Plaster reinforcement with fibers by mineral wool obtained from the recycle of construction and demolition waste

The use of mineral wool is becoming more widespread due to increased acoustic and thermal demands of Spanish Technical Building Code. This increase affects both in rehabilitation and new construction projects. Therefore, waste generation of this type of insulating material is having more importance. The main objective of this research is to study the possibility of recycling fiber obtained from mineral wool of the C&DW as an alternative material to chopped glass fibers that are currently used as reinforcing elements in the prefabricated plaster. To achieve this objective, series are made of plaster E-35 additived with rock wool residue and glass wool residue at different rates of addition. These series are repeated by changing the additive by E fiberglass (length of 25mm) to make a comparative analysis with respect to the series additived with mineral wool waste. All the series are subjected to the test to determine Shore C surface hardness and mechanical testing to determine the compressive and flexural strength. From the results it can be concluded that: with rock wool residue, increases Shore C hardness up to 15% with respect to the glass fiber and 9% with respect to the glass wool, with a percentage of addition 2%. With rock wool residue, weight is decreased by 5% with respect to the glass fiber and 4% with respect to the glass wool waste, with an addition percentage of 4%. For an addition rate of 4%, results in the flexural strength test with fiberglass are 85% higher than those obtained with glass wool residue. However, for a percentage of 1% addition, the results obtained with glass wool residue are 35% higher than those obtained with fiberglass. For an addition rate of 3% results in the compressive strength test with fiberglass are 54% lower than those obtained with rock wool waste and 70% lower than those obtained with glass wool waste. Comparing the two mineral wools, it can be concluded that up to 3% of the addition, the glass wool series results obtained are 10% higher than those additived with rock wool. However, higher percentages of addition show that the results obtained with rock wool are 35% higher than those obtained with glass wool. The general conclusion is that the series additived with mineral wool from C&DW show better results in tests than the ones used nowadays as plaster reinforcement.

Debonding detection of FRP strengthened concrete beams by using impedance measurements and an ensemble PSO adaptive spectral model

An impedance-based midspan debonding identification method for RC beams strengthened with FRP strips is presented in this paper using piezoelectric ceramic (PZT) sensor?actuators. To reach this purpose, firstly, a two-dimensional electromechanical impedance model is proposed to predict the electrical admittance of the PZT transducer bonded to the FRP strips of an RC beam. Considering the impedance is measured in high frequencies, a spectral element model of the bonded-PZT?FRP strengthened beam is developed. This model, in conjunction with experimental measurements of PZT transducers, is used to present an updating methodology to quantitatively detect interfacial debonding of these kinds of structures. To improve the performance and accuracy of the detection algorithm in a challenging problem such as ours, the structural health monitoring approach is solved with an ensemble process based on particle of swarm. An adaptive mesh scheme has also been developed to increase the reliability in locating the area in which debonding initiates. Predictions carried out with experimental results have showed the effectiveness and potential of the proposed method to detect prematurely at its earliest stages a critical failure mode such as that due to midspan debonding of the FRP strip.

Deletion of the loop region of Bcl-2 completely blocks paclitaxel-induced apoptosis

At high concentrations, the tubule poison paclitaxel is able to kill cancer cells that express Bcl-2; it inhibits the antiapoptotic activity of Bcl-2 by inducing its phosphorylation. To localize the site on Bcl-2 regulated by phosphorylation, mutant forms of Bcl-2 were constructed. Mutant forms of Bcl-2 with an alteration in serine at amino acid 70 (S70A) or with deletion of a 60-aa loop region between the α1 and α2 helices (Δloop Bcl-2, which also deletes amino acid 70) were unable to be phosphorylated by paclitaxel treatment of MDA-MB-231 cells into which the genes for the mutant proteins were transfected. The Δloop mutant completely inhibited paclitaxel-induced apoptosis. In cells expressing the S70A mutant, paclitaxel induced about one-third the level of apoptosis seen with wild-type Bcl-2. To evaluate the role of mitogen-activated protein kinases (MAPKs) in Bcl-2 phosphorylation, the activation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 was examined. Paclitaxel-induced apoptosis was associated with phosphorylation of Bcl-2 and activation of ERK and JNK MAPKs. If JNK activation was blocked by transfections with either a stress-activated protein kinase kinase dominant-negative (K→R) gene (which prevents the activation of a kinase upstream of JNK) or MAPK phosphatase-1 gene (which dephosphorylates and inactivates JNK), Bcl-2 phosphorylation did not occur, and the cells were not killed by paclitaxel. By contrast, neither an ERK inhibitor (PD098059) nor p38 inhibitors (SB203580 and SB202190) had an effect on Bcl-2 phosphorylation. Thus, our data show that the antiapoptotic effects of Bcl-2 can be overcome by phosphorylation of Ser-70; forms of Bcl-2 lacking the loop region are much more effective at preventing apoptosis than wild-type Bcl-2 because they cannot be phosphorylated. JNK, but not ERK or p38 MAPK, appear to be involved in the phosphorylation of Bcl-2 induced by paclitaxel.

