963 resultados para CARDIOGENIC-SHOCK
Resumo:
The chapter investigates Shock Control Bumps (SCB) on a Natural Laminar Flow (NLF) aerofoil; RAE 5243 for Active Flow Control (AFC). A SCB approach is used to decelerate supersonic flow on the suction/pressure sides of transonic aerofoil that leads delaying shock occurrence or weakening of shock strength. Such an AFC technique reduces significantly the total drag at transonic speeds. This chapter considers the SCB shape design optimisation at two boundary layer transition positions (0 and 45%) using an Euler software coupled with viscous boundary layer effects and robust Evolutionary Algorithms (EAs). The optimisation method is based on a canonical Evolution Strategy (ES) algorithm and incorporates the concepts of hierarchical topology and parallel asynchronous evaluation of candidate solution. Two test cases are considered with numerical experiments; the first test deals with a transition point occurring at the leading edge and the transition point is fixed at 45% of wing chord in the second test. Numerical results are presented and it is demonstrated that an optimal SCB design can be found to significantly reduce transonic wave drag and improves lift on drag (L/D) value when compared to the baseline aerofoil design.
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This study investigates the application of two advanced optimization methods for solving active flow control (AFC) device shape design problem and compares their optimization efficiency in terms of computational cost and design quality. The first optimization method uses hierarchical asynchronous parallel multi-objective evolutionary algorithm and the second uses hybridized evolutionary algorithm with Nash-Game strategies (Hybrid-Game). Both optimization methods are based on a canonical evolution strategy and incorporate the concepts of parallel computing and asynchronous evaluation. One type of AFC device named shock control bump (SCB) is considered and applied to a natural laminar flow (NLF) aerofoil. The concept of SCB is used to decelerate supersonic flow on suction/pressure side of transonic aerofoil that leads to a delay of shock occurrence. Such active flow technique reduces total drag at transonic speeds which is of special interest to commercial aircraft. Numerical results show that the Hybrid-Game helps an EA to accelerate optimization process. From the practical point of view, applying a SCB on the suction and pressure sides significantly reduces transonic total drag and improves lift-to-drag (L/D) value when compared to the baseline design.
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The paper investigates a detailed Active Shock Control Bump Design Optimisation on a Natural Laminar Flow (NLF) aerofoil; RAE 5243 to reduce cruise drag at transonic flow conditions using Evolutionary Algorithms (EAs) coupled to a robust design approach. For the uncertainty design parameters, the positions of boundary layer transition (xtr) and the coefficient of lift (Cl) are considered (250 stochastic samples in total). In this paper, two robust design methods are considered; the first approach uses a standard robust design method, which evaluates one design model at 250 stochastic conditions for uncertainty. The second approach is the combination of a standard robust design method and the concept of hierarchical (multi-population) sampling (250, 50, 15) for uncertainty. Numerical results show that the evolutionary optimization method coupled to uncertainty design techniques produces useful and reliable Pareto optimal SCB shapes which have low sensitivity and high aerodynamic performance while having significant total drag reduction. In addition,it also shows the benefit of using hierarchical robust method for detailed uncertainty design optimization.
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OBJECTIVE: : Acute traumatic coagulopathy occurs early in hemorrhagic trauma and is a major contributor to mortality and morbidity. Our aim was to examine the effect of small-volume 7.5% NaCl adenocaine (adenosine and lidocaine, adenocaine) and Mg on hypotensive resuscitation and coagulopathy in the rat model of severe hemorrhagic shock. DESIGN: : Prospective randomized laboratory investigation. SUBJECTS: : A total of 68 male Sprague Dawley Rats. INTERVENTION: : Post-hemorrhagic shock treatment for acute traumatic coagulopathy. MEASUREMENTS AND METHODS: : Nonheparinized male Sprague-Dawley rats (300-450 g, n = 68) were randomly assigned to either: 1) untreated; 2) 7.5% NaCl; 3) 7.5% NaCl adenocaine; 4) 7.5% NaCl Mg; or 5) 7.5% NaCl adenocaine/Mg. Hemorrhagic shock was induced by phlebotomy to mean arterial pressure of 35-40 mm Hg for 20 mins (~40% blood loss), and animals were left in shock for 60 mins. Bolus (0.3 mL) was injected into the femoral vein and hemodynamics monitored. Blood was collected in Na citrate (3.2%) tubes, centrifuged, and the plasma snap frozen in liquid N2 and stored at -80°C. Coagulation was assessed using activated partial thromboplastin times and prothrombin times. RESULTS: : Small-volume 7.5% NaCl adenocaine and 7.5% NaCl adenocaine/Mg were the only two groups that gradually increased mean arterial pressure 1.6-fold from 38-39 mm Hg to 52 and 64 mm Hg, respectively, at 60 mins (p < .05). Baseline plasma activated partial thromboplastin time was 17 ± 0.5 secs and increased to 63 ± 21 secs after bleeding time, and 217 ± 32 secs after 60-min shock. At 60-min resuscitation, activated partial thromboplastin time values for untreated, 7.5% NaCl, 7.5% NaCl/Mg, and 7.5% NaCl adenocaine rats were 269 ± 31 secs, 262 ± 38 secs, 150 ± 43 secs, and 244 ± 38 secs, respectively. In contrast, activated partial thromboplastin time for 7.5% NaCl adenocaine/Mg was 24 ± 2 secs (p < .05). Baseline prothrombin time was 28 ± 0.8 secs (n = 8) and followed a similar pattern of correction. CONCLUSIONS: : Plasma activated partial thromboplastin time and prothrombin time increased over 10-fold during the bleed and shock periods prior to resuscitation, and a small-volume (~1 mL/kg) IV bolus of 7.5% NaCl AL/Mg was the only treatment group that raised mean arterial pressure into the permissive range and returned activated partial thromboplastin time and prothrombin time clotting times to baseline at 60 mins.
