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A universal PMSM-driven servo system comprises cascaded PI controllers with a low-pass speed filter for high-frequency disturbance suppression. However, the speed filter and the current loop have received limited attention during the tuning of the speed loop, potentially leading to high-frequency fluctuations or significant resonances in the entire servo system under disturbances. This paper proposes a novel framework of multi-objective optimal tuning for the entire PMSM-driven servo system, focusing on suppressing high-frequency disturbances. The controller parameters to be tuned include the PI gains of the speed loop, the filter time constant and the equivalent time constant of the current loop. The closed-loop cut-off frequency of disturbances is established as a constraint to optimize the speed filter, and the current loop time constant is selected as an objective to improve control smoothness. Experimental results demonstrate that the proposed method can reduce the high-frequency fluctuations of speed and current without causing system resonances.

Summary: Increased blood amino acid levels (hyperaminoacidemia) stimulate pancreas expansion by unclear mechanisms. Here, by genetic and pharmacological disruption of glucagon receptor (GCGR) in mice and zebrafish, we found that the ensuing hyperaminoacidemia promotes pancreatic acinar cell proliferation and cell hypertrophy, which can be mitigated by a low protein diet in mice. In addition to mammalian target of rapamycin complex 1 (mTORC1) signaling, acinar cell proliferation required slc38a5, the most highly expressed amino acid transporter gene in both species. Transcriptomics data revealed the activation signature of yes-associated protein (YAP) in acinar cells of mice with hyperaminoacidemia, consistent with the observed increase in YAP-expressing acinar cells. Yap1 activation also occurred in acinar cells in gcgr−/− zebrafish, which was reversed by rapamycin. Knocking down yap1 in gcgr−/− zebrafish decreased mTORC1 activity and acinar cell proliferation and hypertrophy. Thus, the study discovered a previously unrecognized role of the YAP/Taz pathway in hyperaminoacidemia-induced acinar cell hypertrophy and hyperplasia.

High Modulus Asphalt Mixtures (HMAM) have gained widespread utilization in asphalt pavement construction. It is great critical to study the fatigue characteristics of HMAM. At present, various fatigue test methods are employed in indoor testing to assess HMAM under different mechanical states. Therefore, there is a critical problem that the value of fatigue parameters is not unique in the structural design of HMAM. In this study, three fatigue testing methods were initially used to address the above issues: direct tensile testing, indirect tensile testing, and uniaxial compression testing. These tests help to determine the strength yield surface states at different loading rates. And to reveal the effect of loading rate on the mechanical behavior of HMAM. The results show a power function fit and a good correlation between strength and loading rate. The relationship models of strength with speed for indirect tensile, direct tensile and uniaxial compression tests are SI=3.22(v)0.14, SD=3.22(v)0.15 and SU=3.22(v)0.12, respectively.The higher the loading rate for the three fatigue test results, the greater the expansion of the strength yield surface.The fatigue life (Nf) of HMAM underwent testing, yielding its fatigue effective stress ratio. The relationship between the two was and then established. It is found that the point (1, 1) appears on the backextension line, thus effectively complementing the conventional S-N equation. In addition, the fatigue equations for various fatigue test methods were unified based on effective stress strength ratio and the fatigue life. This paper introduces a novel method for the antifatigue design of HMAM.

Empathy for pain is a key driver of prosocial behavior and is influenced by acute psychosocial stress. However, the role of task-based brain connectivity during acute stress have been neglected. Hence, we aimed to explore the relationship between the magnitude of cortisol response to acute stress and empathy for pain, as well as the neural connectivity mechanisms involved. In this study, 80 healthy participants (37 women and 43 men) were exposed to the acute psychosocial stress paradigm (ScanSTRESS) and were scanned by functional magnetic resonance imaging. Saliva samples were collected to measure the magnitude of cortisol stress response. Subsequently, the participants took part in a pain-video task to assess their empathy for pain. Six participants were excluded because of physical discomfort or excessive head movement in all runs during the task-dependent fMRI scan. Therefore, 33 women and 41 men were included in data analysis. We found that empathy for pain was negatively correlated with the magnitude of cortisol stress response (r = -0.268, p = 0.018) and that the task-based connectivity between the salience network and sensorimotor network, including its sub-network and sub-region, was negatively correlated with the magnitude of cortisol stress response, and positively correlated with empathy for pain. Furthermore, task-based connectivity between the insula and the paracentral lobule mediates the effect of the stress-induced cortisol response on empathy for pain (indirect effect = -0.0152, 95% CI = [-0.036, -0.001], p = 0.036). Our research suggests that empathy is not only correlated with stress-induced glucocorticoids but also tied to the stress-induced reduced communication between basic and higher brain regions.

