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Background: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by amyloid-β peptide (Aβ) deposition. Aβ accumulation induces oxidative stress, leading to mitochondrial dysfunction, apoptosis, and so forth. Octadecaneuropeptide (ODN), a diazepam-binding inhibitor (DBI)-derived peptide, has been reported to have antioxidant properties. However, it is unclear whether ODN has neuroprotective effects in AD. Objective: To profile the potential effects of ODN on AD. Methods: We established a mouse model of AD via microinjection of Aβ in the lateral ventricle. Utilizing a combination of western blotting assays, electrophysiological recordings, and behavioral tests, we investigated the neuroprotective effects of ODN on AD. Results: DBI expression was decreased in AD model mice and cells. Meanwhile, ODN decreased Aβ generation by downregulating amyloidogenic AβPP processing in HEK-293 cells stably expressing human Swedish mutant APP695 and BACE1 (2EB2). Moreover, ODN could inhibit Aβ-induced oxidative stress in primary cultured cells and mice, as reflected by a dramatic increase in antioxidants and a decrease in pro-oxidants. We also found that ODN could reduce oxidative stress-induced apoptosis by restoring mitochondrial membrane potential, intracellular Ca2+ and cleaved caspase-3 levels in Aβ-treated primary cultured cells and mice. More importantly, intracerebroventricular injection of ODN attenuated cognitive impairments as well as long-term potentiation in Aβ-treated mice. Conclusion: These results suggest that ODN may exert a potent neuroprotective effect against Aβ-induced neurotoxicity and memory decline via its antioxidant effects, indicating that ODN may be a potential therapeutic agent for AD.

Hypoxic-ischemic brain damage (HIBD) is among the leading causes of neonatal brain injury. ODN, a peptide derived from diazepam-binding inhibitor (DBI), has potent antioxidant and anti-apoptotic properties. It remains unclear, however, whether ODN is an effective treatment for HIBD. Here, we reported that treatment with ODN (10 ng/day, i.c.v.) alleviated the deficits in myodynamia and motor coordination and cognitive functions in HIBD. Meanwhile, ODN prevented the neuronal loss in the cortex and hippocampus in HIBD rats. In addition, ODN decreased ROS by generating less oxidants and more antioxidants, as reflected by a dramatic increase in total antioxidant capacity, glutathione reductase, and catalase and a marked decrease in H

Alzheimer's disease (AD) is a common neurodegenerative disorder characterized by the accumulation of misfolded amyloid-β (Aβ) peptides, which is caused by an imbalance between Aβ production and clearance. Picroside II (Picr II), the principal active constituent of Picrorhizakurroa Royle ex Benth, possesses a range of pharmacological properties, such as anti-inflammatory, antioxidant, and antiapoptotic effects. However, the exact role of Picr II in AD is not yet fully understood. In this study, we investigated the effects of Picr II on AD and found that it inhibited amyloid precursor protein (APP) processing by enhancing autophagy rather than through the ubiquitin-proteasome pathway, resulting in a reduction in Aβ production. Furthermore, Picr II treatment improved the decline in autophagy, which was due not only to an increase in autophagic flux but also to an increase in the fusion of autophagosomes with lysosomes. Most importantly, daily treatment with Picr II (20 mg/kg, i.p.) throughout the experiment rescued the learning and memory in Aβ-treated mice. Taken together, these results suggest that Picr II may have a potent neuroprotective effect against Aβ-induced memory decline by enhancing autophagy, indicating that Picr II may be a promising therapeutic agent for AD.

