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Scanpaths have played an important role in classic research on reading behavior. Nevertheless, they have largely been neglected in later research perhaps due to a lack of suitable analytical tools. Recently, von der Malsburg and Vasishth (2011) proposed a new measure for quantifying differences between scanpaths and demonstrated that this measure can recover effects that were missed with the traditional eyetracking measures. However, the sentences used in that study were difficult to process and scanpath effects accordingly strong. The purpose of the present study was to test the validity, sensitivity, and scope of applicability of the scanpath measure, using simple sentences that are typically read from left to right. We derived predictions for the regularity of scanpaths from the literature on oculomotor control, sentence processing, and cognitive aging and tested these predictions using the scanpath measure and a large database of eye movements. All predictions were confirmed: Sentences with short words and syntactically more difficult sentences elicited more irregular scanpaths. Also, older readers produced more irregular scanpaths than younger readers. In addition, we found an effect that was not reported earlier: Syntax had a smaller influence on the eye movements of older readers than on those of young readers. We discuss this interaction of syntactic parsing cost with age in terms of shifts in processing strategies and a decline of executive control as readers age. Overall, our results demonstrate the validity and sensitivity of the scanpath measure and thus establish it as a productive and versatile tool for reading research.
In recent years, an increasing number of mutations in what would appear to be 'housekeeping genes' have been identified as having unexpectedly specific defects in multicellular organogenesis. This is also the case for organogenesis in seed plants. Although it is not surprising that loss-of-function mutations in 'housekeeping' genes result in lethality or growth retardation, it is surprising when (1) the mutant phenotype results from the loss of function of a 'housekeeping' gene and (2) the mutant phenotype is specific. In this review, by defining housekeeping genes as those encoding proteins that work in basic metabolic and cellular functions, we discuss unexpected links between housekeeping genes and specific developmental processes. In a surprising number of cases housekeeping genes coding for enzymes or proteins with functions in basic cellular processes such as transcription, post-transcriptional modification, and translation affect plant development.
The development of numerosity estimation: Evidence for a linear number representation early in life
(2015)
Several studies investigating the development of approximate number representations used the number-to-position task and reported evidence for a shift from a logarithmic to a linear representation of numerical magnitude with increasing age. However, this interpretation as well as the number-to-position method itself has been questioned recently. The current study tested 5- and 8-year-old children on a newly established numerosity production task to examine developmental changes in number representations and to test the idea of a representational shift. Modelling of the children's numerical estimations revealed that responses of the 8-year-old children approximate a simple positive linear relation between estimated and actual numbers. Interestingly, however, the estimations of the 5-year-old children were best described by a bilinear model reflecting a relatively accurate linear representation of small numbers and no apparent magnitude knowledge for large numbers. Taken together, our findings provide no support for a shift of mental representations from a logarithmic to a linear metric but rather suggest that the range of number words which are appropriately conceptualised and represented by linear analogue magnitude codes expands during development.
The balance between cellular proliferation and differentiation is a key aspect of development in multicellular organisms. Recent studies on Arabidopsis roots revealed distinct roles for different reactive oxygen species (ROS) in these processes. Modulation of the balance between ROS in proliferating cells and elongating cells is controlled at least in part at the transcriptional level. The effect of ROS on proliferation and differentiation is not specific for plants but appears to be conserved between prokaryotic and eukaryotic life forms. The ways in which ROS is received and how it affects cellular functioning is discussed from an evolutionary point of view. The different redox-sensing mechanisms that evolved ultimately result in the activation of gene regulatory networks that control cellular fate and decision-making. This review highlights the potential common origin of ROS sensing, indicating that organisms evolved similar strategies for utilizing ROS during development, and discusses ROS as an ancient universal developmental regulator.
Methylmercury (MeHg) is an environmental pollutant linked to many neurological defects, especially in developing individuals. The thioredoxin (TRX) system is a key redox regulator affected by MeHg toxicity, however the mechanisms and consequences of MeHg-induced dysfunction are not completely understood. This study evaluated the role of the TRX system in C. elegans susceptibility to MeHg during development. Worms lacking or overexpressing proteins from the TRX family were exposed to MeHg for 1 h at different developmental stage: L1, L4 and adult. Worms without cytoplasmic thioredoxin system exhibited age-specific susceptibility to MeHg when compared to wild-type (wt). This susceptibility corresponded partially to decreased total glutathione (GSH) levels and enhanced degeneration of dopaminergic neurons. In contrast, the overexpression of the cytoplasmic system TRX-1/TRXR-1 did not provide substantial protection against MeHg. Moreover, transgenic worms exhibited decreased protein expression for cytoplasmic thioredoxin reductase (TRXR-1). Both mitochondrial thioredoxin system TRX-2/TRXR-2, as well as other thioredoxin-like proteins: TRX-3, TRX-4, TRX-5 did not show significant role in C. elegans resistance to MeHg. Based on the current findings, the cytoplasmic thioredoxin system TRX-1/TRXR-1 emerges as an important age-sensitive protectant against MeHg toxicity in C. elegans.
