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The over-production of β-amyloid (Aβ) has been strongly correlated to neuronal dysfunction and altered synaptic plasticity in Alzheimer’s disease (AD). Accordingly, it has been proposed that disrupted synaptic transmission and neuronal network instability underlie memory failure that is evident in the early phases of AD. Homeostatic synaptic plasticity (HSP) serves to restrain neuronal activity within a physiological range. Therefore a disruption of this mechanism may lead to destabilization in synaptic and neural circuit function. Here, we report that during HSP by neuronal activity deprivation, application of Aβ results in an aberrant over-response of the up-regulation of AMPA receptor (AMPAR)-mediated synaptic currents and cell-surface AMPAR expression. In the visual cortex, in vivo HSP induced by visual deprivation shows a similar over-response following an Aβ local injection. Aβ increases the expression of GluA2-lacking, calcium permeable AMPARs (CP-AMPARs), which are required for the initiation, but not maintenance of HSP. Both GluA2-lacking and GluA2-containing AMPARs contribute to the Aβ-mediated over-scaling of HSP. We also find that Aβ induces the dissociation of HDAC1 from the miR124 transcription factor EVI1, leading to an up-regulation of miR124 expression and increased amount of CP-AMPARs. Thus, via aberrant stimulation of miR124 expression and biogenesis of CP-AMPARs, Aβ is able to induce an over response in HSP. This Aβ-mediated dysregulation in homeostatic plasticity may play an important role in the pathogenesis of altered neural function and memory deficits in the early stages of AD.

Clinical data have shown women are more susceptible to depression. This study was performed to identify differentially regulated proteins from hippocampus in chronic unpredicted mild stress (CUMS)-exposed male and female young rats. After 7 weeks of CUMS, depressed male (M-D) and female rats (F-D) and unstressed male (M-C) and female controls (F-C) were studied. By proteomics analysis, 74 differential proteins in F-C/M-C, 79 in F-D/M-D, 77 in F-D/F-C, and 32 in M-D/M-C were found. Further, the synapse-related proteins, cytoskeleton protein tau, and stress-related kinases in hippocampus were assayed by Western blotting. F-C rats were found to have lower levels of metabotropic glutamate receptor 1 (mGluR1) and mGluR2 and higher levels of N-methyl-D-aspartate receptor 2B (NR2B), synapsin1, total tau, and dephosphorylated tau than M-C rats. Both F-D and M-D rats had lower levels of glutamate transporter SLC1α2, mGluR1, and mGluR2, and higher levels of total tau and phosphorylated tau than their controls. Compared with their controls, M-D rats had lower NR1 and higher NR2B, and F-D rats had lower NR2A, NR2B, PSD95, and synapsin1. F-C rats had higher JNK and lower phosphorylation levels of ERK at Thr202/Thr204, JNK at Thr183/Thr185, and GSK-3β at Ser9 than M-C ones. Both M-D and F-D rats had decreased phosphorylation of ERK at Thr202/Thr204 and GSK-3β at Ser9, and increased JNK phosphorylation at Thr183/Thr185 compared with their controls. All these data illustrate the biochemical complexity behind the genders, and may also aid in the development of more accurate treatment strategies for depression.

Background Synaptic loss is an early pathological event in Alzheimer’s disease (AD), but its underlying molecular mechanisms remain largely unknown. Recently, microRNAs (miRNAs) have emerged as important modulators of synaptic function and memory. Methods We used miRNA array and quantitative polymerase chain reaction to examine the alteration of miRNAs in AD mice and patients as well as the Morris water maze to evaluate learning and memory in the mice. We also used adeno-associated virus or lentivirus to introduce tyrosine-protein phosphatase non-receptor type 1 (PTPN1) expression of silencing RNAs. Long-term potentiation and Golgi staining were used to evaluate the synaptic function and structure. We designed a peptide to interrupt miR-124/PTPN1 interaction. Results Here we report that neuronal miR-124 is dramatically increased in the hippocampus of Tg2576 mice, a recognized AD mouse model. Similar changes were observed in specific brain regions of affected AD individuals. We further identified PTPN1 as a direct target of miR-124. Overexpression of miR-124 or knockdown of PTPN1 recapitulated AD-like phenotypes in mice, including deficits in synaptic transmission and plasticity as well as memory by impairing the glutamate receptor 2 membrane insertion. Most importantly, rebuilding the miR-124/PTPN1 pathway by suppression of miR-124, overexpression of PTPN1, or application of a peptide that disrupts the miR-124/PTPN1 interaction could restore synaptic failure and memory deficits. Conclusions Taken together, these results identified the miR-124/PTPN1 pathway as a critical mediator of synaptic dysfunction and memory loss in AD, and the miR-124/PTPN1 pathway could be considered as a promising novel therapeutic target for AD patients.