Background: Tauopathies are a group of neurodegenerative disorders, including Alzheimer’s disease (AD) and frontotemporal lobar degeneration with tau pathology. Hyperphosphorylation modification promotes tau protein misfolding and aggregation into neurofibrillary tangles, leading to impairments of synaptic plasticity and learning and memory. However, very limited therapeutic strategies are available. Objective: In the present study, we wanted to investigate the potential effects of Dihydroartemisinin (DHA) on tauopathies. Methods: We constructed adeno-associated virus carrying hTau cDNA (AAVhTau) to establish a mouse model of tauopathy through intrahippocampal microinjection. Using a combination of behavioral test, electrophysiological recording, and western blotting assay, we examined the neuroprotective effects of DHA on learning and memory deficits in mice with tauopathy. Results: DHA improved learning and memory and increased hippocampal CA1 long-term potentiation (LTP) in mice overexpressed human tau (hTau) in the hippocampus. More importantly, further study revealed that DHA could induce protein O-GlcNAcylation modification and reduce protein phosphorylation. O-GlcNAc transferase inhibitor alloxan could suppress DHA-induced protein O-GlcNAcylation, and subsequently prevent therapeutic effect of DHA on the deficits of learning and memory as well as synaptic plasticity in hTau mice. Conclusion: These results indicate that DHA may exert neuroprotective role in tauopathy through a crosstalk between O-GlcNAcylation and phosphorylation, suggesting a potential therapeutic for learning and memory deficits associated with tau pathology.

Aqueous zinc-ion batteries (ZIBs) are considered as a promising energy storage system due to their low cost and high safety merits. However, they suffer from the challenge of uncontrollable dendrite growth due to a non-uniform zinc deposition, which increases internal resistance and causes battery failure. Herein, Ag coating fabricated by a facile surface chemistry route on zinc metal was developed to guide uniform zinc deposition. Ag-coated Zn shows improved electrolyte wettability, a small zinc deposition overpotential, and fast kinetics for zinc deposition/dissolution. Direct optical visualization and scanning electron microscopy images show uniform zinc deposition due to the introduction of Ag coating. As a result, the Ag-coated Zn anode can sustain up to 1450 h of repeated plating/stripping with a low overpotential in symmetric cells at a current density of 0.2 mA cm

Hypoxic-ischemic encephalopathy (HIE) is a main cause of mortality and severe neurologic impairment in the perinatal and neonatal period. However, few satisfactory therapeutic strategies are available. Here, we reported that a rapid nuclear translocation of phosphatase and tensin homolog deleted on chromosome TEN (PTEN) is an essential step in hypoxic-ischemic brain damage (HIBD)- and oxygen-glucose deprivation (OGD)-induced neuronal injures both in vivo and in vitro. In addition, we found that OGD-induced nuclear translocation of PTEN is dependent on PTEN mono-ubiquitination at the lysine 13 residue (K13) that is mediated by neural precursor cell expressed developmentally downregulated protein 4-1 (NEDD4-1). Importantly, we for the first time identified α- and γ-adaptin binding protein (Aagab) as a novel NEDD4-1 regulator to regulate the level of NEDD4-1, subsequently mediating Pten nuclear translocation. Finally, we demonstrated that genetic upregulation of Aagab or application of Tat-K13 peptide (a short interference peptide that flanks K13 residue of PTEN) not only reduced Pten nuclear translocation, but also significantly alleviated the deficits of myodynamia, motor and spatial learning and memory in HIBD model rats. These results suggest that Aagab may serve as a regulator of NEDD4-1-mediated Pten nuclear translocation to promote functional recovery following HIBD in neonatal rats, and provide a new potential therapeutic target to guide the clinical treatment for HIE.

Aqueous zinc-ion batteries (ZIBs) have shown great potential in large-scale energy storage systems due to their economic efficiency and environmental friendliness. However, cathodes for aqueous ZIBs are affected by the slow Zn[Formula: see text] diffusion kinetics and limited capacity. Herein, Mg[Formula: see text]V2O[Formula: see text]H2O (MgVO) nanobelt cathode with a large interlayer spacing of 13.0 Å is prepared via a one-step hydrothermal approach. Furthermore, the pre-intercalated Mg[Formula: see text] can stabilize the crystal structure and prevent Zn[Formula: see text] from being trapped in the lattice. As a result, MgVO cathode delivers a high capacity of 386 mAh g[Formula: see text] at 0.1 A g[Formula: see text], and impressive long-term cycling stability with a capacity retention of 91% after 1500 cycles at 5 A g[Formula: see text]. Moreover, the Zn/[Formula: see text]/MgVO battery can provide a high-energy density of 269 W h kg[Formula: see text] at 0.1 A g[Formula: see text] and a high-power density of 2701 W kg[Formula: see text] at 5 A g[Formula: see text]. The simple preparation and low cost make this cathode show great potential in the applications of large-scale energy storage.

