Defect Emission and Its Dipole Orientation in Layered Ternary Znln2 S4 Semiconductor.

Defect engineering is promising to tailor the physical properties of 2D semiconductors for function-oriented electronics and optoelectronics. Compared with the extensively studied 2D binary materials, the origin of defects and their influence on physical properties of 2D ternary semiconductors are not clarified. Here, the effect of defects on the electronic structure and optical properties of few-layer hexagonal Znln2 S4 is thoroughly studied via versatile spectroscopic tools in combination with theoretical calculations. It is demonstrated that the Zn-In antistructural defects induce the formation of a series of donor and acceptor energy levels and sulfur vacancies induce donor energy levels, leading to rich recombination paths for defect emission and extrinsic absorption. Impressively, the emission of donor-acceptor pair in Znln2 S4 can be significantly tailored by electrostatic gating due to efficient tunability of Fermi level (Ef ). Furthermore, the layer-dependent dipole orientation of defect emission in Znln2 S4 is directly revealed by back focal plane imagining, where it presents obviously in-plane dipole orientation within a dozen-layer thickness of Znln2 S4 . These unique features of defects in Znln2 S4 including extrinsic absorption, rich recombination paths, gate tunability, and in-plane dipole orientation are definitely a benefit to the advanced orientation-functional optoelectronic applications.

The protective effects of melatonin in high glucose environment by alleviating autophagy and apoptosis on primary cortical neurons.

Cognitive dysfunction has been regarded as a complication of diabetes. Melatonin (MLT) shows a neuroprotective effect on various neurological diseases. However, its protective effect on cortical neurons in high glucose environment has not been reported. Our present study aims to observe the protective effect of melatonin on rat cortical neurons and its relationship with autophagy in high glucose environment. The rat primary cortical neurons injury model was induced by high glucose. The CCK-8, flow cytometry, Western blot and immunofluorescence methods were used to examine the cell viability, apoptosis rate and proteins expression. Our results showed that there were no differences in cell viability, apoptosis rate, and protein expression among the control, MLT and mannitol group. The cell viability of the glucose group was significantly lower than that of the control group, and the apoptosis rate of the glucose group was significantly higher than that of the control group. Compared with the glucose group, the glucose + melatonin group showed a significant increase in cell viability and a notable decrease in apoptosis rate. Melatonin concentration of 0.1-1 mmol/L can significantly alleviate the injury of cortical neurons caused by high glucose. Compared with the control group, the glucose group showed a significant reduction of B-cell lymphoma 2 (Bcl-2) protein expression, while remarkable elevations of Bcl2-associated X protein (Bax), cleaved Caspase-3, coiled-coil, myosin-like Bcl2-interacting protein (Beclin-1) and microtubule-associated protein 1 light chain-3B type II (LC3B-II) levels. The neurons pre-administered with melatonin obtained significantly reversed these changes induced by high glucose. The phosphorylation levels of protein kinase B (Akt), mechanistic target of rapamycin kinase (mTOR) and Unc-51 like autophagy activating kinase 1(ULK1) were decreased in the glucose group compared with the control group, whereas significant increase were observed in the glucose + MLT group, compared with the glucose group. These data indicated that melatonin has a neuroprotective effect on cortical neurons under high glucose environment, which may work by activating Akt/mTOR/ULK1 pathway and may be deeply associated with the downregulation of autophagy.

The elemental 2D materials beyond graphene potentially used as hazardous gas sensors for environmental protection.

The intrinsic and electronic properties of elemental two-dimensional (2D) materials beyond graphene are first introduced in this review. Then the studies concerning the application of gas sensing using these 2D materials are comprehensively reviewed. On the whole, the carbon-, nitrogen-, and sulfur-based gases could be effectively detected by using most of them. For the sensing of organic vapors, the borophene, phosphorene, and arsenene may perform it well. Moreover, the G-series nerve agents might be efficiently monitored by the bismuthene. So far, there is still challenge on the material preparation due to the instability of these 2D materials under atmosphere. The synthesis or growth of materials integrated with the technique of surface protection should be associated with the device fabrication to establish a complete process for particular application. This review provides a complete and methodical guideline for scientists to further research and develop the hazardous gas sensors of these 2D materials in order to achieve the purpose of environmental protection.