Summary: Retroactive interference (RI) occurs when new incoming information impairs an existing memory, which is one of the primary sources of forgetting. Although long-term potentiation (LTP) reversal shows promise as the underlying neural correlate, the key molecules that control the sensitivity of memory circuits to RI are unknown, and the developmental trajectory of RI effects is unclear. Here we found that depotentiation in the hippocampal dentate gyrus (DG) depends on GluN2A-containing NMDA receptors (NMDARs). The susceptibility of LTP to disruption progressively increases with the rise in the GluN2A/GluN2B ratio during development. The vulnerability of hippocampus-dependent memory to interference from post-learning novelty exploration is subject to similar developmental regulation by NMDARs. Both GluN2A overexpression and GluN2B downregulation in the DG promote RI-induced forgetting. Altogether, our results suggest that a switch in GluN2 subunit predominance may confer age-related differences to depotentiation and underlie the developmental decline in memory resistance to RI. : Ge et al. report that the NMDA receptor GluN2A/GluN2B subunit ratio determines the sensitivity of strengthened neuronal connections to depotentiation. As the ratio rises during development, memories become more vulnerable to disruption by post-learning interference. These findings help to illuminate the mechanism by which forgetting rates may vary with age. Keywords: forgetting, retroactive interference, depotentiation, NMDA receptor

Hydrocephalus is a neurological condition caused by an abnormal accumulation of cerebrospinal fluid; pharmacological intervention of the disease has been found to elicit a variety of adverse drug reactions (ADRs) in central nervous system (CNS) by unexpectedly targeting certain functional neuroproteins. Here, a systematic neuroprotein drug interactome (SNDI) is created for 11 hydrocephalus drugs/metabolites plus 20 control drugs across 518 druggable pockets on the surface of 472 CNS neuroproteins via a large-scale molecular docking approach. Heuristic clustering analysis of the SNDI profile divides the 31 investigated drug ligands into a distinct panel and a background panel; the former consists of two hydrocephalus drugs (Furosemide and Triamterene) and their respective metabolites (Furosemide glucuronide and Hydroxytriamterene) that are inferred to have generally high affinity towards the whole array of neuroprotein pockets. A total of 13 neuroproteins are enriched in gene ontology semantic mining as putative unexpected targets of the distinct panel, and their intermolecular interactions with hydrocephalus drugs/metabolites are investigated in detail using dynamics simulation and energetics analysis. We also perform kinase assay and viability test to substantiate the interactome analysis. It is found that the Furosemide and Triamterene have significant cytotoxic effects on normal human astrocytes, in which the Triamterene can inhibit the neurokinase ROCK2, a representative of putative unexpected targets, with a high activity, which is comparable with the sophisticated ROCK2 inhibitor Fasudil.

The aberrant activation of CDK5 has been implicated in neuronal death in stroke. The goal of this study is to determine whether knocking down CDK5 by a peptide-directed lysosomal degradation approach is therapeutically effective against stroke. We synthesized a membrane-permeable peptide that specifically binds to CDK5 with a chaperone-mediated autophagy targeting motif (Tat-CDK5-CTM) and tested its therapeutic effects on a mouse model of ischemic stroke. Our results showed that Tat-CDK5-CTM blocked the CDK5-NR2B interaction, resulting in the degradation of CDK5, which in turn prevented calcium overload and neuronal death in cultured neurons. Tat-CDK5-CTM also reduced the infarction area and neuronal loss and improved the neurological functions in MCAO (Middle cerebral artery occlusion) mice. The peptide-directed lysosomal degradation of CDK5 is a promising therapeutic intervention for stroke.

Correction for ‘High-performance UV detectors based on room-temperature deposited amorphous Ga2O3 thin films by RF magnetron sputtering’ by Shun Han et al., J. Mater. Chem. C, 2019, 7, 11834–11844.

