44 resultados para Ignition delays

em Deakin Research Online - Australia


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One important aspect of the economic theory of criminal court delay is to understand how the prosecutor and the defendant make their decisions, and how these respond to changes in trial delay. If both parties jointly maximise expected utility, trial delay may increase or decrease the number of trials, depending upon the decision makers' attitudes towards risk. The main policy implication is that providing the criminal courts with more resources in the form of additional judges and court capacity may lengthen the trial queue rather than shorten it. This is a counterintuitive result contrary to popular belief.

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Court delays are consistently criticised as being inimical to social welfare. However, the theoretical basis for this assertion is not well established in the law and economics literature. As a first step, very little is known about the impact of court delay on the defendant's optimal plea decision. If the defendant is rational in the sense of inter temporally optimising, court delay may increase or decrease the probability of a trial depending on the defendant's bail status. Some empirical support for this theoretical proposition is found using data on plea behaviour for a selection of cases heard in NSW Australia.

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The study examines delay as a crucial factor contributing to maternal mortality, using the conceptual framework of the Three Phases of Delay to explore factors that hinder the provision and utilisation of high quality, timely obstetric care in Kafa Zone, SNNPR, in Ethiopia. The Three Delays constitute the delay in deciding to seek medical care during an obstetric emergency, in reaching a medical facility, and in receiving suitable treatment in a health facility. Various aspects of the Three Delays are evaluated to examine problems of delay, transportation, and the referral system that is considered a vital element of the Ethiopian 'National Reproductive Health Strategy'.

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Glucocorticoids can inhibit pulsatile LH secretion and can delay or even block the preovulatory LH surge. Previous work in ovariectomized ewes has indicated that cortisol can delay the estradiol-induced LH surge in an artificial follicular phase model but the results suggest this effect may be influenced by prior exposure to ovarian steroids. Here we tested the hypothesis that this disruptive effect of cortisol on the positive feedback action of estradiol is dependent on prior exposure to the ovarian steroidal milieu of the estrous cycle. Using long-term ovariectomized ewes, sequential artificial estrous cycles were created in the anestrous season by treatment and subsequent withdrawal of progesterone (CIDRs inserted for 9 d) followed by estradiol implants simulating the pre-ovulatory estradiol rise that induces the LH surge. Following the first artificial estrous cycle, a second cycle was initiated. Progesterone was again administered for 9 d followed by a second artificial follicular phase two weeks later. Beginning 2 hr prior to estradiol administration and ending at 40 hr, animals received either a cortisol infusion (elevate plasma levels to ∼170 ng/ml) or vehicle. Jugular blood was sampled hourly to assess occurrence and timing of the LH surge. Four different treatment sequences were tested (Cycle 1-Cycle 2): cortisol-cortisol; vehicle-cortisol; cortisol-vehicle; and vehicle-vehicle (n=5-6/sequence). If prior exposure to the ovarian steroidal milieu of the estrous cycle was necessary for cortisol to interfere with the positive feedback action of estradiol, then we would predict that cortisol would only delay the LH surge when it was delivered in Cycle 2 but not Cycle 1. Our results failed to support this prediction. Cortisol delayed the surge in both cycles (p<0.01), and the extent of the delay was the same in both Cycles 1 and 2 (4 hrs). Cortisol did not significantly affect surge amplitude in either cycle. These findings reinforce our previous conclusion that cortisol can delay the estradiol-induced LH surge but they do not support the hypothesis that this action of cortisol is dependent upon exposure to the ovarian steroidal milieu of the previous estrous cycle. (NIH-HD-30773)

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Delay in project completion is a major problem in construction that often leads to costly disputes and acrimonious relationships between the parties involved. The primary aim of this investigation was to determine why these delays occur and to develop control measures to minimise their impact.

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Absolute stability of Lurie control systems with multiple time-delays is studied in this paper. By using extended Lyapunov functionals, we avoid the use of the stability assumption on the main operator and derive improved stability criteria, which are strictly less conservative than the criteria in [2,3].

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To evaluate the putative advantages of student self pacing in automated instruction,the studies in this thesis compare the effects of self-paced, and externally-paced, programmed instruction on student accuracy, retention, efficiency, and satisfaction. The results of the experiments show that self-pacing reduced accuracy, retention, and workrates compared to external pacing and indicated that learners often make poor choices about optimum learning conditions. They also show that small changes in the learning environment can result in consistent and substantial changes in learner performance, and that behaviour analysts have an important role to play in the design and implementation of instructional material.

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This paper presents some results on the global exponential stabilization for neural networks with various activation functions and time-varying continuously distributed delays. Based on augmented time-varying Lyapunov-Krasovskii functionals, new delay-dependent conditions for the global exponential stabilization are obtained in terms of linear matrix inequalities. A numerical example is given to illustrate the feasibility of our results.

