36 resultados para Incubation duration


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Braking is a crucial driving task with a direct relationship with crash risk, as both excess and inadequate braking can lead to collisions. The objective of this study was to compare the braking profile of young drivers distracted by mobile phone conversations to non-distracted braking. In particular, the braking behaviour of drivers in response to a pedestrian entering a zebra crossing was examined using the CARRS-Q Advanced Driving Simulator. Thirty-two licensed drivers drove the simulator in three phone conditions: baseline (no phone conversation), hands-free, and handheld. In addition to driving the simulator, each participant completed questionnaires related to driver demographics, driving history, usage of mobile phones while driving, and general mobile phone usage history. The drivers were 18–26 years old and split evenly by gender. A linear mixed model analysis of braking profiles along the roadway before the pedestrian crossing revealed comparatively increased decelerations among distracted drivers, particularly during the initial 20 kph of deceleration. Drivers’ initial 20 kph deceleration time was modelled using a parametric accelerated failure time (AFT) hazard-based duration model with a Weibull distribution with clustered heterogeneity to account for the repeated measures experiment design. Factors found to significantly influence the braking task included vehicle dynamics variables like initial speed and maximum deceleration, phone condition, and driver-specific variables such as licence type, crash involvement history, and self-reported experience of using a mobile phone whilst driving. Distracted drivers on average appear to reduce the speed of their vehicle faster and more abruptly than non-distracted drivers, exhibiting excess braking comparatively and revealing perhaps risk compensation. The braking appears to be more aggressive for distracted drivers with provisional licenses compared to drivers with open licenses. Abrupt or excessive braking by distracted drivers might pose significant safety concerns to following vehicles in a traffic stream.

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This study was designed to identify the neural networks underlying automatic auditory deviance detection in 10 healthy subjects using functional magnetic resonance imaging. We measured blood oxygenation level-dependent contrasts derived from the comparison of blocks of stimuli presented as a series of standard tones (50 ms duration) alone versus blocks that contained rare duration-deviant tones (100 ms) that were interspersed among a series of frequent standard tones while subjects were watching a silent movie. Possible effects of scanner noise were assessed by a “no tone” condition. In line with previous positron emission tomography and EEG source modeling studies, we found temporal lobe and prefrontal cortical activation that was associated with auditory duration mismatch processing. Data were also analyzed employing an event-related hemodynamic response model, which confirmed activation in response to duration-deviant tones bilaterally in the superior temporal gyrus and prefrontally in the right inferior and middle frontal gyri. In line with previous electrophysiological reports, mismatch activation of these brain regions was significantly correlated with age. These findings suggest a close relationship of the event-related hemodynamic response pattern with the corresponding electrophysiological activity underlying the event-related “mismatch negativity” potential, a putative measure of auditory sensory memory.

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It is commonly accepted that regular moderate intensity physical activity reduces the risk of developing many diseases. Counter intuitively, however, evidence also exists for oxidative stress resulting from acute and strenuous exercise. Enhanced formation of reactive oxygen and nitrogen species may lead to oxidatively modified lipids, proteins and nucleic acids and possibly disease. Currently, only a few studies have investigated the influence of exercise on DNA stability and damage with conflicting results, small study groups and the use of different sample matrices or methods and result units. This is the first review to address the effect of exercise of various intensities and durations on DNA stability, focusing on human population studies. Furthermore, this article describes the principles and limitations of commonly used methods for the assessment of oxidatively modified DNA and DNA stability. This review is structured according to the type of exercise conducted (field or laboratory based) and the intensity performed (i.e. competitive ultra/endurance exercise or maximal tests until exhaustion). The findings presented here suggest that competitive ultra-endurance exercise (>4h) does not induce persistent DNA damage. However, when considering the effects of endurance exercise (<4h), no clear conclusions could be drawn. Laboratory studies have shown equivocal results (increased or no oxidative stress) after endurance or exhaustive exercise. To clarify which components of exercise participation (i.e. duration, intensity and training status of subjects) have an impact on DNA stability and damage, additional carefully designed studies combining the measurement of DNA damage, gene expression and DNA repair mechanisms before, during and after exercise of differing intensities and durations are required.