Genistein-3'-sodium sulfonate ameliorates cerebral ischemia injuries by blocking neuroinflammation through the α7nAChR-JAK2/STAT3 signaling pathway in rats.

BACKGROUND: Neuroinflammation plays a pivotal role in the acute progression of cerebral ischemia/reperfusion injury (I/RI). We previously reported that genistein-3'-sodium sulfonate (GSS), a derivative from the extract of the phytoestrogen genistein (Gen), protects cortical neurons against focal cerebral ischemia. However, the molecular mechanism underlying the neuroprotective effects exerted by GSS remains unclear. PURPOSE: The present study focused on the anti-inflammatory effects of GSS following I/RI in rats. STUDY DESIGN: Randomized controlled trial. METHODS: The tMCAO rat model and LPS-stimulated BV2 in vitro model were used. Longa's scare was used to observe neurological function. TTC staining and Nissl staining were used to evaluate brain injury. ELISA, qRT-PCR, Western blotting and immunofluorescent staining methods were used to detect cytokine concentration, mRNA level, protein expression and location. RESULTS: GSS treatment improves neurological function, reduces the volume of cerebral infarction, attenuates proinflammatory cytokines and inactivates the phosphorylation of JAK2 and STAT3 in I/RI rats. Furthermore, GSS increased the expression of α7nAChR. More importantly, the neuroprotective, anti-inflammatory and inhibiting JAK2/STAT3 signaling pathway effects of GSS were counteracted in the presence of alpha-bungarotoxin (α-BTX), an α7nAChR inhibitor, suggesting that α7nAChR is a potential target associated with the anti-inflammatory effects of GSS in the I/RI rats. GSS also inhibited BV2 cells from releasing IL-1ß via the α7nAChR pathway after LPS stimulation. CONCLUSION: GSS protects against cerebral I/RI through the expression of α7nAChR and inhibition of the JAK2/STAT3 pathway. Our findings provide evidence for the role of the cholinergic anti-inflammatory pathway in neuroinflammation and uncover a potential novel mechanism for GSS treatment in ischemic stroke. The downstream signals of GSS, α7nAChR- JAK2/STAT3 could also be potential targets for the treatment of I/RI.

Modulation of 1 MeV electron irradiation on ultraviolet response in MoS2FET.

The material, electrical and ultraviolet optoelectronic properties of few layers bottom molybdenum disulfide (MoS2) field effect transistors (FETs) device was investigated before and after 1 MeV electron irradiation. Due to the participation of SiO2in conduction, we discovered novel photoelectric properties and a relatively long photogenerated carrier lifetime (several tens of seconds). Electron irradiation causes lattice distortion, the decrease of carrier mobility, and the increase of interface state. It leads to the degradation of output characteristics, transfer characteristics and photocurrent of the MoS2FET.

Genistein-3'-sodium sulfonate Attenuates Neuroinflammation in Stroke Rats by Down-Regulating Microglial M1 Polarization through α7nAChR-NF-κB Signaling Pathway.

Microglial M1 depolarization mediated prolonged inflammation contributing to brain injury in ischemic stroke. Our previous study revealed that Genistein-3'-sodium sulfonate (GSS) exerted neuroprotective effects in ischemic stroke. This study aimed to explore whether GSS protected against brain injury in ischemic stroke by regulating microglial M1 depolarization and its underlying mechanisms. We established transient middle cerebral artery occlusion and reperfusion (tMCAO) model in rats and used lipopolysaccharide (LPS)-stimulated BV2 microglial cells as in vitro model. Our results showed that GSS treatment significantly reduced the brain infarcted volume and improved the neurological function in tMCAO rats. Meanwhile, GSS treatment also dramatically reduced microglia M1 depolarization and IL-1ß level, reversed α7nAChR expression, and inhibited the activation of NF-κB signaling in the ischemic penumbra brain regions. These effects of GSS were further verified in LPS-induced M1 depolarization of BV2 cells. Furthermore, pretreatment of α7nAChR inhibitor (α-BTX) significantly restrained the neuroprotective effect of GSS treatment in tMCAO rats. α-BTX also blunted the regulating effects of GSS on neuroinflammation, M1 depolarization and NF-κB signaling activation. This study demonstrates that GSS protects against brain injury in ischemic stroke by reducing microglia M1 depolarization to suppress neuroinflammation in peri-infarcted brain regions through upregulating α7nAChR and thereby inhibition of NF-κB signaling. Our findings uncover a potential molecular mechanism for GSS treatment in ischemic stroke.