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An ongoing challenge in behavioral economics is to understand the variations observed in risk attitudes as a function of their environmental context. Of particular interest is the effect of wealth on risk attitudes. The research in this area has however faced two constraints: the difficulty to study the causal effects of large changes in wealth, and the causal effects of losses on risk behavior. The present paper address this double limitation by providing evidence of the variation of risk attitude after large losses using a natural disaster (Brisbane floods) as the setting for a natural experiment.
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A synthesis is presented of the predictive capability of a family of near-wall wall-normal free Reynolds stress models (which are completely independent of wall topology, i.e., of the distance fromthe wall and the normal-to-thewall orientation) for oblique-shock-wave/turbulent-boundary-layer interactions. For the purpose of comparison, results are also presented using a standard low turbulence Reynolds number k–ε closure and a Reynolds stress model that uses geometric wall normals and wall distances. Studied shock-wave Mach numbers are in the range MSW = 2.85–2.9 and incoming boundary-layer-thickness Reynolds numbers are in the range Reδ0 = 1–2×106. Computations were carefully checked for grid convergence. Comparison with measurements shows satisfactory agreement, improving on results obtained using a k–ε model, and highlights the relative importance of redistribution and diffusion closures, indicating directions for future modeling work.
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The influence of inflow turbulence on the results of Favre–Reynolds-averaged Navier–Stokes computations of supersonic oblique-shock-wave/turbulent-boundary-layer interactions (shock-wave Mach-number MSW ∼2.9), using seven-equation Reynolds-stress model turbulence closures, is studied. The generation of inflow conditions (and the initialization of the flowfield) for mean flow, Reynolds stresses, and turbulence length scale, based on semi-analytic grid-independent boundary-layer profiles, is described in detail. Particular emphasis is given to freestream turbulence intensity and length scale. The influence of external-flow turbulence intensity is studied in detail both for flat-plate boundary-layer flow and for a compression-ramp interaction with large separation. It is concluded that the Reynolds-stress model correctly reproduces the effects of external flow turbulence.
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Due to increased number of terrorist attacks in recent years, loads induced by explosions need to be incorporated in building designs. For safer performance of a structure, its foundation should have sufficient strength and stability. Therefore, prior to any reconstruction or rehabilitation of a building subjected to blast, it is important to examine adverse effects on the foundation caused by blast induced ground shocks. This paper evaluates the effects of a buried explosion on a pile foundation. It treats the dynamic response of the pile in saturated sand, using explicit dynamic nonlinear finite element software LS-DYNA. The blast induced wave propagation in the soil and the horizontal deformation of pile are presented and the results are discussed. Further, a parametric study is carried out to evaluate the effect of varying the explosive shape on the pile response. This information can be used to evaluate the vulnerability of piled foundations to credible blast events as well as develop guidance for their design.
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Introduction The admission to the Intensive Care Unit with a diagnosis of sepsis and/or septic shock is not uncommon. The aim of this article is to present a nursing case review of a patient admitted to the intensive care unit with a diagnosis of septic shock and the use of bedside acid–base formulae to inform clinical decision making. Method We chose to use a case review. This method is useful in reporting unusual or rare cases and is typically seen more in medicine than in nursing. Discussion The gentleman in question was a self-presentation with a short history of fever and worsening shortness of breath. His condition worsened where he required admission to the intensive care unit. The use of ‘advanced’ acid–base interpretation to guide his nursing care provided a platform from which to advance a deeper understanding of the intricacies the critically ill patient often presents. Conclusion The use of case review is enlightening in understanding the disease process and the decision-making that accompanies this. The lessons learnt are applicable to a wider nursing audience because understanding acid–base physiology is beneficial in supporting and advancing critical care nursing practice.
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Breast cancer metastasis to the bone occurs frequently, causing numerous complications including severe pain, fracture, hypercalcemia, and paralysis. Despite its prevalence and severity, few effective therapies exist. To address this, we examined whether the heat shock protein 90 (Hsp90) inhibitor, 17-allylamino-17-demethoxygeldanamycin (17-AAG), would be efficacious in inhibiting breast cancer metastasis to bone. Utilizing the human breast cancer subline, MDA-MB-231SA, previously in vivo selected for its enhanced ability to generate osteolytic bone lesions, we determined that 17-AAG potently inhibited its in vitro proliferation and migration. Moreover, 17-AAG significantly reduced MDA-MB-231SA tumor growth in the mammary-fat pad of nude mice. Despite these findings, 17-AAG enhanced the incidence of bone metastasis and osteolytic lesions following intracardiac inoculation in the nude mouse. Consistent with these findings, 17-AAG enhanced osteoclast formation 2- to 4-fold in mouse bone marrow/osteoblast cocultures, receptor activator of nuclear factor κB ligand (BANKL)-stimulated bone marrow, and RAW264.7 cell models of in vitro osteoclastogenesis. Moreover, the drug enhanced osteoclastogenesis in human cord blood progenitor cells, demonstrating that its effects were not limited to mouse models. In addition to 17-AAG, other Hsp90 inhibitors, such as radicicol and herbimycin A, also enhanced osteoclastogenesis. A pro-osteolytic action of 17-AAG independent of tumor presence was also determined in vivo, in which 17-AAG-treated tumor-naive mice had reduced trabecular bone volume with an associated increase in osteoclast number. Thus, HSP90 inhibitors can stimulate osteoclast formation, which may underlie the increased incidence of osteolysis and skeletal tumor incidence causedby 17-AAG in vivo. These data suggest an important contraindication to the Hsp90 targeted cancer therapy currently undergoing clinical trial.