The objective of the study was to investigate the role of neuregulin-ErbB signaling in neuropathic pain in different types of injury. Neuregulin-1(NRG-1) was injected into animals with either formalin-induced pain model or spared nerve injury (SNI) model. Formalin tests or paw withdrawal tests were performed to study the role of NRG-1 in neuropathic pain. siRNA specific to different erbB receptors were then introduced to test which specific signaling pathway was required for NRG-1 signaling in the different pain models. NRG-1 inhibits neuropathic pain after SNI in a dose-dependent manner, while NRG-1 aggravates formalin-induced neuropathic pain. ErbB2 and erbB4 receptors were activated after neuregulin administration. Knockdown of ErbB2 relieves the aggravation of NRG-1 on formalin-induced neuropathic pain, and knockdown of ErbB4 could relieve the inhibition of NRG-1 on neuropathic pain in the SNI model. NRG-1 has two distinct functions depending on the different receptor activation in different models of neuropathic pain. These novel findings may provide new therapeutic approaches for the treatment of neuropathic pain in different injury types.

Cubic MgZnO thin films were deposited on amorphous quartz substrate by PLD method. Effect of deposition pressure on preferential orientation and optical absorption characteristics of MgZnO thin films were studied. The preferred orientation of cubic MgZnO changed from (2 0 0) to (1 1 1) when deposition pressure increased, and absorption edges of which shift to longer wavelength direction because Mg content of MgZnO thin film decreased. Cubic MgZnO showed much better crystal quality and preferential orientation growth characteristics on proper crystal substrate, because on this substrate the preferred orientation of cubic MgZnO is accordance with that grown in free growth mode on amorphous substrate at special air pressure.

Al-doped ZnO (AZO) thin films were prepared by RF magnetron sputtering on quartz substrates at room temperature in different Ar + H2 ambient. The influence of H2 flow ratio on the structure and optoelectronic properties in AZO films was investigated. The prepared films are hexagonal wurtzite structure with c-axis preferred orientation, and the intensity of (002) peak decreases with the increase of H2 flow ratio. The resistivity significantly decreases with increasing the H2 flow ratio to 1.0 % by almost four orders of magnitude. X-Ray photoelectron spectroscopy and X-ray diffraction measurements exhibit that the effectiveness of Al doping in the substitutional positions is not influenced by H2 addition. We suggest that there exist a large number of acceptors in the films, the introduced H2 will passivate the acceptors, which raises both carrier concentration and Hall mobility. The increase of carrier concentration consequently induces the blue shift of optical absorption edge according to the Burstein-Moss effect.

Exchange protein directly activated by cAMP (Epac) and protein kinase A (PKA) are intracellular receptors for cAMP. Although PKA and its downstream effectors have been studied extensively in the context of drug addiction, whether and how Epac regulates cellular and behavioral effects of drugs of abuse remain essentially unknown. Epac is known to regulate AMPA receptor (AMPAR) trafficking. Previous studies have shown that a single cocaine exposurein vivoleads to an increase in GluA2-lacking AMPARs in dopamine neurons of the ventral tegmental area (VTA). We tested the hypothesis that Epac mediates cocaine-induced changes in AMPAR subunit composition in the VTA. We report that a single cocaine injectionin vivoin wild-type mice leads to inward rectification of EPSCs and renders EPSCs sensitive to a GluA2-lacking AMPAR blocker in VTA dopamine neurons. The cocaine-induced increase in GluA2-lacking AMPARs was absent in Epac2-deficient mice but not in Epac1-deficient mice. In addition, activation of Epac with the selective Epac agonist 8-CPT-2Me-cAMP (8-CPT) recapitulated the cocaine-induced increase in GluA2-lacking AMPARs, and the effects of 8-CPT were mediated by Epac2. We also show that conditioned place preference to cocaine was impaired in Epac2-deficient mice and in mice in which Epac2 was knocked down in the VTA but was not significantly altered in Epac1-deficient mice. Together, these results suggest that Epac2 is critically involved in the cocaine-induced change in AMPAR subunit composition and drug-cue associative learning.SIGNIFICANCE STATEMENTAddictive drugs, such as cocaine, induce long-lasting adaptions in the reward circuits of the brain. A single intraperitoneal injection of cocaine leads to changes in the composition and property of the AMPAR that carries excitatory inputs to dopamine neurons. Here, we provide evidence that exchange protein directly activated by cAMP (Epac), a cAMP sensor protein, is required for the cocaine-induced changes of the AMPAR. We found that the effects of cocaine were mimicked by activation of Epac but were blocked by genetic deletion of Epac. Furthermore, cocaine-cue associative learning was impaired in mice lacking Epac. These findings uncovered a critical role of Epac in regulating the cellular and behavioral actions of cocaine.

