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The flexible domain structure and coexistence of R and T nanodomains are responsible for the enhanced strains and strong relaxor.

Considering the full utilization of energy and pursuing thin-film capacitors with high energy-storage density, the grain size engineering is used to adjust domain size, in order to enhance the energy-storage efficiency and energy-storage density of thin-film capacitors. Therefore, in this work, lead-free Bi0.5Na0.5TiO3 (BNT) films with designed grain size were grown on Nb-doped SrTiO3 (Nb:STO) (001) single-crystalline substrates by modulating the mineralizer concentrations via hydrothermal synthesis. The nature of epitaxial growth near the single-crystalline substrates was proved by transmission electron microscopy (TEM). In addition, the phenomenon of the decrease of grain size and the increase of [100] in-plane orientation with the decline of mineralizer concentrations were clarified by grazing-angle incidence X-ray diffraction (GIXRD) and field emission scanning electron microscope (FESEM). By reducing the grain size, an ultrahigh energy-storage efficiency (η) of 75.56% and superior the recoverable energy-storage density (Wrec) of 16.47 J/cm3 were acquired in pure Bi0.5Na0.5TiO3 films. Furthermore, the fine-grained film exhibits weak dependence on the frequency and has excellent anti-fatigue property. Therefore, hydrothermal synthesis is an efficient, inexpensive, and easy method, which is the most promising way to adjust grain size and energy storage of the film capacitor.

The subthalamic nucleus (STN), substantia nigra pars reticulata (SNr), and pedunculopontine tegmental nucleus (PPTg) are reciprocally connected brain regions that play significant roles in the motor control. However, the electrophysiological relationship among the STN, SNr, and PPTg remains controversial. The present study was designed to further explore the mutual electrophysiological relationship of these brain regions from the perspective of the PPTg-STN-SNr neural circuit. The neuronal activities in the STN and SNr were simultaneously recorded while the PPTg was stimulated in anesthetized rats. The activation of PPTg induced excitatory responses of both the STN and SNr neurons. Comparisons of excitation latencies between the STN and SNr were made to distinguish the excitation evoked from the PPTg-STN-SNr pathway. Additionally, two types of excitatory responses and various inhibitory responses with different latencies in the SNr were recorded. The SNr responses could also be classified into five different response categories, which might attribute to projections within different neural circuits. Neuronal recordings were analyzed in different electrophysiological features (i.e., interspike interval [ISI] mode, ISI asymmetry index, ISI coefficient of variance, firing rate, burst index, and trough peak duration), and different response patterns of neurons had their specific features in neuronal activities. These findings indicated the complex interactions among the STN, SNr, and PPTg electrophysiologically, and provided insights into exploring information transmission mechanisms underlying these circuits.

Octahedral rotation in perovskites and their transformations have a profound influence on their properties. In this work, an easy-to-use model is proposed to reveal the nature of the oxygen octahedral rotation (OOR) changing behaviors at interfacial regions. Different from first principle simulations and symmetry analysis, we establish a general elastic model with a six angle symbol system based on the intrinsic geometry characteristics of the oxygen octahedra network. In the light of the elastic energy generated by octahedral tilting mismatches at interfaces, the systematic analysis is conducted on the changing behavior and mechanism of octahedral rotation with different OOR patterns. Consequently, it is found that there are two forms of basic component angle changing across the interface, i.e. abrupt change and gradual change, depending on the relationship between the directions of the rotational axis of basic component angles and the interface. Furthermore, the coexistence of two forms at the same interface and a special case for gradual change are investigated, which could hardly be identified or predicted by other models and analysis established previously. Generally, the model can be applied to interpret and predict the octahedral rotation changing behavior in perovskites, involving film/substrate heterostructure in epitaxial synthesized thin films, domain boundaries, etc., which agree with the practical examples. Although the model has its limitations due to the complex chemical configuration in 3D oxygen octahedra network, it is expected to be universal for perovskites. Taking the advantage of mathematical simplicity, this model can be a powerful tool for interfacial engineering in perovskites.