Icaritin Alleviates Glutamate-Induced Neuronal Damage by Inactivating GluN2B-Containing NMDARs Through the ERK/DAPK1 Pathway.

Excitatory toxicity due to excessive glutamate release is considered the core pathophysiological mechanism of cerebral ischemia. It is primarily mediated by N-methyl-D-aspartate receptors (NMDARs) on neuronal membranes. Our previous studies have found that icaritin (ICT) exhibits neuroprotective effects against cerebral ischemia in rats, but the underlying mechanism is unclear. This study aims to investigate the protective effect of ICT on glutamate-induced neuronal injury and uncover its possible molecular mechanism. An excitatory toxicity injury model was created using rat primary cortical neurons treated with glutamate and glycine. The results showed that ICT has neuroprotective effects on glutamate-treated primary cortical neurons by increasing cell viability while reducing the rate of lactate dehydrogenase (LDH) release and reducing apoptosis. Remarkably, ICT rescued the changes in the ERK/DAPK1 signaling pathway after glutamate treatment by increasing the expression levels of p-ERK, p-DAPK1 and t-DAPK1. In addition, ICT also regulates NMDAR function during glutamate-induced injury by decreasing the expression level of the GluN2B subunit and enhancing the expression level of the GluN2A subunit. As cotreatment with the ERK-specific inhibitor U0126 and ICT abolishes the beneficial effects of ITC on the ERK/DAPK1 pathway, NMDAR subtypes and neuronal cell survival, ERK is recognized as a crucial mediator in the protective mechanism of ICT. In conclusion, our findings demonstrate that ICT has a neuroprotective effect on neuronal damage induced by glutamate, and its mechanism may be related to inactivating GluN2B-containing NMDAR through the ERK/DAPK1 pathway. This study provides a new clue for the prevention and treatment of clinical ischemic cerebrovascular diseases.

Correction: High-aspect-ratio water-dispersed gold nanowires incorporated within gelatin methacrylate hydrogels for constructing cardiac tissues in vitro.

Correction for 'High-aspect-ratio water-dispersed gold nanowires incorporated within gelatin methacrylate hydrogels for constructing cardiac tissues in vitro' by Xiao-Pei Li et al., J. Mater. Chem. B, 2020, 8, 7213-7224, DOI: .

High-aspect-ratio water-dispersed gold nanowires incorporated within gelatin methacrylate hydrogels for constructing cardiac tissues in vitro.

The field of cardiac tissue engineering has made significant strides in therapeutic and pharmaceutical applications, highlighted by the development of smart biomaterials. Scaffolds with appropriate properties mimicking the nature of a heart matrix will be highly beneficial for cardiac tissue engineering. In this study, high-aspect-ratio water-dispersed gold nanowires (AuNWs) were synthesized and incorporated into gelatin methacrylate (GelMA) hydrogels, demonstrating enhanced electrical conductivity and mechanical properties of the biomaterial scaffolds. Cardiac cells cultured on GelMA-AuNW hybrid hydrogels exhibited better biological activities such as cell viability and maturation state compared to those cultured on GelMA hydrogels. Moreover, cardiomyocytes showed synchronous beating activity and a faster spontaneous beating rate on GelMA-AuNW hybrid hydrogels. Our strategy of integrating high-aspect-ratio water-dispersed gold nanowires within gelatin methacrylate hydrogels provides a favorable biomaterial scaffold to construct functional cardiac tissue for further applications in cardiac tissue engineering and drug screening.

Direct Synthesis of Large-Scale Multilayer TaSe2 on SiO2/Si Using Ion Beam Technology.