Maintaining a proper balance between the glutamate receptor-mediated neuronal excitation and the A type of GABA receptor (GABA

Although lithium metal is regarded as the most promising anode for high energy density lithium ion batteries, the unstable solid-liquid interface during cycling severely shortens the battery lifetime. The Li deposition behavior is greatly influenced by the current density distribution on the surface of the electrode, which is significantly associated with the electrode structure. A well-designed electrode structure plays a key role in stabilizing the solid-liquid interface of the Li metal anode. In this work, a lithiophilic honeycomb-like Ni

The highly conductive and corrosion resistant diffusion layers of niobium, niobium nitrides and niobium carbides have been successfully fabricated on AISI430 stainless steel (430 SS) via a plasma s...

Aqueous zinc-ion batteries (ZIBs) are deemed as the idea option for large-scale energy storage systems owing to many alluring merits including low manufacture cost, environmental friendliness, and high operations safety. However, to develop high-performance cathode is still significant for practical application of ZIBs. Herein, Ba0.23V2O5·1.1H2O (BaVO) nanobelts were fabricated as cathode materials of ZIBs by a typical hydrothermal synthesis method. Benefiting from the increased interlayer distance of 1.31 nm by Ba2+ and H2O pre-intercalated, the obtained BaVO nanobelts showed an excellent initial discharge capacity of 378 mAh·g−1 at 0.1 A·g−1, a great rate performance (e.g., 172 mAh·g−1 at 5 A·g−1), and a superior capacity retention (93% after 2000 cycles at 5 A·g−1).

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases and is currently incurable. Amyloid β protein (Aβ) deposition is the main pathogenesis of AD, and many studies have shown that Aβ accumulation is toxic to neurons, leading to the inflammatory reaction, neuronal apoptosis, and neurofibrillary tangles. Thus, reducing Aβ levels might be a potential therapeutic strategy for AD. Liquiritigenin (LG), a dihydroflavone monomer compound extracted from natural plant licorice, has a variety of biological activities such as antioxidant, anti-tumor, anti-inflammatory and anti-virus. However, the exact function of LG in the pathogenesis of AD is elusive. Here, we reported that LG could significantly attenuate neuronal apoptosis in Aβ-induced N2A cells and APP/PS1 transgenic mice. Our in vivo and in vitro studies revealed that LG could alleviate the inflammation response, reflected by the reduction of NLRP3 and cleaved caspase-1. Meanwhile, we also found that LG was able to shift M1 type microglia towards M2 type microglia in Aβ-induced BV2 cells and AD mice. Furthermore, LG could reduce the Aβ levels by decreasing APP processing and accelerating Aβ clearance in AD mice. More importantly, daily treatment of LG (30 mg/kg day) for 90 days dramatically ameliorated the spatial learning and memory of AD mice. Taken together, these results suggest that LG can reduce the Aβ levels by regulating the M1/M2 transformation of microglia, thereby reversing memory decline during AD development, suggesting that LG may be a potential therapeutic agent for treating AD.

