Activity Coefficients of Organic Solutes at Infinite Dilution in the Ionic Liquids. 2. Organic Solutes in 1‑Hexyl-3-methylimidazolium Nitrate and Gas–Liquid Partitioning and Interfacial Adsorption Using Gas–Liquid Chromatography

This paper reports activity coefficients at infinite dilution for a series of organic solutes in the ionic liquid 1-hexyl-3-methylimidazolium nitrate by gas–liquid chromatography at different temperatures between 313.15 and 363.15 K. The contribution of gas–liquid partitioning and interfacial adsorption to the retention mechanism was estimated by changing the loading of ionic liquid in stationary phase, and the influence of different loading of ionic liquid on the experimental values of activity coefficients at infinite dilution was discussed. The partial molar excess enthalpies at infinite dilution and the solubility parameters of ionic liquid were also calculated from the experimental values of activity coefficients at infinite dilution

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<p>Arbuscular mycorrhizal fungi (AMF) play a crucial role in enhancing the acquisition of immobile nutrients, particularly phosphorus. However, because nitrogen (N) is more mobile in the soil solution and easier to access by plants roots, the role of AMF in enhancing N acquisition is regarded as less important for host plants. Because AMF have a substantial N demand, competition for N between AMF and plants particularly under low N condition is possible. Thus, it is necessary to know whether or not AMF affect N uptake of plants and thereby affect plant growth under field conditions. We conducted a 2-year field trial and pot experiments in a greenhouse by using benomyl to suppress colonization of maize roots by indigenous AMF at both low and high N application rates. Benomyl reduced mycorrhizal colonization of maize plants in all experiments. Benomyl-treated maize had a higher shoot N concentration and content and produced more grain under field conditions. Greenhouse pot experiments showed that benomyl also enhanced maize growth and N concentration and N content when the soil was not sterilized, but had no effect on maize biomass and N content when the soil was sterilized but a microbial wash added, providing evidence that increased plant performance is at least partly caused by direct effects of benomyl on AMF. We conclude that AMF can reduce N acquisition and thereby reduce grain yield of maize in N-limiting soils.</p

Bioactive neolignan, iridoid and flavonoid glycosides from the leaves of <i>Vaccinium bracteatum</i>

Two neolignan glycosides including a new one (1), along with seven iridoid glycosides (3 − 9) and nine flavonoid glycosides (10 − 18), were isolated from the leaves of Vaccinium bracteatum. Their structures were established mainly on the basis of 1D/2D NMR and ESIMS analyses, as well as comparison to known compounds in the literature. The structure of 1 with absolute stereochemistry was also confirmed by chemical degradation and ECD calculation. Selective compounds showed antiradical activity against ABTS and/or DPPH. Moreover, several isolates also suppressed the production of ROS in RAW264.7 cells and exerted neuroprotective effect toward PC12 cells.</p

cPLA₂α deficiency inhibits DSE at parallel fiber-Purkinje cell synapse.

<p>(A) The stimulus protocol with the holding potential (hp) of Purkinje cells and the stimulation timing (stim). The duration of depolarization to 0 mV was 50 ms. Δt between the depolarization and the test stimulus was 5 s. The numbers 1, 2, 3 index control parallel fiber stimuli and 4 labels the test stimulation. The intervals between indexed 1, 2, 3 were 20 s. The intervals between 3 and depolarization was 10 s. (B) Amplitudes of parallel fiber EPSCs derived from one WT Purkinje cell plotted over time for control responses with no preceding prepulse to 0 mV (open circles) and test responses following depolarization (closed circles). Numbered circles (1, 2, 3, 4) correspond to the control and test stimuli in (A), respectively. Representative EPSCs are shown at the right. Stimulus artifacts are blanked for clarity. (C) EPSCs of one KO Purkinje cell plotted over time for control responses with no preceding prepulse to 0 mV (open circles) and test responses following depolarization (closed circles). Representative EPSCs are shown at the right. (D) EPSCs derived from one WT Purkinje cell plotted over time. AACOCF₃ was perfused throughout the experiment, as shown by the bar at top. Control and test responses are shown by open and closed circles, respectively. Representative EPSCs are shown at the right. (E) EPSCs derived from one KO Purkinje cell plotted over time. AACOCF₃ was perfused throughout the experiment, as shown by the bar at top. Control and test responses are shown by open and closed circles, respectively. Representative EPSCs are shown at the right. (F) Bar graphs show the percentage inhibitions of test EPSCs in WT, KO, WT+AACOCF₃ and KO+AACOCF₃. ctrl: control responses (n = 88). WT: 28.3±5.4%; n = 26. KO: 79.4±5.8%; n = 20. WT+AACOCF₃: 75.7±8.3%; n = 22. KO+AACOCF₃: 80.7±6.7%; n = 20. *, P<0.05.</p

MAGL blocks the action of arachidonic acid in DSE.

<p>(A) EPSCs from one WT Purkinje cell plotted over time for control responses (open circles) and test responses (closed circles). Cells were filled with MAGL as indicated by the bar. Representative EPSCs are shown at the right. The percentage inhibition of test EPSCs (89.7±9.1%; n = 21) is shown in (A1). (B) EPSCs from one WT Purkinje cell plotted over time for control (open circles) and test responses (closed circles). Cells were filled with FAAH as indicated by the bar. Representative EPSCs are shown at the right. The percentage inhibition of test EPSCs (28.7±7.1%; n = 23) is shown in (B1). (C) Time courses of percentage changes of parallel fiber EPSC amplitudes derived from KO cells filled with either MAGL (filled circles) or FAAH (open circles). Arachidonic acid (AA) was applied in the bath as indicated by the bar. Arachidonic acid depressed EPSCs in FAAH-filled cells but not MAGL-filled cells. (D) MAGL blocked the rescue of DSE by arachidonic acid in KO cells. KO cells filled with either MAGL (filled circles) or FAAH (open circles) Arachidonic acid restored DSE in KO cells. DSE was induced by the protocol indicated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0041499#pone-0041499-g001" target="_blank">Figure 1A</a> with Δt 5 s. Each data point represents the average percentage inhibition of test EPSC every 2 min. Arachidonic acid was applied in the bath as indicated by the bar. *, P<0.05.</p

BoTx, PPADS, chelerythrine and KT5720 do not influence DSE.

