a national achievement test at baseline and 10–11 years of age. Parents reported on their child’s duration of electronic media use. Results After control for baseline reading, watching more than two hours of television per day at 8–9 years of age predicted a 12-point lower performance in reading at 10–11 years, equivalent to the loss of a third of a year in learning. Using a computer for more than one hour a day predicted a similar 12-point lower numeracy performance. Regarding cross-sectional associations (presumed to capture short-term effects) of media use on numeracy, after controlling for prior media exposure, watching more than two hours of television per day at 10–11 years was concurrently associated with a 12-point lower numeracy score and using a computer for more than one hour per day with a 13-point lower numeracy performance. There was little evidence for concurrent effects on reading. There was no evidence of short- or long-term associations between videogame use and academic performance. Discussion Cumulative television use is associated with poor reading and cumulative computer use with poorer numeracy. Beyond any links between heavy media use and health risks such as obesity, physical activity and mental health, these findings raise a possibility of additional risks of both television and computer use for learning in mid-childhood. These findings carry implications for parents, teachers and clinicians to consider the type and timing of media exposure in developing media plans for children.Peer reviewe

Implementing Electronic Tablet-Based Education of Acute Care Patients

Poor education-related discharge preparedness for patients with heart failure is believed to be a major cause of avoidable rehospitalizations. Technology-based applications offer innovative educational approaches that may improve educational readiness for patients in both inpatient and outpatient settings; however, a number of challenges exist when implementing electronic devices in the clinical setting. Implementation challenges include processes for "on-boarding" staff, mediating risks of cross-contamination with patients' device use, and selling the value to staff and health system leaders to secure the investment in software, hardware, and system support infrastructure. Strategies to address these challenges are poorly described in the literature. The purpose of this article is to present a staff development program designed to overcome challenges in implementing an electronic, tablet-based education program for patients with heart failure

The prevalence of posttraumatic stress disorder in pregnancy and after birth: A systematic review and meta-analysis

BACKGROUND: Previous reviews have provided preliminary insights into risk factors and possible prevalence of Post-traumatic Stress Disorder (PTSD) postpartum with no attempt to examine prenatal PTSD. This study aimed to assess the prevalence of PTSD during pregnancy and after birth, and the course of PTSD over this time. METHODS: PsychINFO, PubMed, Scopus and Web of Science were searched using PTSD terms crossed with perinatal terms. Studies were included if they reported the prevalence of PTSD during pregnancy or after birth using a diagnostic measure. RESULTS: 59 studies (N =24267) met inclusion criteria: 35 studies of prenatal PTSD and 28 studies of postpartum PTSD (where 4 studies provided prevalence of PTSD in pregnancy and postpartum). In community samples the mean prevalence of prenatal PTSD was 3.3% (95%, CI 2.44-4.54). The majority of postpartum studies measured PTSD in relation to childbirth with a mean prevalence of 4.0% (95%, CI 2.77-5.71) in community samples. Women in high-risk groups were at more risk of PTSD with a mean prevalence of 18.95% (95%, CI 10.62-31.43) in pregnancy and 18.5% (95%, CI 10.6-30.38) after birth. Using clinical interviews was associated with lower prevalence rates in pregnancy and higher prevalence rates postpartum. LIMITATIONS: Limitations include use of stringent diagnostic criteria, wide variability of PTSD rates, and inadequacy of studies on prenatal PTSD measured in three trimesters. CONCLUSIONS: PTSD is prevalent during pregnancy and after birth and may increase postpartum if not identified and treated. Assessment and treatment in maternity services is recommended

A network analysis to identify mediators of germline-driven differences in breast cancer prognosis

cited By 0Identifying the underlying genetic drivers of the heritability of breast cancer prognosis remains elusive. We adapt a network-based approach to handle underpowered complex datasets to provide new insights into the potential function of germline variants in breast cancer prognosis. This network-based analysis studies similar to 7.3 million variants in 84,457 breast cancer patients in relation to breast cancer survival and confirms the results on 12,381 independent patients. Aggregating the prognostic effects of genetic variants across multiple genes, we identify four gene modules associated with survival in estrogen receptor (ER)-negative and one in ER-positive disease. The modules show biological enrichment for cancer-related processes such as G-alpha signaling, circadian clock, angiogenesis, and Rho-GTPases in apoptosis.Peer reviewe

