The low-birth-weight infant remains at much higher risk of mortality than the infant with normal weight at birth. In the neonatal period, when most infant deaths occur, the proportion of low-birth-weight infants, especially those with very low weight, is the major determinant of the magnitude of the mortality rates. Furthermore, differences in low-birth-weight rates account for the higher neonatal mortality rates observed in some groups, particularly those characterized by socioeconomic disadvantages. Much of the recent decline in neonatal mortality can be attributed to increased survival among low-birth-weight infants, apparently as a result of hospital-based services. The application of these services is currently considered cost-effective, although whether this will continue to be true in the future is unclear because of the increased survival of very tiny infants. Although low-birth-weight infants remain at increased risk of both postneonatal mortality and morbidity in infancy and early childhood, the risk is substantially smaller than that of neonatal death. In addition, these adverse later outcomes have not offset the gains achieved in the neonatal period. Nonetheless, the increased survival of high-risk infants raises concern about their future requirements for special medical and educational services and about the stress on their families. Despite increased access to antenatal services, only moderate declines in the proportion of low-birth-weight infants has been observed, and almost no change has occurred in the proportion of those with very low weight at birth. In addition, in many areas of the country the birth-weight-specific neonatal mortality rates are similar for groups at high and low risk of neonatal death. In view of these findings, continuation of the current decline in neonatal mortality and reduction of the mortality differentials between high- and low-risk groups require the identification and more effective implementation of strategies for the prevention of low-weight births.

High-intensity exercise can result in up to a 1,000-fold increase in the rate of ATP demand compared to that at rest (Newsholme et al., 1983). To sustain muscle contraction, ATP needs to be regenerated at a rate complementary to ATP demand. Three energy systems function to replenish ATP in muscle: (1) Phosphagen, (2) Glycolytic, and (3) Mitochondrial Respiration. The three systems differ in the substrates used, products, maximal rate of ATP regeneration, capacity of ATP regeneration, and their associated contributions to fatigue. In this exercise context, fatigue is best defined as a decreasing force production during muscle contraction despite constant or increasing effort. The replenishment of ATP during intense exercise is the result of a coordinated metabolic response in which all energy systems contribute to different degrees based on an interaction between the intensity and duration of the exercise, and consequently the proportional contribution of the different skeletal muscle motor units. Such relative contributions also determine to a large extent the involvement of specific metabolic and central nervous system events that contribute to fatigue. The purpose of this paper is to provide a contemporary explanation of the muscle metabolic response to different exercise intensities and durations, with emphasis given to recent improvements in understanding and research methodology.

Context Genetic factors play an important role in the etiology of both autism spectrum disorders (ASD) and autistic traits. However, little is known about the etiologic consistency of autistic traits across levels of severity. Objective We compared the etiology of typical variation in autistic traits with extreme scoring groups (including top 1%) which mimicked the prevalence of diagnosed ASD in the largest twin study of autistic traits to date. Design Twin study employing phenotypic analysis and genetic model-fitting in the total sample and extreme scoring groups (top 5%, 2.5%, 1%). Setting A nationally-representative general population twin sample from the United Kingdom. Participants The families of 5,988 12-year-old pairs in the Twin Early Development Study. Main Outcome Measure Autistic traits as assessed by the Childhood Autism Spectrum Test. Results Moderate to high heritability was found for autistic traits in the general population (52% for females; 76% for males). High heritability was found in extreme scoring groups. There were no differences in heritability among extreme groups or between the extreme groups and the general population. A continuous liability shift towards autistic trait affectedness was seen in the cotwins of individuals scoring in the top 1%, suggesting shared etiology between extreme scores and normal variation. Conclusions This evidence of similar etiology across normal variation and the extremes has implications for molecular genetic models of ASD and for conceptualizing ASD as the quantitative extreme of a neurodevelopmental continuum.

The findings in the HLBW INT group provide support for preschool education to make long-term changes in a diverse group of children who are at developmental risk. The lack of observable benefit in the LLBW group raises questions about the biological and educational factors that foster or inhibit sustained effects of early educational intervention.

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