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Traffic congestion has been a growing issue in many metropolitan areas during recent years, which necessitates the identification of its key contributors and development of sustainable strategies to help decrease its adverse impacts on traffic networks. Road incidents generally and crashes specifically have been acknowledged as the cause of a large proportion of travel delays in urban areas and account for 25% to 60% of traffic congestion on motorways. Identifying the critical determinants of travel delays has been of significant importance to the incident management systems which constantly collect and store the incident duration data. This study investigates the individual and simultaneous differential effects of the relevant determinants on motorway crash duration probabilities. In particular, it applies parametric Accelerated Failure Time (AFT) hazard-based models to develop in-depth insights into how the crash-specific characteristic and the associated temporal and infrastructural determinants impact the duration. AFT models with both fixed and random parameters have been calibrated on one year of traffic crash records from two major Australian motorways in South East Queensland and the differential effects of determinants on crash survival functions have been studied on these two motorways individually. A comprehensive spectrum of commonly used parametric fixed parameter AFT models, including generalized gamma and generalized F families, have been compared to random parameter AFT structures in terms of goodness of fit to the duration data and as a result, the random parameter Weibull AFT model has been selected as the most appropriate model. Significant determinants of motorway crash duration included traffic diversion requirement, crash injury type, number and type of vehicles involved in a crash, day of week and time of day, towing support requirement and damage to the infrastructure. A major finding of this research is that the motorways under study are significantly different in terms of crash durations; such that motorway exhibits durations that are on average 19% shorter compared to the durations on motorway. The differential effects of explanatory variables on crash durations are also different on the two motorways. The detailed presented analysis confirms that, looking at the motorway network as a whole, neglecting the individual differences between roads, can lead to erroneous interpretations of duration and inefficient strategies for mitigating travel delays along a particular motorway.

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Background Longer breastfeeding duration appears to have a protective effect against childhood obesity. This effect may be partially mediated by maternal feeding practices during the first years of life. However, the few studies that have examined links between breastfeeding duration and subsequent feeding practices have yielded conflicting results. Objective Using a large sample of first-time mothers and a newly validated, comprehensive measure of maternal feeding (the Feeding Practices and Structure Questionnaire1), this study examined associations between breastfeeding duration and maternal feeding practices at child age 24 months. Methods Mothers (n = 458) enrolled in the NOURISH trial2 provided data on breastfeeding at child age 4, 14 and 24 months, and on feeding practices at 24 months. Structural Equation Modelling was used to examine associations between breastfeeding duration and five non-responsive and four structure-related ‘authoritative’ feeding practices, adjusting for a range of maternal and child characteristics. Results The model showed acceptable fit (χ2/df = 1.68; RMSEA = .04, CFI = .91 and TLI = .89) and longer breastfeeding duration was negatively associated with four out of five non-responsive feeding practices and positively associated with three out of four structure-related feeding practices. Overall, these results suggest that mothers who breastfeed longer reported using more appropriate feeding practices. Conclusion These data demonstrate an association between longer breastfeeding duration and authoritative feeding practices characterised by responsiveness and structure, which may partly account for the apparent protective effect of breastfeeding on childhood obesity.

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The detailed molecular mechanisms underlying the regulation of sleep duration in mammals are still elusive. To address this challenge, we constructed a simple computational model, which recapitulates the electrophysiological characteristics of the slow-wave sleep and awake states. Comprehensive bifurcation analysis predicted that a Ca2+-dependent hyperpolarization pathway may play a role in slow-wave sleep and hence in the regulation of sleep duration. To experimentally validate the prediction, we generate and analyze 21 KO mice. Here we found that impaired Ca2+-dependent K+ channels (Kcnn2 and Kcnn3), voltage-gated Ca2+ channels (Cacna1g and Cacna1h), or Ca2+/calmodulin-dependent kinases (Camk2a and Camk2b) decrease sleep duration, while impaired plasma membrane Ca2+ ATPase (Atp2b3) increases sleep duration. Pharmacological intervention and whole-brain imaging validated that impaired NMDA receptors reduce sleep duration and directly increase the excitability of cells. Based on these results, we propose a hypothesis that a Ca2+-dependent hyperpolarization pathway underlies the regulation of sleep duration in mammals.