Control of Compensation Temperature in CoGd Films through Hydrogen and Oxygen Migration under Gate Voltage.

Electrical control of magnetic properties is crucial for low-energy memory and logic spintronic devices. We find that the magnetic properties of ferrimagnetic CoGd can be altered through ionic liquid gating. Gate voltages manipulate the opposite magnetic moments in Co and Gd sublattices and induce a giant magnetic compensation temperature change of more than 200 K in Pt/CoGd/Pt heterostructures. The electrically controlled dominant magnetic sublattice allows voltage-induced magnetization switching. Both experiments and theoretical calculations demonstrate that the significant modulations of compensation temperature are relevant to the reduced Gd moments due to the presence of hydrogen ions at positive voltages as well as the enhanced Co moments and reduced Gd moments due to the injection of oxygen ions at negative voltages. These findings expand the possibilities for all-electric and reversible magnetization control in the field of spintronics.

Electrical Control of Magnetism through Proton Migration in Fe3O4/Graphene Heterostructure.

Ion migration has direct and crucial bearing on the crystal lattice field, electron filling, orbital occupation and spin polarization, which in turn changes the physical properties. Electric field is an effective way to control ion migration, but it may include simultaneous movement of multiple ions and increase the complexity of the system. Therefore, controllable and selective single ion migration with an unambiguous mechanism is highly desired. Here, the magnetic moments of Fe3O4 could be reversibly controlled by ionic liquid gating on the basis of migration of pure protons. A bilayer graphene could serve as an ion sieve, allowing only protons rather than oxygen ions or hydroxyl groups to participate in the gating process, thus guaranteeing the reversibility of magnetic property changes. This work is expected to supply an ideal arena for electrically sketching the functionalities of solid state materials based on the selective ion migration.

Tumor-promoting mechanisms of macrophage-derived extracellular vesicles-enclosed microRNA-660 in breast cancer progression.

INTRODUCTION: Breast cancer metastasis is the main cause of cancer-related death in women worldwide. Current therapies have remarkably improved the prognosis of breast cancer patients but still fail to manage metastatic breast cancer. Here, the present study was set to explore the role of microRNA (miR)-660 from tumor-associated macrophages (TAMs) in breast cancer, particularly in metastasis. MATERIALS AND METHODS: We collected breast cancer tissues and isolated their polarized macrophages as well as extracellular vesicles (EVs), in which we measured the expression of miR-660, Kelch-like Protein 21 (KLHL21), and nuclear factor-κB (NF-κB) p65. Breast cancer cells were transfected with miR-660 mimic, miR-660 inhibitor, and sh-KLHL21 and then the cells were co-cultured with EVs or TAMs followed by detection of invasion and migration. Finally, mouse model of breast cancer was established to detect the effect of miR-660 or KLHL21 on metastasis by measuring the lymph node metastasis (LNM) foci in femur and lung. RESULTS: KLHL21 was poorly expressed, whereas miR-660 was highly expressed in breast cancer tissues and cells. Of note, low KLHL21 expression or high miR-660 expression was related to poor overall survival. EVs-contained miR-660 was identified to bind to KLHL21, reducing the binding between KLHL21 and inhibitor kappa B kinase ß (IKKß) to activate the NF-κB p65 signaling pathway. Interestingly, EV-loaded miR-660 from TAMs could be internalized by breast cancer cells. Moreover, silencing of KLHL21 increased the number of lung LNM foci in vivo, while EVs-contained miR-660 promoted cancerous cell invasion and migration. DISCUSSION: Taken altogether, our work shows that TAMs-EVs-shuttled miR-660 promotes breast cancer progression through KLHL21-mediated IKKß/NF-κB p65 axis.

Fluorometric determination of antioxidant capacity in human plasma by using upconversion nanoparticles and an inner filter effect mechanism.