Study region: Dongting Lake, Southern China. Study focus: Lakes play a crucial role in Sustainable Development Goal (SDG) 6, which focuses on water-related ecosystems. Here, we devised a methodology to estimate Dongting Lake water storage and analyze their dynamic changes for monitoring SDG 6.6.1 from 2001 to 2020. This study not only provide a geospatial perspective for monitoring water storage for SDG 6.6.1 under the climate oscillations and human impacts in a large floodplain lake but also provide an important scientific basis for improving the optimal allocation of water resources of the Dongting Lake area. New hydrological insights: Remote sensing data are preferable for establishing water storage models during dry seasons, whereas water level is more reliable during wet seasons. Over the past 20 years, average annual water storage in the lake regions has displayed relatively stable fluctuations with an upward trend since 2015. During the wet season, East Dongting Lake has the largest storage capacity, while most of the water resources are concentrated in South Dongting Lake during the dry season. The water storage deviation reached up to 20 %, with a notable negative deviation of more than 10 % during 2011–2015 caused by a severe drought. Related to the stable operation of the Three Gorges Project and the conservation policy initiated by the Chinese government, Dongting Lake is in a stable and recovery period.

Sleep deprivation has been demonstrated to exert widespread and intricate impacts on the brain network. The human brain network is a modular network composed of interconnected nodes. This network consists of provincial hubs and connector hubs, with provincial hubs having diverse connectivities within their own modules, while connector hubs distribute their connectivities across different modules. The latter is crucial for integrating information from various modules and ensuring the normal functioning of the modular brain. However, there has been a lack of systematic investigation into the impact of sleep deprivation on brain connector hubs. In this study, we utilized functional connectivity from resting-state functional magnetic resonance imaging, as well as structural connectivity from diffusion-weighted imaging, to systematically explore the variation of connector hub properties in the cerebral cortex after one night of sleep deprivation. The normalized participation coefficients (PCnorm) were utilized to identify connector hubs. In both the functional and structural networks, connector hubs exhibited a significant increase in average PCnorm, indicating the diversity enhancement of the connector hub following sleep deprivation. This enhancement is associated with increased network cost, reduced modularity, and decreased small-worldness, but enhanced global efficiency. This may potentially signify a compensatory mechanism within the brain following sleep deprivation. The significantly affected connector hubs were primarily observed in both the Control Network and Salience Network. We believe that the observed results reflect the increasing demand on the brain to invest more effort at preventing performance deterioration after sleep loss, in exchange for increased communication efficiency, especially involving systems responsible for neural resource allocation and cognitive control. These results have been replicated in an independent dataset. In conclusion, this study has enhanced our understanding of the compensatory mechanism in the brain response to sleep deprivation. This compensation is characterized by an enhancement in the connector hubs responsible for inter-modular communication, especially those related to neural resource and cognitive control. As a result, this compensation comes with a higher network cost but leads to an improvement in global communication efficiency, akin to a more random-like network manner.

Abstract Aberrant coagulation and thrombosis are associated with severe COVID-19 post-SARS-CoV-2 infection, yet the underlying mechanism remains obscure. Here we show that serum levels of SARS-CoV-2 envelope (E) protein are associated with coagulation disorders of COVID-19 patients, and intravenous administration of the E protein is able to potentiate thrombosis in mice. Through protein pull-down and mass spectrometry, we find that CD36, a transmembrane glycoprotein, directly binds with E protein and mediates hyperactivation of human and mouse platelets through the p38 MAPK-NF-κB signaling pathway. Conversely, the pharmacological blockade of CD36 or p38 notably attenuates human platelet activation induced by the E protein. Similarly, the genetic deficiency of CD36, as well as the pharmacological inhibition of p38 in mice, significantly diminishes E protein-induced platelet activation and thrombotic events. Together, our study reveals a critical role for the CD36-p38 axis in E protein-induced platelet hyperactivity, which could serve as an actionable target for developing therapies against aberrant thrombotic events related to the severity and mortality of COVID-19.