Black phosphorus (BP) has emerged as a promising two-dimensional (2D) material for next generation transistor applications due to its superior carrier transport properties. Among other issues, achieving reduced subthreshold swing and enhanced hole mobility simultaneously remains a challenge which requires careful optimization of the BP/gate oxide interface. Here, we report the realization of high performance BP transistors integrated with HfO2 high-k gate dielectric using a low temperature CMOS process. The fabricated devices were shown to demonstrate a near ideal subthreshold swing (SS) of ~69 mV/dec and a room temperature hole mobility of exceeding >400 cm2/Vs. These figure-of-merits are benchmarked to be the best-of-its-kind, which outperform previously reported BP transistors realized on traditional SiO2 gate dielectric. X-ray photoelectron spectroscopy (XPS) analysis further reveals the evidence of a more chemically stable BP when formed on HfO2 high-k as opposed to SiO2, which gives rise to a better interface quality that accounts for the SS and hole mobility improvement. These results unveil the potential of black phosphorus as an emerging channel material for future nanoelectronic device applications.

The entorhinal cortex (EC) is one of the most vulnerable brain regions that is attacked during the early stage of Alzheimer's disease (AD). Here, we report that the synaptic terminals of pyramidal neurons in the EC layer II (ECIIPN) directly innervate CA1 parvalbumin (PV) neurons (CA1PV) and are selectively degenerated in AD mice, which exhibit amyloid-β plaques similar to those observed in AD patients. A loss of ECIIPN-CA1PV synapses disables the excitatory and inhibitory balance in the CA1 circuit and impairs spatial learning and memory. Optogenetic activation of ECIIPN using a theta burst paradigm rescues ECIIPN-CA1PV synaptic defects and intercepts the decline in spatial learning and memory. These data reveal a novel mechanism of memory loss in AD mice via the selective degeneration of the ECIIPN-CA1PV pathway.

Figure S1â S6. (PDF 1580 kb)

Alzheimer’s disease (AD) is a late-onset progressive neurodegenerative disorder that leads to cognitive, memory and behavioural impairments. Substantial evidence indicates that disrupted neuronal calcium homeostasis is an early event in AD that could mediate synaptic dysfunction and neuronal toxicity. Sodium calcium exchangers (NCXs) play important roles in regulating intracellular calcium, and accumulated data suggests that reduced NCX function, following aberrant proteolytic cleavage of these exchangers, may contribute to neurodegeneration. This review, characterizes the expression and activity of NCX as a prominent feature of AD brain, identifies the molecular mechanisms underlying the effects of NCX isoforms, and pinpoints the molecular determinants responsible for the effects of NCX. Our findings suggest that calpain mediates cleavage of NCX3 in AD brain and therefore that reduced NCX3 activity contributes to the sustained increases in intraneuronal calcium concentrations that are associated with caspase-12 activation and neuronal death in AD.

Chronic intake of nicotine can impair hippocampal plasticity, but the underlying mechanism is poorly understood. Here, we demonstrate that chronic nicotine administration in adult rats inactivates the cyclic AMP-response element binding protein (CREB), a transcription factor that regulates neurogenesis and other plasticity-related processes necessary for learning and memory. Consequently, we showed that impaired CREB signaling is associated with a significant decline in the production of new neurons in the dentate gyrus. Combining retrovirus labeling with gene expression approaches, we found that chronic nicotine administration reduces the number of adult-generated granule neurons by decreasing the survival of newborn cells but not the proliferation of progenitor cells. Additionally, we found that retroviral-mediated expression of a constitutively active CREB in the dentate gyrus rescues survival of newborn cells and reverses the nicotine-induced decline in the number of mature granule neurons. Prolonged nicotine exposure also compromises CREB activation and reduces the viability of progenitor cells in vitro, thereby suggesting that nicotine may exert its adverse effects directly on immature cells in vivo. Taken together, these data demonstrate that inhibition of CREB activation is responsible for the nicotine-induced impairment of hippocampal plasticity.

EPAC proteins are the guanine nucleotide exchange factors that act as the intracellular receptors for cyclic AMP. Two variants of EPAC genes including EPAC1 and EPAC2 are cloned and are widely expressed throughout the brain. But, their functions in the brain remain unknown. Here, we genetically delete EPAC1 (EPAC1(-/-)), EPAC2 (EPAC2(-/-)), or both EPAC1 and EPAC2 genes (EPAC(-/-)) in the forebrain of mice. We show that EPAC null mutation impairs long-term potentiation (LTP) and that this impairment is paralleled with the severe deficits in spatial learning and social interactions and is mediated in a direct manner by miR-124 transcription and Zif268 translation. Knockdown of miR-124 restores Zif268 and hence reverses all aspects of the EPAC(-/-) phenotypes, whereas expression of miR-124 or knockdown of Zif268 reproduces the effects of EPAC null mutation. Thus, EPAC proteins control miR-124 transcription in the brain for processing spatial learning and social interactions.