The multilayer 1T-TaSe2 is successfully synthesized by annealing a Se-implanted Ta thin film on the SiO2/Si substrate. Material analyses confirm the 1T (octahedral) structure and the quasi-2D nature of the prepared TaSe2. Temperature-dependent resistivity reveals that the multilayer 1T-TaSe2 obtained by our method undergoes a commensurate charge-density wave (CCDW) transition at around 500 K. This synthesis process has been applied to synthesize MoSe2 and HfSe2 and expanded for synthesis of one more transition-metal dichalcogenide (TMD) material. In addition, the main issue of the process, that is, the excess metal capping on the TMD layers, is solved by the reduction of thickness of the as-deposited metal thin film in this work.

Electron radiation effects on the structural and electrical properties of MoS2 field effect transistors.

The effects of space radiation on the structural and electrical properties of MoS2 field effect transistors (FETs) were investigated. The 1 MeV electronically equivalent International Space Station (ISS) track was used to apply fluence equivalent to the orbital for 10 (1.0 × 1012 cm-2) and 30 years (3.0 × 1012 cm-2) using the AP8 and AE8 models. X-ray photoelectron spectroscopy (XPS), Raman and photoluminescence (PL) spectra were recorded before and after irradiation. Electron irradiation produced strong desulfurization effects in MoS2 FETs. The PL spectra before and after irradiation did not change significantly, while the [Formula: see text] and A1g Raman modes were red- and blue-shifted, respectively. The XPS results demonstrated a strong desulfurization effect of the electron beam on MoS2. This reduction indicates a much higher amount of irradiation-induced S vacancies compared to Mo vacancies. The electrical characteristics of the device were measured before and after irradiation. The increase in the channel leakage current after irradiation was attributed to the oxide trapping positive charges. MoS2 FETs irradiated by the electron-beam demonstrated a decreased current. This phenomenon can be attributed to the combination of the states at the SiO2/MoS2 interfaces and Coulomb scattering. Our study provides a deeper understanding of the influence of 1 MeV electron-beam irradiation on MoS2-based nano-electronic devices for future space applications.

Modulation of electronic and optical properties by surface vacancies in low-dimensional ß-Ga2O3.

Calculations using the Heyd-Scuseria-Ernzerhof screened hybrid functional reveal the detailed influence that surface vacancies have on the electronic and optical properties of low-dimensional (LD) ß-Ga2O3. Vacancies manifest subtle changes to the electronic characteristics as oxygen states predominate the valence band at the surface. Dielectric functions at the surface are found to increase with vacancies and defects. A broad impact on optical properties, such as absorption coefficients, reflectivity, refractive indices, and electron loss, is seen with increased vacancy defects. Both visible and infrared regions show direct correlation with vacancies while there is a marked decrease in the deep ultraviolet (UV) region. These calculations on the ß-Ga2O3 model system may guide the rational design of two-dimensional optical devices with minimized van der Waals forces.

Easy Applied Gelatin-Based Hydrogel System for Long-Term Functional Cardiomyocyte Culture and Myocardium Formation.

Harnessing biomaterials for in vitro tissue construction has long been a research focus because of its powerful potentials in tissue engineering and pharmaceutical industry. Myocardium is a critical cardiac tissue with complex multiple muscular layers. Considering the specific characters of native cardiac tissues, it is necessary to design a biocompatible and biomimetic platform for cardiomyocyte culture and myocardium formation with sustained physiological function. In this study, we developed gelatin-based hydrogels chemically cross-linked by genipin, a biocompatible cross-linker, as cell culture scaffolds. Moreover, to achieve and maintain the functionality of myocardium, for instance, well-organized cardiomyocytes and synchronized contractile behavior, we fabricated gelatin-based hydrogels with patterned microstructure using a microcontact printing technique. Furthermore, graphene oxide (GO), with unprecedented physical and chemical properties, has also been incorporated into gelatin for culturing cardiomyocytes. Our results show that micropatterned genipin-cross-linked gelatin hydrogels are very helpful to promote alignment and maturation of neonatal rat ventricular cardiomyocytes. More interestingly, the presence of GO significantly enhances the functional performance of cardiomyocytes, including an increase in contraction amplitude and cardiac gene expression. The cultured cardiomyocytes reach a well-synchronized contraction within 48 h of cell seeding and keep beating for up to 3 months. Our study provides a new and easy-to-use gelatin-based scaffold for improving physiological function of engineered cardiac tissues, exhibiting promising applications in cardiac tissue engineering and drug screening.