Adolescent transport and unintentional injuries: a systematic analysis using the Global Burden of Disease Study 2019

Background: Globally, transport and unintentional injuries persist as leading preventable causes of mortality and morbidity for adolescents. We sought to report comprehensive trends in injury-related mortality and morbidity for adolescents aged 10–24 years during the past three decades. Methods: Using the Global Burden of Disease, Injuries, and Risk Factors 2019 Study, we analysed mortality and disability-adjusted life-years (DALYs) attributed to transport and unintentional injuries for adolescents in 204 countries. Burden is reported in absolute numbers and age-standardised rates per 100 000 population by sex, age group (10–14, 15–19, and 20–24 years), and sociodemographic index (SDI) with 95% uncertainty intervals (UIs). We report percentage changes in deaths and DALYs between 1990 and 2019. Findings: In 2019, 369 061 deaths (of which 214 337 [58%] were transport related) and 31·1 million DALYs (of which 16·2 million [52%] were transport related) among adolescents aged 10–24 years were caused by transport and unintentional injuries combined. If compared with other causes, transport and unintentional injuries combined accounted for 25% of deaths and 14% of DALYs in 2019, and showed little improvement from 1990 when such injuries accounted for 26% of adolescent deaths and 17% of adolescent DALYs. Throughout adolescence, transport and unintentional injury fatality rates increased by age group. The unintentional injury burden was higher among males than females for all injury types, except for injuries related to fire, heat, and hot substances, or to adverse effects of medical treatment. From 1990 to 2019, global mortality rates declined by 34·4% (from 17·5 to 11·5 per 100 000) for transport injuries, and by 47·7% (from 15·9 to 8·3 per 100 000) for unintentional injuries. However, in low-SDI nations the absolute number of deaths increased (by 80·5% to 42 774 for transport injuries and by 39·4% to 31 961 for unintentional injuries). In the high-SDI quintile in 2010–19, the rate per 100 000 of transport injury DALYs was reduced by 16·7%, from 838 in 2010 to 699 in 2019. This was a substantially slower pace of reduction compared with the 48·5% reduction between 1990 and 2010, from 1626 per 100 000 in 1990 to 838 per 100 000 in 2010. Between 2010 and 2019, the rate of unintentional injury DALYs per 100 000 also remained largely unchanged in high-SDI countries (555 in 2010 vs 554 in 2019; 0·2% reduction). The number and rate of adolescent deaths and DALYs owing to environmental heat and cold exposure increased for the high-SDI quintile during 2010–19. Interpretation: As other causes of mortality are addressed, inadequate progress in reducing transport and unintentional injury mortality as a proportion of adolescent deaths becomes apparent. The relative shift in the burden of injury from high-SDI countries to low and low–middle-SDI countries necessitates focused action, including global donor, government, and industry investment in injury prevention. The persisting burden of DALYs related to transport and unintentional injuries indicates a need to prioritise innovative measures for the primary prevention of adolescent injury. Funding: Bill & Melinda Gates Foundation

The BRCA2 c.68-7T > A variant is not pathogenic: A model for clinical calibration of spliceogenicity.

Although the spliceogenic nature of the BRCA2 c.68-7T>A variant has been demonstrated, its association with cancer risk remains ontroversial. In this study, we accurately quantified by real-time PCR and digital PCR the BRCA2 isoforms retaining or missing exon 3. In addition, the combined odds ratio for causality of the variant was estimated using genetic and clinical data, and its associated cancer risk was estimated by case-control analysis in 83,636 individuals. Co-occurrence in trans with pathogenic BRCA2 variants was assessed in 5,382 families. Exon 3 exclusion rate was 4.5-fold higher in variant carriers (13%) than controls (3%), indicating an exclusion rate for the c.68-7T>A allele of approximately 20%. The posterior probability of pathogenicity was 7.44 x 10-115. There was neither evidence for increased risk of breast cancer (OR 1.03; 95% CI 0.86-1.24), nor for a deleterious effect of the variant when co-occurring with pathogenic variants. Our data provide for the first time robust evidence of the non-pathogenicity of the BRCA2 c.68-7T>A. Genetic and quantitative transcript analyses together inform the threshold for the ratio between functional and altered BRCA2 isoforms compatible with normal cell function. These findings might be exploited to assess the relevance for cancer risk of other BRCA2 spliceogenic variants