Background Accumulation of amyloid-β (Aβ) peptides, generated from amyloid-β precursor protein (AβPP) amyloidogenic processing, is one of the most salient disease hallmarks of Alzheimer's disease (AD). Nicotine is able to promote α-secretase-mediated AβPP nonamyloidogenic processing and increase the release of sAβPPα and C-terminal fragment of 83 amino acids (C83). However, the potential molecular mechanism remains elusive. Objective The aim of the present study was to investigate the effect of nicotine on AβPP processing in SH-SY5Y cells that stably express human Swedish mutant AβPP695 (SH-SY5Y-AβPP695). Methods The expression of AβPP and its C-terminal fragments including C99, C89, and C83, was measured in SH-SY5Y-AβPP695 cells treated with nicotine for 6 h. Protein kinase C (PKC) antagonist Ro30-8220 or agonist PMA was used to determine the role of PKC in AβPP processing. Lentivirus-mediated shRNA targeting receptor for activated C-kinase 1 (RACK1) gene was added into the media to knockdown RACK1 expression, and then AβPP processing was examined. Results The results showed that 6 h of nicotine exposure increased the expression of α-secretase (ADAM10) and C83 in a dose dependent manner. While the β-secretase (BACE1), AβPP amyloidogenic processing products C89 and C99 as well as Aβ peptides (including Aβ40 and Aβ42) remained unchanged. We also found that nicotine elevated the expression of phosphorylated PKC (P-PKC) and RACK1 on the cytomembrane. PKC antagonist Ro30-8220 treatment prevented the increase of ADAM10 and C83 by nicotine. Genetic knockdown RACK1 significantly inhibited P-PKC, and consequently abolished the increase of ADAM10 and C83 by nicotine. Conclusion Taken together, these results indicate that nicotine effectively promotes AβPP nonamyloidogenic processing via RACK1-dependent activation of PKC in SH-SY5Y-AβPP695 cells and could be a potential molecule for AD treatment.

Maternal sleep deprivation (MSD) has been suggested to be associated with increased frequency of neurodevelopmental disorders in offspring in both humans and animal models. However, the underlying cellular and molecular mechanism is still unclear. We have recently reported that MSD at different stages of pregnancy impairs the emotional and cognitive functions, and suppresses hippocampal CA1 long-term potentiation (LTP) in the offspring rats. Here, we report that the MSD induced LTP impairment at the CA1 hippocampus of the offspring rats is associated with increased long-term depression (LTD) and reduced expression of postsynaptic GluA2-containing α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs). Importantly, we found that inhibition of AMPAR endocytosis by a synthetic peptide Tat-GluA23Y (3 μmol/kg, i.p.) not only increased level of AMPARs and reduced LTD, but also restored LTP. Moreover, treatment with Tat-GluA23Y peptide markedly alleviated the MSD-induced impairments of spatial learning and memory; and decreased depressive- and anxiety-like behaviors in the offspring. Together, our findings suggest that the MSD-induced postsynaptic AMPAR endocytosis causally contributes to the impairments of hippocampal synaptic plasticity, thereby disrupting the emotional and cognitive functions in the offspring.

In defect engineering, doping and vacancy are effective ways to improve the electrochemical performance of electrode material. For the first time, we introduce N dopants and tunable oxygen vacancies into electrolytic MnO2 with graphite as skeleton by a simple wet ball milling. The nanocomposites (NEG) exhibit excellent rate performance under various current densities. The density functional theory (DFT) calculations and climbing image-nudged elastic band (CI-NEB) demonstrate the interstitial N dopants can improve electronic conductivity and lithium-ion diffusion. This research will facilitate the deep understanding of the mechanism of lithium-ion diffusion and provide a novel idea for the study on the defect engineering.

Alzheimer's disease (AD) is the most common cause of progressive cognitive impairment in the aged. The aggregation of the amyloid β-protein (Aβ) is a hallmark of AD and is linked to synapse loss and cognitive impairment. Capsaicin, a specific agonist of the transient receptor potential vanilloid 1 (TRPV1), has been proven to ameliorate stress-induced AD-like pathological and cognitive impairments, but it is unclear whether TRPV1 activation can affect cognitive and synaptic functions in Aβ-induced mouse model of AD. In this study, we investigated the effects of TRPV1 activation on spatial memory and synaptic plasticity in mice treated with Aβ. To induce AD-like pathological and cognitive impairments, adult C57Bl/6 mice were microinjected with Aβ42 (100 μM, 2.5 μl/mouse, i.c.v.). Two weeks after Aβ42 microinjection, spatial learning and memory as well as hippocampal long-term potentiation (LTP) were examined. The results showed that Aβ42 microinjection significantly impaired spatial learning and memory in the Morris water maze and novel object recognition tests compared with controls. These behavioral changes were accompanied by synapse loss and impaired LTP in the CA1 area of hippocampus. More importantly, daily capsaicin (1 mg/kg, i.p.) treatment throughout the experiment dramatically improved spatial learning and memory and synaptic function, as reflected by enhanced hippocampal LTP and reduced synapse loss, whereas the TRPV1 antagonist capsazepine (1 mg/kg, i.p.) treatment had no effects on cognitive and synaptic function in Aβ42-treated mice. These results indicate that TRPV1 activation by capsaicin rescues cognitive deficit in the Aβ42-induced mouse model of AD both structurely and functionally.

Mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) is an essential negative regulator of MAPKs by dephosphorylating MAPKs at both tyrosine and threonine residues. Dysregulation of the MAPK signaling pathway has been associated with Alzheimer’s disease (AD). However, the role of MKP-1 in AD pathogenesis remains elusive. Here, we report that MKP-1 levels were decreased in the brain tissues of patients with AD and an AD mouse model. The reduction in MKP-1 gene expression appeared to be a result of transcriptional inhibition via transcription factor specificity protein 1 (Sp1) cis-acting binding elements in the MKP-1 gene promoter. Amyloid-β (Aβ)-induced Sp1 activation decreased MKP-1 expression. However, upregulation of MKP-1 inhibited the expression of both Aβ precursor protein (APP) and β-site APP-cleaving enzyme 1 by inactivating the extracellular signal-regulated kinase 1/2 (ERK)/MAPK signaling pathway. Furthermore, upregulation of MKP-1 reduced Aβ production and plaque formation and improved hippocampal long-term potentiation (LTP) and cognitive deficits in APP/PS1 transgenic mice. Our results demonstrate that MKP-1 impairment facilitates the pathogenesis of AD, whereas upregulation of MKP-1 plays a neuroprotective role to reduce Alzheimer-related phenotypes. Thus, this study suggests that MKP-1 is a novel molecule for AD treatment.

Alzheimer's disease (AD) is one of the most common causes of neurodegenerative diseases in the elderly. The accumulation of amyloid‐β (Aβ) peptides is one of the pathological hallmarks of AD and leads to the impairments of synaptic plasticity and cognitive function. The transient receptor potential vanilloid 1 (TRPV1), a nonselective cation channel, is involved in synaptic plasticity and memory. However, the role of TRPV1 in AD pathogenesis remains largely elusive. Here, we reported that the expression of TRPV1 was decreased in the brain of APP23/PS45 double transgenic AD model mice. Genetic upregulation of TRPV1 by adeno‐associated virus (AAV) inhibited the APP processing and Aβ deposition in AD model mice. Meanwhile, upregulation of TRPV1 ameliorated the deficits of hippocampal CA1 long‐term potentiation (LTP) and spatial learning and memory through inhibiting GluA2‐containing α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor (AMPAR) endocytosis. Furthermore, pharmacological activation of TRPV1 by capsaicin (1 mg/kg, i.p.), an agonist of TRPV1, dramatically reversed the impairments of hippocampal CA1 LTP and spatial learning and memory in AD model mice. Taken together, these results indicate that TRPV1 activation effectively ameliorates cognitive and synaptic functions through inhibiting AMPAR endocytosis in AD model mice and could be a novel molecule for AD treatment., Aging reduces TRPV1 activity to lead to AMPAR endocytosis and active APP processing to promote Aβ deposition. Increased AMPAR endocytosis and Aβ result in LTP impairment and subsequently induce memory deficits. Genetic upregulation or pharmacological activation of TRPV1 is able to reverse AD‐related neuropathologies in AD model mice.