Ultra-fast annealing manipulated spinodal nano-decomposition in Mn-implanted Ge.

In the present work, millisecond-range flash lamp annealing is used to recrystallize Mn-implanted Ge. Through systematic investigations of structural and magnetic properties, we find that the flash lamp annealing produces a phase mixture consisting of spinodally decomposed Mn-rich ferromagnetic clusters within a paramagnetic-like matrix with randomly distributed Mn atoms. Increasing the annealing energy density from 46, via 50, to 56 J cm-2 causes the segregation of Mn atoms into clusters, as proven by transmission electron microscopy analysis and quantitatively confirmed by magnetization measurements. According to x-ray absorption spectroscopy, the dilute Mn ions within Ge are in d 5 electronic configuration. This Mn-doped Ge shows paramagnetism, as evidenced by the unsaturated magnetic-field-dependent x-ray magnetic circular dichroism signal. Our study reveals how spinodal decomposition occurs and influences the formation of ferromagnetic Mn-rich Ge-Mn nanoclusters.

Interaction between hydrogen and gallium vacancies in ß-Ga2O3.

In this paper, the revised Heyd-Scuseria-Ernzerhof screened hybrid functional (HSE06) is used to investigate the interaction between hydrogen with different concentrations and gallium vacancies in ß-Ga2O3. The hydrogen can compensate a gallium vacancy by forming hydrogen-vacancy complex. A gallium vacancy can bind up to four hydrogen atoms, and formation energies decrease as the number of hydrogen atoms increases. Hydrogen prefers to bind with three coordinated oxygen. The bonding energy and annealing temperatures of complexes containing more than two hydrogen atoms are computed, and show relatively high stability. In addition, vacancy concentrations increase with the increasing vapor pressures. This paper can effectively explain the hydrogen impact in ß-Ga2O3.

3'-Daidzein sulfonate sodium provides neuroprotection by promoting the expression of the α7 nicotinic acetylcholine receptor and suppressing inflammatory responses in a rat model of focal cerebral ischemia.

In a previous study using a rat model of focal cerebral ischemia/reperfusion (I/R) injury, we found that 3'-Daidzein sulfonate sodium (DSS), a derivative of daidzein, exerts neuroprotective effects by alleviating brain edema and reducing levels of interleukin (IL)-6. The present study was designed to further examine the potential mechanisms of the neuroprotective properties of DSS in a rat model of cerebral I/R injury. We found that treatment with DSS ameliorated neurological deficit, infarct size, and cerebral water content in rats with cerebral I/R injury. Moreover, treatment with DSS significantly reduced the levels of IL-1ß, IL-6, and tumor necrosis factor (TNF)-α in serum and in the ischemic penumbra. Additionally, DSS treatment increased the expression of nicotinic acetylcholine receptor alpha 7 (α7nAChR), and inhibited the expression of glial fibrillary acidic protein, phosphorylated p65 nuclear factor κB, and phosphorylated inhibitor of NF-κBα, suggesting that DSS provides neuroprotection by suppressing inflammatory responses after focal cerebral I/R injury. Notably, α-bungarotoxin, an antagonist of α7nAChR, reversed the neuroprotective effects of DSS after cerebral I/R injury, suggesting that inhibition of α7nAChR expression is sufficient for reversal of the neuroprotective effects of DSS. In conclusion, we found that DSS treatment provides neuroprotection by promoting α7nAChR expression in a rat model of focal cerebral ischemia, thus establishing α7nAChR as a potential therapeutic target in cerebral I/R injury.

MicroRNA-34a modulates the Notch signaling pathway in mice with congenital heart disease and its role in heart development.

