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Abstract The development of highly efficient and durable alkaline hydrogen evolution reaction (HER) catalysts is crucial for achieving high-performance practical anion exchange membrane water electrolyzer (AEMWE) at ampere-level current density. Herein, we report a design concept by employing Ga single atoms as an electronic bridge to stabilize the Ru clusters for boosting alkaline HER performance in practical AEMWE. Experimental and theoretical results collectively reveal that the bridged Ga sites trigger strong metal-support interaction for the homogeneous distribution of Ru clusters with high density, as well as optimize the Ru–H bond strength due to the electron transfer between Ru and Ga for enhanced intrinsic HER activity. Moreover, the oxophilic Ga sites near the Ru clusters tend to adsorb the hydroxyl species and accelerate the water dissociation for sufficient proton supplement in an alkaline medium. The Ru–GaSA/N–C catalyst exhibits a low overpotential of 4 ± 1 mV (10 mA cm−2) and high mass activity of 9.3 ± 0.5 A mg−1 Ru at −0.05 V vs RHE. In particular, the Ru–GaSA/N–C-based AEMWE in 1 M KOH delivers a voltage of only 1.74 V to reach an industrial current density of 1 A cm−2, and can steadily operate at 1 A cm−2 for more than 170 h.

Unmanned aerial vehicle (UAV) confrontation scenarios play a crucial role in the study of agent behavior selection and decision planning. Multi-agent reinforcement learning (MARL) algorithms serve as a universally effective method guiding agents toward appropriate action strategies. They determine subsequent actions based on the state of the agents and the environmental information that the agents receive. However, traditional MARL settings often result in one party agent consistently outperforming the other party due to superior strategies, or both agents reaching a strategic stalemate with no further improvement. To solve this issue, we propose a semi-static deep deterministic policy gradient algorithm based on MARL. This algorithm employs a centralized training and decentralized execution approach, dynamically adjusting the training intensity based on the comparative strengths and weaknesses of both agents’ strategies. Experimental results show that during the training process, the strategy of the winning team drives the losing team’s strategy to upgrade continuously, and the relationship between the winning team and the losing team keeps changing, thus achieving mutual improvement of the strategies of both teams. The semi-static reinforcement learning algorithm improves the win-loss relationship conversion by 8% and reduces the training time by 40% compared with the traditional reinforcement learning algorithm.

ABSTRACT: The study investigated the effects of feed efficiency (residual feed intake, RFI and residual intake and gain, RIG) on the production performance of small-sized meat ducks. Ninety ducks with intermediate and extreme (high and low) RFI values were selected from 1,083 male ducks of similar body weight, and the 3 groups were then redivided according to RIG. For both efficiency measures, the feed conversion ratio (FCR) and average daily feed intake (ADFI) of efficient ducks were significantly lower than those of inefficient ducks (P < 0.05), while the residual body weight gain (RG) was significantly higher in efficient ducks (P < 0.05). Inefficient-RFI animals showed greater skin fat yield (P < 0.05), but no other differences in carcass traits were observed (P > 0.05). RIG had positive effects on the pH1 value of the breast muscle (P < 0.05), but feed efficiency did not affect the other meat quality traits (P > 0.05). With regard to blood biochemical parameters, efficient ducks had significantly lower triglycerides (TG) (P < 0.05). Correlation analysis demonstrated that RFI was positively correlated with average daily feed intake and feed conversion ratio (P < 0.05), while RIG exhibited a strong negative correlation with both (P < 0.05). The average daily body weight gain was positively correlated with RIG (P < 0.05). RIG had a positive effect on the pH1 value of the breast muscle (P < 0.05). Furthermore, triglyceride and high-density lipoprotein cholesterol levels correlated with both efficiency classifications (P < 0.05). Overall, the efficiency measures did not affect the carcass and meat quality of small-sized meat ducks but could identify ducks with lower feed consumption and fast growth.

