Fluorine-Modulated MXene-Derived Catalysts for Multiphase Sulfur Conversion in Lithium-Sulfur Battery.

Fluorine owing to its inherently high electronegativity exhibits charge delocalization and ion dissociation capabilities; as a result, there has been an influx of research studies focused on the utilization of fluorides to optimize solid electrolyte interfaces and provide dynamic protection of electrodes to regulate the reaction and function performance of batteries. Nonetheless, the shuttle effect and the sluggish redox reaction kinetics emphasize the potential bottlenecks of lithium-sulfur batteries. Whether fluorine modulation regulate the reaction process of Li-S chemistry? Here, the TiOF/TiC MXene nanoribbons with a tailored F distribution were constructed via an NHF fluorinated method.

MXene materials in electrochemical energy storage systems.

MXenes, due to their unique geometric structure, rich elemental composition, and intrinsic physicochemical properties, have multi-functional applications. In the field of electrochemical energy storage, MXenes can be used as active components, conductive agents, supports, and catalysts in ion-intercalated batteries, metal-sulfur batteries, and supercapacitors. The electrochemical performance of MXene materials is closely related to their distinctive physical and chemical properties, which depend on their geometry, surface functional groups, and elemental composition.

Architecture of integrated solid-state zinc-ion battery based on sodium alginate gelation.

How to construct a new electrode/electrolyte interface structure in solid-state batteries (SSBs), enhance interface stability, and improve the cycling performance of SSBs is a great challenge for the development of SSBs. Here, an all-in-one "interface-free" structure was developed. This interfacial structure constructs a full-interface hydrogen bonding network through the abundant hydrogen bond donors and acceptors in the cathode and electrolyte to enhance the interfacial stability and avoid interfacial failure during charging and discharging, and generates cathode-electrolyte interface (CEI) in-situ to effectively regulate zinc ion transport.

Dendritic distribution of autophagosomes underlies pathway-selective induction of LTD.

The mechanism of long-term depression (LTD), a cellular substrate for learning, memory, and behavioral flexibility, is extensively studied in Schaffer collateral (SC) synapses, with inhibition of autophagy identified as a key factor. SC inputs terminate at basal and proximal apical dendrites, whereas distal apical dendrites receive inputs from the temporoammonic pathway (TAP). Here, we demonstrate that TAP and SC synapses have a shared LTD mechanism reliant on NMDA receptors, caspase-3, and autophagy inhibition.

CoO nanoparticles loaded on carbon spheres with synergistic effects for effective inhibition of shuttle effect in Li-S batteries.

Lithium-sulfur (Li-S) batteries, as one of the new energy storage batteries, show immense potential due to their high theoretical specific capacity and theoretical energy density. However, there are still some problems to be solved, among which the shuttle effect of lithium polysulfides is one extremely serious issue with respect to the industrial application of Li-S batteries. Rational design of electrode materials with effective catalytic conversion ability is an effective route to accelerate the conversion of lithium polysulfides (LiPSs).

Cobalt Nanoparticles Loaded on MXene for Li-S Batteries: Anchoring Polysulfides and Accelerating Redox Reactions.

Catalysis is regarded as an effective strategy to fundamentally increase sulfur utilization, accelerating the kinetics of the transformation between lithium polysulfides (LiPSs) and lithium sulfide (Li S) on a substrate. However, the intermodulation of catalysts and sulfur species is elusive, which is limited to the comprehensive analysis of electrochemical performance in the dynamic reaction process. Herein, cobalt nanoparticles loaded on MXene nanosheets (Co/Ti C) are selected as sulfur hosts and the representative catalyst.

Analysis of Th-cell subsets in local and systemic environments from experimental periodontitis rats.

Objectives: The objective of this study was to explore the effect of periodontitis on Th-cell subsets in local and systemic environments.

Methods: A total of 32 male Sprague-Dawley rats were randomly divided into periodontitis and control groups. Silk ligatures were applied to the mandibular first (M1) molars in the periodontitis group.

Enucleation combined with guided bone regeneration in small and medium-sized odontogenic jaw cysts.