The objective of the study was to elucidate the mechanism by which microRNA-34a (miR-34a) influences heart development and participates in the pathogenesis of congenital heart disease (CHD) by targeting NOTCH-1 through the Notch signaling pathway. Forty D7 pregnant mice were recruited for the purposes of the study and served as the CHD (n=20, successfully established as CHD model) and normal (n=20) groups. The positive expression of the NOTCH-1 protein was evaluated by means of immunohistochemistry. Embryonic endocardial cells (ECCs) were assigned into the normal, blank, negative control (NC), miR-34a mimics, miR-34a inhibitors, miR-34a inhibitors+siRNA-NOTCH-1, siRNA-NOTCH-1, miR-34a mimics+NOTCH-1 OE and miR-34a mimics+crispr/cas9 (mutant NOTCH-1) groups. The expressions of miR-34a, NOTCH-1, Jagged1, Hes1, Hey2 and Csx in cardiac tissues and ECCs were determined by both RT-qPCR and western blotting methods. MTT assay and flow cytometry were conducted for cell proliferation and apoptosis measurement. A dual luciferase reporter assay was applied to demonstrate that NOTCH-1 was the target gene of miR-34a. In comparison to the normal group, the expressions of miR-34a, Jagged1, Hes1 and Hey2 displayed up-regulated levels, while the expressions of NOTCH-1 and Csx were down-regulated in the CHD group. Compared with the blank and NC groups, the miR-34a mimics and siRNA-NOTCH-1 groups displayed reduced expressions of NOTCH-1 and Csx as well as a decreased proliferation rate, higher miR-34a, Jagged1, Hes1 and Hey2 expressions and an increased rate of apoptosis; while an reverse trend was observed in the miR-34a inhibitors group. The expressions of MiR-34a recorded increased levels in the miR-34a mimics+NOTCH-1 OE and miR-34a mimics+crispr/cas9 (mutant NOTCH-1) groups, however no changes in the expressions of NOTCH-1, Jagged1, Hes1, Hey2, Csx, as well as cell proliferation and apoptosis were observed when compared to the blank and NC groups. The results of our study demonstrated that miR-34a increases the risk of CHD through its downregulation of NOTCH-1 by modulating the Notch signaling pathway.

Estimation of tea catechin levels using micellar electrokinetic chromatography: a quantitative approach.

A simple, inexpensive micellar electrokinetic chromatography (MEKC) method with UV detection was used to determine seven catechins and one xanthine (caffeine) in tea. All the compounds were successfully separated (15kV) within a 15-min migration period with a high number of theoretical plates (>8.0×10(4)) in a running buffer (pH 7) containing 10mmoll(-1) sodium tetraborate, 4mmoll(-1) sodium phosphate, and 25mmoll(-1) SDS. The regression lines of all standard catechins were linear within the range of 0.03-4µgml(-1). Green tea infused at 95°C for 10min showed higher levels of catechins (especially epigallocatechin galate, epicatechin gallate, and epicatechin) than tea infused at 80°C. In addition, major differences were observed in the levels of catechins in the first and second infusions (both brewed at 95°C for 10min). Finally, green tea leaves were infused separately with tap water, deionised water, spring water, reverse osmosis water, and distilled water at 95°C, and the catechin content of the infusions was investigated by the proposed method. In the infusion brewed with tap water, catechins appeared to be epimerisation from the epistructure to the nonepistructure. This epimerisation may take place more readily in tap water than in distilled water owing to the complexity of the ions present in tap water.

Gold nanosponges: green synthesis, characterization, and cytotoxicity.

A simply approach for the synthesis of Au nanostructures in tea infusions at room temperature is developed. By controlling the concentrations of tea infusions, Au nanostructures in various shapes and sizes have been prepared. From 1 x (original concentration) and 0.01 x (100 times diluted) tea infusions, 52.2 +/- 8.1 nm Au nanosponges (T-Au NSs) and 23 +/- 2 nm spherical Au nanoparticles (T-Au NPs) were prepared. The phytochemicals present on the surface of T-Au NSs were proved by surface-assisted laser desorption/ionization mass spectrometry, Fourier transform infrared spectrometry and capillary electrophoresis coupled with UV detection. The energy-dispersive X-ray spectroscopy and powder X-ray diffraction data reveal pure crystalline structures of the T-Au NSs. The dark field scattering images observe that the T-Au NSs have significant affinity toward HeLa cells. The cytotoxicity of T-Au NSs on HeLa cells is through caspase-3 activation.