Abstract Background We aimed to address the shortage of evidence regarding the safety of the local resection approach by comparing long-term oncological outcomes between patients managed by local resection and those who underwent radical resection. Methods This was a propensity-score matched cohort analysis study that included patients of all ages diagnosed with locally advanced rectal cancer (LARC) who had received neoadjuvant chemoradiotherapy (nCRT) at the Fujian Medical University Union Hospital and Fujian Medical University Affiliated Zhangzhou Hospital, China, between Jan 10, 2011, to Dec 28, 2021. Partial patients with a significant downstage of the tumor were offered management with the local resection approach, and most of the rest were offered radical resection if eligible. Findings One thousand six hundred ninety-three patients underwent radical resection after nCRT, and another 60 patients performed local resection. The median follow-up times were 44.0 months (interquartile range = 4–107 months). After propensity-core matching (PSM), in the Kaplan–Meier curves, local resection (n = 56) or radical resection (n = 211) was not significantly associated with 1-, 3-, and 5-year cumulative incidence of overall survival (OS) (HR = 1.103, 95% CI: 0.372 ~ 3.266), disease-free survival (DFS) ((HR = 0.972, 95% CI: 0.401 ~ 2.359), local recurrence (HR = 1.044, 95% CI: 0.225 ~ 4.847), and distant metastasis (HR = 0.818, 95% CI: 0.280 ~ 2.387) (all log-rank P > 0.05). Similarly, multivariate Cox regression analysis indicates that local excision still was not an independent risk factor for OS (HR = 0.863, 95% CI: 0.267 ~ 2.785, P = 0.805) and DFS (HR = 0.885, 95% CI: 0.353 ~ 2.215, p = 0.794). Conclusion Local resection can be a management option in selected patients with middle-low rectal cancer after nCRT for LARC and without loss of oncological safety at five years.

Insufficient glucagon signalling results in hyperaminoacidemia, which drives adaptive proliferation of glucagon-producing α cells. Here the authors report that the amino acid sensitive calcium sensing receptor (CaSR) is necessary for α cell proliferation via Gq signalling during hyperaminoacidemia.

Objectives: Pancreatic beta cells secrete insulin postprandially and during fasting to maintain glucose homeostasis. Although glucose-stimulated insulin secretion (GSIS) has been extensively studied, much less is known about basal insulin secretion. Here, we performed a genome-wide CRISPR/Cas9 knockout screen to identify novel regulators of insulin secretion. Methods: To identify genes that cell autonomously regulate insulin secretion, we engineered a Cas9-expressing MIN6 subclone that permits irreversible fluorescence labeling of exocytic insulin granules. Using a fluorescence-activated cell sorting assay of exocytosis in low glucose and high glucose conditions in individual cells, we performed a genome-wide CRISPR/Cas9 knockout screen. Results: We identified several members of the COMMD family, a conserved family of proteins with central roles in intracellular membrane trafficking, as positive regulators of basal insulin secretion, but not GSIS. Mechanistically, we show that the Commander complex promotes insulin granules docking in basal state. This is mediated, at least in part, by its function in ITGB1 recycling. Defective ITGB1 recycling reduces its membrane distribution, the number of focal adhesions and cortical ELKS-containing complexes. Conclusions: We demonstrated a previously unknown function of the Commander complex in basal insulin secretion. We showed that by ITGB1 recycling, Commander complex increases cortical adhesions, which enhances the assembly of the ELKS-containing complexes. The resulting increase in the number of insulin granules near the plasma membrane strengthens basal insulin secretion.

In the previous 10 years, researchers have suggested a critical role for the brain reward system in stress resilience. However, no study has provided an empirical link between activity in the mesostriatal reward regions during stress and the recovery of cortisol stress response. Moreover, although reward sensitivity as a trait has been demonstrated to promote stress resilience, it remains unclear whether it modulates the brain reward system in stress resilience and how this effect is achieved by the inherent neuroendocrine system. To investigate these uncertainties, 70 young adults were recruited to participate in a ScanSTRESS task, and their brain imaging data and saliva samples (for cortisol assay) were collected during the task. In addition, we assessed reward sensitivity, cortisol awakening response, and intrinsic functional connectivity of the brain in all the participants. We found that left putamen activation during stress exposure positively predicted cortisol recovery. In addition, reward sensitivity was positively linked with activation of the left putamen, and this relationship was serially mediated by the cortisol awakening response and right hippocampus-left inferior frontal gyrus intrinsic connectivity. These findings suggest that reward sensitivity modulates reward pathways in stress resilience through the interplay of the diurnal stress response system and network of the hippocampus-prefrontal circuitry. Summarily, the current study built a model to highlight the dynamic and multifaceted interaction between pertinent allostatic factors in the reward-resilience pathway and uncovered new insight into the resilience function of the mesostriatal reward system during stress.

