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[Display omitted] The emerging of solar-driven interfacial evaporation provides new opportunities to alleviate the shortage of fresh water resource. Nevertheless, in practical solar desalination, salt precipitation will lead to the decrease of evaporation rate due to reduced light absorption and blocked evaporation channels of evaporator. It still remains a challenge to eliminate salt accumulation and simultaneously maintain high-efficient evaporation. In this work, a solar evaporator was prepared based on reduced graphene oxide and chitosan coated honeycomb-structured fabric (rCHF). The rCHF showed a high light absorbance of 97.2% due to enhanced light trapping of the honeycomb structure and ultra-low thermal conductivity of 0.044 W m−1 K−1. Furthermore, the temperature gradient generated inside the honeycomb unit can induce the Marangoni effect, which led to the site-specific salt crystallization on rCHF in seawater evaporation. As a result, the rCHF realized an excellent solar evaporation rate of 2.02 kg m-2h−1 under one sun irradiation (1 kW m−2). The site-specific salt crystallization on the surface of rCHF ensured stable evaporation even in 20% brine, and the isolated salt can be removed by natural dissolution owing to the excellent hydrophilicity of rCHF. This work provides a new perspective for the design of solar evaporator for practical solar seawater desalination. [ABSTRACT FROM AUTHOR]

Highlights: [•] Scaffolds of the post-synaptic density (PSD) organize glutamate receptor complexes. [•] Genetic manipulations of PSD scaffolds alter synaptic plasticity and complex behavior. [•] PSD scaffolds control distinct cognitive and affective behaviors. [•] Mutations of PSD scaffolds contribute to symptoms of psychiatric diseases. [ABSTRACT FROM AUTHOR]

The thermal conductivities of f-BNNS/EP composites were significantly improved and the interfacial thermal resistances were dramatically reduced due to the improvement of f-BNNS dispersion and compatibility with the epoxy matrix by amino acid functionalization. [Display omitted] The practical applications of boron nitride nanosheet (BNNS) are dramatically limited by the harsh exfoliation and surface functionalization conditions due to the hydrophobic and chemically inert nature. This issue can be improved by selecting efficient modifiers with hydrophilic groups. A green and scalable amino acid-assisted ball milling method is presented to exfoliate and functionalize BNNS simultaneously. The different interactions between BNNS and four amino acids (tryptophan (Trp), phenylalanine (Phe), arginine (Arg), lysine (Lys)) are thoroughly investigated to rationalize the thermal and mechanical properties of their corresponding epoxy (EP) composites. Trp and Phe display higher functionalization degree and dispersibility of BNNS than Arg and Lys thanks to the additional π-π interactions between the aromatic groups and BNNS. Moreover, both BNNS-Trp/EP and BNNS-Phe/EP exhibit higher cross-plane thermal conductivity of 2.1 and 1.96 W m−1 K−1 at 30 wt% filler loading. In addition, the mechanical strengths of all these amino acids functionalized BNNS filled epoxy composites are significantly enhanced due to stronger interfacial interactions between fillers and epoxy matrix. Thus, this work paves the way for the facile mass production of functionalized BNNS and expedites their applications in thermal interface materials of electronic components. [ABSTRACT FROM AUTHOR]

Aberrant energy metabolism in the brain is a common pathological feature in the preclinical Alzheimer's Disease (AD). Recent studies have reported the early elevations of glycolysis-involved enzymes in AD brain and cerebrospinal fluid according to a large-scale proteomic analysis. It's well-known that astrocytes exhibit strong glycolytic metabolic ability and play a key role in the regulation of brain homeostasis. However, its relationship with glycolytic changes and cognitive deficits in early AD patients is unclear. Here, we investigated the mechanisms by which astrocyte glycolysis is involved in early AD and its potential as a therapeutic target. Our results suggest that Aβ-activated microglia can induce glycolytic-enhanced astrocytes in vitro , and that these processes are dependent on the activation of the AKT-mTOR-HIF-1α pathway. In early AD models, the increase in L-lactate produced by enhanced glycolysis of astrocytes leads to spatial cognitive impairment by disrupting synaptic plasticity and accelerating Aβ aggregation. Furthermore, we find rapamycin, the mTOR inhibitor, can rescue the impaired spatial memory and Aβ burden by inhibiting the glycolysis-derived L-lactate in the early AD models. In conclusion, we highlight that astrocytic glycolysis plays a critical role in the early onset of AD and that the modulation of glycolysis-derived L-lactate by rapamycin provides a new strategy for the treatment of AD. [Display omitted] • Aβ-activated microglia can induce the reactive astrocytes with enhanced glycolysis in vitro. • Persistently glycolysis-derived L-lactate influx can impair spatial cognition and accelerate Aβ aggregation. • Enhanced glycolysis in reactive astrocyte is dependent on the activation of AKT-mTOR-HIF-1α pathway. • Rapamycin can rescue the impaired spatial memory and Aβ burdens by inhibiting glycolysis-derived L-lactate in AD models. [ABSTRACT FROM AUTHOR]