Lithium metal is considered as the ultimate anode candidate for next-generation high-energy storage systems due to its ultrahigh specific capacity and low reduction potential. However, the practical application of lithium metal anode is severely impeded by uncontrollable lithium dendrite growth. In this work, a three-dimensional (3D) N-doped carbon fiber (NCF) network with ion/electron-conductivity has been fabricated by electrospinning the polyacrylonitrile solution and subsequent thermal treatment. The 3D NCF as an interlayer covering on the lithium anode is used to regulate the lithium plating/stripping behavior, accommodating partially deposited Li to realize lithium dendrite-free deposition on the lithium anode. Benefiting from these, the symmetrical cell of Li anode protected by NCF (Li@NCF) delivers long duration time (>1200 h) with a low initial nucleation overpotential (30 mV) at the current density of 1 mA cm−2. In addition, the full cell of Li@NCF||LiFePO4 exhibits excellent capacity retention of 114.6 mAh cm−2 over 360 cycles at the current density of 1 C. This strategy contributes a step forward for dendrite-free lithium metal batteries.

Tin dioxide (SnO2) is a promising anode material candidate for lithium-ion batteries (LIBs), yet its practical application is hindered by severe volume expansion and inferior conductivity. Here, we proposed a facile way for preparing self-assemble SnO2 porous nanotubes by electrospinning and subsequent thermal treatments. The nanosized SnO2 particles anchored on the wall of tube provide abundant reaction sites for the electrochemical reaction, and plenty of internal space of hollow structure effectively accommodates the volume expansion. Besides, the tubular structure is intact after 100 cycles at the current density of 200 mA g−1, implying the robust structure can accommodate the volume expansion well. Due to the above advantages, SnO2 porous nanotubes as the anode of LIBs display excellent reversible capacity, superior rate performance and good cycling stability. This self-assemble porous tubular structure provides an efficient route to restrain the volume expansion of anode materials in electrochemical reactions for advanced LIBs.

Aqueous Zn-ion batteries (ZIBs) have received increasing attention because of their high safety, low cost and environmental benignity. However, the development of high-performance cathode materials using for zinc-ion de/intercalation is still a challenge. In this work, V2O5@polyaniline (V2O5@PANI) nanocomposites were synthesized by the polymerization of aniline and V2O5. Due to the organic-inorganic compatibility, V2O5@PANI exhibits a good electrochemical performance serving as cathode material for ZIBs, which displays a high specific capacity (361 mAh g−1 at 0.1 A g−1) and an excellent cycling stability (93.8% capacity retention after 1000 cycles).

Alzheimer's disease (AD) is a neurodegenerative disease characterized by the deposition of amyloid-β peptides (Aβ). Aβ accumulation leads to the formation of neurofibrillary tangles, inflammation, axonal injury, synapse loss, and neuronal apoptosis. Thus, reducing Aβ levels should exert a neuroprotective effect against AD. Ginsenoside Rf, an extract from Panax notoginseng, has potent anti-fatigue, anti-nociception, anti-oxidation, and anti-inflammation properties. However, it is unclear whether ginsenoside Rf is effective in the treatment of AD. Here, we reported that ginsenoside Rf could significantly attenuate Aβ-induced apoptosis in N2A cells, as reflected by a dramatic increase in mitochondrial membrane potential and decrease in Ca2 + concentration, reactive oxygen species, and active caspase-3 expression. Meanwhile, ginsenoside Rf could alleviate the Aβ-induced inflammation reaction, such as the decrease of interferon-gamma (IFN-γ) and active caspase-1 expression and the increase of interleukin-13. Furthermore, we also found that Rf is able to accelerate Aβ clearance and subsequently reduces Aβ level in N2A cells stably transfected with human Swedish mutant APP695 (N2A-APP). More importantly, daily Rf treatment (20 mg/kg, i.p.) throughout the experiment dramatically improved spatial learning and memory in Aβ42-induced mouse model of AD. Taken together, these results indicate that ginsenoside Rf may decrease Aβ-induced neurotoxicity and memory decline via anti-inflammatory response during AD development, suggesting that Rf may be a potential therapeutic agent for treating AD.