Exposure to high manganese (Mn) levels may damage the basal ganglia, leading to a syndrome analogous to Parkinson's disease, with motor and cognitive impairments. The molecular mechanisms underlying Mn neurotoxicity, particularly during development, still deserve further investigation. Herein, we addressed whether early-life Mn exposure affects motor coordination and cognitive function in adulthood and potential underlying mechanisms. Male Wistar rats were exposed intraperitoneally to saline (control) or MnCl2 (5, 10 or 20 mg/kg/day) from post-natal day (PND) 8-12. Behavioral tests were performed on PND 60-65 and biochemical analysis in the striatum and hippocampus were performed on PND14 or PND70. Rats exposed to Mn (10 and 20 mg/kg) performed significantly worse on the rotarod test than controls indicating motor coordination and balance impairments. The object and social recognition tasks were used to evaluate short-term memory. Rats exposed to the highest Mn dose failed to recognize a familiar object when replaced by a novel object as well as to recognize a familiar juvenile rat after a short period of time. However, Mn did not alter olfactory discrimination ability. In addition, Mn-treated rats displayed decreased levels of non-protein thiols (e.g. glutathione) and increased levels of glial fibrillary acidic protein (GFAP) in the striatum. Moreover, Mn significantly increased hippocampal glutathione peroxidase (GPx) activity. These findings demonstrate that acute low-level exposure to Mn during a critical neurodevelopmental period causes cognitive and motor dysfunctions that last into adulthood, that are accompanied by alterations in antioxidant defense system in both the hippocampus and striatum. (C) 2015 Elsevier Inc. All rights reserved.
The aim of this study was a longitudinal description of the ontogeny of the adult electric organ of Campylomormyrus rhynchophorus which produces as adult an electric organ discharge of very long duration (ca. 25 ms). We could indeed show (for the first time in a mormyrid fish) that the electric organ discharge which is first produced early during ontogeny in 33-mm-long juveniles is much shorter in duration and has a different shape than the electric organ discharge in 15-cm-long adults. The change from this juvenile electric organ discharges into the adult electric organ discharge takes at least a year. The increase in electric organ discharge duration could be causally linked to the development of surface evaginations, papillae, at the rostral face of the electrocyte which are recognizable for the first time in 65-mm-long juveniles and are most prominent at the periphery of the electrocyte.
Leaf senescence represents a key developmental process through which resources trapped in the photosynthetic organ are degraded in an organized manner and transported away to sustain the growth of other organs including newly forming leaves, roots, seeds, and fruits. The optimal timing of the initiation and progression of senescence are thus prerequisites for controlled plant growth, biomass accumulation, and evolutionary success through seed dispersal. Recent research has uncovered a multitude of regulatory factors including transcription factors, micro-RNAs, protein kinases, and others that constitute the molecular networks that regulate senescence in plants. The timing of senescence is affected by environmental conditions and abiotic or biotic stresses typically trigger a faster senescence. Various phytohormones, including for example ethylene, abscisic acid, and salicylic acid, promote senescence, whereas cytokinins delay it. Recently, several reports have indicated an involvement of auxin in the control of senescence, however, its mode of action and point of interference with senescence control mechanisms remain vaguely defined at present and contrasting observations regarding the effect of auxin on senescence have so far hindered the establishment of a coherent model. Here, we summarize recent studies on auxin-related genes that affect senescence in plants and highlight how these findings might be integrated into current molecular-regulatory models of senescence.
Introduction: Gait speed is one of the most commonly and frequently used parameters to evaluate gait development. It is characterized by high variability when comparing different steps in children. The objective of this study was to determine intra-individual gait speed variability in children.
Methods: Gait speed measurements (6-10 trials across a 3 m walkway) were performed and analyzed in 8263 children, aged 1-15 years. The coefficient of variation (CV) served as a measure for intra-individual gait speed variability measured in 6.6 +/- 1.0 trials per child. Multiple linear regression analysis was conducted to evaluate the influence of age and body height on changes in variability. Additionally, a subgroup analysis for height within the group of 6-year-old children was applied.
Results: A successive reduction in gait speed variability (CV) was observed for age groups (age: 1-15 years) and body height groups (height: 0.70-1.90 m). The CV in the oldest subjects was only one third of the CV (CV 6.25 +/- 3.52%) in the youngest subjects (CV 16.58 +/- 10.01%). Up to the age of 8 years (or 1.40 m height) there was a significant reduction in CV over time, compared to a leveling off for the older (taller) children.
Discussion: The straightforward approach measuring gait speed variability in repeated trials might serve as a fundamental indicator for gait development in children. Walking velocity seems to increase to age 8. Enhanced gait speed consistency of repeated trials develops up to age 15.