One of the most important issues related to adiabatic shear failure is the correlation among temperature elevation, adiabatic shear band (ASB) formation and the loss of load capacity of the material. ...Our experimental results show direct evidence that ASB forms several microseconds after stress collapse and temperature rise reaches its maximum about 30 μs after ASB formation. This observation indicates that temperature rise cannot be the cause of ASB. Rather, it might be the result of adiabatic shear localization. As such, the traditional well-accepted thermal-softening mechanism of ASB needs to be reconsidered.
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In this paper, we aim to deal with the cooperative tracking problem for a group of nonlinear systems with actuator faults and external disturbance/model uncertainty. The faults in the actuator are ...allowed to be in arbitrary forms such as actuator degradation, amplification, or even total failure. Moreover, the disturbance/model uncertainty under consideration is of Lipschitz type by assuming that the derivative of disturbance/model uncertainty is uniformly bounded. Then, provided that the actuator has sufficient healthy components when the faults happen, we employ the integral sliding mode technique to design the controller that can tolerate the actuator faults, meanwhile the external disturbance can also be rejected. The controller design is separated into two steps. First, a nominal controller is designed such that the estimated disturbance/model uncertainty from disturbance observer is completely rejected and the desired performance is guaranteed. Second, by the integral sliding mode control technique, a compensating controller is designed such that the matched estimation error of actuator faults and the external disturbance/model uncertainty can be compensated. The designed controller, formed by the sum of the nominal controller and compensating controller, finally proves to guarantee practical synchronization of nonlinear systems. Simulations demonstrate the effectiveness of our theoretical findings.
Summary
Salinity stress enhances reactive oxygen species (ROS) accumulation by activating the transcription of NADPH oxidase genes such as RbohD, thus mediating plant developmental processes, ...including seed germination. However, how salinity triggers the expression of ROS‐metabolism‐related genes and represses seed germination has not yet been fully addressed.
In this study, we show that Abscisic Acid‐Insensitive 4 (ABI4), a key component in abscisic acid (ABA) signaling, directly combines with RbohD and Vitamin C Defective 2 (VTC2), the key genes involved in ROS production and scavenging, to modulate ROS metabolism during seed germination under salinity stress.
Salinity‐induced ABI4 enhances RbohD expression by physically interacting with its promoter, and subsequently promotes ROS accumulation, thus resulting in cell membrane damage and a decrease in seed vigor. Additional genetic evidence indicated that the rbohd mutant largely rescues the salt‐hypersensitive phenotype of ABI4 overexpression seeds. Consistently, the abi4/vtc2 double mutant showed the salt‐sensitive phenotype, similar to the vtc2 mutant, suggesting that both RbohD and VTC2 are epistatic to ABI4 genetically.
Altogether, these results suggest that the salt‐induced RbohD transcription and ROS accumulation is dependent on ABI4, and that the ABI4‐RbohD/VTC2 regulatory module integrates both ROS metabolism and cell membrane integrity, ultimately repressing seed germination under salinity stress.
Acute respiratory distress syndrome (ARDS) threatens the survival of critically ill patients, the mechanisms of which are still unclear. Neutrophil extracellular traps (NETs) released by activated ...neutrophils play a critical role in inflammatory injury. We investigated the role of NETs and the underlying mechanism involved in acute lung injury (ALI). We found a higher expression of NETs and cyclic GMP-AMP synthase-stimulator of interferon genes (
) in the airways, which was reduced by Deoxyribonuclease I (DNase I) in ALI. The administration of the
inhibitor H-151 also significantly relieved inflammatory lung injury, but failed to affect the high expression of NETs in ALI. We isolated
neutrophils from bone marrow and acquired
neutrophils by inducing HL-60 to differentiate. After the PMA interventions, exogenous NETs were obtained from such extracted neutrophils. Exogenous NETs intervention in vitro and in vivo resulted in airway injury, and such inflammatory lung injury was reversed upon degrading NETs with or inhibiting
with H-151 as well as siRNA
. In conclusion,
participates in regulating NETs-mediated inflammatory pulmonary injury, which is expected to be a new therapeutic target for ARDS/ALI.