Identification of a BRCA2-Specific modifier locus at 6p24 related to breast cancer risk

Common genetic variants contribute to the observed variation in breast cancer risk for BRCA2 mutation carriers; those known to date have all been found through population-based genome-wide association studies (GWAS). To comprehensively identify breast cancer risk modifying loci for BRCA2 mutation carriers, we conducted a deep replication of an ongoing GWAS discovery study. Using the ranked P-values of the breast cancer associations with the imputed genotype of 1.4 M SNPs, 19,029 SNPs were selected and designed for inclusion on a custom Illumina array that included a total of 211,155 SNPs as part of a multi-consortial project. DNA samples from 3,881 breast cancer affected and 4,330 unaffected BRCA2 mutation carriers from 47 studies belonging to the Consortium of Investigators of Modifiers of BRCA1/2 were genotyped and available for analysis. We replicated previously reported breast cancer susceptibility alleles in these BRCA2 mutation carriers and for several regions (including FGFR2, MAP3K1, CDKN2A/B, and PTHLH) identified SNPs that have stronger evidence of association than those previously published. We also identified a novel susceptibility allele at 6p24 that was inversely associated with risk in BRCA2 mutation carriers (rs9348512; per allele HR = 0.85, 95% CI 0.80-0.90, P = 3.9×10−8). This SNP was not associated with breast cancer risk either in the general population or in BRCA1 mutation carriers. The locus lies within a region containing TFAP2A, which encodes a transcriptional activation protein that interacts with several tumor suppressor genes. This report identifies the first breast cancer risk locus specific to a BRCA2 mutation background. This comprehensive update of novel and previously reported breast cancer susceptibility loci contributes to the establishment of a panel of SNPs that modify breast cancer risk in BRCA2 mutation carriers. This panel may have clinical utility for women with BRCA2 mutations weighing options for medical prevention of breast cancer

Genome-wide association analysis of more than 120,000 individuals identifies 15 new susceptibility loci for breast cancer.

Genome-wide association studies (GWAS) and large-scale replication studies have identified common variants in 79 loci associated with breast cancer, explaining ∼14% of the familial risk of the disease. To identify new susceptibility loci, we performed a meta-analysis of 11 GWAS, comprising 15,748 breast cancer cases and 18,084 controls together with 46,785 cases and 42,892 controls from 41 studies genotyped on a 211,155-marker custom array (iCOGS). Analyses were restricted to women of European ancestry. We generated genotypes for more than 11 million SNPs by imputation using the 1000 Genomes Project reference panel, and we identified 15 new loci associated with breast cancer at P < 5 × 10(-8). Combining association analysis with ChIP-seq chromatin binding data in mammary cell lines and ChIA-PET chromatin interaction data from ENCODE, we identified likely target genes in two regions: SETBP1 at 18q12.3 and RNF115 and PDZK1 at 1q21.1. One association appears to be driven by an amino acid substitution encoded in EXO1.BCAC is funded by Cancer Research UK (C1287/A10118, C1287/A12014) and by the European Community's Seventh Framework Programme under grant agreement 223175 (HEALTH-F2-2009-223175) (COGS). Meetings of the BCAC have been funded by the European Union COST programme (BM0606). Genotyping on the iCOGS array was funded by the European Union (HEALTH-F2-2009-223175), Cancer Research UK (C1287/A10710, C8197/A16565), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer program and the Ministry of Economic Development, Innovation and Export Trade of Quebec, grant PSR-SIIRI-701. Combination of the GWAS data was supported in part by the US National Institutes of Health (NIH) Cancer Post-Cancer GWAS initiative, grant 1 U19 CA148065-01 (DRIVE, part of the GAME-ON initiative). For a full description of funding and acknowledgments, see the Supplementary Note.This is the author accepted manuscript. The final version is available from NPG via http://dx.doi.org/10.1038/ng.324