GluN2A and GluN2B, two predominant Glu2N subunits of NMDARs in hippocampus and cortex, display distinct organization and mobility in the neuronal surface. Here, authors show Rph3A, a GluN2A-specific binding protein, undergoes liquid-liquid phase separation, which regulate mobility, synaptic and extrasynaptic surface clustering, synaptic localization and synaptic response of GluN2A.

Swarm models hold significant importance as they provide the collective behavior of self-organized systems. Boids model is a fundamental framework for studying emergent behavior in swarms systems. It addresses problems related to simulating the emergent behavior of autonomous agents, such as alignment, cohesion, and repulsion, to imitate natural flocking movements. However, traditional models of Boids often lack pinning and the adaptability to quickly adapt to the dynamic environment. To address this limitation, we introduce reinforcement learning into the framework of Boids to solve the problem of disorder and the lack of pinning. The aim of this approach is to enable drone swarms to quickly and effectively adapt to dynamic external environments. We propose a method based on the Q-learning network to improve the cohesion and repulsion parameters in the Boids model to achieve continuous obstacle avoidance and maximize spatial coverage in the simulation scenario. Additionally, we introduce a virtual leader to provide pinning and coordination stability, reflecting the leadership and coordination seen in drone swarms. To validate the effectiveness of this method, we demonstrate the model’s capabilities through empirical experiments with drone swarms, and show the practicality of the RL-Boids framework.

A tunable and efficient strategy was adopted to synthesize highly porous nano-structured CuO−carbonized composites (CuxO@C) using Cu3(BTC)2 as a sacrificial template. The as-synthesized CuO nanocomposites exhibited hollow octahedral structures, a large surface area (89.837 m2 g−1) and a high proportion of Cu2O active sites distributed on a carbon frame. Based on DFT calculations, both the Cu atoms on the surface (CuS) and oxygen vacancy (OV) exhibited strong chemical reactivity. On the perfect CuO (111), the CuS transferred charge to O atoms on the surface and SO2 molecules. A strong adsorption energy (−1.41 eV) indicated the existence of the chemisorption process. On the oxygen-deficient CuO (111), the O2 preferably adsorbed on OV and then formed SO3 by bonding with SO2, followed by the cleavage of the O−O bond. Furthermore, the CuO nanocomposites exhibited an excellent ratio of S/Cu in SO2 removal experiments compared with CuO nanoparticles produced by coprecipitation.

Neuromuscular junction is a synapse between motoneurons and skeletal muscles, where acetylcholine receptors (AChRs) are concentrated to control muscle contraction. Studies of this synapse have contributed to our understanding of synapse assembly and pathological mechanisms of neuromuscular disorders. Nevertheless, underlying mechanisms of NMJ formation was not well understood. To this end, we took a novel approach – studying mutant genes implicated in congenital myasthenic syndrome (CMS). We showed that knock-in mice carrying N88K, a prevalent CMS mutation of Rapsyn (Rapsn), died soon after birth with profound NMJ deficits. Rapsn is an adapter protein that bridges AChRs to the cytoskeleton and possesses E3 ligase activity. In investigating how N88K impairs the NMJ, we uncovered a novel signaling pathway by which Agrin-LRP4-MuSK induces tyrosine phosphorylation of Rapsn, which is required for its self-association and E3 ligase activity. Our results also provide insight into pathological mechanisms of CMS.

Adult neurogenesis in the hippocampus may represent a form of plasticity in brain functions including mood, learning and memory. However, mechanisms underlying neural stem/progenitor cells (NSPCs) proliferation are not well understood. We found that Agrin, a factor critical for neuromuscular junction formation, is elevated in the hippocampus of mice that are stimulated by enriched environment (EE). Genetic deletion of the Agrn gene in excitatory neurons decreases NSPCs proliferation and increases depressive-like behavior. Low-density lipoprotein receptor-related protein 4 (Lrp4), a receptor for Agrin, is expressed in hippocampal NSPCs and its mutation blocked basal as well as EE-induced NSPCs proliferation and maturation of newborn neurons. Finally, we show that Lrp4 interacts with and activates receptor tyrosine kinase-like orphan receptor 2 (Ror2); and Ror2 mutation impairs NSPCs proliferation. Together, these observations identify a role of Agrin-Lrp4-Ror2 signaling for adult neurogenesis, uncovering previously unexpected functions of Agrin and Lrp4 in the brain.

