Understanding neurodevelopment in premature infants: applied chaos theory.
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The recent explosion of transgenic zebrafish lines in the literature demonstrates the value of this model system for detailed in vivo analysis of gene regulation and morphogenetic movements. The optical clarity and rapid early development of zebrafish provides the ability to follow these events as they occur in live, developing embryos. This article will review the development of transgenic technology in zebrafish as well as the current and future uses of transgenic zebrafish to explore the dynamic environment of the developing vertebrate embryo.
The aim of this experiment was to test the capacity of children to develop anticipation at various stages of their growth. We studied the learning process of an artificial co-ordination by means of a procedure of double unloading in two groups of children, and a group of adults. Elbow-joint angle measurement was used to assess for the improvement of the forearm stabilization through the six learning sessions. The main results report a developmental sequence of the acquisition of anticipatory postural adjustments (APA) similar to the one established for the ontogenesis of APA. A difference in learning dynamics, but also in the final level of performance, is reported between children aged 5-6 and children aged 7-8 years. The improvement occurring at the age of 7 years probably indicates maturation of internal representations, favourable to the faster setting up of operational anticipated control.
A complex orchestration of stem-cell specification, expansion and differentiation is required for the proper development of the nervous system. Although progress has been made on the role of individual genes in each of these processes, there are still unresolved questions about how gene function translates to the dynamic assembly of cells into tissues. Recently, stem-cell biology has emerged as a bridge between the traditional fields of cell biology and developmental genetics. In addition to their potential therapeutic role, stem cells are being exploited as experimental 'logic chips' that integrate information and exhibit self-organizing properties. Recent studies provide new insights on how morphogenic signals coordinate major stem cell decisions to regulate the size, shape and cellular diversity of the nervous system.
The specificity of facial processing impairment in autistic children, particularly in the domain of emotion, is still debated. The aim of our study was to assess the influence of motion on facial expression recognition in young autistic children. Thirteen autistic children (M age: 69.38 months) were matched for gender and developmental level with a control group of 13 normal children (M age: 40.53 months). They were compared on their ability to match videotaped "still," "dynamic," and "strobe" emotional and nonemotional facial expressions with photographs. Results indicate that children with autism do not perform significantly worse than their controls in any of our experimental conditions. Compared to previous studies showing lower performance in autistic than in control children when presented with static faces, our data suggest that slow dynamic presentations facilitate facial expression recognition by autistic children. This result could be of interest to parents and specialists involved in education and reeducation of these children.
In muscle spindles of the cat, independent control of dynamic and static components of the response of the primary sensory ending to stretch is provided by separate motor inputs to the various kinds of intrafusal muscle fibre: dynamic axons (gamma or beta) to the bag1 fibres and static axons to the bag2 (typically gamma only) and chain (gamma or beta) fibres. Nonlinear summation of separately evoked effects during combined stimulation of dynamic and static motor axons appears to be due to mutual resetting by antidromic invasion of separate encoding sites, leading to partial occlusion of the momentarily lesser response by the greater. The encoding sites are thought to be located within the primary ending's preterminal branches which from first-order level are normally segregated to the bag1 fibre and to the bag2 and chain fibres. Here we describe the analysis of a special case that arose in a histophysiological study which had shown that the degree of occlusion was related to the minimum number of nodes between the putative encoding sites. Three-dimensional reconstruction of the primary ending revealed that the terminals of one chain fibre were derived entirely from the first-order branch that supplied the bag1 fibre, including one terminal that was shared directly with the bag1 (sensory cross-terminal). The other first-order branch supplied the bag2 and remaining chain fibres as normal. The degree of occlusion seen during simultaneous stimulation of a dynamic beta axon and a static gamma axon indicated that the encoding sites were separated by both first-order branches. Schematic reconstruction of the motor innervation revealed that the static gamma axon was most unlikely to have supplied the chain fibre which shared sensory terminals with the bag1, but that these fibres also shared a motor input with histological characteristics of beta type. Ramp-frequency stimulation of the dynamic beta axon at constant length evoked a driving effect which persisted after fatiguing the extrafusal component and was therefore explicable on the basis of the observed pattern of motor innervation, though the identity of the axon could not be conclusively proved. Individually, instances of shared sensory terminals and motor input of bag1 and chain fibres are rare in the cat; their combination in a single spindle with correlated physiology is described here for the first time. The observation is considered in relation to the importance of dynamic and static segregation in motor control, since it may imply that there is a lower limit to the degree of segregation that the developmental programme can provide.