Opioid relapse is generally caused by the recurrence of context-induced memory reinstatement of reward. However, the internal mechanisms that facilitate and modify these processes remain unknown. One of the key regions of the reward is the nucleus accumbens (NAc) which receives glutamatergic projections from the dorsal hippocampus CA1 (dCA1). It is not yet known whether the dCA1 projection to the NAc shell regulates the context-induced memory recall of morphine. Here, we used a common model of addiction-related behavior conditioned place preference paradigm, combined with immunofluorescence, chemogenetics, optogenetics, and electrophysiology techniques to characterize the projection of the dCA1 to the NAc shell, in context-induced relapse memory to morphine. We found that glutamatergic neurons of the dCA1 and gamma aminobutyric acidergic (GABA) neurons of the NAc shell are the key brain areas and neurons involved in the context-induced reinstatement of morphine memory. The dCA1-NAc shell glutamatergic input pathway and the excitatory synaptic transmission of the dCA1-NAc shell were enhanced via the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) when mice were re-exposed to environmental cues previously associated with drug intake. Furthermore, chemogenetic and optogenetic inactivation of the dCA1-NAc shell pathway decreased the recurrence of long- and short-term morphine-paired context memory in mice. These results provided evidence that the dCA1-NAc shell glutamatergic projections mediated the context-induced memory recall of morphine. [Display omitted] • The neurons of the dCA1 and NAc shells were activated in a morphine-paired context. • The dCA1-NAc shell glutamatergic input pathway was enhanced in a morphine-paired context. • The excitatory synaptic transmission from the dCA1 to the NAc shell was mediated by AMPAR. • Inhibition of dCA1-NAc shell glutamatergic projection restrained the context-induced relapse memory in mice. [ABSTRACT FROM AUTHOR]

• IQGAP1 was involved in fear memory. • IQGAP1/ERK mediated histone posttranslational modifications and memory formation via HDAC2. • IQGAP1 −/− mice exhibited decreased histone phosphorylation and acetylation. Epigenetic mechanisms of learning and memory are particularly interesting topics in neuroscience that have recently been investigated. As shown in our previous study, IQGAP1, a scaffolding protein of MAPK, is involved in fear memory through interactions with GluN2A-containing NMDA receptors and the ERK1/2 cascade. However, researchers have not determined whether histone posttranslational modifications are regulated by the IQGAP1/ERK signaling pathway. We performed in vivo studies using IQGAP1 −/− and IQGAP1 +/+ mice to provide insights into the specific functions of IQGAP1 in memory processes and the precise mechanisms underlying its regulatory effects. IQGAP1 −/− mice exhibited impaired fear memory, decreased levels of phosphorylated ERK1/2 and histone H3S10, decreased acetylation of H3K14, and decreased c-Fos expression in the hippocampus compared to IQGAP1 +/+ mice after fear conditioning. HDAC2 was significantly enriched at the c-fos gene promoter in IQGAP1 −/− mice. Correspondingly, the disruption of the epigenetic regulation induced by ERK1/2 signaling through an intra-hippocampal injection of the MEK antagonist U0126 or GluN2A-selective pharmacological antagonist NVP-AAM077 blocked context-dependent memory formation, while no changes were observed after treatment with the GluN2B-selective antagonist Ro25-6981. The administration of SAHA, a non-specific HDAC inhibitor, or knock-down of HDAC2 with shHDAC2-AAV in the dorsal hippocampus significantly rescued the impaired fear memory formation, H3S10 phosphorylation, H3K14 acetylation, and c-Fos expression in IQGAP1 −/− mice. Thus, we postulated that the IQGAP1/ERK-dependent mechanism regulating histone posttranslational modifications via HDAC2 potentially underlies memory formation. [ABSTRACT FROM AUTHOR]