Glucose-stimulated insulin secretion (GSIS) from pancreatic β-cells is potentiated by cAMP-elevating agents, such as the incretin hormone glucagon-like peptide-1 (GLP-1), and cAMP exerts its insulin secretagogue action by activating both protein kinase A (PKA) and the cAMP-regulated guanine nucleotide exchange factor designated as Epac2. Although prior studies of mouse islets demonstrated that Epac2 acts via Rap1 GTPase to potentiate GSIS, it is not understood which downstream targets of Rap1 promote the exocytosis of insulin. Here, we measured insulin secretion stimulated by a cAMP analog that is a selective activator of Epac proteins in order to demonstrate that a Rap1-regulated phospholipase C-epsilon (PLC-ε) links Epac2 activation to the potentiation of GSIS. Our analysis demonstrates that the Epac activator 8-pCPT-2'-O-Me-cAMP-AM potentiates GSIS from the islets of wild-type (WT) mice, whereas it has a greatly reduced insulin secretagogue action in the islets of Epac2 (-/-) and PLC-ε (-/-) knockout (KO) mice. Importantly, the insulin secretagogue action of 8-pCPT-2'-O-Me-cAMP-AM in WT mouse islets cannot be explained by an unexpected action of this cAMP analog to activate PKA, as verified through the use of a FRET-based A-kinase activity reporter (AKAR3) that reports PKA activation. Since the KO of PLC-ε disrupts the ability of 8-pCPT-2'-O-Me-cAMP-AM to potentiate GSIS, while also disrupting its ability to stimulate an increase of β-cell [Ca2+]i, the available evidence indicates that it is a Rap1-regulated PLC-ε that links Epac2 activation to Ca2+-dependent exocytosis of insulin.

Zinc oxide (ZnO) films were deposited onto Si to form n-ZnO/p-Si heterojunctions. Under the illumination of by both ultraviolet (UV) light and sunlight, obvious photovoltaic behavior was observed. It was found that the conversion efficiency of the heterojunctions increased significantly with increasing thickness of the ZnO film, and the mechanism for light-harvesting in the heterojunctions is discussed. The results suggest that ZnO films may be helpful to increasing the harvesting of UV photons, thus decreasing the thermalization loss of UV energy in Si-based solar cells.

We present a low-temperature optical study of the large-area monolayer WS2 grown by chemical vapor deposition (CVD). Power-dependent photoluminescence (PL) measurements were conducted, and temperature-dependent PL spectra were measured in the range of 3 to 300 K. With the comparative PL bands obtained, a stronger trion emission in the edge region was detected to be the key difference. Sulfur vacancies (SVs) were observed to increase in density along the growth direction and found to be the main source of the large population of local charge carriers. The monolayer WS2 exhibited an upper bound for the trion binding energy of 18 meV in the edge region.

Owing to the low doping concentration of nitrogen and strong compensation of intrinsic donors, the attainment of highly conductive p-type ZnO films remains one of the largest challenges for the application of ZnO. An approach has been proposed to increase the doping concentration of nitrogen in ZnO by exposing the ZnO:N films in the ambient of nitrogen plasma periodically in this paper. Hall measurements and photoluminescence spectroscopy indicate that this approach is effective in improving the hole concentration in ZnO films. Under the optimized conditions, a p-type ZnO film with a hole concentration of 1.68 × 1018 cm−3 has been achieved.

Synaptic mechanism in Alzheimer’s disease: a selective degeneration of an excitatory synaptic pathway in the CA1 hippocampus that controls spatial learning and memory in Alzheimer’s disease

SummaryN-methyl-D-aspartate (NMDA) receptors constitute a major subtype of glutamate receptors at extrasynaptic sites that link multiple intracellular catabolic processes responsible for irreversible neuronal death. Here, we report that cerebral ischemia recruits death-associated protein kinase 1 (DAPK1) into the NMDA receptor NR2B protein complex in the cortex of adult mice. DAPK1 directly binds with the NMDA receptor NR2B C-terminal tail consisting of amino acid 1292-1304 (NR2BCT). A constitutively active DAPK1 phosphorylates NR2B subunit at Ser-1303 and in turn enhances the NR1/NR2B receptor channel conductance. Genetic deletion of DAPK1 or administration of NR2BCT that uncouples an activated DAPK1 from an NMDA receptor NR2B subunit in vivo in mice blocks injurious Ca2+ influx through NMDA receptor channels at extrasynaptic sites and protects neurons against cerebral ischemic insults. Thus, DAPK1 physically and functionally interacts with the NMDA receptor NR2B subunit at extrasynaptic sites and this interaction acts as a central mediator for stroke damage.