Polymorphisms in the oxytocin receptor (

For the sake of excellent strain performance for actuator application, Sn-modified Bi0.5Na0.5TiO3–Bi0.5K0.5TiO3 (BNT–BKT) ceramics were designed and prepared by solid-state reaction method. The crystal structures and microstructures of Bi0.5(Na0.75K0.25)0.5(Ti1−xSnx)O3 (abbreviated as BNKT–xSn, x = 0, 0.02, 0.05, 0.08) were systematically investigated together with their strain performance. It is found that all the compositions possessed a single perovskite structure phase by X-ray diffraction patterns. With increasing Sn content, the ferroelectric phase with mainly tetragonal structure gradually transformed into the ergodic relaxor phase in pseudocubic structure with nanodomains further confirmed by high-resolution transmission electron microscope images. Both the P–E and I–E loops confirmed this structural change and the coexistence of ferroelectric phase and ergodic relaxor phase at x = 0.02, where a large strain of 0.37% was achieved with low hysteresis (21.8%). By analyzing the bipolar and unipolar strain curves and the origin of strain, we believe that the large strain is contributed to the phase transition from ferroelectric phase into ergodic relaxor phase, and the low hysteresis is beneficial from the existence of ergodic relaxor phase, which should pave a way for future developing high-performance actuators.

Pb1−0.5xNbx((Zr0.52Sn0.48)0.955Ti0.045)1−xO3(PNZST-100x (x = 0.01, 0.02, 0.03, 0.04)) antiferroelectric (AFE) ceramics were prepared using a solid-state method. X-ray diffraction analysis indicates a structural evolution from the tetragonal phase to the pseudocubic phase. When x = 0.02, the ceramic exhibits an enhanced energy storage density of 1.37 J/cm3, and a strain, with 0–1 switching characteristics, of 0.22%. Selected-area electron diffraction (SAED), high-resolution transmission electron microscopy imaging, and in-situ TEM analyses indicate that there are two kinds of superlattice reflections, including the 1/2(hkl) superlattice reflection (h, k, and l: all odd) and 1/6.67(a* + b*) one-dimensional incommensurate superlattice reflections. The origin of the 1/2(hkl) superlattice reflection was the tilting of a-a-a- oxygen octahedra. Therefore, the 1/2(hkl) reflections were no longer superlattice reflections, but fundamental reflections in the trigonal system; hence, the reciprocal vector was re-expressed as $$H\, = \,ha^{*} \, + \,kb^{*} \, + \,lc^{*} \, \pm \,1/6.67\left( {a^{*} \, + \,b^{*} } \right),$$ where h, k, and l are integers and (− h + k + l) = 3n. The incommensurate structure of the PNZST-2 ceramic originated from the displacement of Pb2+.

BACKGROUND Colorectal cancer (CRC) is the second most commonly diagnosed cancer in females and the third in males worldwide. Although existing evidence explained some critical functions of the single genetic abnormality in the pathogenesis of CRC, the function of interactors involved in the colon-specific regulatory network, especially DNA methylation regulated network is still poorly understood. MATERIAL AND METHODS In this work, matched gene expression and DNA methylation samples of CRC patients were retrieved. Differential gene expression and methylation analyses were performed. In addition, gene expression and DNA methylation were integrated into a colon-specific regulatory gene network, detecting the epigenetically regulated gene modules which drive CRC through an underlying epigenetic mechanism. Finally, the colon-specific DNA methylation-regulated gene modules were validated using an independent set of CRC patients. RESULTS Differential gene expression analysis demonstrated the upregulation of the cell cycle and DNA replication and downregulation of cGMP-PKG signaling pathway and calcium signaling pathway in CRC. Differentially methylated regions (DMRs) showed the different levels of methylation in promoters, CpG islands, and genes in CRC. In addition, gene expression and DNA methylation were integrated into a colon-specific regulatory gene network, detecting 8 epigenetically regulated gene modules which drive CRC through an underlying epigenetic mechanism. Interestingly, 2 of the colon-specific DNA methylation-regulated gene modules showed a significant predictive ability for the survival of an independent set of CRC patients. CONCLUSIONS The results of this study could open a new era and aid the development of novel therapeutic targets for the treatment of CRC patient.