B-cell receptor-associated protein 31 (BAP31) has been shown to overexpress in a wide range type of cancers. The present study aims to investigate the role of BAP31 on migration in lung cancer. Results showed that the migration of BAP31 knockdown cells was weaken than the control cells. Applying TGFβ to treat BAP31 knockdown cells could reduce cell migration. The enhancement on proliferation by TGFβ treatment was downregulated after BAP31 knockdown. The cell death and G0/G1 phase arrest was increased in the cells with TGFβ and BAP31 siRNA treatment when compared with TGFβ treatment alone. Gene expression analysis showed that Bax/Bcl2, MLKL and LC3 was upregulated in the cells with combinatorial treatment of TGFβ and BAP31 siRNA. In addition, BAP31 was shown to regulate multiple signaling pathways, especially for Wnt signaling. It found that BAP31 knockdown cells treated with TGFβ decreased β-catenin cytosolic expression and nuclear localization. Wnt signaling activator BIO could restore the downregulation of proliferation by BAP31 knockdown. This finding suggested that BAP31 regulated cancer cell migration is possibly involved with cell death mechanisms and Wnt signaling.

Magnesium, an essential mineral micronutrient, plays a role in the activation of various transporters and enzymes. The present study aimed to investigate the possibility of applying magnesium to enhance the efficacy of cisplatin which is still ranked as one of the major chemotherapeutic drugs for bladder cancer patients. Results showed that the survival rate and colony formation of bladder cancer cells were reduced by combinatorial treatment with cisplatin and magnesium chloride (MgCl2). The proportion of apoptotic cells was also increased in UC3 bladder cancer cells treated with a combination of cisplatin and MgCl2. Most importantly, a marked decrease in nuclear β-catenin was observed in cells that received cisplatin treatment. In addition, the nuclear β-catenin in cisplatin treated cells was further down-regulated by supplementing MgCl2. 6-bromoindirubin-3′-oxime (BIO), an inhibitor of glycogen synthase kinase-3 (GSK-3) that activates the Wnt/β-catenin signaling pathway by modulating β-catenin activity, was thus applied to further exploit the role of this signaling pathway in magnesium aided cancer treatment. The survival rate of bladder cancer cells was decreased by BIO treatment at concentrations of 1.0, 2.5 and 5.0 μM accompanied by increased β-catenin expression. However, the expression of β-catenin in MgCl2-treated cells was lower than in untreated cells under the same BIO concentration. The expression of cleaved caspase-3, cleaved caspase-9 and microtubule-associated protein 1 light chain 3- II (LC3-II) was highest in cells treated with MgCl2 and 5.0 μM BIO among the examined groups. Our findings reveal that magnesium could contribute to cisplatin-based chemotherapy by moderately regulating the Wnt/β-catenin signaling pathway.

Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by the persistent presence of antiphospholipid antibodies (aPL) and thrombotic or obstetric events. Given the heterogeneity of the clinical manifestations, it is likely that genetic and acquired factors are involved in the pathogenesis of APS. The inherited polymorphisms of the thrombophilic gene, including methylenetetrahydrofolate reductase (MTHFR) C677T, type 1 plasminogen activator inhibitor (PAI-1) 4G/5G, factor V Leiden (FVL) G1691A, prothrombin (PT) G20210A, antithrombin (AT), and fibrinogen (Fg) polymorphisms, were analyzed in 67 aPL(+) patients from the Chinese Han population, including 41 APS patients and 26 persistent aPL carriers. The MTHFR C677T genotypes of 105 healthy controls, and the PAI-1 4G/5G polymorphism of 120 healthy controls, from the Chinese Han population were acquired for this study. Both the MTHFR C677T genotype (χ2 = 10.67, p = 0.004) and C/T allele distribution (χ2 = 5.92, p = 0.019) between the aPL(+) patients and healthy controls were found to be significantly different. Furthermore, we observed that the patients with at least one T allele had a higher risk of arterial thrombosis (CT vs. CC, OR 11.00, p= 0.025; CT + TT vs. CC, OR 10.27, p = 0.018). The C677T mutation of MTHFR is a risk factor for arterial thrombosis in Chinese Han patients with APS.