Background: The odontogenic jaw cyst is a cavity containing liquid, semifluid or gaseous components, with the development of the disease. In recent years, with the rapid development of oral materials and the transformation of treatment of jaw cysts, more options are available for treatment of postoperative bone defect of jaw cysts. Guided bone regeneration (GBR) places biomaterials in the bone defect, and then uses biofilm to separate the proliferative soft tissue and the slow-growing bone tissue to maintain the space for bone regeneration, which is widely used in the field of implantology.

Mitophagy in the basolateral amygdala mediates increased anxiety induced by aversive social experience.

Psychosocial stress is a common risk factor for anxiety disorders. The cellular mechanism for the anxiogenic effect of psychosocial stress is largely unclear. Here, we show that chronic social defeat (CSD) stress in mice causes mitochondrial impairment, which triggers the PINK1-Parkin mitophagy pathway selectively in the amygdala.

Dysbindin-1 regulates mitochondrial fission and gamma oscillations.

Mitochondria are cellular ATP generators. They are dynamic structures undergoing fission and fusion. While much is known about the mitochondrial fission machinery, the mechanism of initiating fission and the significance of fission to neurophysiology are largely unclear.

The BAD-BAX-Caspase-3 Cascade Modulates Synaptic Vesicle Pools via Autophagy.

The BAD-BAX-caspase-3 cascade is a canonical apoptosis pathway. Macroautophagy ("autophagy" hereinafter) is a process by which organelles and aggregated proteins are delivered to lysosomes for degradation. Here, we report a new function of the BAD-BAX-caspase-3 cascade and autophagy in the control of synaptic vesicle pools.

Autophagy controls the induction and developmental decline of NMDAR-LTD through endocytic recycling.

NMDA receptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form of synaptic plasticity. Its expression is mediated by the removal of AMPA receptors from postsynaptic membranes. Under basal conditions, endocytosed AMPA receptors are rapidly recycled back to the plasma membrane.

Potentiation of Divergent Medial Amygdala Pathways Drives Experience-Dependent Aggression Escalation.

Heightened aggression can be serious concerns for the individual and society at large and are symptoms of many psychiatric illnesses, such as post-traumatic stress disorder. The circuit and synaptic mechanisms underlying experience-induced aggression increase, however, are poorly understood. Here we find that prior attack experience leading to an increase in aggressive behavior, known as aggression priming, activates neurons within the posterior ventral segment of the medial amygdala (MeApv).

Clinical significance of nuclear localisation of agrin in lung adenocarcinoma.

Agrin has recently been identified as a novel oncogene that is overexpressed in several types of human cancers. However, its role in lung cancer has not yet been investigated. The purpose of the current study was to investigate agrin protein expression in lung cancer and evaluate its clinicopathological and prognostic significance.

Effects of the presence and absence of amino acids on translation, signaling, and long-term depression in hippocampal slices from Fmr1 knockout mice.

Fragile X syndrome (FXS) is caused by silencing of the FMR1 gene and consequent absence of its protein product, fragile X mental retardation protein (FMRP). FMRP is an RNA-binding protein that can suppress translation. The absence of FMRP leads to symptoms of FXS including intellectual disability and has been proposed to lead to abnormalities in synaptic plasticity.

MiR-27a targets DKK2 and SFRP1 to promote reosseointegration in the regenerative treatment of peri-implantitis.

In the inflamed microenvironment of peri-implantitis, limited osteogenesis on the implant surface impedes well-established reosseointegration using current clinical therapies. MicroRNAs (miRNAs) function as potent molecular managers that may simultaneously regulate multiple endogenous processes such as inflammation and osteogenesis. The delivery of miRNAs may provide a way to effectively treat some diseases.

MicroRNA sequence analysis identifies microRNAs associated with peri-implantitis in dogs.

Peri-implantitis, which is characterized by dense inflammatory infiltrates and increased osteoclast activity, can lead to alveolar bone destruction and implantation failure. miRNAs participate in the regulation of various inflammatory diseases, such as periodontitis and osteoporosis. Therefore, the present study aimed to investigate the differential expression of miRNAs in canine peri-implantitis and to explore the functions of their target genes.

miR-26a and miR-384-5p are required for LTP maintenance and spine enlargement.