Background The population in Jiamusi has been reported to have the highest prevalence of colorectal cancer (CRC) in China. The genetic causal-effect for this occurrence among the residents remains unclear. Given the long cold seasons with people wearing more clothes and reduced UV exposure, we aimed to study the association between the vitamin D metabolism-related gene CYP24A1 polymorphism and CRC susceptibility. Method A case-control study was conducted that included 168 patients with CRC and 710 age-matched healthy individuals as the control group. Plausible susceptible variations were sought and clinical phenotypic-genotype association analysis was performed. Results Overall, two CYP24A1 polymorphisms, rs6013905 AX (P = 0.02, OR = 1.89, 95%CI: 1.09–3.29) and rs2762939 GX (P = 0.02, OR = 1.52, 95%CI: 1.08–2.13) were significantly associated with CRC in the Jiamusi population. In the female group, three CYP24A1 polymorphisms, rs6013905 AX (P = 0.04, OR = 2.59, 95%CI: 1.03–6.49), rs2762939 GX (P = 0.01, OR = 2.35, 95%CI: 1.25–4.42), and rs6068816 GG (P = 0.05, OR = 1.89, 95%CI: 0.99–3.59) carriers were significantly associated with CRC. In clinical phenotypic-genotype analysis, rs6013905 GG (P = 0.05, OR = 4.00, 95%CI: 0.92–17.48) and rs2762939 GX (P = 0.03, OR = 4.87, 95%CI: 1.00–23.69) carriers were significantly associated with poorly differentiated CRC, while CYP24A1 rs6068816 AX was significantly associated with the tumor type (P = 0.02, OR = 2.08, 95%CI: 1.10–3.96) and location (P = 0.04, OR = 2.24, 95%CI: 1.05–4.77). Conclusion CYP24A1 gene polymorphism may be a genetic risk factor attributable to the highest prevalence of CRC in Jiamusi people. Individuals with CYP24A1 gene polymorphism may have an increased barrier for vitamin D absorption, thus contributing to the risk of CRC development.

The suppression of inappropriate actions is critical for flexible behavior. Cortical-basal ganglia networks provide key gating mechanisms for action suppression, yet the specific roles of neuronal subpopulations are poorly understood. Here, we examine Arkypallidal (‘‘Arky’’) and Prototypical (‘‘Proto’’) globus pallidus neurons during a Stop task, which requires abrupt cancellation of an imminent action. We first establish that Arky neurons can be identified by their firing properties across the natural sleep/wake cycle. We then show that Stop responses are earlier and stronger in the Arky compared to the Proto subpopulation. In contrast to other basal ganglia neurons, pallidal Stop responses are selective to Stop, rather than Go, cues. Furthermore, the timing of these Stop responses matches the suppression of developing striatal Go-related activity. Our results support a two-step model of action suppression: actions-inpreparation are first paused via a subthalamic-nigral pathway, then cancelled via Arky GABAergic projections to striatum.

We consider a quantum spin Hall (QSH) insulator strip touching on one s-wave superconductor sandwiched between two ferromagnetic insulators and study its scattering processes, tunneling conductance, and noise power by using an extended Bogoliubov-de Gennes scattering formalism. It is demonstrated that interedge coupling and noncollinear magnetizations allow for producing the usual and novel crossed Andreev reflections (ARs), respectively, and thus the corresponding spin-singlet and -triplet pairing entanglements. Moreover, by proper tuning of the band structures of the ferromagnetic layers, under the resonance bias voltage, not only perfect but also fully spin-polarized crossed AR at any magnetic orientational angle α is exhibited, which can be experimentally confirmed by the tunneling conductance and noise power. Particularly, the perfect and fully spin-polarized modulation between the spin-singlet and -triplet Andreev entanglements could be performed by α at certain energy values, which suggest that the setup can act as a topological superconducting spintronic device with such a manipulation function.