The balance between free oxygen radicals and antioxidant defense systems is usually assessed by an antioxidant capacity assay. A rapid and sensitive antioxidant capacity assay is described here. It is making use of NaYF4:Yb/Er@NaYF4 core-shell upconversion nanoparticles (UCNPs) and potassium permanganate (KMnO4). In this strategy, added KMnO4 reduces the green (540 nm) emission of the UCNPs (under 980 nm photoexcitation) due to an inner filter effect. The antioxidants cysteine, ascorbic acid and glutathione (GSH) reduce the intense purple color of KMnO4 because it is reduced to Mn(II) ion. Hence, the green upconversion fluorescence is restored after the addition of antioxidants. Figures of merit for this assay (for the case of GSH) include a detection limit of 3.3 µM, a detection range that extends from 10 µM to 2.5 mM, and an assay time of a few seconds. The assay was applied to the evaluation of antioxidant capacity in human plasma samples spiked with GSH and gave satisfactory repeatability and specificity. Graphical abstract Schematic presentation of a fluorometric assay based on inner filter effect (IFE) between upconversion nanoparticles (UCNPs) and potassium permanganate (KMnO4) for the determination of antioxidant capacity in human plasma.

Synthesis and Luminescence Properties of a Novel Yellow-White Emitting NaLa(MoO4)2: Dy3+, Li+ Phosphor.

Intense yellow-white NaLa(MoO4)2: Dy3+ phosphors co-doped with Li+ ions have been successfully synthesized via facile sol-gel combustion approach. The dependence of the crystal structure and crystallinity, particle morphology, photoluminescence property, fluorescent lifetime and absolute quantum efficiency of the as-prepared phosphors has been investigated. Stable yellow-white emission from 440 nm to 600 nm and higher absolute quantum efficiency were studied on Dy3+ doped NaLa(MoO4)2, Dy3+ and Li+ co-doped NaLa(MoO4)2, respectively. Surprisingly, only a small amount of Li+ can lead to a remarkable increase of the PL intensity and the quantum efficiency. Especially, along with 0.75 mol% Li+ ions induced in the NaLa(MoO4)2: Dy3+ phosphors, the absolute quantum efficiency increased from 13.8% to 22%, and the possible mechanism has been deeply discussed. Outstanding luminescence properties have certified that NaLa(MoO4)2: Dy3+, Li+ phosphors are promising candidates as new yellow-white components for optical devices.

UV Light Illumination Can Improve the Sensing Properties of LaFeO3 to Acetone Vapor.

The synthesized LaFeO3 nanocrystalline sensor powders show positive response to sensing acetone vapor at 200 °C. The responses to acetone vapor (at 0.5, 1, 2, 5, 10 ppm) are 1.18, 1.22, 1.89, 3.2 and 7.83. To make the sensor operate at a lower optimum temperature, UV light illumination 365 nm is performed. Response of the sensor has a larger improvement under 365 nm UV light illumination than without it. The responses to acetone vapor (at 0.5, 1, 2, 5, 10 ppm) are 1.37, 1.85, 3.16, 8.32 and 14.1. Furthermore, the optimum operating temperature is reduced to 170 °C. As the relative humidity increases, the resistance and sensitivity of sensor are reduced. The sensor shows good selectivity toward acetone when compared with other gases. Since the detection of ultralow concentrations of acetone vapor is possible, the sensor can be used to preliminarily judge diabetes in the general public, as a high concentration of acetone is exhaled in breath of diabetic patients. The sensor shows a good stability, which is further enhanced under UV light illumination. The sensor shows better stability when under 365 nm UV light illumination. Whether under light illumination or not. The LaFeO3 material shows good performance as a sensor when exposed to acetone vapor.

Optical-magnetic bifunctional properties and mechanistic insights on upconversion of NaYF4:Yb,Ho,Tm@NaGdF4 with a tunable nanodumbbell morphology.

The energy-upconversion of lanthanide-doped nanoparticles with a core-shell structure can be utilized to enhance and tune optical properties and can generate multifunctionality in a single system. Herein, the core-shell nanoparticles NaYF4:Yb,Ho,Tm@NaGdF4 were prepared by thermally decomposing lanthanide acetylacetonate precursors. Through modifying the molar ratio of the core and shell, nanodumbbell-shaped particles with different sizes and morphologies were precisely synthesized. The formation mechanism and the heterogeneous epitaxial growth process of the nanodumbbell-shaped particles were studied. After coating the shell layer, upconversion luminescence intensities, spectral purity and fluorescence lifetimes were improved. Furthermore, the magnetic performance of the core-shell nanoparticles was characterized. The optical-magnetic bifunctional upconversion core-shell particles with programmable shape and multiple properties provide an ideal platform for the preparation of nanodumbbell-shaped particles and the promotion of upconversion materials for biomedical research.