Lasing action is realized in a ZnO/GaN heterojunction by employing a MgO interlayer. The MgO layer can confine electrons in the ZnO layer, while holes can pass through the MgO layer and enter into the n-ZnO layer from the p-GaN layer. The threshold of the lasing action is as low as 0.8 mA.

Summary Aberrant cell-cycle activity and DNA damage are emerging as important pathological components in various neurodegenerative conditions. However, their underlying mechanisms are poorly understood. Here, we show that deregulation of histone deacetylase 1 (HDAC1) activity by p25/Cdk5 induces aberrant cell-cycle activity and double-strand DNA breaks leading to neurotoxicity. In a transgenic model for neurodegeneration, p25/Cdk5 activity elicited cell-cycle activity and double-strand DNA breaks that preceded neuronal death. Inhibition of HDAC1 activity by p25/Cdk5 was identified as an underlying mechanism for these events, and HDAC1 gain of function provided potent protection against DNA damage and neurotoxicity in cultured neurons and an in vivo model for ischemia. Our findings outline a pathological signaling pathway illustrating the importance of maintaining HDAC1 activity in the adult neuron. This pathway constitutes a molecular link between aberrant cell-cycle activity and DNA damage and is a potential target for therapeutics against diseases and conditions involving neuronal death.

In this paper, we have prepared Schottky type ZnO metal–semiconductor–metal (MSM) ultraviolet (UV) detector. The structural, electrical, and optical measurements were carried out. The detector exhibited a peak responsivity of 0.337 A/W at 360 nm and the dark current was about 1 nA under 3 V bias. An ultraviolet–visible rejection ratio was obtained about more than four orders of magnitude from the fabricated detector. The 10–90% rise and fall time were 20 ns and 250 ns, respectively. We proposed that the detector had shown a gain, which was attributed to the trapping of hole carriers at the semiconductor–metal interface.

Ni thin films were electrodeposited on n-Si (100) substrate from the electrolytes containing Ni(CH 3 COO) 2 and CH 3 COONH 4 at room temperature. The scanning electron microscope images of the films reveals the uniform distribution of the nickel all over the substrate surface, which illustrates that the fine Ni films on large scales could be obtained through the method of electrodeposition. Vibrating sample magnetometer measurement with the applied field parallel to the surface shows obvious hysteresis loops of the magnetic thin films. The morphology and magnetism of the Ni thin films evolves with the deposition time increasing. The effect of deposition conditions on the properties of the Ni thin films is investigated.

Mg x Zn 1− x O alloy films were prepared on sapphire substrates using Ar and N 2 as the sputtering gases. The effect of the sputtering gas on the structural, optical and electrical properties of the Mg x Zn 1− x O films was studied. By using N 2 as the sputtering gas, the Mg x Zn 1− x O film shows p-type conductivity and the band gap is larger than that employing Ar as the sputtering gas. The reason for this phenomenon is thought to be related to the reaction between N–O or N–Zn, and the N-doping.

ZnO nanorods of 25 nm with quite homogeneous size and shape have been fabricated by introducing ZnO sols as nucleation centers prior to the hydrothermal reaction. The samples were characterized by scanning electron microscope, transmission electron microscope, X-ray diffraction, photoluminescence and resonant Raman spectra. After ZnO sols are introduced, the width of the resulting nanorods decreases above an order of magnitude and the aspect ratio increases 5 times. The increase of the intensity ratio of ultraviolet to visible emissions in room-temperature photoluminescence spectrum and the decrease of the Raman linewidths show the improvement in the quality of ZnO nanorods. Influences of the number of seed nuclei and the aging time of ZnO sols on the morphology of ZnO nanorods are discussed.

Neurogenesis continues throughout adulthood in the central nervous system in mammals. Cerebral ischemia induces neurogenesis in the subventricular zone and dentate gyrus. New neurons migrate to the granule cell layer of dentate gyrus or to the damaged CA1 region and striatum, where they differentiate into mature neurons and re-establish connections. Ischemic insults also promote axonal sprouting in ischemic penumbra. Neurogenesis and axonal sprouting may contribute to functional recovery after cerebral ischemia.