In the grant-free massive machine-type communication (mMTC) scenario, a key challenge is the joint device activity detection and data decoding. The sporadic nature of mMTC makes compressed sensing a promising solution to the activity detection problem. However, the typical two-phase coherent transmission scheme, which divides channel training and data decoding into two separate phases, suffers performance losses, especially when only a few bits of data are transmitted by each active device. This paper follows a newly proposed non-coherent transmission scheme in which the data bits are embedded in the pilot sequences and the BS simultaneously detects active devices and decodes the embedded data bits without explicit channel estimation. To exploit statistical channel information and the specific structure of the sparsity pattern introduced by the non-coherent transmission scheme, i.e., only one row in each section can be non-zero, we propose a receiving method based on the approximate message passing (AMP) algorithm with non-separable minimum mean-squared error denoisers specifically designed for the problem. The corresponding state evolution equations, which can be used to predict the section error rate (SER) performance, is obtained and simplified under certain assumptions. We also derive closed-form expressions of the SER performance based on the state evolution results. Finally, numerical simulations are given to validate the accuracy of the performance analysis and to show the superiority of the proposed receiving method over the conventional method based on AMP with separable denoisers in the literature.

Geared motor-driven lower limb exoskeletons (LLEs) are widely researched to assist paraplegic patients with spinal cord injury in recovering locomotion ability. In order to achieve a compact exoskeleton joint design while avoiding increasing the mechanical complexity of the exoskeleton frame, this study presents a design of an LLE with compact and modular actuation. A synchronous drive and a gear drive as transmissions are used to distribute hip and knee actuators, respectively, ensuring a compact axial width. The modular design of joint actuators enables it simple to separately design or select the ergonomic exoskeleton frames. A paradigm of the LLE design is comprehensively provided, including the requirement analysis, mechanical, electrical and control system design, which can be a reference of the early development of the exoskeleton prototype. The performance of the LLE is preliminarily validated by the benchtop tests including the closed-loop speed bandwidth test and the swing test and one healthy human subject experiments including walking with the LLE disenabling all motors and walking assisted by the LLE. The results of the benchtop tests validate that the LLE has enough bandwidth of closed-loop speed, satisfactory repeatability, high precision, good antijamming capability and strong torque capacity. The results of the healthy human subject experiments validate a harmonic interaction and a good integration between the user and the ergonomic mechanical system, good performance of the electrical and control system in joints motion control of the LLE. The prototype of the LLE smoothly and successfully assists the healthy human subject in walking on the level ground. The proposed LLE is promising to be applied to assist paraplegic patients in recovering the walking ability.

This paper introduces the analysis, design and preliminary evaluation of a self-integrated parallel elastic actuator (PEA) with an electric motor and a flat spiral spring in parallel to drive the hip joint of lower limb exoskeletons for power-efficient walking assistance. Firstly, we quantitatively analyze the reason why the parallel elasticity (PE) placed at the sagittal hip joint can reduce the motor power requirement during walking assistance, which contributes to the theory of PEA development and application. The design of the PEA is then introduced in detail. The novelty of the design is that the actuator is reduced in size by integrating the spring into the motor, and the requirement of spring stiffness is significantly reduced by placing the spring directly parallel to the motor shaft. Furthermore, both the simulation based on dynamic modeling and benchtop experiment are conducted preliminarily to evaluate the performance of the PEA with nine spring stiffnesses in a range from 0 - 5.29 mN·m/rad regarding two indexes including the average and maximum positive electrical power of the motor. Their results show that the two indexes become smaller when the PE is attached and decrease as the spring stiffness increases. When the PE with a stiffness of 5.29 mN·m/rad is attached, the actuator obtains the largest reduction rate of 11.99 and 16.84 % in the average (root mean square) and maximum positive electrical power of the motor in the simulation and 10.3 and 26.25 % in the experiment, respectively. Those results provide evidence for the applicability of the newly designed PEA in driving a lower limb exoskeleton with high power efficiency during walking assistance for paraplegic patients with complete loss in walking ability.