Efficient Synthesis of Highly Photoluminescent Short Dendritic CdSeS/ZnS Quantum Dots for Biolabeling.

A convenient and efficient approach is reported to synthesize CdSeS with low-cost and low-toxic materials. The influence of the Se/S ratio and reaction time on the photoluminescent properties of CdSeS QDs is investigated through researching the temporal evolution of the absorption and the emission. Following, the high photoluminescent short dendritic green-emitting CdSeS/ZnS QDs are prepared using the method inspired by the successive ion layer adsorption and reaction procedure, which are composed of a CdSeS core and ZnS branches. Transmission electronic microscopy and X-ray diffraction show that the CdSeS/ZnS QDs is in a cubic zinc blende structure. The photoluminescence intensity increase significantly when the ZnS branches form as a result of the charge carriers being confined in the core. The photoluminescence quantum yield of the obtained CdSeS/ZnS core-shell QDs can be up to 90%, which is much higher than that of initial CdSeS QDs (39%). In addition, CdSeS/ZnS QDs have good photoluminescence intensity after they are transferred from organic solvent into aqueous media through ligand replacement using mercaptoacetic acid. Afterwards, the E. Coli O-157 are not only successfully conjugated with CdSeS/ZnS QDs but also present clear images under UV irradiation.

Linearly Polarized Broadband Emission and Multiwavelength Lasing in Solution-Processed Quantum Dots.

A miniature laser with linear polarization is a long sought-after component of photonic integrated circuits. In particular, for multiwavelength polarization lasers, it supports simultaneous access to multiple, widely varying laser wavelengths in a small spatial region, which is of great significance for advancing applications such as optical computing, optical storage, and optical sensing. However, there is a trade-off between the size of small-scale lasers and laser performance, and multiwavelength co-gain of laser media and multicavity micromachining in the process of laser miniaturization remain as significant challenges. Herein, room-temperature linearly polarized multiwavelength lasers in the visible and near-infrared wavelength ranges are demonstrated, by fabricating random cavities scattered with silica in an Er-doped Cs2Ag0.4Na0.6In0.98Bi0.02Cl6 double-perovskite quantum dots gain membrane. By regulating the local symmetry and enabling effective energy transfer in nanocrystals, multiwavelength lasers with ultralow thresholds are achieved at room temperature. The maximum degree of polarization reaches 0.89. With their advantages in terms of miniaturization, ultralow power consumption, and adaptability for integration, these lasers offer a prospective light source for future photonic integrated circuits aimed at high-capacity optical applications.

A Critical Role for γCaMKII in Decoding NMDA Signaling to Regulate AMPA Receptors in Putative Inhibitory Interneurons.

CaMKII is essential for long-term potentiation (LTP), a process in which synaptic strength is increased following the acquisition of information. Among the four CaMKII isoforms, γCaMKII is the one that mediates the LTP of excitatory synapses onto inhibitory interneurons (LTPE→I). However, the molecular mechanism underlying how γCaMKII mediates LTPE→I remains unclear. Here, we show that γCaMKII is highly enriched in cultured hippocampal inhibitory interneurons and opts to be activated by higher stimulating frequencies in the 10-30 Hz range. Following stimulation, γCaMKII is translocated to the synapse and becomes co-localized with the postsynaptic protein PSD-95. Knocking down γCaMKII prevents the chemical LTP-induced phosphorylation and trafficking of AMPA receptors (AMPARs) in putative inhibitory interneurons, which are restored by overexpression of γCaMKII but not its kinase-dead form. Taken together, these data suggest that γCaMKII decodes NMDAR-mediated signaling and in turn regulates AMPARs for expressing LTP in inhibitory interneurons.

HOXD9 transcriptionally induced UXT facilitate breast cancer progression via epigenetic modification of RND3.

