Reading and writing are crucial for many aspects of modern life but up to 1 in 10 children are affected by dyslexia [1, 2], which can persist into adulthood. Family studies of dyslexia suggest heritability up to 70% [3, 4], yet no convincing genetic markers have been found due to limited study power [5]. Here, we present a genome-wide association study representing a 20-fold increase in sample size from prior work, with 51,800 adults self-reporting a dyslexia diagnosis and 1,087,070 controls. We identified 42 independent genome-wide significant loci: 17 are in genes linked to or pleiotropic with cognitive ability/educational attainment; 25 are novel and may be more specifically associated with dyslexia. Twenty-three loci (12 novel) were validated in independent cohorts of Chinese and European ancestry. We confirmed a similar genetic aetiology of dyslexia between sexes, and found genetic covariance with many traits, including ambidexterity, but not neuroanatomical measures of language-related circuitry. Causal analyses revealed a directional effect of dyslexia on attention deficit hyperactivity disorder and bidirectional effects on socio-educational traits but these relationships require further investigation. Dyslexia polygenic scores explained up to 6% of variance in reading traits in independent cohorts, and might in future enable earlier identification and remediation of dyslexia.
Previous research has indicated that education influences cognitive development, but it is unclear what, precisely, is being improved. Here, we tested whether education is associated with cognitive test score improvements via domain-general effects on general cognitive ability (g), or via domain-specific effects on particular cognitive skills. We conducted structural equation modeling on data from a large (n = 1,091), longitudinal sample, with a measure of intelligence at age 11 years and 10 tests covering a diverse range of cognitive abilities taken at age 70. Results indicated that the association of education with improved cognitive test scores is not mediated by g, but consists of direct effects on specific cognitive skills. These results suggest a decoupling of educational gains from increases in general intellectual capacity.
This study compares different approaches to measuring the number of nurse practitioners (NPs) providing primary care services using data from the 2012 U.S. National Sample Survey of Nurse Practitioners, North Carolina licensing data from 2011, and a 2010 California survey of nurse practitioners and nurse midwives. Estimates of the number and share of NPs providing primary care depend on how one defines primary care. If the definition is based on the field of NP education, the estimated shares in primary care specialties are 83.5% in North Carolina and 90.7% in California; if the definition is based on current or past fields of certification, the estimated shares are 79.9% in North Carolina and 74.5% nationally. The estimated number is even smaller if one considers employment setting (58.4% in North Carolina, 66.8% in California, and 67.8% nationally), and shrinks to about half of NPs if focusing on current field of clinical specialization.
The metabolic capability for the complete oxidation of glucose, i.e. aerobic glycolysis, is highly developed in the brains of neurologically mature (precocial) species at birth, whereas this activity is severely limited in the brains of neurologically immature (non-precocial) species such as the rat and human. The latter utilize a mixture of glucose and ketone bodies for synthetic and energetic activities and the advent of neurological competence associated with the capability for complete dependence on and oxidation of glucose must await the development of key enzymes such as the pyruvate dehydrogenase complex (PDHC). A similar relationship appears to exist with respect to the development of neurological maturity of different brain regions in a single species, the rat. The development of the enzymes of energy metabolism of neonatal rat brain will be discussed with respect to the energy fuels available to the neonatal brain. In particular mechanisms by which the PDHC develops in neonatal brain will be evaluated. Evidence suggests that this is due to a specific increase in enzyme protein in contrast to a general increase in mitochondrial activity.
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