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Alkalosis enhances human exercise performance, and reduces K+ loss in contracting rat muscle. We investigated alkalosis effects on K+ regulation, ionic regulation and fatigue during intense exercise in nine untrained volunteers. Concentric finger flexions were conducted at 75% peak work rate (-3 W) until fatigue, under alkalosis (Alk, NaHCO3, 0.3 g kg−1) and control (Con, CaCO3) conditions, 1 month apart in a randomised, double-blind, crossover design. Deep antecubital venous (v) and radial arterial (a) blood was drawn at rest, during exercise and recovery, to determine arterio-venous differences for electrolytes, fluid shifts, acid–base and gas exchange. Finger flexion exercise barely perturbed arterial plasma ions and acid–base status, but induced marked arterio-venous changes. Alk elevated [HCO3] and PCO2, and lowered [H+] (P < 0.05). Time to fatigue increased substantially during Alk (25 ± 8%, P < 0.05), whilst both [K+]a and [K+]v were reduced (P < 0.01) and [K+]a-v during exercise tended to be greater (P= 0.056, n= 8). Muscle K+ efflux at fatigue was greater in Alk (21.2 ± 7.6 µmol min−1, 32 ± 7%, P < 0.05, n= 6), but peak K+ uptake rate was elevated during recovery (15 ± 7%, P < 0.05) suggesting increased muscle Na+,K+-ATPase activity. Alk induced greater [Na+]a, [Cl]v, muscle Cl influx and muscle lactate concentration ([Lac]) efflux during exercise and recovery (P < 0.05). The lower circulating [K+] and greater muscle K+ uptake, Na+ delivery and Cl uptake with Alk, are all consistent with preservation of membrane excitability during exercise. This suggests that lesser exercise-induced membrane depolarization may be an important mechanism underlying enhanced exercise performance with Alk. Thus Alk was associated with improved regulation of K+, Na+, Cl and Lac.

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Wild waterfowl populations form a natural reservoir of Avian Influenza (AI) virus, and fears exist that these birds may contribute to an AI pandemic by spreading the virus along their migratory flyways. Observational studies suggest that individuals infected with AI virus may delay departure from migratory staging sites. Here, we explore the epidemiological dynamics of avian influenza virus in a migrating mallard (Anas platyrhynchos) population with a specific view to understanding the role of infection-induced migration delays on the spread of virus strains of differing transmissibility. We develop a host-pathogen model that combines the transmission dynamics of influenza with the migration, reproduction and mortality of the host bird species. Our modeling predicts that delayed migration of individuals influences both the timing and size of outbreaks of AI virus. We find that (1) delayed migration leads to a lower total number of cases of infection each year than in the absence of migration delay, (2) when the transmission rate of a strain is high, the outbreak starts at the staging sites at which birds arrive in the early part of the fall migration, (3) when the transmission rate is low, infection predominantly occurs later in the season, which is further delayed when there is a migration delay. As such, the rise of more virulent AI strains in waterfowl could lead to a higher prevalence of infection later in the year, which could change the exposure risk for farmed poultry. A sensitivity analysis shows the importance of generation time and loss of immunity for the effect of migration delays. Thus, we demonstrate, in contrast to many current transmission risk models solely using empirical information on bird movements to assess the potential for transmission, that a consideration of infection-induced delays is critical to understanding the dynamics of AI infection along the entire flyway.

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Summary We examined the independent contributions of First Nations ethnicity and lower income to post-fracture mortality. A similar relative increase in mortality associated with fracture appears to translate into a larger absolute increase in post-fracture mortality for First Nations compared to non-First Nations peoples. Lower income also predicted increased mortality post-fracture.

Introduction First Nations peoples have a greater risk of mortality than non-First Nations peoples. We examined the independent contributions of First Nations ethnicity and income to mortality post-fracture, and associations with time to surgery post-hip fracture.

Methods Non-traumatic fracture cases and fracture-free controls were identified from population-based administrative data repositories for Manitoba, Canada (aged ≥50 years). Populations were retrospectively matched for sex, age (within 5 years), First Nations ethnicity, and number of comorbidities. Differences in mortality post-fracture of hip, wrist, or spine, 1996–2004 (population 1, n = 63,081), and the hip, 1987–2002(Population 2, n = 41,211) were examined using Cox proportional hazards regression to model time to death. For hip fracture, logistic regression analyses were used to model the probability of death within 30 days and 1 year.

Results Population 1: First Nations ethnicity was associated with an increased mortality risk of 30–53 % for each fracture type. Lower income was associated with an increased mortality risk of 18–26 %. Population 2: lower income predicted mortality overall (odds ratio (OR) 1.15, 95 % confidence interval (CI) 1.07–1.23) and for hip fracture cases (OR 1.18, 95%CI 1.05–1.32), as did older age, male sex, diabetes, and >5 comorbidities (all p ≤ 0.01). Higher mortality was associated with pertrochanteric fracture (OR 1.14, 95 % CI 1.03–1.27), or surgery delay of 2–3 days (OR 1.34, 95 % CI 1.18–1.52) or ≥4 days (OR 2.35, 95 % CI 2.07–2.67).

Conclusion A larger absolute increase in mortality post-fracture was observed for First Nations compared to non-First Nations peoples. Lower income and surgery delay >2 days predicted mortality post-fracture. These data have implications regarding prioritization of healthcare to ensure targeted, timely care for First Nations peoples and/or individuals with lower income.