The rediscovery of Mendel's laws a century ago launched the science that William Bateson called "genetics," and led to a new view of evolution combining selection, particulate inheritance, and the newly characterized phenomenon of "mutation." This "mutationist" view clashed with the earlier view of Darwin, and the later "Modern Synthesis," by allowing discontinuity, and by recognizing mutation (or more properly, mutation-and-altered-development) as a source of creativity, direction, and initiative. By the mid-20th century, the opposing Modern Synthesis view was a prevailing orthodoxy: under its influence, "evolution" was redefined as "shifting gene frequencies," that is, the sorting out of pre-existing variation without new mutations; and the notion that mutation-and-altered-development can exert a predictable influence on the course of evolutionary change was seen as heretical. Nevertheless, mutationist ideas re-surfaced: the notion of mutational determinants of directionality emerged in molecular evolution by 1962, followed in the 1980s by an interest among evolutionary developmental biologists in a shaping or creative role of developmental propensities of variation, and more recently, a recognition by theoretical evolutionary geneticists of the importance of discontinuity and of new mutations in adaptive dynamics. The synthetic challenge presented by these innovations is to integrate mutation-and-altered-development into a new understanding of the dual causation of evolutionary change--a broader and more predictive understanding that already can lay claim to important empirical and theoretical results--and to develop a research program appropriately emphasizing the emergence of variation as a cause of propensities of evolutionary change.
This paper summarises and interrelates the findings of a large-scale multidisciplinary investigation to assess the influence of exercise on the development of the equine musculoskeletal system in general and of osteochondrosis in particular, up to age 5 months. Forty-three foals, genetically predisposed to develop OC, were divided into 3 exercise groups: box-rest, box-rest with training and free pasture exercise. At 5 months, all foals were weaned and 8 foals per group were subjected to euthanasia for postmortem examination. The remaining 19 foals were placed together and subjected to euthanasia at age 11 months. Foals were clinically and radiographically monitored during life, muscle and tendon biopsies were taken and gait analysed kinematically. After euthanasia, all major musculoskeletal tissue components (bone, articular cartilage, tendon and muscle) were analysed extensively using a wide variety of techniques. Radiographic monitoring of the stifle and hock joints and postmortem analysis of all diarthrodial joints led to the conclusion that osteochondrosis is a dynamic and very common process in which lesions cannot only develop, but may regress spontaneously during the 'windows of susceptibility' of the various joints, making the clinically diagnosed forms of osteochondrosis into the tip of an iceberg. Closure of the 'window of susceptibility' may be determined by the metabolic status of the chondrocyte which was shown to be inferior in older lesions. Exercise had no influence on the number of lesions, but was related to the distribution of lesions within the joint. There was some evidence that growth rate may be one of the most important intrinsic factors that determine the occurrence of OC. Lack of exercise (box-rest) generally delayed the development of the tissues that make up the equine musculoskeletal system. This was evident in bone mineral density (BMD) at various sites, chemical composition of tendon and of articular cartilage, and in the development of gait. In most cases, this delay was compensated for when box confinement was lifted after 5 months. However, there were indications that this was not true for some collagen characteristics of articular cartilage where the withholding of exercise at early age may therefore have a lifelong effect. The training protocol used (rather high-intensity exercise superimposed on a basic box-rest regimen) appeared to have long lasting negative effects, affecting chondrocyte viability long after the training protocol had ended. A same tendency was seen in bone (decrease in BMD) and tendons (decreases in proteoglycan and hyaluronic acid content). It is concluded that, during the first months postpartum, the equine musculoskeletal system passes through a very dynamic period of growth-related development and intense alteration. In this period, the system is vulnerable to adverse influences that may result in developmental orthopaedic disease. However, regenerative capacity is still high, also in those tissues that are notorious for their lack of repair capacity in the mature individual, such as articular cartilage and tendon. Exercise seems to be an important factor in the determination of the final make-up (and hence biomechanical strength) of these tissues and, therefore, is a potentially powerful tool for the enhancement of injury resistance.
NF-E2-related factor 3 (Nrf3) is a recently identified member of a family of transcription factors homologous to the Drosophila "cap 'n' collar" or CNC protein. The cnc gene is located immediately 3' to the Drosophila homeobox gene cluster and has been shown to regulate at least one of those genes, deformed. Likewise, human and mouse CNC homologues are located immediately 3' to each of the four Hox complexes, although no genetic interactions have yet been demonstrated in vertebrates. Work presented here demonstrates that Nrf3, adjacent to the Hox A cluster, is expressed during early development of the chicken embryo. Expression begins in the presumptive heart myocardium from the time of cardiac tube fusion through the looping process. Nrf3 transcripts then disappear from the heart and are next observed in the myotomal compartment of maturing somites, restricted to the medial portion along the rostrocaudal axis and fading after muscle precursors migrate. Central nervous system expression appears gradually and persists at low levels in ventricular neuroepithelial cells until at least embryonic day 6. Strong expression is observed in the early epiphysis, in the collecting ducts of the developing kidney and in individual cells of the yolk sac, underlying blood islands. This is the first description using in situ hybridization of the expression of a CNC family member and its dynamics through the course of early development.
