Nucleation of the electroactive γ phase and enhancement of the optical transparency in low filler content poly(vinylidene)/clay nanocomposites

Poly(vinylidene fluoride), PVDF, based nanocomposites with different clays structures have been processed by solvent casting and melt crystallisation. Depending on the melting temperature of the polymer, the nanocomposite recrystalises in the electroactive or non electroactive β-phase of the polymer. This fact is related to the thermal behaviour of the clay. For montmorillonite clay, the full crystallisation of the electroactiveγ-phase occurs for clay contents lower than 0.5 wt%, allowing the nanocomposites to maintain the mechanical properties of the polymer matrix. The electroactivity of the material has been proven by measuring the piezoelectric d33 response of the material. The obtained value of d33 is -7 pC/N, lower than in β-PVDF obtained by mechanical stretching, but still among the largest coefficients obtained for polymers. Further, the optical transmittance in the visible range is strongly enhanced with respect to the transmittance of the pure polymer. Finally, it is demonstrated that the nucleation of the β-phase can be also obtained in other clays, such as in kaolinite and laponite.Fundação para a Ciência e a Tecnologia (FCT) - NANO/NMed-SD/0156/2007, PTDC/CTM/69316/2006, PTDC/CTM-NAN/112574/2009, SFRH/BD/62507/2009.FEDER funds through the "Programa Operacional Factores de Competitividade – COMPETECOST Action MP1003, the ‘European Scientific Network for Artificial Muscles’ (ESNAM)

MHO1, an Evolutionarily Conserved Gene, Is Synthetic Lethal with PLC1; Mho1p Has a Role in Invasive Growth

The novel protein Memo (Mediator of ErbB2 driven cell motility) was identified in a screen for ErbB2 interacting proteins and found to have an essential function in cell motility. Memo is evolutionarily conserved with homologs found in all branches of life; the human and yeast proteins have a similarity of >50%. In the present study we used the model organism S. cerevisiae to characterize the Memo-homologue Mho1 (Yjr008wp) and to investigate its function in yeast. In a synthetic lethal screen we found MHO1 as a novel synthetic lethal partner of PLC1, which encodes the single phospholipase C in yeast. Double-deleted cells lacking MHO1 and PLC1, proliferate for up to ten generations. Introduction of human Memo into the memoΔplc1Δ strain rescued the synthetic lethal phenotype suggesting that yeast and human proteins have similar functions. Mho1 is present in the cytoplasm and the nucleus of yeast cells; the same distribution of Memo was found in mammalian cells. None of the Memo homologues have a characteristic nuclear localization sequence, however, a conserved nuclear export sequence is found in all. In mammalian cells, blocking nuclear export with Leptomycin B led to nuclear Memo accumulation, suggesting that it is actively exported from the nucleus. In yeast MHO1 expression is induced by stress conditions. Since invasive growth in S. cerevisiea is also stress-induced, we tested Mho1's role in this response. MHO1 deletion had no effect on invasion induced by nutrient deprivation, however, Mho1 overexpression blocked the invasive ability of yeast cells, suggesting that Mho1 might be acting in a dominant negative manner. Taken together, our results show that MHO1 is a novel synthetic lethal interactor with PLC1, and that both gene products are required for proliferation. Moreover, a role for Memo in cell motility/invasion appears to be conserved across species

Correction: The Effect of Protandim® Supplementation on Athletic Performance and Oxidative Blood Markers in Runners.

[This corrects the article DOI: 10.1371/journal.pone.0160559.]