High-quality oxidized pellets are the basis to achieve high-efficiency utilization of vanadium–titanium magnetite (VTM) ores. Bentonite was used as a binder of VTM. The main phase composition of VTM is titanomagnetite and ilmenite. When the amount of bentonite is 1%, the compressive strength and dropping strength of VTM pellets can meet the requirements. To improve metallurgical properties, the pellets need to be roasted. The best conditions for roasting are as follows: calcination temperature of 1523 K and a calcination time of 20 min. The consolidation mechanism, phase transformation, and crystal structure transformation of VTM in the process of oxidation roasting are also explained.

The dopaminergic neuromodulator system is fundamental to brain functions. Abnormal dopamine (DA) pathway is implicated in psychiatric disorders, including schizophrenia (SZ) and autism spectrum disorder (ASD). Mutations in Cullin 3 (CUL3), a core component of the Cullin-RING ubiquitin E3 ligase complex, have been associated with SZ and ASD. However, little is known about the function and mechanism of CUL3 in the DA system. Here, we show that CUL3 is critical for the function of DA neurons and DA-relevant behaviors in male mice. CUL3-deficient mice exhibited hyperactive locomotion, deficits in working memory and sensorimotor gating, and increased sensitivity to psychostimulants. In addition, enhanced DA signaling and elevated excitability of the VTA DA neurons were observed in CUL3-deficient animals. Behavioral impairments were attenuated by dopamine D2 receptor antagonist haloperidol and chemogenetic inhibition of DA neurons. Furthermore, we identified HCN2, a hyperpolarization-activated and cyclic nucleotide-gated channel, as a potential target of CUL3 in DA neurons. Our study indicates that CUL3 controls DA neuronal activity by maintaining ion channel homeostasis and provides insight into the role of CUL3 in the pathogenesis of psychiatric disorders. [ABSTRACT FROM AUTHOR]

Wnt signaling plays a critical role in production and differentiation of neurons and undergoes a progressive reduction during cortical development. However, how Wnt signaling is regulated is not well understood. Here we provide evidence for an indispensable role of neddylation, a ubiquitylation-like protein modification, in inhibiting Wnt/β-catenin signaling. We show that β-catenin is neddylated; and inhibiting β-catenin neddylation increases its nuclear accumulation and Wnt/β-catenin signaling. To test this hypothesis in vivo, we mutated Nae1, an obligative subunit of the E1 for neddylation in cortical progenitors. The mutation leads to eventual reduction in radial glia progenitors (RGPs). Consequently, the production of intermediate progenitors (IPs) and neurons is reduced, and neuron migration is impaired, resulting in disorganization of the cerebral cortex. These phenotypes are similar to those of β-catenin gain-of-function mice. Finally, suppressing β-catenin expression is able to rescue deficits of Nae1 mutant mice. Together, these observations identified a mechanism to regulate Wnt/β-catenin signaling in cortical development. [ABSTRACT FROM AUTHOR]

Amyloid-β (Aβ) deposition occurs years before cognitive symptoms appear and is considered a cause of Alzheimer's disease (AD). The imbalance of Aβ production and clearance leads to Aβ accumulation and Aβ deposition. Increasing evidence indicates an important role of astrocytes, the most abundant cell type among glial cells in the brain, in Aβ clearance. We explored the role of low-density lipoprotein receptor-related protein 4 (LRP4), a member of the LDLR family, in AD pathology. We show that Lrp4 is specifically expressed in astrocytes and its levels in astrocytes were higher than those of Ldlr and Lrp1, both of which have been implicated in Aβ uptake. LRP4 was reduced in postmortem brain tissues of AD patients. Genetic deletion of the Lrp4 gene augmented Aβ plaques in 5xFAD male mice, an AD mouse model, and exacerbated the deficits in neurotransmission, synchrony between the hippocampus and PFC, and cognition. Mechanistically, LRP4 promotes Aβ uptake by astrocytes likely by interacting with ApoE. Together, our study demonstrates that astrocytic LRP4 plays an important role in Aβ pathology and cognitive function. [ABSTRACT FROM AUTHOR]