High-quality near-ultraviolet (UV) light-emitting diodes (LEDs) used InGaN/GaN multiple quantum wells (MQWs) have been grown on ScMgAlO4 substrates by plasma enhanced metalorganic chemical vapor deposition (PEMOCVD). The structural properties and optoelectronic properties of InGaN/GaN MQWs are characterized carefully. The full-width at half-maximums (FWHMs) for GaN(0002) and GaN(10–12) X-ray rocking curves are 180 and 190 arcsec, respectively, indicating high crystalline quality of GaN epitaxial films. The as-grown InGaN/GaN MQWs with sharp and abrupt hetero-interfaces have been also obtained and confirmed by high-resolution X-ray diffraction and high-resolution transmission electron microscopy measurements. Meanwhile, there is a photoluminescence peak at 385 nm with an FWHM of 23.2 nm at 300 K and the internal quantum efficiency (IQE) for these InGaN/GaN MQWs is measured to be as high as 79.8%, revealing the high optoelectronic properties. This work sheds light on the preparation of high-performance near-UV LEDs for the application of UV curing, lighting, etc.

Schwann cells are integral components of vertebrate neuromuscular synapses; in their absence, pre-synaptic nerve terminals withdraw from post-synaptic muscles, leading to muscle denervation and synapse loss at the developing neuromuscular junction (NMJ). Here, we report a rescue of muscle denervation and neuromuscular synapses loss in type III Neuregulin 1 mutant mice (CRD-Nrg1−/−), which lack Schwann cells. We found that muscle denervation and neuromuscular synapse loss were prevented in CRD-Nrg1−/−mice when presynaptic activity was blocked by ablating a specific gene, such as Snap25 (synaptosomal-associated 25 kDa protein) or Chat (choline acetyltransferase). Further, these effects were mediated by a pathway that requires postsynaptic acetylcholine receptors (AChRs), because ablating Chrna1 (acetylcholine receptor α1 subunit), which encodes muscle-specific AChRs in CRD-Nrg1−/−mice also rescued muscle denervation. Moreover, genetically ablating muscle dihydropyridine receptor (DHPR) β1 subunit (Cacnb1) or ryanodine receptor 1 (Ryr1) also rescued muscle denervation and neuromuscular synapse loss in CRD-Nrg1−/−mice. Thus, these genetic manipulations follow a pathway–from presynaptic to postsynaptic, and, ultimately to muscle activity mediated by DHPRs and Ryr1. Importantly, electrophysiological analyses reveal robust synaptic activity in the rescued, Schwann-cell deficient NMJs in CRD-Nrg1−/−Cacnb1−/−or CRD-Nrg1−/−Ryr1−/−mutant mice. Thus, a blockade of synaptic activity, although sufficient, is not necessary to preserve NMJs that lack Schwann cells. Instead, a blockade of muscle activity mediated by DHRPs and Ryr1 is both necessary and sufficient for preserving NMJs that lack Schwann cells. These findings suggest that muscle activity mediated by DHPRs/Ryr1 may destabilize developing NMJs and that Schwann cells play crucial roles in counteracting such a destabilizing activity to preserve neuromuscular synapses during development., Author summary Nerve cells (neurons) communicate with each other through specialized focal connections called synapses. Synapses are commonly assembled into a tripartite structure composed of pre- and post-synaptic neurons, and a glial cell that is closely associated with both pre- and post-synaptic components. At the vertebrate neuromuscular synapse (the neuromuscular junction, NMJ), the tripartite structure is composed of a nerve terminal, a muscle fiber and a glial cell called the terminal Schwann cell. Previous studies have shown that Schwann cells are vital to the NMJ–without Schwann cells, the NMJ fails to form. Here, we report unexpected findings that bipartite NMJs can be established in vivo, in the absence of Schwann cells. These results were accomplished by ablating specific genes in mice, ultimately resulting in a total blockade of muscle activity. Thus, Schwann cells become dispensable for the NMJ if muscle activity is blocked. These findings suggest that muscle activity normally destabilizes the NMJ during synapse formation and that Schwann cells play crucial roles in NMJ formation by opposing this muscle-derived destabilizing activity in order to preserve the developing neuromuscular synapses.

