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Hydrated and anhydrous LiB11H14salts are prepared through a facile approach. Liquid-like Li+conductivity (10−2S cm−1) is observed for a-LiB11H14·(H2O)nat 60 °C. LiB11H14·2H2O is classified as a new class of ionic liquid as it melts near 70 °C.

Solid-state sodium batteries have attracted great attention owing to their improved safety, high energy density, large abundance and low cost of sodium compared to the current Li-ion batteries. Sodium-boranes have been studied as potential solid-state electrolytes and the search for new materials is necessary for future battery applications. Here, a facile and cost-effective solution-based synthesis of Na

Metal boron-hydrogen compounds are considered as promising solid electrolyte candidates for the development of all-solid-state batteries (ASSB), owing to the high ionic conductivity exhibited bycloso- andnido-boranes. In this study, an optimised low cost preparation method of MB11H14·(H2O)n, (M = Li and Na) and KB11H14is proposed and analysed. The formation of the B11H14−salt is pH-dependent, and H3O+competes with small ionic radii cations, such as Li+and Na+, to produce a hydronium salt of B11H14−, which forms B11H13OH−upon heating. The use of diethyl ether to extract B11H14−salt from the aqueous medium during synthesis is an important step to avoid hydrolysis of the compound upon drying. The proposed method of synthesis results in LiB11H14and NaB11H14coordinated with water, whereas KB11H14is anhydrous. Hydrated LiB11H14·(H2O)nand NaB11H14·(H2O)nexhibit exceptional ionic conductivities at 25 °C, 1.8 × 10−4S cm−1and 1.1 × 10−3S cm−1, respectively, which represent some of the highest solid-state Li+and Na+conductivities at room temperature. The salts also exhibit oxidative stability of 2.1 Vvs.Li+/Li and 2.6 Vvs.Na+/Na, respectively. KB11H14undergoes a reversible polymorphic structural transition to a metastable phase before decomposing. All synthesisednido-boranes decompose at temperatures greater than 200 °C.

One of the main obstacles to studying the pathophysiology of lymphedema development is the lack of appropriate experimental models. Fol-lowing up on a mouse-tail method that has been described, we performed changes to the method which made it easier to perform in our hands and demonstrated similar results. Twenty C57Black mice were operated on using the previous tech-nique and euthanized after 3 or 6 weeks. Another twenty mice were submitted to the new technique developed in our laboratory and euthanized at the same time points. Tissue samples were collected from the proximal part of the tail (control) and from the distal part (lymphedema) for both mod-els. Animals in both operative groups developed marked edema in the distal part of the tail. This was characterized by lymph vessels dilation, edema, inflammatory cell infiltration, and adipose tissue deposition. Lymphedema was detected after 3 weeks in both models, reaching its maximum after 6 weeks. Adipocytes detected by histology (Oil red O staining) and molecular markers for adipogenesis, lymphangiogenesis and inflam-mation (lipin 1 and 2, SLP76, and F4-80) were demonstrated to be increased equally in both models. In conclusion, both models provide a reliable method to study lymphedema pathophys-iology. However, our modified technique is easier and faster to perform while still providing reliable and consistent results.

We report, for the first time, members of the Y xPr2- xO3 system with non-bixbyite or defect fluorite structures. The synthesis, structure, phase transitions, and high temperature reactivity of the trigonal A-type and monoclinic B-type structures are reported along with those of the cubic C-type phase (bixbyite). Combined powder X-ray and neutron diffraction Rietveld refinements are used to report structural details of all three reported phases. Phase transitions are investigated, showing a clear dependence on average cation size. Using neutron diffraction, phase transitions are followed in situ, revealing that all high temperature phases are quenchable. In-situ powder X-ray diffraction experiments in flowing oxygen allow insights into mechanistic details of redox processes in the reported phases. In contrast to the C-type cubic bixbyite, the trigonal A-type and monoclinic B-type structures do not allow for topotactic oxygen uptake, displaying instead a phase transition to either the bixbyite C-type capable of accommodating additional oxide anions or the direct oxidation to the cubic defect fluorite structure. The findings reported here agree with the accepted lanthanide sesquioxide phase diagrams and provide exceptional control of phases. The work is important for the prediction of structures, and the synthetic control needed for rational design of functional materials.