Long-term potentiation (LTP) is a form of synaptic plasticity that results in enhanced synaptic strength. It is associated with the formation and enlargement of dendritic spines-tiny protrusions accommodating excitatory synapses. Both LTP and spine remodelling are crucial for brain development, cognition and the pathophysiology of neurological disorders.

NMDA receptor-dependent LTD is required for consolidation but not acquisition of fear memory.

NMDA receptor-dependent long-term depression (NMDAR-LTD) is a form of synaptic plasticity leading to long-lasting decreases in synaptic strength. NMDAR-LTD is essential for spatial and working memory, but its role in hippocampus-dependent fear memory has yet to be determined. Induction of NMDAR-LTD requires the activation of caspase-3 by cytochrome c.

miR-191 and miR-135 are required for long-lasting spine remodelling associated with synaptic long-term depression.

Activity-dependent modification of dendritic spines, subcellular compartments accommodating postsynaptic specializations in the brain, is an important cellular mechanism for brain development, cognition and synaptic pathology of brain disorders. NMDA receptor-dependent long-term depression (NMDAR-LTD), a prototypic form of synaptic plasticity, is accompanied by prolonged remodelling of spines. The mechanisms underlying long-lasting spine remodelling in NMDAR-LTD, however, are largely unclear.

Electrophysiological effects of SKF83959 on hippocampal CA1 pyramidal neurons: potential mechanisms for the drug's neuroprotective effects.

Although the potent anti-parkinsonian action of the atypical D₁-like receptor agonist SKF83959 has been attributed to the selective activation of phosphoinositol(PI)-linked D₁ receptor, whereas the mechanism underlying its potent neuroprotective effect is not fully understood. In the present study, the actions of SKF83959 on neuronal membrane potential and neuronal excitability were investigated in CA1 pyramidal neurons of rat hippocampal slices. SKF83959 (10-100 µM) caused a concentration-dependent depolarization, associated with a reduction of input resistance in CA1 pyramidal neurons.

Metaplastic regulation of long-term potentiation/long-term depression threshold by activity-dependent changes of NR2A/NR2B ratio.

In vivo experience induces changes in synaptic NMDA receptor (NMDAR) subunit components, which are correlated with subsequent modifications of synaptic plasticity. However, little is known about how these subunit changes regulate the induction threshold of subsequent plasticity. At hippocampal Schaffer collateral-CA1 synapses, we first examined whether a recent history of neuronal activity could affect subsequent synaptic plasticity through its actions on NMDAR subunit components.

Distinct trafficking and expression mechanisms underlie LTP and LTD of NMDA receptor-mediated synaptic responses.

Although an increasing number of studies have demonstrated the plasticity of NMDA receptor-mediated synaptic transmission, little is known about the molecular mechanisms that underlie this neurologically important process. In a study of NMDAR-mediated synaptic responses in hippocampal Schaffer-CA1 synapses whose AMPA receptor (AMPAR) activity is totally blocked, we uncovered differences between the trafficking mechanisms that underlie the long-term potentiation (LTP) and long-term depression (LTD) that can be induced in these cells under these conditions. The LTP-producing protocol failed to induce a change in the amplitude of NMDAR-mediated postsynaptic currents (NMDAR EPSCs) in the first 5-10 min, but induced gradual enhancement of NMDAR EPSCs thereafter that soon reached a stable magnitude.

Synaptic metaplasticity through NMDA receptor lateral diffusion.

Lateral diffusion of glutamate receptors was proposed as a mechanism for regulating receptor numbers at synapses and affecting synaptic functions, especially the efficiency of synaptic transmission. However, a direct link between receptor lateral diffusion and change in synaptic function has not yet been established. In the present study, we demonstrated NMDA receptor (NMDAR) lateral diffusion in CA1 neurons in hippocampal slices by detecting considerable recovery of spontaneous or evoked EPSCs from the block of (+)-MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate], an irreversible NMDAR open-channel blocker.