<p>(A) EPSCs from one WT Purkinje cell plotted over time for control (open circles) and test responses (closed circles). Representative EPSCs are shown at the right. Internal BoTx was applied as indicated by the bar. The percentage inhibition of test EPSCs (27.8±9.5%; n = 17) is shown in (A1). (B) EPSCs from one WT Purkinje cells plotted over time for control (open circles) and test responses (closed circles). Representative EPSCs are shown at right. The percentage inhibition of test EPSCs (29.2±9.1%; n = 25) is shown in (B1). (C) and (D), Control (open circles) and test (closed circles) EPSCs from two WT Purkinje cells are plotted over time. Representative EPSCs are shown at the right. Representative EPSCs are shown at the right. (C1) and (D1) show DSE amplitudes in chelerythrine (28.7±10.3%; n = 18) and KT5720 (29.2±10.1%; n = 18), respectively. DSE in WT cells (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0041499#pone-0041499-g001" target="_blank">Figure 1E</a>; gray bar) is replotted in (C1) and (D1) for comparison. Applications of BoTx, PPADS, chelerythrine and KT5720 are indicated by bars. Stimulus artifacts of EPSCs are blanked for clarity. *, P<0.05.</p

A proposed model for DSE.

<p>A proposed model for 2-AG release and DSE at parallel fiber-Purkinje cell synapse. Strikethrough texts show the molecules unrelated to DSE, as demonstrated in the present work. See Discussion for explanation.</p

Paxilline reverses the blockade of DSE by internal K⁺.

<p>(A) EPSCs from one WT Purkinje cell plotted over time for control responses (open circles) and test responses (closed circles). Representative EPSCs are shown at the right. Internal K⁺ was applied as indicated by the bar. The percentage inhibition of test EPSCs (89.3±10.4%; n = 26) is shown in (A1). (B) EPSCs from one WT Purkinje cell plotted over time for control (open circles) and test responses (closed circles). Representative EPSCs are shown at the right. Internal K⁺ plus external apamin was applied as indicated by the bar. The percentage inhibition of test EPSCs (89.2±9.9%; n = 20) is shown in (B1). (C) EPSCs from one WT Purkinje cell plotted over time for control (open circles) and test responses (closed circles). Representative EPSCs are shown at the right. Internal K⁺ plus external paxilline was applied as indicated by the bar. The percentage inhibition of test EPSCs (36.6±8.4%; n = 22) is shown in (C1). *, P<0.05.</p

Zinc exposure decreases NR1 clusters and NMDA currents.

<p>Cultured hippocampal neurons were immunostained for NR1. (A) Representative images of clustering of NR1 in control, NBQX+nimodipine and Zn+NBQX+nimodipine groups. For each image, a higher magnification shows the dendritic segment (enclosed in white box) studded with numerous clusters, indexed by white arrows. Scale bar, 50 µm. (B) and (C) show the quantification of (A). Both the number and mean intensity of NR1 clusters were significantly decreased after zinc treatment. The mean intensities were 85.4±4.0 (control; n = 27), 90.2±4.0 (NBQX+nimodipine; n = 24), and 71.5±4.0 (Zn+NBQX+nimodipine; n = 27). (D) Representative whole-cell currents in response to agonist solution containing 30 µM NMDA, 10 µM glycine, 1 µM TTX, 10 µM bicuculline, 10 µM NBQX and 1 µM strychnine in cultured pyramidal cells from control, NBQX+nimodipine and Zn+NBQX+nimodipine groups. The averaged peak amplitude of NMDA currents in Zn+NBQX+nimodipine group was reduced, as shown in (E). *, P<0.05, **, P<0.01.</p

NBQX+nimodipine prevent cell death in chronic zinc exposure.

<p>(A) Typical 10× and 40× bright field pictures of hippocampal neurons of control, NBQX+nimodipine and Zn+NBQX+nimodipine groups at DIV6 and DIV 14. Scale bar, 50 µm. (B) Hippocampal cells were immunostained with tau (green) and DAPI (blue) in control, NBQX+nimodipine and Zn+NBQX+nimodipine groups at DIV14. Merge is the superimposition of Tau and DAPI signals. Note that there was no difference in the dendritic branching and nucleus morphology among three groups. Scale bar, 50 µm. (C) Mitochondrial function was measured in control, NBQX+nimodipine and Zn+NBQX+nimodipine groups. The red and green signals represent the JC-1 monomer (monomer) and JC-1 J-aggregate (J-aggregate), respectively. Merge is the superimposition of red and green signals. Scale bar, 50 µm. The quantification is shown in the right. The mitochondrial membrane potential (Δψ) of cultured cells in each group was calculated as the fluorescence ratio of red to green. Y axis represents the percent change of Δψ in NBQX+nimodipine (99.4±9.9%; n = 9) and Zn+NBQX+nimodipine (107.9±9.6%; n = 10) compared to control. (D) MTT assay derived from cells in control, NBQX+nimodipine and Zn+NBQX+nimodipine groups at DIV14. The ratios (NBQX+nimodipine and Zn+NBQX+nimodipine) were calculated by normalization to control (N = 3).</p