We address an efficient scheme to generate single circularly polarized attosecond pulse using spatially inhomogeneous fields in the vicinity of metallic nanostructures from atom media with nonvanishing angular quantum number. Based on the numerical solution of a two-dimensional time-dependent Schrodinger equation, it is shown that using linearly polarized plasmonic fields, the harmonic intensity of two orthogonal polarization components, i.e., harmonics polarized parallel and perpendicular to the driving fields polarization direction, is comparable. Moreover, the relative phase between the two components is about π / 2 . As a result, near-circularly polarized isolated attosecond extreme ultraviolet or X-ray pulses can be directly produced.

Many chronic neuroscience studies require neural probes that can reliably record with a large number of electrodes in a densely configured array. Previous works have shown that adverse tissue reaction can be significantly reduced as probe shanks are scaled down toward subcellular dimensions. In addition, flexible probes can mitigate shear stress-induced tissue damage due to micromotion. However, both size reduction and flexibility compromise probe's ability to penetrate the pia mater, especially when many electrodes are distributed across multiple probe shanks. In this paper, we present a method to lithographically pattern a biodegradable silk coating that provides temporary mechanical stiffness for the surgical insertion of flexible probes without any conventional design constraints on the probe size, shape, or material. After insertion, the silk is completely dissolved in the tissue, only leaving the flexible minimum-geometry probes inside the brain. We validated the design by successfully inserting silk-backed 64-channel parylene probes into the motor cortex of Long-Evans rats (n = 6) and recorded in vivo neural activity for six weeks.

Studies have implied that the circadian oscillation of mitogen-activated protein kinase (MAPK) signal pathways is crucial for hippocampus-dependent memory. NF1 mouse models (Nf1 heterozygous null mutants; Nf1 +/−) displayed enhanced MAPK activity in the hippocampus and resulted in memory deficits. We assumed a link between MAPK pathways and hippocampal rhythmic oscillations, which have never been explored in Nf1 +/− mice. We demonstrated that the level of extracellular signal–regulated kinases 1 and 2 (ERK1/2) phosphorylation in Nf1 +/− mice were significantly higher at nighttime than at daytime. Moreover, the in vivo recording revealed that for the Nf1 +/− group, the power spectral density of theta rhythm significantly decreased and the firing rates of pyramidal neurons increased. Our results indicated that the hippocampal MAPK oscillation and theta rhythmic oscillations in Nf1 +/− mice were disturbed and hinted about a possible mechanism for the brain dysfunction in Nf1 +/− mice. Electronic supplementary material The online version of this article (doi:10.1186/s13041-017-0309-8) contains supplementary material, which is available to authorized users.

In vivo recording in CA1 demonstrates alterations in hippocampal rhythmic oscillations and firing rates in Nf1 +/− mice. a The local field potentials (LFPs) recordings in CA1(WT mice). First trace- unfiltered LFPs, second trace- alpha oscillations (filtered 7–12 Hz). b Histograms show the averaged power spectral density of the neuronal rhythmic oscillations (alpha). Data are expressed as mean ± SEM (WT, n = 5; Nf1 +/− , n = 5). Two-way analysis of variance with repeated measures and post hoc Bonferroni tests was used to evaluate differences in local field potential power spectrum density in day and night recordings in Nf1 +/− and WT groups. ***p

The correlation is shown between theta oscillation and MAPK level in hippocampus. The averaged power spectral density of the neuronal rhythmic oscillations (theta) was shown. The pErk1/2 expression in Nf1 +/â mice and littermates WT mice were evaluated by western blot analysis at day and night. (PDF 421Â kb)

Alzheimer's disease (AD) is pathologically characterized by deposition of β-amyloid (Aβ) peptides, which closely correlates with the balance of nerve growth factor (NGF)-related TrkA/p75NTR signaling. (−)-Epigallocatechin-3-gallate (EGCG) is used for prevention and treatment of many neurodegenerative diseases, including AD. However, whether the neuroprotective effects of EGCG treatment were via modulating the balance of TrkA/p75NTR signaling was still unknown. In this study, we found that EGCG treatment (2 mg · kg –1 · day –1) dramatically ameliorated the cognitive impairments, reduced the overexpressions of Aβ(1–40) and amyloid precursor protein (APP), and inhibited the neuronal apoptosis in the APP/PS1 mice. Interestingly, the EGCG treatment enhanced the relative expression level of NGF by increasing the NGF/proNGF ratio in the APP/PS1 mice. Moreover, after EGCG treatment, TrkA signaling was activated by increasing the phosphorylation of TrkA following the increased phosphorylation of c-Raf, ERK1/2, and cAMP response element-binding protein (CREB), simultaneously the p75NTR signaling was significantly inhibited by decreasing the p75ICD expression, JNK2 phosphorylation, and cleaved-caspase 3 expression, so that the Aβ deposits and neuronal apoptosis in the hippocampus were inhibited.

