Air traffic flow management (ATFM) is the key driver of efficient aviation. It aims at balancing traffic demand against airspace capacity by scheduling aircraft, which is critical for air navigation ...service providers in delivering secure and sustainable air transport. Nowadays, the scale of scheduled aircraft grows dramatically along with the sharp increase in air traffic demand, which brings heavy pressure to efficient scheduling. Regarding safety and efficiency as two fundamental objectives of air transport, this paper proposes a cooperative co-evolutionary algorithm to solve large-scale multi-objective ATFM problems. First, a new multi-objective co-evolution framework with an evolving external archive is devised, in which the subcomponents collaborate with each other via the knee solution of the archive. Second, a novel fuzzy decomposition method is specifically designed to split the large-scale ATFM problem into small-size subcomponents by utilizing the spatiotemporal correlations of aircraft. During optimization, the proposed algorithm can continuously receive feedback from the optimization process and make the decomposition more likely better suited to the problem. Third, a new contribution-based probabilistic resource allocation mechanism is developed to automatically assign the computing resources to the unbalanced subcomponents. Finally, a test suite with different scales extracted from real air traffic data is created. Extensive experimental results show that, given the same number of fitness evaluations, the proposed algorithm significantly outperforms the state-of-the-art baselines in terms of effectiveness on all the benchmark instances.
Air traffic flow management plays a crucial role in efficient aviation. Most existing studies assume the flight speed as constant throughout the trip, leading to ineffective fixed-speed schedules. To ...address this issue, we propose a new problem model, which allows variable speed control to improve the flexibility and maneuverability of the management. In addition, we consider two conflicting objectives, which are minimizing the total flight delays and conflicts between flights, where the conflicts depend on the flight 4D trajectories (3D position plus time). To solve this new challenging problem, we propose a novel multi-objective evolutionary algorithm with new problem-specific individual representation and search operators. Specifically, the multi-chromosomes encoding scheme is designed to adapt to different types of operations. Then, to search the huge search space effectively, we develop a hybrid crossover operator that recombines the parents based on their flight routes. Furthermore, to balance the exploration and exploitation, we develop a new mutation strategy to utilize the heterogeneous search potential of different individuals. For exploitation, the knee individual in the Pareto front is improved by a new time shift operator for exploitation, and other non-dominated solutions are mutated by fixed-route mutation. For exploration, the dominated solutions are mutated randomly. To verify the effectiveness, we compare it with the real air traffic flow management schedules and the state-of-the-art algorithms on a range of real-world air traffic datasets. Extensive results show that the proposed algorithm can significantly outperform the baselines in generating safe and efficient 4D trajectories.
The purpose of this study was to explore the effects of tumor necrosis factor-α (TNF-α) on ventricular fibrillation (VF) in rats with acute myocardial infarction (AMI). Rats were randomly classified ...into AMI group, sham operation group and recombinant human tumor necrosis factor receptor:Fc fusion protein (rhTNFR:Fc) group. Spontaneous and induced VFs were recorded. Monophasic action potentials (MAPs) among different zones of myocardium were recorded at eight time points before and after ligation and MAP duration dispersions (MAPDds) were calculated. Then expression of TNF-α among different myocardial zones was detected. After ligation of the left anterior descending coronary artery, total TNF-α expression in AMI group began to markedly increase at 10 min, reached a climax at 20–30min, and then gradually decreased. The time-windows of VFs and MAPDds in the border zone performed in a similar way. At the same time-point, the expression of TNF-α in the ischemia zone was greater than that in the border zone, and little in the non-ischemia zone. Although the time windows of TNF-α expression, the MAPDds in the border zone and the occurrence of VFs in the rhTNFR:Fc group were similar to those in the AMI group, they all decreased in the rhTNFR:Fc group. Our findings demonstrate that TNF-α could enlarge the MAPDds in the border zone, and promote the onset of VFs.
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•An environmentally friendly CS-BP flame-retardant coating was synthesized by an electrostatic assembly method;•The CS-BP coating was tightly adhered to the surface of PUF through ...hydrogen bonding and electrostatic interaction;•The CS-BP significantly enhanced the fire resistance and photothermal conversion capability of PUF;•CS enhanced the catalytic carbonization and free radical quenching effect of BP.
A novel surface coating based on chitosan (CS) modified black phosphorus (BP) is obtained through layer-by-layer self-assembly and applied to flame-retardant rigid polyurethane foam (PUF). The CS-BP coating tightly adheres to the PUF surface through hydrogen bonding and electrostatic interaction, improving the PUF's thermal stability, photothermal conversion performance and fire safety performance without compromising its mechanical properties. The 9L-CS-BP/PUF exhibits reduced the peak of CO2 release, PHRR, and THR by 36.7%, 39.5%, and 28.8%, respectively, while increasing its residual carbon content by 35.2%. Moreover, a systematic comparison is made between the residual carbon inside and on the surface before and after combustion, and the results indicate that a large number of P-O-C structures and phosphoric acid derivatives are generated on the surface. The surface carbon layer formed by CS-BP effectively inhibited the thermo-oxidative degradation process of inner PUF. In the gas phase, modification of CS increases both the temperature range for the release of phosphorus-containing compounds during BP pyrolysis and the release of non-combustible gases during combustion, synergistically enhancing the gas-phase flame retardancy of CS-BP coating. This study provides a new approach to enhance the flame retardancy efficiency and broaden the application of BP-based flame retardants.