BACKGROUND: Ubiquitously expressed transcript (UXT) is a prefoldin-like protein. It was reported that UXT played vital role in several cancer types. However, functional role of UXT in breast cancer need further investigation. METHODS: mRNA level or protein level of were determined by qRT-PCR or western blots. Proliferation of breast cancer cells was evaluated by CCK-8 assay and EdU assay. Migrative and invasive ability of cells were determined by wound healing assay and transwell assay. Transcriptional activation of UXT was determined by dual luciferase activity. The enrichment of H3K27me3 and EZH2 on the promoter of RND3 was evaluated by ChIP assay. The methylation of RND3 promoter was determined by MSP assay. In vivo function of UXT was evaluated by xenograft model. RESULTS: Our results indicated that UXT was elevated in breast cancer and associated with poor prognosis. HOXD9 elevated expression of UXT via transcriptional activation. UXT knockdown impaired the proliferation, migration and invasion. Rescue experiments suggested that UXT promoted malignant phenotypes of breast cancer cells via epigenetically repressing RND3. Moreover, UXT promoted tumorigeneses and metastasis of breast cancer cell in vivo. CONCLUSION: Inhibition of UXT impaired proliferation and metastasis of cancer cell via promoting RND3. Moreover, UXT epigenetically repressed the expression of RND3 via recruiting EZH2 in the promoter of RND3.

Luminescence, energy transfer, colour modulation and up-conversion mechanisms of Yb3+, Tm3+ and Ho3+ co-doped Y6MoO12.

A series of novel up-conversion luminescent Yb3+/Ln3+ (Tm3+, Ho3+, Tm3+/Ho3+)-doped Y6MoO12 (YMO) nanocrystals were synthesized using the sol-gel method. The consistent spherical morphology of the nanocrystals with different doping ratios was found to be profiting from the homogenisation and rapid agglomeration of the composition in the gel state and calcining process. The X-ray diffraction (XRD) and field-emission scanning electron microscope images were employed to confirm perfect crystallinity and uniform morphology. Photoluminescence spectra and decay curves were used to characterize the optical properties of the synthesized samples. The YMO:Yb3+/Ln3+ (Tm3+, Ho3+, Tm3+/Ho3+) nanocrystals were excited by near-infrared photons and emitted photons distributed in blue, green, and red bands with a wide colour gamut, and even white colour, by optimising the relative doping concentrations of the activator ions. The energy conversion mechanism in the up-conversion process was studied using power-dependent luminescence and is depicted in the energy level diagram. In addition, 70% of the luminescence intensity of YMO can be preserved after annealing at 700 °C, and the temperature sensing was tested in the range 298-498 K. These merits of multicolour emissions in the visible region and good stability endow the as-prepared nanocrystals with potential applications in the fields of optical data storage, encryption, sensing, and other multifunctional photonic technologies.

Rational designing of oscillatory rhythmicity for memory rescue in plasticity-impaired learning networks.

In the brain, oscillatory strength embedded in network rhythmicity is important for processing experiences, and this process is disrupted in certain psychiatric disorders. The use of rhythmic network stimuli can change these oscillations and has shown promise in terms of improving cognitive function, although the underlying mechanisms are poorly understood. Here, we combine a two-layer learning model, with experiments involving genetically modified mice, that provides precise control of experience-driven oscillations by manipulating long-term potentiation of excitatory synapses onto inhibitory interneurons (LTPE→I). We find that, in the absence of LTPE→I, impaired network dynamics and memory are rescued by activating inhibitory neurons to augment the power in theta and gamma frequencies, which prevents network overexcitation with less inhibitory rebound. In contrast, increasing either theta or gamma power alone was less effective. Thus, inducing network changes at dual frequencies is involved in memory encoding, indicating a potentially feasible strategy for optimizing network-stimulating therapies.

Spectroscopic identification of interactions of formaldehyde with bovine serum albumin.

The mechanism of formaldehyde-protein interactions was investigated by determining the effects of formaldehyde on the common protein bovine serum albumin (BSA). The effects at the molecular level were determined by fluorescence, ultraviolet absorption, and circular dichroism (CD) spectrometry. Formaldehyde could decrease the amount of alpha-helix, leading to loosening of the protein skeleton. In the loose structure, internal amino acids are exposed and the characteristic fluorescence of BSA is obviously quenched. The spectroscopic results reveal that formaldehyde exposure induces changes in the microenvironment and conformation of serum albumin, which could lead to toxic effects on the organism.