Several limitations have recently been described for lucigenin, a probe frequently used to assess the activity of vascular NAD(P)H oxidase, a major superoxide source. The preferential reducing substrate of such oxidase remains unclear. We assessed whether lucigenin artifacts could affect detection of NAD(P)H oxidase activity. Initial chemiluminescence assays were performed with vascular rings or homogenates at 5, 50, or 250 μM concentrations. Results showed preferential signals with NADPH (vs. NADH) with 5 and 50 μM lucigenin, which were blocked by diphenylene iodonium (DPI), superoxide dismutase (SOD), or its cell-permeable mimetic MnTBAP. With 250 μM lucigenin, the relative signal with NADH became larger than with NADPH, and was poorly inhibited by all three antagonists above. All SOD/DPI-resistant signals were effectively blocked by the electron acceptor nitrobluetetrazolium. Spin trapping with DMPO showed an approximate doubling of DMPO-OH radical adduct signal upon addition of 5 μM lucigenin to homogenates incubated with either NADPH or NADH. With 50 or 250 μM lucigenin, much larger increases were observed with NADH, as opposed to NADPH. Furthermore, oxygen consumption measurements showed analogous results. In summary, our data suggest that: (i) Lucigenin redox-cycling is detectable in vascular tissue even at 5 μM concentrations, while at 250 μM redox-cycling becomes predominant and is markedly increased when NADH is the assayed substrate; and (ii) With 250 μM lucigenin, preferentially with NADH, signals are further overestimated by direct, oxidase-dependent, superoxide-independent two-electron transfer. Therefore, previous reports of preferential NADH affinity of the vascular oxidase may have been due to these artifacts.

Hamburger is a meat-based food that is easy to prepare and is widely consumed. It can be enriched using different ingredients, such as chia's by-product, which is rich in omega-3. Chemometrics is a very interesting tool to assess the influence of ingredients in the composition of foods. A complete factorial design 2(2) (two factors in two levels) with duplicate was performed to investigate the influence of the factors (1) concentration of textured soy proteins (TSP) and (2) concentration of chia flour partially defatted (CFPD) as a partial replacement for the bovine meat and porcine fat mix in hamburgers.The results of proximal composition, lipid oxidation, fatty acids sums, ratios, and nutritional indexes were used to propose statistical models. The factors TSP and CFPD were significant, and the increased values contributed to improve the composition in fatty acids, crude protein, and ash. Principal components analysis distinguished the samples with a higher content of chia. In desirability analysis, the highest level of TSP and CFPD was described as the optimal region, and it was not necessary to make another experimental point.The addition of chia's by-product is an alternative to increase the α-linolenic contents and to obtain nutritionally balanced food.

SUMMARYSeroprevalence ofToxocaraandTaenia soliumand risk factors for infection with these parasites were explored in a long-term rural settlement in São Paulo state, Brazil. An ELISA for the detection of anti-ToxocaraIgG and IgE and anti-T. soliumcysticerci was standardized usingToxocaraexcretory-secretory antigens (TES) obtained from the cultured second-stage larvae ofT. canisand by vesicular fluid antigen fromTaenia crassiceps cysticerci(VF). For cysticercosis, the reactive ELISA samples were assayed by Western blot using 18 kDa and 14 kDa proteins purified from VF. Out of 182 subjects, 25 (13·7%) presented anti-ToxocaraIgG and a positive correlation between total IgE and the reactive index of specific anti-TES IgE (P=0·0265) was found amongst the subjects found seropositive for anti-ToxocaraIgG. In these individuals 38·0% showed ocular manifestations. The frequency of anti-T. soliumcysticerci confirmed by Western blot was 0·6%. Seropositivity forToxocarawas correlated with low educational levels and the owning of dogs. Embryonated eggs ofToxocaraspp. were found in 43·3% of the analysed areas.