The gel polymer electrolyte (GPE) is a promising substitution for traditional liquid electrolytes. However, GPE is still troubled mainly by its sluggish ionic conductivity and inferior interfacial ...compatibility with electrodes. Herein, a phosphorus-modified GPE was fabricated by in situ incorporation of black phosphorus (BP) nanosheets into a poly(methyl methacrylate) (PMMA) matrix during the self-polymerization of monomers. The developed GPE exhibited high ionic conductivity (1.083 mS·cm–1 at 30 °C), an enhanced Li+ transference number (0.43), and a wide electrochemical stability window (5.2 V vs Li+/Li), while good thermal stability and improved flame retardancy can also be achieved. Differential scanning calorimeter measurements confirmed that the crystallinity of the PMMA matrix was not changed as BP nanosheets were incorporated. Further investigation proved that BP nanosheets contained in PMMA segments effectively immobilized the anions to decrease the coordination number around Li+. As a result, Li+ ion transport through the GPE was facilitated, which promoted the uniform stripping/plating of lithium while cycling the lithium symmetry cell. Based on the phosphorus-modified GPE, the Li|LiFePO4 and Li|LiNi0.5Co0.2Mn0.3O2 batteries and graphite|LiFePO4 soft-package battery exhibited encouraging electrochemical performances and safety properties.
Abstract To investigate the basis of ischemia-induced bradycardia (< 60 beats/min), we isolated pacemaker cells from the rabbit sinoatrial node and exposed them to ischemic-like conditions, including ...omission of glucose, pH 6.6, and either 5.4 or 10 mM KCl to evaluate the role of increased serum K. A perforated-patch technique was employed to test the hypothesis that the arrhythmia is caused by attenuation of inward currents that contribute to the diastolic depolarization. After exposure to “ischemic” Tyrode containing 5.4 mM KCl, the pacemaker cells exhibited 13% slower beat rates and action potentials with 6-mV greater overshoots and 44% longer durations. In contrast, after exposure to “ischemic” Tyrode containing 10 mM KCl, the pacemaker cells exhibited a 7-mV depolarization of the maximum diastolic potential but no significant change in the overshoot. Beat rates were slowed by 43%, and the action potentials were prolonged by 46%. “Ischemic” Tyrode containing 5.4 mM KCl increased L-type Ca current, decreased T-type Ca current and reduced Ni-sensitive inward current tails (presumably Na–Ca exchange current), even after treatment with 40 μM ryanodine to block Ca release from the sarcoplasmic reticulum. “Ischemic” Tyrode containing 10 mM KCl increased hyperpolarization-activated inward current at diastolic potentials and reduced the slowly activating component, but not the rapidly activating component, of delayed rectifier K current. Our results suggest that reductions of inward Na–Ca exchange current and T-type Ca current contribute to “ischemia”-induced “bradycardia” in sinoatrial node pacemaker cells.
Acute lung injury (ALI) is a critical clinical condition with a high mortality rate, characterized with excessive uncontrolled inflammation and apoptosis. Recently, microRNAs (miRNAs) have been found ...to play crucial roles in the amelioration of various inflammation-induced diseases, including ALI. However, it remains unknown the biological function and regulatory mechanisms of miRNAs in the regulation of inflammation and apoptosis in ALI. The aim of this study is to identify and evaluate the potential role of miRNAs in ALI and reveal the underlying molecular mechanisms of their effects. Here, we analyzed microRNA expression profiles in lung tissues from LPS-challenged mice using miRNA microarray. Because microRNA-27a (miR-27a) was one of the miRNAs being most significantly downregulated, which has an important role in regulation of inflammation, we investigated its function. Overexpression of miR-27a by agomir-27a improved lung injury, as evidenced by the reduced histopathological changes, lung wet/dry (W/D) ratio, lung microvascular permeability and apoptosis in the lung tissues, as well as ameliorative survival of ALI mice. This was accompanied by the alleviating of inflammation, such as the reduced total BALF cell and neutrophil counts, decreased levels of tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-6) interleukin-1β (IL-1β) and myeloperoxidase (MPO) activity in BAL fluid. Toll-like receptor 4 (TLR4), an important regulator of the nuclear factor kappa-B (NF-κB) signaling pathway, was identified as a novel target of miR-27a in RAW264.7 cells. Furthermore, our results showed that LPS stimulation increased the expression of MyD88 and NF-κB p65 (p-p65), but inhibited the expression of inhibitor of nuclear factor-κB-α (IκB-α), suggesting the activation of NF-κB signaling pathway. Further investigations revealed that agomir-miR-27a reversed the promoting effect of LPS on NF-κB signaling pathway. The results here suggested that miR-27a alleviates LPS-induced ALI in mice via reducing inflammation and apoptosis through blocking TLR4/MyD88/NF-κB activation.