The triple-branch signal detection (TBSD) scheme can eliminate multiple-user interference (MUI) without fixed in-phase cross-correlation (IPCC) stipulation in the spectral-amplitude-coding optical code division multiple access (SACOCDMA) systems. In this paper, we modify the traditional TBSD scheme and theoretically analyze the principle of the MUI elimination. Then, the bit-error-rate (BER) performance of the modified TBSD scheme is investigated under multiple transmission rates. The results show that the modified TBSD employing the codes with unfixed IPCC can achieve simultaneous optical code recognition and MUI elimination in the SAC-OCDMA.

Developing skeletal myofibers in vertebrates are intrinsically “pre-patterned” for motor nerve innervation. However, the intrinsic factors that regulate muscle pre-patterning remain unknown. Here we show that a functional skeletal muscle dihydropyridine receptor (DHPR, the L-type Ca2+ channel in muscle) is required for muscle pre-patterning during the development of the neuromuscular junction (NMJ). Targeted deletion of the β1 subunit of DHPR (Cacnb1) in mice leads to muscle pre-patterning defects, aberrant innervation and precocious maturation of the NMJ. Reintroducing the Cacnb1 gene into Cacnb1−/− muscles reverses the pre-patterning defects and restores normal development of the NMJ. The mechanism by which DHPRs govern muscle pre-patterning is independent of their role in excitation-contraction coupling (E-C coupling), but requires Ca2+ influx through the L-type Ca2+ channel. Our findings demonstrate that the skeletal muscle DHPR retrogradely regulates the patterning and formation of the NMJ.

PurposeThe purpose of this paper is to present a new approach for selecting the good heavy oil reservoirs to develop preferentially, which can avoid the huge economical loss resulted from wrong decision.Design/methodology/approachA new method of ranking the development priority of heavy oil reservoir is present, in which the neural network is applied for the first time to acquire reservoir parameters' weights through training samples and the genetic algorithm is used to optimize the joint weighs of neurons in case that neural network falling into local minimum. Additionally, the paper establishes subordinate function of every parameter. Eventually, comprehensive evaluation values of all heavy oil reservoirs are obtained.FindingsThe method can ensure the veracity and creditability of the parameters' weights, avoid the randomicity brought by experts.Research limitations/implicationsAccessibility of the data of many heavy oil reservoirs is the main limitation.Practical implicationsA very useful and new method for the decision makers of heavy oil reservoirs development.Originality/valueThe new approach of ranking the development priority of heavy oil reservoir based on the neural network and the genetic algorithm. The paper is aimed at the leaders who manage the development of heavy oil reservoirs.

L-3-n-butylphthalide (L-NBP), an extract from seeds of Apium graveolens Linn (Chinese celery), has been shown to have neuroprotective effects on cerebral ischemic, vascular dementia and amyloid-beta (Abeta)-induced animal models by inhibiting oxidative injury, neuronal apoptosis and glial activation, regulating amyloid-beta protein precursor (AbetaPP) processing and reducing Abeta generation. The objective of this study was to investigate the effects of L-3-n-butylphthalide on memory impairment and the expression of brain neurotrophic derived factor (BNDF), kinaseB (TrkB), phosphatidylinositol 3 kinase (PI3K) and Akt in APP/PS1 double transgenic mouse models. APP/PS1 double transgenic mice were administered 30 mg/kg•d L-NBP and 10 mg/kg•d L-NBP for one month. The learning and memory ability were studied using the water maze test. Protein expression and transcript levels of genes in the mice hippocampus were evaluated using western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR), respectively. The results demonstrated that both 30 mg/kg•d L-NBP and 10 mg/kg•d L-NBP doses of L-NBP significantly increased memory capability and the expression of hippocampal BDNF/TrkB/PI3K/AKT in mice The results suggested that L-NBP treatment may reverse memory impairment in APP/PS1 transgenic mice, and BDNF/TrkB/PI3K/AKT, may be involved in this process.