Microfilaments (actin filaments) regulate various dynamic events during meiotic maturation. Relatively, little is known about the regulation of microfilament organization in mammalian oocytes. Proline-rich tyrosine kinase2 (Pyk2), a protein tyrosine kinase related to focal adhesion kinase (FAK) is essential in actin filaments organization. The present study was to examine the expression and localization of Pyk2, and in particular, its function during rat oocyte maturation. For the first time, by using Western blot and confocal laser scanning microscopy, we detected the expression of Pyk2 in rat oocytes and found that Pyk2 and Try402 phospho-Pyk2 were localized uniformly at the cell cortex and surrounded the germinal vesicle (GV) or the condensed chromosomes at the GV stage or after GV breakdown. At the metaphase and the beginning of anaphase, Pyk2 distributed asymmetrically both in the ooplasm and the cortex with a marked staining associated with the chromosomes and the region overlying the meiotic spindle. At telophase, Pyk2 was observed in the cleavage furrows in addition to its cortex and cytoplasm localization. The dynamics of Pyk2 were similar to that of F-actin, and this kinase was found to co-localize with microfilaments in several developmental stages during rat oocyte maturation. Microinjection of Pyk2 antibody demolished the microfilaments assembly and also inhibited the first polar body (PB1) emission. These findings suggest an important role of Pyk2 for rat oocyte maturation by regulating the organization of actin filaments.
The scores on 22 items of the Purdue Perceptual-motor Survey, administered to 567 normal school children of mean IQ 103 and mean age of 116 mo., were subjected to R-factor analysis by the method of principal factoring with orthogonal varimax rotation. The analysis led to the definition of 10 factors: J, ocular control; K, dynamic balance; L, visual-motor fluency; M, chalkboard; N, unilateral-bilateral coordination; O, upper-lower body differentiation; P, form perception; Q, developmental maturation; R, sex; and S, spatial body perception. The results provide cross-validation for previous studies on the perceptual-motor attributes of normal school children.
In a review of existing literature, compound narcolepsy is shown to involve not only problems of sleep regulation, but also autonomic, hormonal, emotional, and possibly motor and cognitive dysfunctions, strongly implicating the hypothalamus, limbic system, and possibly the striatum and cortex in the disorder. Neurochemical studies and the pattern of narcoleptic symptoms support the idea of a dynamic imbalance between dopamine and acetylcholine in the etiology of the disorder. What is known about the natural history of compound narcolepsy suggests a developmental course beginning with fluctuations in dopamine release, followed by supersensitivity of dopamine autoreceptors, and later followed by a pattern of intrinsic oscillations and reciprocal "overshoots" in release of dopamine and acetylcholine to account for the typical sequence of appearance of narcoleptic symptoms.
We are studying the functional roles of neuronal gap junctional coupling during development, using motor neurons and their synapses with muscle fibers as a model system. At neuromuscular synapses, several studies have shown that the relative pattern of activity among motor inputs competing for innervation of the same target muscle fiber determines how patterns of innervation are sculpted during the first weeks after birth. We asked whether gap junctional coupling among motor neurons modulates the relative timing of motor neuron activity in awake, behaving neonatal mice. We found that the activity of motor neurons innervating the same muscle is temporally correlated perinatally, during the same period that gap junction-mediated electrical and dye coupling are present. In vivo blockade of gap junctions abolished temporal correlations in motor neuron activity, without changing overall motor behavior, motor neuron activity patterns or firing frequency. Together with preliminary studies in mice lacking gap junction protein Cx40, our data suggest that developmentally regulated gap junctional coupling among motor and other neurons affects the activity in nascent neural circuits and thus in turn affects synaptic connectivity. Dynamic monitoring of dye coupling can be used to explore this possibility in normal mice and in mice lacking gap junction proteins during embryonic and neonatal development.
In experimental ecosystems that accommodate perch fry (Perca fluviatilis), significant structural changes within the benthic communities occurred under the effect of fish feeding on oligochaetes and on the larvae of chidonomids and other insects. Perch fry began to consume benthic animals at early developmental stages (C1-C2). The transition to regular feeding under experimental condition occurred at the D2-E stage (days 30-40), when the benthic community reached a developmental peak. The quantitative parameters characterizing the compositions of perch stomach contents and the main groups of zoobenthos closely correlated with each other. The dynamics of quantitative parameters of these animal groups (except for mollusks) proved to be determined both by the specific features of their life cycles and by the degree of consumption.