There is a growing interest in the pathophysiology of processes involving vascular cell injury and redox signaling, particularly with superoxide generation. Lucigenin chemiluminescence has been extensively used as a method to assess superoxide production and its underlying enzymatic mechanisms in many biological systems, the most studied one being the vascular NAD(P)H oxidase. Recent evidence suggests substantial limitations of this probe because of artifactual superoxide generation. To investigate if lucigenin concentration could affect the detection of vascular NAD(P)H oxidase activity we performed studies with lucigenin chemiluminescence, oxygen consumption and electron paramagnetic resonance (EPR) spectroscopy for superoxide generation detection with vascular homogenates and different concentrations of lucigenin (5, 50 and 250 μM). The NAD(P)H oxidase blocker diphenylene iodonium (DPI, 20 μM), SOD (500 IU/ml), catalase (500 IU/ml) and the electron acceptor NBT were also used to characterize lucigenin behavior in a vascular system. Our data showed that lucigenin alone, with 5 μM, induced a 2-fold increase in oxygen consumption, while with 250 μM oxygen consumption increased 5-fold. Superoxide generation, assessed by EPR spectroscopy, also increased progressively with 5, 50 and 250 μM lucigenin. These effects were particularly enhanced by addition of NADH, but occurred also with NADPH. Chemiluminescence studies showed that with 5 and 50 μM lucigenin there is greater NADPH induced signal than NADH, while 250 μM lucigenin yields a 1.5-fold greater signal with NADH than with NADPH. Furthermore, all NADPH-driven luminescent signals were inhibited by SOD, DPI, and NBT, as well as NADH-driven luminescence with 5 μM lucigenin. On the other hand, with lucigenin 250 μM, NADH-driven luminescence could not be blocked by SOD or DPI, but was completely inhibited by NBT. Catalase did not show any inhibitory effect on NADPH-induced luminescence, but inhibited 30% of NADH-driven signals. In conclusion, lucigenin even at low doses undergoes redoxcycling reactions, which are favored by NADH generating artifactual superoxide. Furthermore, it is possible that lucigenin acts as a direct electron acceptor from vascular enzymatic sources other than the superoxide-generating NAD(P)H oxidase, and detects also hydrogen peroxide generated by a vascular NADH oxidase.

The effects of mercury on vascular smooth muscle results in vasoconstriction, but the mechanism of this action is not elucidated yet. To investigate this issue we examined the effects of HgCl(2) in the isolated rat tail vascular bed. The tail artery was dissected, cannulated, and perfused at a constant flow (2.5 ml/min) with Krebs solution plus EDTA 0.03 mM at 36 degrees C. After equilibration for 30 min the effects of increasing concentrations of HgCl(2) (0.5, 1, 2, 5, and 10 microM) on the perfusion pressure were investigated. Concentrations of HgCl(2), 2 microM and above, significantly increased perfusion pressure. Blockade of alpha receptors (prazosin 84 ng/ml) did not alter the responses to HgCl(2), suggesting that the metal does not induce the release of neurotransmitters from sympathetic nerve terminals. To investigate the possible role of endothelium on the vasoconstriction produced by HgCl(2), preparations were precontracted with 10(-7) M phenylepherine or perfused with 5 microM HgCl(2) for 20 min. Acetylcholine-vasodilated preparations precontracted with phenylepherine demonstrating the integrity of the endothelial nitric oxide-releasing mechanism. In contrast, after perfusion with 5 microM HgCl(2), the vasodilation produced by acetylcholine was abolished. In the presence of either phenylephrine or HgCl(2) the effects of sodium nitroprusside remained unchanged. Pretreatment with 30 microM indomethacin fully prevented the HgCl(2)-induced vasoconstriction. However, the endothelium-dependent vasodilation in response to acetylcholine was significantly reduced after indomethacin plus HgCl(2) treatment, meanwhile the vasodilation produced by nitroprusside remained unchanged. Pretreatment with L-arginine (1 mM) did not prevent the vasoconstriction induced by HgCl(2), nor did it restore the ability of acetylcholine to produce vasodilation, and it did not alter the response to sodium nitroprusside. The possibility of HgCl(2)'s actions mediated by the formation of free radicals was also investigated. The administration of 10 mM histidine significantly reduced the vasoconstrictor response if used before HgCl(2) treatment without improving the reduced vasodilation produced by acetylcholine. These results are consistent with the hypothesis that the vasoconstriction produced by HgCl(2) may be mediated by the formation of superoxide anions, stimulating the production of a COX-derived vasoconstrictor agent and by reducing the endothelial vasodilator activity.