12 research outputs found

    Unveiling the Semicoherent Interface with Definite Orientation Relationships between Reinforcements and Matrix in Novel Al<sub>3</sub>BC/Al Composites

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    High-strength lightweight Al-based composites are promising materials for a wide range of applications. To provide high performance, a strong bonding interface for effective load transfer from the matrix to the reinforcement is essential. In this work, the novel Al<sub>3</sub>BC reinforced Al composites have been in situ fabricated through a liquid–solid reaction method and the bonding interface between Al<sub>3</sub>BC and Al matrix has been unveiled. The HRTEM characterizations on the Al<sub>3</sub>BC/Al interface verify it to be a semicoherent bonding structure with definite orientation relationships: (0001)<sub>Al<sub>3</sub>BC</sub>//(11̅1)<sub>Al</sub>;[112̅0]<sub>Al<sub>3</sub>BC</sub>//[011]<sub>Al</sub>. Periodic arrays of geometrical misfit dislocations are also observed along the interface at each (0001)<sub>Al<sub>3</sub>BC</sub> plane or every five (11̅1)<sub>Al</sub> planes. This kind of interface between the reinforcement and the matrix is strong enough for effective load transfer, which would lead to the evidently improved strength and stiffness of the introduced new Al<sub>3</sub>BC/Al composites

    Excellent Catalytic Effects of Graphene Nanofibers on Hydrogen Release of Sodium alanate

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    One of the most technically challenging barriers to the widespread commercialization of hydrogen-fueled devices and vehicles remains hydrogen storage. More environmentally friendly and effective nonmetal catalysts are required to improve hydrogen sorption. In this paper, through a combination of experiment and theory, we evaluate and explore the catalytic effects of layered graphene nanofibers toward hydrogen release of light metal hydrides such as sodium alanate. Graphene nanofibers, especially the helical kind, are found to considerably improve hydrogen release from NaAlH<sub>4</sub>, which is of significance for the further enhancement of this practical material for environmentally friendly and effective hydrogen storage applications. Using density functional theory, we find that carbon sheet edges, regardless of whether they are of zigzag or armchair type, can weaken Al–H bonds in sodium alanate, which is believed to be due to a combination of NaAlH<sub>4</sub> destabilization and dissociation product stabilization. The helical form of graphene nanofibers, with larger surface area and curved configuration, appears to benefit the functionalization of carbon sheet edges. We believe that our combined experimental and theoretical study will stimulate more explorations of other microporous or mesoporous nanomaterials with an abundance of exposed carbon edges in the application of practical complex light metal hydride systems

    Remodeling of Hyperpolarization-Activated Current, I<sub>h</sub>, in Ah-Type Visceral Ganglion Neurons Following Ovariectomy in Adult Rats

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    <div><p>Hyperpolarization-activated currents (I<sub>h</sub>) mediated by hyperpolarization-activated cyclic nucleotide-gated (HCN) channels modulate excitability of myelinated A− and Ah-type visceral ganglion neurons (VGN). Whether alterations in I<sub>h</sub> underlie the previously reported reduction of excitability of myelinated Ah-type VGNs following ovariectomy (OVX) has remained unclear. Here we used the intact nodose ganglion preparation in conjunction with electrophysiological approaches to examine the role of I<sub>h</sub> remodeling in altering Ah-type neuron excitability following ovariectomy in adult rats. Ah-type neurons were identified based on their afferent conduction velocity. Ah-type neurons in nodose ganglia from non-OVX rats exhibited a voltage ‘sag’ as well as ‘rebound’ action potentials immediately following hyperpolarizing current injections, which both were suppressed by the I<sub>h</sub> blocker ZD7288. Repetitive spike activity induced afterhyperpolarizations lasting several hundreds of milliseconds (termed post-excitatory membrane hyperpolarizations, PEMHs), which were significantly reduced by ZD7288, suggesting that they resulted from transient deactivation of I<sub>h</sub> during the preceding spike trains. Ovariectomy reduced whole-cell I<sub>h</sub> density, caused a hyperpolarizing shift of the voltage-dependence of I<sub>h</sub> activation, and slowed I<sub>h</sub> activation. OVX-induced I<sub>h</sub> remodeling was accompanied by a flattening of the stimulus frequency/response curve and loss of PEMHs. Also, HCN1 mRNA levels were reduced by ∼30% in nodose ganglia from OVX rats compared with their non-OVX counterparts. Acute exposure of nodose ganglia to 17beta-estradiol partly restored I<sub>h</sub> density and accelerated I<sub>h</sub> activation in Ah-type cells. In conclusion, I<sub>h</sub> plays a significant role in modulating the excitability of myelinated Ah-type VGNs in adult female rats.</p></div

    I<sub>h</sub> in myelinated Ah-type VGNs from adult, non-ovariectomized rats.