MiR-200c promotes papillary thyroid cancer cell proliferation, migration, and invasion by downregulating PTEN.

MiR-200c has been reported in several types of human cancer. Nevertheless, the expression profile and biological functions of miR-200c remain uncovered papillary thyroid cancer (PTC). The expression level of miR-200c was evaluated in PTC tissues using RT-qPCR. Survival analysis was performed in a cohort of 88 PTC patients. The effects of miR-200c on cell proliferation, migration, and invasion capacities were analyzed using CCK-8 and transwell assays. Target genes of miR-200c were assessed using luciferase reporter assay, RT-qPCR, Western blot and rescue experiments. MiR-200c was found to be upregulated in human PTC tissues and closely associated with pN stage and distant metastasis. High expression of miR-200c was associated with poor clinical prognosis in PTC patients. Whilst overexpression of miR-200c was demonstrated to promote the proliferation, migration, and invasion of PTC cells; knockdown of miR-200c showed an opposite inhibitory effect. Bioinformatics analysis and luciferase reporter assays confirmed that PTEN is a downstream target of miR-200c. Functional assays demonstrated that PTC cell proliferation, migration, and invasion were promoted by miR-200c via negative regulation of PTEN. Finally, overexpression of PTEN was shown to partially reverse the tumor promoting effect of miR-200c. In conclusion, this study indicates that miR-200c is a crucial prognostic biomarker of PTC, and that targeting of miR-200c/ PTEN axis may be of therapeutic significance in PTC patients.

Excitation-transcription coupling via synapto-nuclear signaling triggers autophagy for synaptic turnover and long-lasting synaptic depression.

For network rewiring and information storage in the brain, late phase long-term synaptic depression (L-LTD) requires the long-lasting reorganization of cellular resources. We found that activation of GRIN/NMDAR recruits transcription-dependent autophagy for synaptic turnover to support L-LTD. Activity-dependent CRTC1 synapto-nuclear translocation increases nuclear CRTC1 that competes with FXR for binding to CREB; this in turn enhances the direct binding between CRTC1-CREB and macroautophagy/autophagy gene promoters. Synergistic actions of CRTC1-CREB are preferentially turned on by LTD-inducing stimuli and switched off by genetic knockdown of CREB or CRTC1, or acutely activating FXR. Disrupted CRTC1-CREB signaling impairs activity-driven loss of surface GRIA/AMPARs and DLG4/PSD-95, and selectively prevents GRIN/NMDAR-dependent L-LTD, which are rescued by enhancing MTOR-regulated autophagy. These findings suggest a novel mechanism in L-LTD, in which brief synaptic activities recruit long-lasting autophagy through excitation-transcription coupling for ensuing synaptic remodeling.

Warm white-light emitting silica films prepared using lead-free double perovskite QDs.

Lead-free double perovskite has attracted widespread attention due to its good stability and non-toxicity. In this work, Cs2AgxNa1-xInCl6 quantum dots were synthesized via a thermal injection method using non-toxic precursors. Based on the wide spectrum of self-bound excitons, the quantum dots achieved white light emission. Bi-doped Cs2AgxNa1-xInCl6 quantum dots with excellent luminescence performance have the same cubic structure, and they have a larger Stokes shift. The cubic perovskite space group is Fm3[combining macron]m, and [NaCl6], [AgCl6] and [InCl6] octahedrons alternately appear in the cubic structure. The photoluminescence quantum yield of Cs2AgxNa1-xInCl6 is improved by doping with a small amount of Bi; the PL QY increased to 57.3% with an obvious emission peak at 600 nm. The stability and luminescence intensity of perovskite QDs were further enhanced by SiO2 coating and a Cs2AgxNa1-xInCl6:Bi-SiO2 thin film was prepared using perhydropolysilazane as the precursor. The materials have huge application potential in the field of white light emission and display.