This study was aimed to establish an experimental mouse model of combined transgenic inhibition of both multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and inward rectifier ...potassium current (Ik1), and to observe whether the specific inhibition of both CaMKII and Ik1 can bring about any effects on cardiac remodeling. Mice were divided into 4 groups: wild type (WT), CaMKII inhibited (AC3-I), Ik1 inhibited (Kir2.1-AAA) and combined inhibition of both CaMKII and Ik1 (AC3-I+Kir2.1-AAA). Mice in each group received electrocardiogram (ECG) and echocardiography examination. ECG in the condition of isoproterenol (ISO) injection was also checked. The whole cell patch clamp technique was used to measure Ik1 and the transient outward potassium current (Ito) from enzymatically isolated myocytes of left ventricle. In the condition of basal status, no significant changes of heart rate, PR interval and QRS interval were observed. No mouse showed ventricular arrhythmias in all of the 4 groups. After IS
Two human repeated insult patch tests were carried out in Shanghai and Mumbai in 2011. Even using the same protocol in two cities, thete was still some difference between them. What was the key point ...in HRIPT? Display omitted
► Two HRIPTs in same protocol were carried out in Shanghai and Mumbai. ► There remains to be clear distinction between the results of the two cities. ► Greater attention should be paid to factors that influence the results of HRIPT. ► Those factors are the meteorological impact and the ethnicity of the subject.
Human repeated insult patch test (HRIPT) is regarded as one of the confirmatory test in determining the safety of skin sensitizers. A number of important factors should be considered when conducting and interpreting the results of the HRIPT.
To investigate for probable critical factors that influence the results of HRIPT with the same protocol in Shanghai and Mumbai.
Two HRIPTs were carried out in Shanghai and Mumbai in 2011. Six identical products and 1% sodium lauryl sulfate were tested. Two Chinese dermatologists performed the grading in the two cities. Climate conditions of Shanghai and Mumbai were also recorded.
For four lower reaction ratio products, cumulative irritation scores in the induction phase were higher in individuals whose ethnicity was Indian rather than Chinese. Reaction ratio of the same four products was highly correlated to the climatic parameters. The other two higher reaction ratio products and the positive control had no difference between the two ethnicities.
Greater attention ought to be paid to the impact of climate on the results of HRIPT, especially for the mild irritation cosmetics when giving the interpretation. Greater emphasis also needs to be placed on the ethnicity of the subjects.
1 Department of Cell Physiology and Molecular Biophysics, Texas Tech University Health Sciences Center, Lubbock, Texas; and 2 Department of Cardiology, Institute of Cardiovascular Diseases, Ion ...Channelopathy Research Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Submitted 24 April 2007
; accepted in final form 29 August 2007
Ischemic-like conditions (a glucose-free, pH 6.6 Tyrode solution bubbled with 100% N 2 ) enhance L-type Ca current ( I Ca,L ) in single pacemaker cells (PCs) isolated from the rabbit sinoatrial node (SAN). In contrast, studies of ventricular myocytes have shown that acidic extracellular pH, as employed in our "ischemic" Tyrode, reduces I Ca,L . Therefore, our goal was to explain why I Ca,L is increased by "ischemia" in SAN PCs. The major findings were the following: 1 ) blockade of Ca-induced Ca release with ryanodine, exposure of PCs to BAPTA-AM, or replacement of extracellular Ca 2+ with Ba 2+ failed to prevent the ischemia-induced enhancement of I Ca,L ; 2 ) inhibition of protein kinase A with H-89, or calcium/calmodulin-dependent protein kinase II with KN-93, reduced I Ca,L but did not prevent its augmentation by ischemia; 3 ) ischemic Tyrode or pH 6.6 Tyrode shifted the steady-state inactivation curve in the positive direction, thereby reducing inactivation; 4 ) ischemic Tyrode increased the maximum conductance but did not affect the activation curve; 5 ) in rabbit atrial myocytes isolated and studied with exactly the same techniques used for SAN PCs, ischemic Tyrode reduced the maximum conductance and shifted the activation curve in the positive direction; pH 6.6 Tyrode also shifted the steady-state inactivation curve in the positive direction. We conclude that the acidic pH of ischemic Tyrode enhances I Ca,L in SAN PCs, because it increases the maximum conductance and reduces inactivation. Furthermore, the opposite results obtained with rabbit atrial myocytes cannot be explained by differences in cell isolation or patch-clamp techniques.
acidosis; protein kinase A; calcium/calmodulin-dependent protein kinase II; calcium-induced inactivation; rabbit atrial myocytes
Address for reprint requests and other correspondence: Y-M Du, Dept. of Cell Physiology and Molecular Biophysics, Texas Tech Univ. Health Sciences Ctr., 3601 4th St., Lubbock, TX 79430 (e-mail: yimeidu{at}hotmail.com )
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