Neurotrophic factor NRG1 and its receptor ErbB4 play a role in GABAergic circuit assembly during development. ErbB4 null mice possess fewer interneurons, have decreased GABA release, and show impaired behavior in various paradigms. In addition, NRG1 and ErbB4 have also been implicated in regulating GABAergic transmission and plasticity in matured brains. However, current ErbB4 mutant strains are unable to determine whether phenotypes in adult mutant mice result from abnormal neural development. This important question, a glaring gap in understanding NRG1-ErbB4 function, was addressed by using two strains of mice with temporal control of ErbB4 deletion and expression, respectively. We found that ErbB4 deletion in adult mice impaired behavior and GABA release but had no effect on neuron numbers and morphology. On the other hand, some deficits due to the ErbB4 null mutation during development were alleviated by restoring ErbB4 expression at the adult stage. Together, our results indicate a critical role of NRG1-ErbB4 signaling in GABAergic transmission and behavior in adulthood and suggest that restoring NRG1- ErbB4 signaling at the postdevelopmental stage might benefit relevant brain disorders. [ABSTRACT FROM AUTHOR]

During aging, acetylcholine receptor (AChR) clusters become fragmented and denervated at the neuromuscular junction (NMJ). Underpinning molecular mechanisms are not well understood. We showed that LRP4, a receptor for agrin and critical for NMJ formation and maintenance, was reduced at protein level in aged mice, which was associated with decreased MuSK tyrosine phosphorylation, suggesting compromised agrin-LRP4-MuSK signaling in aged muscles. Transgenic expression of LRP4 in muscles alleviated AChR fragmentation and denervation and improved neuromuscular transmission in aged mice. LRP4 ubiquitination was augmented in aged muscles, suggesting increased LRP4 degradation as a mechanism for reduced LRP4. We found that sarcoglycan α (SGα) interacted with LRP4 and delayed LRP4 degradation in cotransfected cells. AAV9-mediated expression of SGα in muscles mitigated AChR fragmentation and denervation and improved neuromuscular transmission in aged mice. These observations support a model where compromised agrin- LRP4-MuSK signaling serves as a pathological mechanism of age-related NMJ decline and identify a novel function of SGa in stabilizing LRP4 for NMJ stability in aged mice. [ABSTRACT FROM AUTHOR]

The excitability of interneurons requires Nav1.1, the α subunit of the voltage-gated sodium channel. Nav1.1 deficiency and mutations reduce interneuron excitability, a major pathological mechanism for epilepsy syndromes. However, the regulatory mechanisms of Nav1.1 expression remain unclear. Here, we provide evidence that neddylation is critical to Nav1.1 stability. Mutant mice lacking Nae1, an obligatory component of the E1 ligase for neddylation, in parvalbumin-positive interneurons (PVINs) exhibited spontaneous epileptic seizures and premature death. Electrophysiological studies indicate that Nae1 deletion reduced PVIN excitability and GABA release and consequently increased the network excitability of pyramidal neurons (PyNs). Further analysis revealed a reduction in sodium-current density, not a change in channel property, in mutant PVINs and decreased Nav1.1 protein levels. These results suggest that insufficient neddylation in PVINs reduces Nav1.1 stability and thus the excitability of PVINs; the ensuing increased PyN activity causes seizures in mice. Consistently, Nav1.1 was found reduced by proteomic analysis that revealed abnormality in synapses and metabolic pathways. Our findings describe a role of neddylation in maintaining Nav1.1 stability for PVIN excitability and reveal what we believe is a new mechanism in the pathogenesis of epilepsy. [ABSTRACT FROM AUTHOR]