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    <p><b>A</b>) Vagal stimulation-evoked transmembrane action potential in a myelinated Ah-type vagal ganglion neuron (VGN). The value for the conduction velocity (CV) measured between the stimulation and recording site was indicative of an Ah-type cell. <b>B</b>) Transmembrane action potential recorded from the same neuron as in (<b>A</b>) and its first derivative over time (blue trace). Note the presence of a repolarization ‘hump’. <b>C</b>) Examples of membrane potential responses of an Ah-type VGN to a depolarizing and a hyperpolarizing current injection step. The cell was first injected with 150 pA current step, giving rise to repetitive action potential firing, which ceased upon termination of the current injection (blue trace). A −120 pA step current injection caused membrane hyperpolarization (blue trace), which gradually increased to its maximum value (−130 mV, dot in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0071184#pone-0071184-g004" target="_blank">Figure 4C</a>) and then depolarized slowly (−96 mV, sag) despite continued current injection. Return of the membrane potential to baseline was associated with the occurrence of a spontaneous action potential. Gray traces show the membrane potential changes in response to a positive and negative current step injection in the presence of the I<sub>h</sub> blocker ZD7288 (10 microM/L). ZD7288 suppressed spontaneous action potential discharge during depolarizing current injection, and reduced the sag potential (difference between peak membrane potential and endpulse potential). <b>D</b>) Plots of the peak vs. endpulse voltage as a function of the magnitude of the hyperpolarizing step current injection under control and following application of ZD7288. ZD7288 suppressed sag potentials in Ah-type neurons. Date are mean ±1 SD. <i>n</i> = 6 cells for each data point, *<i>P</i><0.05 and **<i>P</i><0.01 <i>vs</i>. control (Ctrl).</p

    Effect of 1.0 microM 17beta-estradiol (17beta-E<sub>2</sub>) on I<sub>h</sub> in myelinated Ah-type VGNs from ovariectomized (OVX) rats.

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    <p>See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0071184#pone-0071184-t001" target="_blank">Table 1</a> for explanation of V<sub>1/2</sub>, S<sub>1/2</sub>, and activation time constant (Tau). Data are mean ±1 SD with *<i>P</i><0.05 <i>vs</i> control, <i>n</i> = 5 VGN from 5 ganglion preparations.</p

    Classification of afferent VGN subtypes and characterization of hyperpolarization-activated current (I<sub>h</sub>).

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    <p>CV: fiber conduction velocity; WCC: whole-cell capacitance; I<sub>h</sub>: current density measured at the end of a 1-s voltage step to −120 mV; V<sub>1/2</sub> and S<sub>1/2</sub>: half-activation voltage and slope, respectively, of the activation curve; Tau: activation time constant at −120 mV. Data are mean ±1 SD, *<i>P</i><0.05 and **<i>P</i><0.01 <i>vs</i> A-type, <sup>‡</sup><i>P</i><0.05 and <sup>‡‡</sup><i>P</i><0.01 <i>vs</i> Ah− type, and <sup>†</sup><i>P</i><0.05 and <sup>††</sup><i>P</i><0.01 <i>vs</i> Non-OVX.</p

    The I<sub>h</sub> blocker ZD7288 reduces peak PEMH amplitude in A-type VGNs.

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    <p>In the absence of ZD7288, a 1-s train of vagal stimulation at 50 Hz causes a PEMH. (<b>A</b>). Exposure to 1 microM ZD7288 causes no change in the stimulus/response pattern but markedly reduces the peak PEMH amplitude. Numbers at the beginning and end denote RMP and most negative membrane potential during PEMH, respectively. (<b>B</b>). Scale bars in (<b>A</b>) also apply to (<b>B</b>).</p

    Characterization of I<sub>h</sub> in VGNs from adult, non-ovariectomized rats.

