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Nb 999 Buy

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Vanadium and niobium cation-water complexes, V+(H2O) and Nb+(H2O), are produced by laser vaporization in a pulsed supersonic expansion, mass selected in a time-of-flight spectrometer, and studied with infrared photodissociation spectroscopy using rare gas atom (Ar, Ne) complex predissociation. The vibrational bands measured in the O-H stretching region contain K-type rotational sub-band structure, which provides insight into the structures of these complexes. However, rotational sub-bands do not exhibit the simple patterns seen previously for other metal ion-water complexes. The A rotational constants are smaller than expected and the normal 3:1 intensity ratios for K = odd:even levels for independent ortho:para nuclear spin states are missing for some complexes. We relied on highly correlated internally contracted multi-reference configuration interaction and Coupled Cluster [CCSD(T)] electronic structure calculations of those complexes with and without the rare gas atoms to investigate these anomalies. Rare gas atoms were found to bind via asymmetric motifs to the hydrated complexes undergoing large amplitude motions that vibrationally average to the quasi-C2v symmetry with a significant probability off the C2 axis, thus explaining the reduced A values. Both vanadium and niobium cations exhibit unusually strong nuclear spin coupling to the hydrogen atoms of water, the values of which vary with their electronic state. This catalyzes ortho-para interconversion in some complexes and explains the rotational patterns. The rate of ortho-para relaxation in the equilibrated complexes must therefore be greater than the collisional cooling rate in the supersonic expansion (about 106 s-1).

Optimized coefficients of the Gibbs free energy expression for each stable phase of the binary Nb-Si have been obtained, using the Thermo-Calc program for this purpose. The Nb3Si, alphaNb(5)Si(3), NbSi2 and Diamond (Si) have been modeled as stoichiometric phases and the liquid L, BCC (Nb) and the betaNb(5)Si(3) phases as solutions, with the excess term described using the Redlich-Kister formalism. The Si solubility in the betaNb(5)Si(3) phase has been modeled according to two possibilities: (i) Si substituting for Nb and (ii) vacancies in the Nb positions. The calculated diagrams compare well with the experimental information taken from the literature.

aHubei Provincial Key Laboratory for Protection and Application of Special Plants in Wuling Area of China, College of Life Science, South-Central University for Nationalities, Wuhan, Hubei, P.R. China

In recent years, research has identified over 90 major R genes of rice blast disease and more than 20 of those R genes have been isolated.[4] Among them, 17 R genes, Pib, Pi-ta, Pik-h, Pi2, Pi9, Piz-t, Pi36, Pi37, Pik-m, Pid3, Pi5, Pit, Pbl, Pi-sh, Pik, Pik-p and Pia, belong to a large R gene family, which encodes nucleotide-binding sites and leucine-rich repeat (NBS-LRR) proteins; in addition, Pid-2 encodes receptor-like kinase proteins [5] and the partial resistance gene pi21 encodes a proline-rich protein.[6]

Extensive research has been reported on innate plant immunity and various defence responses against microbial pathogen attack mediated through multiple signalling pathways. Such defence responses are a key requirement for the induction of a set of pathogenesis-related proteins (PRs). PRs are defined as plant proteins that are induced specifically in pathological or stress situations; the production and accumulation of PRs represent an essential component of the active plant defence repertoire.[7] One of the critical signalling pathways leading to stress response is performed through salicylic acid (SA), which is constitutively present in high levels in rice.[8,9] In addition, a large body of genetic and molecular evidence has shown that jasmonates, including jasmonic acid (JA) and methyl jasmonate, also provide essential and important endogenous signals that are implicated in induced resistance to pathogen infection.[10] Moreover, abscisic acid (ABA) has also been identified as a signalling molecule and has been implicated as a component in PR gene(s) regulation in plants.[11] RAR1, a zinc-binding protein, is another key component involved in diverse R resistance in plants.[12] RAR1 interacts directly with SGT1 (for suppression of the G2 allele of Skp1) and HSP90, which are essential for disease resistance mediated by diverse R proteins.[13]

In the field resistance response, OsWRKY45 was upregulated at 24 h in both cultivars, AA and AA-pi21 (Figure 1). The OsWRKY45 expression further increased significantly at 48 h and reached a much higher level (63-fold of the background level) in the susceptible AA line than in the resistant AA-pi21 one (about 25-fold of the background level). In KHS, OsWRKY45 could not be induced at 24 h but could increase 13-fold after 48 h, whereas in KHR, the expression levels increased 14.5-fold after 24 h and 3.7-fold after 48 h (Figure 1). In other words, OsWRKY45 was upregulated in all of the tested lines, but its levels of expression in the resistant cultivars were much lower than that in the respective susceptible ones. Only in the resistant KHR, the expression level of WRKY45 was higher than in the susceptible KHS. Thus, it can be speculated that probably only Pikahei is involved in the SA signalling pathway.

In our study, at the tested time point, OsPR1b was shown to be upregulated in four lines (NB, NB-Pib, NB-Pizt and NB-Pik). However, much higher expression levels were shown at 48 h p.i. than at 24 h p.i. No expression was observed in NB-Pita2 at the three time points. OsPR1b was significantly induced by 48 h p.i. in AA and AA-pi21; however, the expression level in AA-pi21 was higher than that in AA (Figure 4). Strangely, OsPR1b was not expressed in lines KHS and KHR, and an experimental error was ruled out. PBZ1 was significantly elevated at 24 h in five lines (NB-Pib, NB-Pizt, NB-Pik, NB-Pita2 and AA-pi21), peaking at 48 h at approximately 340-, 155-, 156-, 45- and 35-fold, respectively (Figure 5). Compared with NB, the expression level of PBZ1 in the resistant lines was lower. The expression profiles of PBZ1 in AA and AA-pi21 were similar to that of OsPR1b. However, PBZ1 was upregulated with expression levels in KHS higher than those in KHR (Figure 5).

Our results showed that OsRAR1 expression levels were downregulated in all of the tested lines, except for NB-Pita2 and KHR (Figure 6). In addition, OsSGT1 was upregulated in five lines (NB-Pib, NB-Pizt, NB-Pik, NB-Pita2 and KHR) to 2-, 2-, 2-, 2.5- and 4.5-fold of their background by 24 h p.i. (Figure 7). They subsequently decreased rapidly by 48 h p.i in NB, NB-Pib, NB-Pizt, NB-Pik and NB-Pita2. OsSGT1 was upregulated in two lines: AA and AA-pi21. The expression levels were 1.6-fold at 24 h in AA and 2.6-fold at 48 h in AA-pi21, demonstrating a substantial increase in the resistant line AA-pi21 (Figure 7). OsSGT1 was induced at 24 h in two lines (KHR and KHS), where the expression level of KHR was much higher than in KHS.

The expression patterns of OsHSP90 were similar in all of the tested lines, demonstrating upregulation at 24 h to 1.5-, 2.7-, 6.7-, 2.1 and 4.1-fold in NB, NB-Pib, NB-Pizt, NB-Pik and NB-Pita2, respectively (Figure 8). OsHSP90 was upregulated to 1.8-, 2.8-, 1.2- and 1.6-fold of the corresponding background levels by 24 h p.i. in AA, AA-pi21, KHS and KHR, respectively. However, the gene was downregulated by 48 h p.i. in all of the tested lines.

This research was supported by grants from the National Science Foundation of China [grant number 31370306]; Project from Department of Human Resources and Social Security of China [grant number BZY12005]; the National Transgenic Research Project [grant number 2014ZX08009004B]; Hubei Provincial National Science Project [grant number 2013CFA098]. 041b061a72


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