Inner filter effect between upconversion nanoparticles and Fe(ii)-1,10-phenanthroline complex for the detection of Sn(ii) and ascorbic acid (AA).

Dual-function and multi-function sensors can use the same material or detection system to achieve the purpose of detection of two or more substances. Due to their high sensitivity and specificity, dual-function and multi-function sensors have potential applications in many fields. In this article, we designed a dual-function sensor to detect Sn(ii) and ascorbic acid (AA) based on the inner filter effect (IFE) between NaYF4:Yb,Er@NaYF4@PAA (UCNPs@PAA) and Fe(ii)-1,10-phenanthroline complex. Fe(ii)-1,10-phenanthroline complex has strong absorption in most of the ultraviolet-visible light range (350 nm-600 nm), and this absorption band overlaps with the green emission peak of UCNPs@PAA at 540 nm; Fe(ii)-1,10-phenanthroline complex can significantly quench the green light emission of UCNPs@PAA. When Sn(ii) or AA is added to the UCNPs@PAA/Fe(iii)/1,10-phenanthroline, they can reduce Fe(iii) to Fe(ii). Fe(ii) can react with 1,10-phenanthroline to form an orange complex, thereby quenching the green light emission of UCNPs@PAA. And the quenching efficiency is related to the concentration of Sn(ii) and AA; there is a linear relationship between quenching efficiency and the concentration of Sn(ii) and AA, within a certain concentration range the detection limits of this dual-function sensor for Sn(ii) and AA are 1.08 µM and 0.97 µM, respectively. In addition, the dual-function sensor can also detect Sn(ii) and AA in tap and spring water.

Neuronal activity recruits the CRTC1/CREB axis to drive transcription-dependent autophagy for maintaining late-phase LTD.

Cellular resources must be reorganized for long-term synaptic plasticity during brain information processing, in which coordinated gene transcription and protein turnover are required. However, the mechanism underlying this process remains elusive. Here, we report that activating N-methyl-d-aspartate receptors (NMDARs) induce transcription-dependent autophagy for synaptic turnover and late-phase long-term synaptic depression (L-LTD), which invokes cytoplasm-to-nucleus signaling mechanisms known to be required for late-phase long-term synaptic potentiation (L-LTP). Mechanistically, LTD-inducing stimuli specifically dephosphorylate CRTC1 (CREB-regulated transcription coactivator 1) at Ser-151 and are advantaged in recruiting CRTC1 from cytoplasm to the nucleus, where it competes with FXR (fed-state sensing nuclear receptor) for binding to CREB (cAMP response element-binding protein) and drives autophagy gene expression. Disrupting synergistic actions of CREB and CRTC1 (two essential L-LTP transcription factors) impairs transcription-dependent autophagy induction and prevents NMDAR-dependent L-LTD, which can be rescued by constitutively inducing mechanistic target of rapamycin (mTOR)-dependent autophagy. Together, these findings uncover mechanistic commonalities between L-LTP and L-LTD, suggesting that synaptic activity can tune excitation-transcription coupling for distinct long-lasting synaptic remodeling.

Gating of hippocampal rhythms and memory by synaptic plasticity in inhibitory interneurons.

Mental experiences can become long-term memories if the hippocampal activity patterns that encode them are broadcast during network oscillations. The activity of inhibitory neurons is essential for generating these neural oscillations, but molecular control of this dynamic process during learning remains unknown. Here, we show that hippocampal oscillatory strength positively correlates with excitatory monosynaptic drive onto inhibitory neurons (E→I) in freely behaving mice. To establish a causal relationship between them, we identified γCaMKII as the long-sought mediator of long-term potentiation for E→I synapses (LTPE→I), which enabled the genetic manipulation of experience-dependent E→I synaptic input/plasticity. Deleting γCaMKII in parvalbumin interneurons selectively eliminated LTPE→I and disrupted experience-driven strengthening in theta and gamma rhythmicity. Behaviorally, this manipulation impaired long-term memory, for which the kinase activity of γCaMKII was required. Taken together, our data suggest that E→I synaptic plasticity, exemplified by LTPE→I, plays a gatekeeping role in tuning experience-dependent brain rhythms and mnemonic function.