The Effect of Protandim^® Supplementation on Athletic Performance and Oxidative Blood Markers in Runners

<div><p>The purpose of this study determined if oral supplementation of Protandim^® (a nutraceutical) for 90 days improved 5-km running performance and reduced serum thiobarbituric acid-reacting substances (TBARS) at rest, an indicator of oxidative stress. Secondary objectives were to measure whole blood superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPX), at rest and 10 minutes after completion of the race before and after supplementation as well as quality of life. In a double-blind, randomized, placebo controlled trial, 38 runners [mean (SD) = 34 (7) yrs; BMI = 22 (2) kg/m²] received either 90 days of Protandim^® [1 pill a day, n = 19)] or placebo (n = 19). Randomization was done in blocks of two controlling for sex and 5-km baseline performance. A 5-km race was performed at baseline and after 90 days of supplementation, with blood samples taken before and 10-min after each race. Fasting blood samples were acquired at baseline, after 30, 60, and 90 days of supplementation. TBARS, SOD, GPX, and GSH were assayed in an out-of-state accredited lab. Running performance was not altered by Protandim^® or placebo [20.3 (2.1) minutes, with an -8 (33) seconds change in 5-km time regardless of group]. There was no change in TBARS, SOD, or GPX (at rest) after three months of Protandim^® supplementation compared to placebo. However, in a subgroup ≥ 35 years of age, there was a 2-fold higher increase in SOD in those taking Protandim^® for three months compared to those on placebo (<i>p</i> = 0.038). The mean post-race change in TBARS (compared to pre-race) increased by about 20% in half of the subjects, but was not altered between groups, even after three months of supplementation. Quality of life was also not different between the two conditions. In conclusion, Protandim^® did not (1) alter 5-km running time, (2) lower TBARS at rest (3) raise antioxidant enzyme concentrations compared to placebo (with exception of SOD in those ≥ 35 years old) or, (4) affect quality of life compared to placebo.</p><p><b><i>Trial Registration</i>:</b> ClinicalTrials.gov <a href="https://clinicaltrials.gov/ct2/results?term=NCT02172625&Search=Search" target="_blank">NCT02172625</a></p></div

The long terms effects of supplementation on glutathione peroxidase and total glutathione content from whole blood (rest, fasted state).

<p>There was no difference between groups for either variable (<i>p</i> = 0.66 for glutathione peroxidase, <i>p</i> = 0.52 for whole blood glutathione). The asterisk* signifies statistical significance at 57 days post-supplementation (<i>p</i> = 0.00) compared to the baseline value after adjustments for multiple comparisons. Mean values represented by circles, error bars represent SD. The x-axis represents the mean (SD) of the number of days post-supplementation.</p

The measured week to week coefficient of variation in the blood variables.

<p>All blood variables were measured by Genova Diagnostics (n = 38).</p

The long terms effects of supplementation on the cysteine to cysteine ratio and the cysteine to sulfate ratio (rest, fasted state).

<p>There was no difference between groups for either variable (<i>p</i> = 0.30 for the cysteine to cysteine ratio, <i>p</i> = 0.69 for the cysteine to sulfate ratio). For the cysteine to sulfate ratio, there was a difference at 57 days post-supplementation compared to baseline (<i>p</i> = 0.00). Mean values represented by circles, error bars represent SD.</p

Individual changes in superoxide dismutase (SOD) in runners ≥ 35 years of age (range = 35 to 46 years of age).

<p>Those taking Protandim^® for 88 days (n = 8) showed a 2-fold higher increase in SOD compared to the 11 runners taking the placebo (Group x Time interaction effect, <i>p</i> = 0.038). The effect size for the between group change between Protandim^® and placebo was +1.00 (Bias corrected, Hedges) (95% CI of the effect size = 0.03 to 1.96) in favor of Protandim^®.</p

Individual changes in lipid peroxides between groups before the supplementation period and after 88 days of supplementation.

<p>The baseline period is an average of both baseline days prior to supplementation. In total, 19 subjects (50%) showed increases in TBARS from pre-race to post-race ranging from 0.1 to 4.4 μmol/L [mean increase = +1.7 (SD 1.4) μmol/L or ~20%]. Supplementation with Protandim^® did not lessen the increase in lipid peroxidation compared to placebo.</p