In order to advance the understanding of brain functions, it is critical to manipulate and monitor the neural circuitry in the cellular level. Supporting optogenetics, silicon probes with monolithically integrated waveguides and electrodes were designed and validated with in-vivo recording of photo-induced neural activity. For chronic applications, we developed a technology that utilizes a biodegradable silk coating to support probes with unique geometries and flexibility for reduced tissue reactions. Consistent recording has been observed for 5 weeks in rats.

Many chronic brain implants would benefit from a neural probe with many densely configured electrodes with stable recording quality. We present a novel strategy to scale up the number of electrodes with minimized risk of proportionally increasing the adverse foreign body reactions. A flexible parylene probe having 64 electrodes has been designed and fabricated with unique geometries for reduced tissue reactions. Biocompatible silk fibroin was patterned to provide a biodegradable mechanical support of the flexible probe during insertion. We validated the design with in vivo recording in rats and observed no significant deterioration in recording quality for over 5 weeks.

Salient cues can prompt the rapid interruption of planned actions. It has been proposed that fast, reactive behavioral inhibition involves specific basal ganglia pathways, and we tested this by comparing activity in multiple rat basal ganglia structures during performance of a stop-signal task. Subthalamic nucleus (STN) neurons showed low-latency responses to Stop cues, irrespective of whether actions were successfully canceled or not. By contrast, neurons downstream in the substantia nigra pars reticulata (SNr) responded to Stop cues only in trials with successful cancellation. Recordings and simulations together indicate that this sensorimotor gating arises from the relative timing of two distinct inputs to neurons in the SNr dorsolateral “core” subregion: cue-related excitation from STN and movement-related inhibition from striatum. Our results support race models of action cancellation, with successful stopping requiring Stop cue information to be transmitted from STN to SNr before increased striatal input creates a point of no return.

Background Alzheimer’s disease (AD), an age-related neurodegenerative disorder, is the predominant form of dementia in the elderly, clinically characterized by cognitive impairment and pathologically characterized by extracellular senile plaques largely composed of b-amyloid (Ab) peptide. The overburden of b-amyloid (Ab )d eposition in AD is associated with peroxidation which plays an important role in neuronal dysfunction. APP/PS1 double transgenic mice, which display significant learning and memory impairments and the typical pathological changes such as numerous Ab deposition, are ideal model to mimic the symptoms of AD. (-)-Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenolic constituent in green tea, which has ironchelating, anti-inflammatory, antioxidant and anticancer activities. However, it remains unclear whether EGCG improves learning and memory impairments by attenuating peroxidation in APP/PS1 double transgenic mice. Therefore, we evaluated the relationships between the ameliorated memory dysfunctions and the inhibited peroxidative levels in APP/PS1 transgenic mice after EGCG treatment. Methods APP/PS1 mice at the age of 9 months, randomly distributed into EGCG-treated APP/PS1 group (EGCG group) or APP/PS1 group, and age-matched wild-type mice (C57 BL/6J, WT group) were assigned as aging control. Mice were intragastrically administered EGCG (2 mg/ kg) or vehicle (distilled water) once daily for 4 weeks. Memory function was evaluated in Morris Water Maze (MWM) and passive avoidance test (PAT). The contents of malondialdehyde (MDA), and the activities of total superoxide dismutase (t-SOD) and glutathione peroxidase (GSH-Px) in hippocampus were examined using lipid preoxidation MDA assay kit, total superoxide dismutase assay kit with WST-1, and total glutathione peroxidase assay kit, respectively. The protein expression of inducible nitric-oxide synthase (iNOS) in the hippocampus was measured by Western blot. Results In PAT, the shorter latency and the increased error time to enter the dark compartment of APP/PS1 group were found compared with WT group (P