In this work, the working mechanism of the CO2–H2O flow corrosion of mild carbon steel is investigated by a two-dimensional simulation. Three models including a mass transfer model, an ...electrochemical model, and a convection–diffusion model are integrated to study the comprehensive working mechanisms. Several factors including temperature, pH, CO2 partial pressure, and flow velocity are considered. The results show that the flow corrosion increases with increasing temperature, decreasing pH or increasing CO2 partial pressure. As the temperature reaches above 60 °C, H2O reduction of the cathode becomes significant in the CO2–H2O flow corrosion. The cathode reaction of the corrosion at low pH is dominated by H+ reduction and sensitive to flow velocity, while with the increase of pH, H2CO3 plays an obvious buffer role to supplement H+. The effect of the flow velocity on CO2–H2O flow corrosion increases with the temperature, where the flow turbulence is found to play an important role in promoting corrosion enhancement.
Moderate traumatic brain injury (TBI) in children often happen when there's a sudden blow to the frontal bone, end with long unconscious which can last for hours and progressive cognitive deficits. ...However, with regard to the influences of moderate TBI during children adulthood, injury-induced alterations of locomotive ability, long-term memory performance, and hippocampal electrophysiological firing changes have not yet been fully identified. In this study, lateral fluid percussion (LFP) method was used to fabricate moderate TBI in motor and somatosensory cortex of the 6-weeks-old mice. The motor function, learning and memory function, extracellular CA1 neural spikes were assessed during acute and subacute phase. Moreover, histopathology was performed on day post injury (DPI) 16 to evaluate the effect of TBI on tissue and cell morphological changes in cortical and hippocampal CA1 subregions. After moderate LFP injury, the 6-weeks-old mice showed severe motor deficits at the early stage in acute phase but gradually recovered later during adulthood. At the time points in acute and subacute phase after TBI, novel object recognition (NOR) ability and spatial memory functions were consistently impaired in TBI mice; hippocampal firing frequency and burst probability were hampered. Analysis of the altered burst firing shows a clear hippocampal theta rhythm drop. These electrophysiological impacts were associated with substantially lowered NOR preference as compared to the sham group during adulthood. These results suggest that moderate TBI introduced at motorsenory cortex in 6-weeks-old mice causes obvious motor and cognitive deficits during their adulthood. While the locomotive ability progressively recovers, the cognitive deficits persisted while the mice mature as adult mice. The cognitive deficits may be attributed to the general suppressing of whole neural network, which could be labeled by marked reduction of excitability in hippocampal CA1 subregion.
Microorganisms drive much of the marine nitrogen (N) cycle, which jointly controls the primary production in the global ocean. However, our understanding of the microbial communities driving the ...global ocean N cycle remains fragmented. Focusing on "who is doing what, where, and how?", this study draws a clear picture describing the global biogeography of marine N-cycling microbial communities by utilizing the
Oceans shotgun metagenomes. The marine N-cycling communities are highly variable taxonomically but relatively even at the functional trait level, showing clear functional redundancy properties. The functional traits and taxonomic groups are shaped by the same set of geo-environmental factors, among which, depth is the major factor impacting marine N-cycling communities, differentiating mesopelagic from epipelagic communities. Latitudinal diversity gradients and distance-decay relationships are observed for taxonomic groups, but rarely or weakly for functional traits. The composition of functional traits is strongly deterministic as revealed by null model analysis, while a higher degree of stochasticity is observed for taxonomic composition. Integrating multiple lines of evidence, in addition to drawing a biogeographic picture of marine N-cycling communities, this study also demonstrated an essential microbial ecological theory-determinism governs the assembly of microbial communities performing essential biogeochemical processes; the environment selects functional traits rather than taxonomic groups; functional redundancy underlies stochastic taxonomic community assembly.
A critical question in microbial ecology is how the complex microbial communities are formed in natural ecosystems with the existence of thousands different species, thereby performing essential ecosystem functions and maintaining ecosystem stability. Previous studies disentangling the community assembly mechanisms mainly focus on microbial taxa, ignoring the functional traits they carry. By anchoring microbial functional traits and their carrying taxonomic groups involved in nitrogen cycling processes, this study demonstrated an important mechanism associated with the complex microbial community assembly. Evidence shows that the environment selects functional traits rather than taxonomic groups, and functional redundancy underlies stochastic taxonomic community assembly. This study is expected to provide valuable mechanistic insights into the complex microbial community assembly in both natural and artificial ecosystems.