FeSe films have been grown on GaAs (001) substrates by low-pressure metal organic vapor deposition at different temperatures. X-ray diffraction analysis indicated that the FeSe films grown at substrate temperatures (Ts) between 220 and 340°C were preferentially oriented with tetragonal structure. It was not possible to deposit films at Ts above 400°C. The atomic molar ratios of Se∕Fe increased with increasing the flow rate of H2Se∕Fe(CO)5 and the growth temperature. The electronic property results showed that the conductive type of FeSe could be adjusted by controlling the growth temperature. The coercivity of FeSe decreased with increasing the growth temperature from 220to300°C due to the improvement of crystal quality.

Cd 1 - x Fe x S and Cd 1 - x - y Fe x Zn y S thin films were grown by low-pressure metal organic chemical vapor deposition (LP-MOCVD) on c - Al 2 O 3 substrates. The films fabricated at 360 ∘ C under an hydrogen pressure of 76 Torr had hexagonal structure with only one (0 0 0 2) diffraction peak. The samples with low doping content have sharp absorption edges. It is found that the absorption edge and the emission peak positions of the Cd 1 - x - y Fe x Zn y S film shift to high energy due to the Zn-doping. The band gap energy could be tuned in a wide range with the change of Zn content. The broadening of the Cd 1 - x - y Fe x Zn y S emission peak could be attributed to the alloy fluctuations and the shallow defect in the samples.

Effect of a polarized P(VDF-TrFE) ferroelectric polymer gating on AlGaN/GaN metal-oxide-semiconductor high-electron-mobility transistors (MOS-HEMTs) was investigated. The P(VDF-TrFE) gating in the source/drain access regions of AlGaN/GaN MOS-HEMTs was positively polarized (i.e., partially positively charged hydrogen were aligned to the AlGaN surface) by an applied electric field, resulting in a shift-down of the conduction band at the AlGaN/GaN interface. This increases the 2-dimensional electron gas (2-DEG) density in the source/drain access region of the AlGaN/GaN heterostructure and thereby reduces the source/drain series resistance. Detailed material characterization of the P(VDF-TrFE) ferroelectric film was also carried out using the atomic force microscopy (AFM), X-ray Diffraction (XRD) and ferroelectric hysteresis loop measurement.

Ginsenoside compound K (GCK), the main metabolite of protopanaxadiol constituents of Panax ginseng, easily produces alkali metal adduct ions during mass spectrometry particularly with lithium. Accordingly, we have developed a rapid and sensitive liquid chromatography–tandem mass spectrometric method for analysis of GCK in human plasma based on formation of a lithium adduct. The analyte and paclitaxel (internal standard) were extracted from 50 µL human plasma using methyl tert-butyl ether. Chromatographic separation was performed on a Phenomenex Gemini C18 column (50 mm×2.0 mm; 5 μm) using stepwise gradient elution with acetonitrile–water and 0.2 mmol/L lithium carbonate at a flow rate of 0.5 mL/min. Detection was performed in the positive ion mode using multiple reaction monitoring of the transitions at m/z 629→449 for the GCK-lithium adduct and m/z 860→292 for the adduct of paclitaxel. The assay was linear in the concentration range 1.00–1000 ng/mL (r2>0.9988) with intra- and inter-day precision of ±8.4% and accuracy in the range of −4.8% to 6.5%. Recovery, stability and matrix effects were all satisfactory. The method was successfully applied to a pharmacokinetic study involving administration of a single GCK 50 mg tablet to healthy Chinese volunteers., Graphical abstract Ginsenoside compound K (GCK), the main metabolite of protopanaxadiol constituents of Panax ginseng, easily produces alkali metal adduct ions during mass spectrometry particularly with lithium. Accordingly, a rapid and sensitive liquid chromatography–tandem mass spectrometric method was developed for analysis of GCK in human plasma based on formation of a lithium adduct. The method was successfully applied to a pharmacokinetic study involving administration of a single GCK 50 mg tablet to healthy Chinese volunteers.

In district 4 of the Tahe Oilfield, the Ordovician Yingshan Formation was most petroliferous. Marine carbonate rocks with big thickness were widespread. Secondary pores, including dissolution pores, fractures and caves, served as the main reservoir spaces, while primary pores were poorly developed. According to modern karst hydraulic unit theory, a conceptual model of karst was established. Three palaeo-hydraulic zones were identified:vadose zone (including infiltration sub-zone and percolation sub-zone), phreatic zone and tranquil zone. The distribution of reservoirs was described using stochastic seismic inversion technology. The reservoirs were controlled by palaeo-hydraulic zones vertically and karst landforms horizontally, which was proved by field work.