Regional coverage reconnaissance is a signiflcant means of obtaining the important targets in the region and a prerequisite for the precision strike. The research status of LAVs (Loitering Air Vehicles) regional coverage is analyzed in his paper, and the detector model is built which is applicable to LAV. By analyzing the difierent ways how circular target region should be divided, a conclusion is obtained that the total distance is shortest and the total turning number is least in the parallel split manner; according to the indicators requirements of turning radius and reconnaissance radius, LAV turning method is appropriately given; the objective function of this problem is established and the constraints are determined correspondingly, then this problem had been optimized with MOPSOA (Multi-object Particle Swarm Optimization Algorithm); the obtained path plan after optimization is ideal.

Our previous study has shown that pentobarbital causes memory deficits and impairs hippocampal synaptic plasticity. The Tat-GluA23Y peptide (GluA23Y) prevents activity-dependent α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) endocytosis. It enables early-phase long-term potentiation (LTP) to proceed to late-phase LTP allowing short-term memory to convert to long-term memory. The purpose of this study is to explore the potential effects of GluA23Y on pentobarbital-induced memory deficits through behavioral and electrophysiological paradigms. We found that in vivo intrahippocampal infusion of GluA23Y (100μM, 1μl per hippocampus) 30min prior to pentobarbital administration (8mM, 1μl per hippocampus) significantly rescued the pentobarbital-induced deficit of memory retrieval in rats during the Morris water maze test. Pre-incubation of GluA23Y (10μM) partially rescued bath application of pentobarbital-induced synaptic transmission of the CA3-CA1 pathway in hippocampal slices. More importantly, GluA23Y selectively upregulated the synaptic GluA2 expression that was suppressed by pentobarbital. Together, these results suggest that inhibition of GluA2-containing AMPAR endocytosis by GluA23Y increases the pentobarbital-suppressed basal synaptic transmission by upregulating the synaptic GluA2, and then subsequently alleviates spatial memory deficits. Therefore, inhibition of AMPAR endocytosis may be a potential therapeutic way to treat memory disorders caused by anesthetics.

Atopic dermatitis (AD) is a common chronic inflammatory skin disorder, and patients with AD suffer from severe psychological stress, which markedly increases the prevalence rate of depression and anxiety disorders in later life. Fluoxetine, a selective serotonin reuptake inhibitor, has recently been reported to exert anti-inflammatory and immunosuppressive effects. However, it is unclear whether fluoxetine is effective in the treatment of AD through reducing psychological stress and inflammatory reaction. Here, we reported that a BALB/c mouse model of AD was induced by application of 2,4‑dinitrochlorobenzene (DNCB) onto hairless dorsal skin. Chronic fluoxetine treatment (10 mg/kg per day, i.p.) significantly attenuated AD-like symptoms, as reflected by a dramatic decrease in scratching bouts, as well as a decrease in anxiety- and depressive-like behaviors. Furthermore, these behavioral changes were accompanied by a significant decrease in epidermal thickness, the number of mast cells in skin tissue, mRNA levels of interleukin-4 (IL-4) and IL-13 in the spleen, as well as serum immunoglobulin E (IgE) in the DNCB-treated mice by treatment with fluoxetine. Taken together, these results indicate that fluoxetine may suppress psychological stress and inflammatory response during AD development, and subsequently ameliorate AD symptoms, suggesting that fluoxetine may be a potential therapeutic agent against AD in clinic.

The measurement method for shooting in the rear using single camera and intersection measurement on plane using two cameras were presented in order to solve the problem of small field coverage for shooting orthogonally using the camera in the test of effective distance for the grenade fuze. The distance of the exploded bullets in the X direction and the quantitative denotation of the error due to the spread of the projectile in the Z direction were obtained for the single camera, and the position of the exploded bullets were obtained accurately in the X direction and in the Z direction for intersection measurement using two cameras on two-dimension plane. First, the measurement formula was deduced, and the error due to the spread of the projectile in the Z direction for the single camera was analyzed, then, the intersection measurement method using two cameras on plane was validated by the experiment, the results show that the absolute error are less than 6cm.