Aflatoxin B1 (AFB1) is the most dangerous and abundant mycotoxin, which is toxic to almost all animals, and poultry is more sensitive to AFB1 toxicity. Ingesting AFB1-contaminated feed can cause ...significant liver damage and brings serious harm to poultry, which greatly restricts the development of the poultry industry. The present research was implemented to explore the intervention effect and its mechanism of taraxasterol on liver damage induced by AFB1 in broiler chickens. The liver damage model in broiler chickens was established by feeding 0.5 mg/kg AFB1 feed, and taraxasterol (25, 50 and 100 mg/kg BW, respectively) was given in the drinking water for 21 days. The growth performance, liver function, oxidative stress, apoptosis and autophagy were evaluated. The results showed that taraxasterol increased BW and reduced feed-to-gain ratio of broiler chickens induced by AFB1. Taraxasterol improved the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyltransferase (GGT), total bilirubin (TBIL) and alkaline phosphatase (ALP), and attenuated hepatic histopathological changes induced by AFB1. Meantime, taraxasterol down-regulated cytochrome P450 (CYP450) enzyme system CYP1A1 and CYP2A6 mRNA expression, inhibited the overproduction of reactive oxygen species (ROS) and malondialdehyde (MDA), and enhanced the activities of antioxidant enzymes glutathione (GSH) and catalase (CAT) and the content of antioxidant superoxide dismutase (SOD) of the liver in broiler chickens induced by AFB1. Furthermore, taraxasterol up-regulated the mRNA and protein expression of hepatic nuclear factor E2 related factor 2 (Nrf2), heme oxygenase 1 (HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO1), and down-regulated the expression of hepatic kelch like ECH associated protein 1 (Keap1) induced by AFB1 in Keap1/Nrf2 signaling pathway. The ultrastructural observation and RT-qPCR results found that taraxasterol inhibited apoptosis of hepatocytes, up-regulated the expression of B-cell lymphoma-2 (Bcl-2) mRNA and down-regulated the expression of Bax and caspase3 mRNA. Further, taraxasterol restored the autophagy of hepatocytes and down-regulated the mRNA expression of phosphatidylinositol 3-kinase K (PI3K), protein kinase B (AKT) and mammalian target of rapamycin (mTOR) in AFB1-induced liver of broiler chickens. The above results indicate that taraxasterol alleviates liver damage induced by AFB1 in broiler chickens through regulation of Keap1/Nrf2 signaling pathway to exert its antioxidant effect, mitochondrial apoptosis pathway to improve anti-apoptotic ability and PI3K/AKT/mTOR pathway to restore autophagy.
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•Taraxasterol alleviated aflatoxin B1-induced liver damage in broiler chickens.•Taraxasterol inhibited oxidative stress via activating Nrf2/Keap1 pathway.•Taraxasterol improved anti-apoptotic ability via inhibiting apoptosis pathway.•Taraxasterol restored autophagy via inhibiting PI3K/AKT/mTOR pathway.
The typical semi conductivity and few active sites of hydrogen evolution of 2H MoSe2 severely restrict its electrocatalytic hydrogen evolution performance. At the same time, the 1T MoSe2 has metal ...conductivity and plentiful hydrogen evolution sites, making it feasible to optimize the electrocatalytic hydrogen evolution behavior of MoSe2 using phase engineering. In this study, we, through a simple one-step hydrothermal method, composed 1T/2H MoSe2, and then used newly emerging transition metal carbides with several atomic-layer thicknesses Ti3C2Tx to improve the conductivity of a MoSe2-based electrocatalyst. Finally, MoSe2@Ti3C2Tx was successfully synthesized, according to the control of the additional amount of Ti3C2Tx, to form a proper MoSe2/ Ti3C2Tx heterostructure with a better electrochemical HER performance. As obtained MoSe2@4 mg-Ti3C2Tx achieved a low overpotential, a small Tafel slope and this work offers additional insight into broadened MoSe2 and MXenes-based catalyst’s electrochemical application.
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