In Situ Preparation of rGO-Cement Using Thermal Reduction Method and Performance Study.

In this study, the combination of freeze-drying and high-temperature thermal reduction methods was employed to in situ prepare reduced graphene oxide (rGO)-Cement based on graphene oxide (GO)-Cement. The electrical conductivity and mechanical properties of the rGO-Cement were investigated. Microscopic analysis methods such as Raman spectra, X-ray photoelectron spectroscopy (XPS), and scanning electron microscopy (SEM) were used to confirm the successful transformation of GO-Cement to rGO-Cement. The research results demonstrated that with an increase in rGO content, the electrical resistivity of the rGO-Cement decreased first and then increased, reaching a percolation threshold at the dosage of 0.7 wt.%. The compressive strength and flexural strength of the rGO-Cement increased first and then decreased. The optimal dosage of rGO was 0.7%. The in situ preparation of rGO-Cement using the thermal reduction method holds a great potential for various applications, providing new ideas and methods for the modification and enhancement of cement materials.

Noteworthy perspectives on microglia in neuropsychiatric disorders.

Microglia are so versatile that they not only provide immune surveillance for central nervous system, but participate in neural circuitry development, brain blood vessels formation, blood-brain barrier architecture, and intriguingly, the regulation of emotions and behaviors. Microglia have a profound impact on neuronal survival, brain wiring and synaptic plasticity. As professional phagocytic cells in the brain, they remove dead cell debris and neurotoxic agents via an elaborate mechanism. The functional profile of microglia varies considerately depending on age, gender, disease context and other internal or external environmental factors. Numerous studies have demonstrated a pivotal involvement of microglia in neuropsychiatric disorders, including negative affection, social deficit, compulsive behavior, fear memory, pain and other symptoms associated with major depression disorder, anxiety disorder, autism spectrum disorder and schizophrenia. In this review, we summarized the latest discoveries regarding microglial ontogeny, cell subtypes or state spectrum, biological functions and mechanistic underpinnings of emotional and behavioral disorders. Furthermore, we highlight the potential of microglia-targeted therapies of neuropsychiatric disorders, and propose outstanding questions to be addressed in future research of human microglia.

Esketamine ameliorates post-stroke anxiety by modulating microglial HDAC3/NF-κB/COX1 inflammatory signaling in ischemic cortex.

Post-stroke anxiety (PSA) is a kind of affective disorder occurring after a stroke, with anxiety as the primary clinical manifestation. PSA's mechanism is unclear, and there are few prevention and treatment measures. Our previous study found that HDAC3 could activate NF-κB signaling through mediated p65 deacetylation, which further influenced microglia activation. That implies HDAC3 may be the key mediator in ischemic stroke mice and modulates anxiety susceptibility to stress. This study established a PSA model in male C57BL/6 mice through photothrombotic stroke combined with chronic restrain stress. We focused on exploring whether esketamine administration can alleviate anxiety-like behavior and neuroinflammation, which may be associated with inhibiting HDAC3 expression and NF-κB pathway activation. The results showed that esketamine administration alleviated anxiety-like behavior in PSA mice. And the results showed that esketamine alleviated cortical microglial activation, altered microglial number, and kept morphology features. Furthermore, the results showed that the expression of HDAC3, phosphor-p65/p65, and COX1 significantly decreased in esketamine-treated PSA mice. Besides, we also found that esketamine reduced PGE2 expression, one of the primary regulators of negative emotions. Interestingly, our results indicate that esketamine reduced the perineuronal net (PNN) number in the pathological process of PSA. In conclusion, this study suggests esketamine could alleviate microglial activation, reduces inflammatory cytokine, and inhibits the expression of HDAC3 and NF-κB in the cortex of PSA mice to attenuate anxiety-like behavior. Our results provided a new potential therapeutic target for applying esketamine to PSA.

The role of gamma oscillations in central nervous system diseases: Mechanism and treatment.

Gamma oscillation is the synchronization with a frequency of 30-90 Hz of neural oscillations, which are rhythmic electric processes of neuron groups in the brain. The inhibitory interneuron network is necessary for the production of gamma oscillations, but certain disruptions such as brain inflammation, oxidative stress, and metabolic imbalances can cause this network to malfunction. Gamma oscillations specifically control the connectivity between different brain regions, which is crucial for perception, movement, memory, and emotion. Studies have linked abnormal gamma oscillations to conditions of the central nervous system, including Alzheimer's disease, Parkinson's disease, and schizophrenia. Evidence suggests that gamma entrainment using sensory stimuli (GENUS) provides significant neuroprotection. This review discusses the function of gamma oscillations in advanced brain activities from both a physiological and pathological standpoint, and it emphasizes gamma entrainment as a potential therapeutic approach for a range of neuropsychiatric diseases.