The treatment of a case of encopresis of six years duration in a boy now ten years of age demonstrates how physiological and dynamical processes in personal relationships combine in a common evolution. Through this the encopresis has become chronic and has lead to other instances of developmental retardation in the form of inadequate school performance. The fundamental concept behind the psychotherapeutical treatment stems from the recognition of an inner connection between the current symptoms, the chronic nature of the disease and the lack of success of previous disciplinary, medical and psychotherapeutical attempts at a solution.
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OBJECTIVE: The United States is a highly mobile society, with family relocation rates double those of Great Britain and Germany. The objective of this study was to describe the impact of frequent family moves on reported rates of delay in growth or development, learning disorders, school failure, and frequent behavioral problems in US school-age children. DESIGN AND SETTING: We analyzed data on 9915 six- to 17-year-old children of families responding to the 1988 National Health Interview Survey, a nationally representative sample of families and children. OUTCOME MEASURES: Parents were asked to report the total number of moves the index child had experienced during his or her lifetime. Total moves were adjusted for the child's age in years. Children were divided into two groups: never moved/infrequent relocation (below the 90th percentile for age-adjusted moves) and frequent relocation (above the 90th percentile for age-adjusted moves). The parent was asked if the child had ever had a learning disability or a delay in growth or development, had ever failed a grade, or had four or more frequently occurring behavioral problems as described by a behavioral problems checklist. RESULTS: The measures of both child dysfunction and family relocation were independently associated with multiple sociodemographic characteristics such as poverty, race, and family structure. Frequent relocation was associated with higher rates of all measures of child dysfunction; 23% of children who moved frequently had repeated a grade vs 12% of children who never or infrequently moved. Eighteen percent of children who moved frequently had four or more behavioral problems vs 7% of children who never or infrequently moved. Use of logistic regression to control for potential confounding covariates demonstrated that children who moved frequently were 77% more likely to be reported to have four or more behavioral problems (odds ratio, 1.77; 95% confidence interval, 1.37 to 2.29) and were 35% more likely to have failed a grade (odds ratio, 1.35; 95% confidence interval, 1.06 to 1.72), but no more likely to have had delays in growth or development or a learning disorder. CONCLUSIONS: After adjusting for other covariates, frequent family relocation was associated with an increased risk of children failing a grade in school and four or more frequently occurring behavioral problems.
In this paper we investigate the consequences of size-dependent competition among the individuals of a consumer population by analyzing the dynamic properties of a physiologically structured population model. Only 2 size-classes of individuals are distinguished: juveniles and adults. Juveniles and adults both feed on one and the same resource and hence interact by means of exploitative competition. Juvenile individuals allocate all assimilated energy into development and mature on reaching a fixed developmental threshold. The combination of this fixed threshold and the resource-dependent developmental rate, implies that the juvenile delay between birth and the onset of reproduction may vary in time. Adult individuals allocate all assimilated energy to reproduction. Mortality of both juveniles and adults is assumed to be inversely proportional to the amount of energy assimilated. In this setting we study how the dynamics of the population are influenced by the relative foraging capabilities of juveniles and adults. In line with results that we previously obtained in size-structured consumer-resource models with pulsed reproduction, population cycles primarily occur when either juveniles or adults have a distinct competitive advantage. When adults have a larger per capita feeding rate and are hence competitively superior to juveniles, population oscillations occur that are primarily induced by the fact that the duration of the juvenile period changes with changing food conditions. These cycles do not occur when the juvenile delay is a fixed parameter. When juveniles are competitively superior, two different types of population fluctuations can occur: (1) rapid, low-amplitude fluctuations having a period of half the juvenile delay and (2) slow, large-amplitude fluctuations characterized by a period, which is roughly equal to the juvenile delay. The analysis of simplified versions of the structured model indicates that these two types of oscillations also occur if mortality and/or development is independent of food density, i.e. in a situation with a constant juvenile developmental delay and a constant, food-independent background mortality. Thus, the oscillations that occur when juveniles are more competitive are induced by the juvenile delay per se. When juveniles exert a larger foraging pressure on the shared resource, maturation implies an increase not only in adult density, but also in food density and consequently fecundity. Our analysis suggests that this correlation in time between adult density and fecundity is crucial for the occurrence of population cycles when juveniles are competitively superior.