The catastrophic outbreak of coronavirus disease 2019 (COVID-19) is currently a public emergency. Adult-onset Still’s disease (AOSD) is an autoinflammatory disease characterized by life-threatening complications. Systemic hyperinflammation and cytokine storm play a critical role in the pathogenesis of both COVID-19 and AOSD. We aimed to compare the similarities and differences focusing on ferritin and cytokine levels between severe COVID-19 and active AOSD. A literature search was performed using the databases PubMed, EMBASE, and Web of Science to collect the levels of cytokine including IL-1β, IL-6, IL-18, TNF-α, IL-10, and ferritin in severe COVID-19 patients. After extracting available data of indicators of interest, we acquired these statistics with a single-arm meta-analysis. Furthermore, a comparison was conducted between 52 patients with active AOSD in our center and severe COVID-19 patients from databases. The levels of IL-6 and IL-10 were higher in severe COVID-19 compared with those in active AOSD. There were no significant differences on the cytokine of IL-1β and TNF-α. Fold changes of IL-18 were defined as the mean expression level ratio of severe COVID-19 to healthy controls in the COVID-19 study and active AOSD to healthy controls in our study, individually. Although the fold change of IL-18 in patients with AOSD was significantly higher than patients with severe COVID-19 (fold change: 594.00 vs 2.17), there was no statistical comparability. In addition, the level of ferritin was higher in active AOSD in comparison with severe COVID-19. Our findings suggest that severe COVID-19 and active AOSD have differences in cytokine panel and ferritin level, indicating the pathogenic role of ferritin in overwhelming inflammation. And it paves the way to make efficacy therapeutic strategy targeting the hyperinflammatory process in COVID-19 according to AOSD management, especially in severe COVID-19.

When planning lunar rover missions, it is important to develop intuition and driving skills for unfamiliar environments before incurring the costs of reaching the moon. Simulators make it possible to operate in environments that have the physical characteristics of target locations without the expense of extensive physical tests. This paper proposes a motion simulation and human–computer interaction system based on a parallel mechanism to realize high-fidelity manned lunar rover simulations. The system consists of an interactive operating platform and a lunar surface simulation environment based on Unity3D. To make the 6-DOF platform simulate the posture changes of the rover, we improved the motion simulation algorithm. We designed a posture adjustment system and built virtual sensors to help astronauts perceive the lunar environment. Finally, this paper discusses the method for the realization of the multi-channel human–computer interaction system; astronauts can interactively control the rover through five channels. Experiments show that this system can realize high-fidelity rover simulation and improve the efficiency of human-computer interaction.

Surface property is an important factor that is widely considered in crystal growth and design. It is also found to play a critical role in changing the constitutive law seen in the classical elasticity theory for nanomaterials. Through molecular static simulations, this work presents the calculation of surface properties (surface energy density, surface stress and surface stiffness) of some typical cubic and hexagonal crystals: face-centered-cubic (FCC) pure metals (Cu, Ni, Pd and Ag), body-centered-cubic (BCC) pure metals (Mo and W), diamond Si, zincblende GaAs and GaN, hexagonal-close-packed (HCP) pure metals (Mg, Zr and Ti), and wurzite GaN. Sound agreements of the bulk and surface properties between this work and the literature are found. New results are first reported for the surface stiffness of BCC pure metals, surface stress and surface stiffness of HCP pure metals, Si, GaAs and GaN. Comparative studies of the surface properties are carried out to uncover trends in their behaviors. The results in this work could be helpful to the investigation of material properties and structure performances of crystals.

Acute lung injury (ALI) is a severe clinical disease marked by dysregulated inflammation response and has a high rate of morbidity and mortality. Macrophages, which play diverse roles in the inflammatory response, are becoming therapeutic targets in ALI. In this study we investigated the effects of dehydrocostus lactone (DHL), a natural sesquiterpene, on macrophage activation and LPS-induced ALI. The macrophage cell line RAW264.7 and primary lung macrophages were incubated with DHL (0, 3, 5, 10 and 30 μmol/L) for 0.5 h and then challenged with LPS (100 ng/mL) for up to 8 hours. C57BL/6 mice were intratracheally injected with LPS (5 mg/kg) to induce acute lung injury (ALI) and then treated with a range of DHL doses intraperitoneally (5 to 20 mg/kg). The results showed that DHL inhibited LPS-induced production of proinflammatory mediators such as iNOS, NO, and cytokines including TNF-α, IL-6, IL-1β, and IL-12 p35 by suppressing the activity of NF-κB via p38 MAPK/MK2 and Akt signaling pathway in macrophages. The in vivo results revealed that DHL significantly attenuated LPS-induced pathological injury and reduced cytokines expression in the lung. NF-κB, p38 MAPK/MK2 and Akt signaling molecules were also involved in the anti-inflammatory effect. Collectively, our findings suggested that DHL is a promising agent for alleviating LPS-induced ALI.