HDAC3-Regulated PGE2 Production by Microglia Induces Phobic Anxiety Susceptibility After Stroke and Pointedly Exploiting a Signal-Targeted Gamma Visual Stimulation New Therapy.

BACKGROUND: Phobic anxiety present after stroke (called poststroke anxiety, PSA) can hamper the rehabilitation of patients and disrupt their usual activities. Besides, the symptoms and mechanisms of PSA are different from those in nonstroke populations that have generalized anxiety disorder. What's more, the treatment approaches for phobic anxiety are confined to unitary or general methods with poor efficiency. METHODS: Behavioural test screen combined bioinformatics analysis explored molecular changes between generalized anxiety disorder in nonstroke mice (restraint stress, RS) and photothrombotic stroke mice exposed to environmental stress (PTS + RS, mimicking PSA). Multiple molecular biological and neurobiological methods were employed to explain mechanisms in vitro and in vivo. And exploiting gamma flicker stimulation device for therapy. RESULTS: Microglial (MG) overactivation is a prominent characteristic of PTS + RS. HDAC3 was mainly upregulated in activated-microglia from damaged cortex and that local prostaglandin E2 (PGE2) production increased in MG via HDAC3-mediated activation of NF-κB signalling by p65 deacetylation. A high content of PGE2 in damaged ischaemic cortex could diffuse freely to amygdala, eliciting anxiety susceptibility of PSA via EP2. Importantly, gamma flicker stimulation relieved anxious behaviour of PTS + RS by modulating the HDAC3/Cox1/EP2 network at some extent. CONCLUSIONS: HDAC3-regulated PGE2 production by microglia constitutes phobic anxiety susceptibility after stroke and a protective approach of gamma visual stimulation can be a candidate new therapy.

The triple role of rongalite in aminosulfonylation of aryldiazonium tetrafluoroborates: synthesis of N-aminosulfonamides via a radical coupling reaction.

A simple and convenient method for N-aminosulfonamide synthesis from the cross-coupling of aryldiazonium tetrafluoroborates and rongalite under metal-free, oxidant-free, and room-temperature conditions is reported. This method does not require an external amine source, with the aryldiazonium tetrafluoroborates participating as both an aryl radical and a potential amine source in the transformation. Mechanistic studies revealed that rongalite could act as a radical initiator, a sulfur dioxide surrogate and a reducing reagent simultaneously in this reaction.

[Effects of reduced nitrogen application and soybean intercropping on nitrogen balance of sugarcane field].

A four-year (2010-2013) field experiment was carried out to explore the effects of three planting patterns (sugarcane, soybean monoculture and sugarcane-soybean 1:2 intercropping) with two nitrogen input levels (300 and 525 kg . hm-2) on soybean nitrogen fixation, sugarcane and soybean nitrogen accumulation, and ammonia volatilization and nitrogen leaching in sugarcane field. The results showed that the soybean nitrogen fixation efficiency (NFE) of sugarcane-soybean inter-cropping was lower than that of soybean monoculture. There was no significant difference in NFE among the treatments with the two nitrogen application rates. The nitrogen application rate and inter-cropping did not remarkably affect nitrogen accumulation of sugarcane and soybean. The ammonia volatilization of the reduced nitrogen input treatment was significantly lower than that of the conventional nitrogen input treatment. Furthermore, there was no significant difference in nitrogen leaching at different nitrogen input levels and among different planting patterns. The sugarcane field nitrogen balance analysis indicated that the nitrogen application rate dominated the nitrogen budget of sugarcane field. During the four-year experiment, all treatments leaved a nitrogen surplus (from 73.10 to 400.03 kg . hm-2) , except a nitrogen deficit of 66.22 kg . hm-2 in 2011 in the treatment of sugarcane monoculture with the reduced nitrogen application. The excessive nitrogen surplus might increase the risk of nitrogen pollution in the field. In conclusion, sugarcane-soybean intercropping with reduced nitrogen application is feasible to practice in consideration of enriching the soil fertility, reducing nitrogen pollution and saving production cost in sugarcane field.