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    <p><b>A</b>), <b>B</b>), and <b>C</b>) Hyperpolarization-evoked currents recorded from an A−, Ah− and C-type neuron (panel A, B and C, respectively). Cells were subjected to a twin-pulse protocol, wherein they were held between −40 and −130 mV in steps of 5 mV for 1 second, and then clamped to −80 mV for 600 ms before return to the holding potential of −40 mV. The interval between each twin-pulse was 1 s. In the A− and Ah-type neuron, step hyperpolarizations evoked inward currents that had an instantaneous component followed by a slowly activating component, whereas the initial instantaneous component was not observed in the C-type neuron. The magnitude of hyperpolarization-evoked currents was largest in the A-type cell, intermediate in the Ah-type cell, and smallest in the C-type cell. Clamping the cell to −80 mV caused slowly activating or slowly deactivating tail currents, depending on the voltage of the preceding clamp step. <b>D</b>), Plots of hyperpolarization-evoked current densities as a function of voltage for all three neuronal subtypes. Endpulse currents were used for analyses. Data are mean ±1 SD. <b>E</b>) Activation curves obtained from tail current recordings as shown in (<b>A</b>), (<b>B</b>) and (<b>C</b>). Sigmoid fittings indicated half maximal activation at −88.0±3.14 mV, −92.4±4.5 mV, and −106±12.8 mV (<i>P</i><0.01 by ANOVA) in A-, Ah−, and C-type cells, respectively (denoted by the downward arrows). Slopes of the activation curves were S<sub>1/2</sub> = 6.14±1.22 mV, 6.13±0.98 mV, and 7.14±2.2 mV, <i>P</i>>0.05 by ANOVA ). <b>F</b>), Plots of inward current densities elicited during hyperpolarizations to potentials ranging from −40 to −80 mV. Scale bars in (<b>C</b>) also apply for (<b>A</b>) and (<b>B</b>). Data are mean ±1 SD, *<i>P</i><0.05 and **<i>P</i><0.01 vs Ah-type, <sup>#</sup><i>P</i><0.05 and <sup>##</sup><i>P</i><0.01 vs C-type. <b>G</b>) Time constants of Ih activation as a function of voltage in A and Ah type neurons. Time constants were obtained by monoexponential fit of the current traces in (<b>A</b>) and (<b>B</b>). Values are mean ± SD. *<i>P</i><0.05 and **<i>P</i><0.01 vs A-type.</p

    Hyperpolarization increases, whereas ZD7288 reduces, both PEMH amplitude in and excitability of Ah-type VGNs.

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    <p><b>A</b>) Transmembrane potentials recorded under zero current-clamp condition in an Ah-type neuron before, during and after application of a train of vagal stimuli at 75 Hz. A 1∶1 stimulus/response ratio was sustained throughout the vagal stimulation episode. The peak amplitude of the evoked action potentials progressively decreased to a new steady state value at the end of the pulse train. No PEMH was observed. <b>B</b>) Sustained application of a hyperpolarizing current throughout vagal stimulation attenuated the reduction in peak amplitude of evoked action potentials in a train of 75 Hz and induced a PEMH. Hyperpolarizing currents were applied throughout the recordings, including the post-tetanic period. <b>C</b>) Further increase in the vagal stimulation frequency failed to induce a stable 1∶1 stimulus/response pattern under zero current-clamp conditions, rather a 3∶2 cycle developed, i.e. every third stimulus did not trigger an action potential. No PEMH was induced. <b>D</b>) Injection of a hyperpolarizing current resulted in restoration of a 1∶1 stimulus/response pattern throughout most of the train duration with only brief, intermittent 2∶1 cycles, and induced a large PEMH. Hyperpolarizing currents were applied throughout the recordings, including the post-tetanic period. <b>E</b>) and <b>F</b>) In a separate Ah-type neuron, application of ZD7288 (1 microM) eliminated the PEMH. <b>G</b>) and <b>H</b>) In another Ah-type VGN, a 1-s train of vagal stimulation at 50 Hz evoked action potentials at a 1∶1 stimulus/response ratio and a small-amplitude PEMH. Application of 10 microM ZD7288 to the preparation resulted in loss of a stable 1∶1 stimulus/response pattern and also abolished the PEMH. Scale bars in (<b>C</b>) also apply for (<b>A</b>), (<b>B</b>), and (<b>D</b>); scale bars in (<b>G</b>) are also applied to (<b>E</b>), (<b>F</b>), and (<b>H</b>).</p

    Electrical properties of myelinated A-type vagal ganglion neurons in the nodose ganglion preparation of adult non-ovariectomized rats.

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    <p><b>A</b>) Vagal stimulation-evoked transmembrane action potential in a myelinated A-type vagal ganglion neuron (VGN). The value for the conduction velocity (CV) measured between the stimulation and recording site was indicative of an A-type cell. <b>B</b>) Transmembrane action potential recorded from the same neuron as in (<b>A</b>) and its first derivative over time (blue trace). <b>C</b>) – <b>E</b>) Post-excitatory membrane hyperpolarization (PEMH) following 1-s trains of vagal stimulation at 20 (<b>C</b>), 50 (<b>D</b>), and 100 Hz (<b>E</b>). Numbers at the end of each trace denote most negative value of the membrane potential during each PEMH. <b>F</b>) – <b>H</b>) PEMHs induced by 1-s trains of vagal stimulation at 100 Hz superimposed on different degrees of RMP hyperpolarization. Hyperpolarizing currents were applied throughout the recordings, including the post-tetanic period. Numbers at the beginning and end of each trace denote RMP and most negative membrane potential value during PEMH, respectively. Scale bars in (<b>E</b>) also apply to (<b>C</b>) – (<b>H</b>).</p
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