The energy band alignment between HfAlO and GaN (0001) was characterized using high-resolution x-ray photoelectron spectroscopy (XPS). The HfAlO was deposited using a metal-organic chemical vapor deposition (MOCVD) gate cluster. A valence band offset of 0.38 eV and a conduction band offset of 2.22 eV were obtained across the HfAlO/GaN heterointerface without any passivation. With in situ SiH4 passivation (vacuum anneal+SiH4 treatment) on the GaN surface right before HfAlO deposition, the valence band offset and the conduction band offset across the HfAlO/GaN heterointerface were found to be 0.51 eV and 2.09 eV, respectively. The difference in the band alignment is believed to be dominated by the core level up-shift or chemical shift in the GaN substrate as a result of different interlayers (ILs) formed by the two surface preparations. ASTAR (Agency for Sci., Tech. and Research, S’pore) Accepted version

High-quality (1 1 0) Fe films with thickness of 200 nm were grown on Al 2 O 3 (0 0 0 6) substrates by low-pressure metal organic chemical vapor deposition (LP-MOCVD). The effects of residual carbon and post-annealing treatment on magnetic properties of Fe films were studied. X-ray photoelectron spectroscopy (XPS) measurements revealed that almost all the interstitial carbon atoms in Fe films can be removed by annealing at temperature of 600 °C. Vibrating sample magnetometer (VSM) showed that the in-plane (out-of-plane) coercivity of the film annealed at 600 °C is clearly larger (smaller) than that of as-grown one, which can be assigned to the tensile stress relaxation due to the removal of carbon. As the annealing temperature increased from 600 to 750 °C, the in-plane coercivity decreased while the out-of-plane coercivity increased. Meanwhile, the in-plane remanence ratios increased rapidly with the increase of annealing temperature, but the out-of-plane remanence ratios changed slightly. The origin of the changes of magnetic properties with annealing temperatures was discussed.

Thin iron films have been grown on (001) GaAs substrates by low pressure metal organic chemical vapor deposition (LP-MOCVD) at different temperatures with the pressure of 150 Torr. X-ray diffraction (XRD) analysis showed that all films have only one strong diffraction peak (110). The surface of Fe film became smooth with increasing the growth temperature. Magnetization measurements showed that the Fe films grown at different temperatures were ferromagnetic with easy axis parallel to the film surface and hard axis perpendicular to the substrates. The field dependence of magnetization along two axes showed a remarkable difference, implying that the samples have strong magnetic anisotropy. Furthermore, when the applied magnetic field is perpendicular to the Fe surface, a sharp jump in the hysteresis loop could be observed, followed by a broad shoulder, which is related to the interface effect, the existence of carbon and the formation of 180∘/90∘ magnetic domains.

ZnO nanostructures, including nanotowers, nanovolcanoes, nanorods, nanotubes, and nanoflowers, have been grown by using the hydrothermal technique. Most of the ZnO nanostructures show the perfect hexagonal cross section and well-faceted top and side surfaces. The basic chemistry and growth mechanism are discussed. By increasing the reaction time, the volcano-like and tube-like ZnO structures were formed due to the Ostwald ripening process and the selective adsorption of the complexes. By using the seed layer, the dense-arrayed, regular oriented ZnO nanorods were obtained due to the decreased nucleation barrier and the abundant interfaces as well as the increasing surface roughness.

Well-faceted hexagonal ZnO nanotubes were synthesized by a simple hydrothermal method and the subsequent aging process without any catalysts or templates. The formation of the tubular structure is closely linked to the polarity of ZnO and the selective adsorption behavior of Zn2+ amino complexes. The surface-related optical properties were studied with use of Raman and photoluminescence spectra. It was found that the oxygen vacancy-related visible emission intensity decreased while surface defect-related visible emission intensity increased when the nanotubes were annealed in oxygen ambient. The anomalous enhancement of PL integrated intensity with the temperature shows fairly high surface state density existing in ZnO nanotubes.

Nonionic polymer poly (vinylpyrrolidone) (PVP) was firstly mixed into oxygenated zinc chloride electrolyte to modulate the crystal growth and morphology of ZnO from electrodeposition. Arrays of ZnO hexagonal prisms with well-defined (0 0 0 1) end facets and { 1 0 1 ¯ 0 } side facets were grown perpendicularly onto p-type Si substrates using the simple and economic route. It was observed that the concentration of PVP played an important role in the final morphology and size of ZnO crystals. The optical studies indicated that the addition of PVT not only influenced crystal growth habit but also improved the optical properties of ZnO.