The tetravalent guanylhydrazone CNI-1493 blocks the toxic effects of interleukin-2 without diminishing antitumor efficacy

The use of interleukin 2 (IL-2) as an antineoplastic agent has been limited by the serious toxicities that accompany the doses necessary for a tumor response. Elevation of nitric oxide (NO) and tumor necrosis factor (TNF) both have been implicated in IL-2 toxicities. CNI-1493, a tetravalent guanylhydrazone, is an inhibitor of macrophage activation including the synthesis of TNF and other cytokines. Doses of CNI-1493 as low as 1 mg/kg/day conferred complete protection against fatal toxicity of IL-2 with IL-2 doses tenfold higher than the safely tolerated level in Sprague–Dawley rats. Moreover, typical pathologic changes in the lungs, kidneys, and the liver caused by IL-2 infusion were blocked by cotreatment with CNI-1493. When animals bearing established hepatomas were given IL-2 and CNI-1493 combination therapy, 10 of 10 hepatomas regressed from 1 cm3 to <1 mm3. Intracytoplasmic TNF levels were increased in normal tissues from IL-2 treated animals, and treatment with CNI-1493 maintained TNF at control levels. The degree of apoptosis measured by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling staining of tumors following IL-2 therapy was not reduced compared with IL-2 cotreated with CNI-1493. In contrast, apoptosis in the liver and lung parenchyma following IL-2 therapy was blocked completely by cotreatment with CNI-1493. Taken together, these data showed that low and infrequent doses of CNI-1493 markedly protected animals from IL-2 systemic toxicities whereas not affecting tumor response to IL-2 therapy. With the protection afforded by CNI-1493 treatment, IL-2 therapy dose levels could be increased to provide significant antitumor effects in animals with established hepatomas.

Phentolamine block of KATP channels is mediated by Kir6.2

The ATP-sensitive K+-channel (KATP channel) plays a key role in insulin secretion from pancreatic β cells. It is closed both by glucose metabolism and the sulfonylurea drugs that are used in the treatment of noninsulin-dependent diabetes mellitus, thereby initiating a membrane depolarization that activates voltage-dependent Ca2+ entry and insulin release. The β cell KATP channel is a complex of two proteins: Kir6.2 and SUR1. The former is an ATP-sensitive K+-selective pore, whereas SUR1 is a channel regulator that endows Kir6.2 with sensitivity to sulfonylureas. A number of drugs containing an imidazoline moiety, such as phentolamine, also act as potent stimulators of insulin secretion, but their mechanism of action is unknown. We have used a truncated form of Kir6.2, which expresses independently of SUR1, to show that phentolamine does not inhibit KATP channels by interacting with SUR1. Instead, our results argue that phentolamine may interact directly with Kir6.2 to produce a voltage-independent reduction in channel activity. The single-channel conductance is unaffected. Although the ATP molecule also contains an imidazoline group, the site at which phentolamine blocks is not identical to the ATP-inhibitory site, because phentolamine block of an ATP-insensitive mutant (K185Q) is normal. KATP channels also are found in the heart where they are involved in the response to cardiac ischemia: they also are blocked by phentolamine. Our results suggest that this may be because Kir6.2, which is expressed in the heart, forms the pore of the cardiac KATP channel.

A Role for Cadherin-5 in Regulation of Vascular Endothelial Growth Factor Receptor 2 Activity in Endothelial Cells

FLK-1/vascular endothelial growth factor receptor 2 (VEGFR-2) is one of the receptors for VEGF. In this study we examined the effect of cell density on activation of VEGFR-2. VEGF induces only very slight tyrosine phosphorylation of VEGFR-2 in confluent (95–100% confluent) pig aortic endothelial (PAE) cells. In contrast, robust VEGF-dependent tyrosine phosphorylation of VEGFR-2 was observed in cells plated in sparse culture conditions (60–65% confluent). A similar cell density-dependent phenomenon was observed in different endothelial cells but not in NIH-3T3 fibroblast cells expressing VEGFR-2. Stimulating cells with high concentrations of VEGF or replacing the extracellular domain of VEGFR-2 with that of the colony-stimulating factor 1 receptor did not alleviate the sensitivity of VEGFR-2 to cell density, indicating that the confluent cells were probably not secreting an antagonist to VEGF. Furthermore, in PAE cells, ectopically introduced platelet-derived growth factor α receptor could be activated at both high and low cell density conditions, indicating that the density effect was not universal for all receptor tyrosine kinases expressed in endothelial cells. In addition to lowering the density of cells, removing divalent cations from the medium of confluent cells potentiated VEGFR-2 phosphorylation in response to VEGF. These findings suggested that cell–cell contact may be playing a role in regulating the activation of VEGFR-2. To this end, pretreatment of confluent PAE cells with a neutralizing anti-cadherin-5 antibody potentiated the response of VEGFR-2 to VEGF. Our data demonstrate that endothelial cell density plays a critical role in regulating VEGFR-2 activity, and that the underlying mechanism appears to involve cadherin-5.

Characterization of residual structure in the thermally denatured state of barnase by simulation and experiment: Description of the folding pathway

Residual structure in the denatured state of a protein may contain clues about the early events in folding. We have simulated by molecular dynamics the denatured state of barnase, which has been studied by NMR spectroscopy. An ensemble of 104 structures was generated after 2 ns of unfolding and following for a further 2 ns. The ensemble was heterogeneous, but there was nonrandom, residual structure with persistent interactions. Helical structure in the C-terminal portion of helix α1 (residues 13–17) and in helix α2 as well as a turn and nonnative hydrophobic clustering between β3 and β4 were observed, consistent with NMR data. In addition, there were tertiary contacts between residues in α1 and the C-terminal portion of the β-sheet. The simulated structures allow the rudimentary NMR data to be fleshed out. The consistency between simulation and experiment inspires confidence in the methods. A description of the folding pathway of barnase from the denatured to the native state can be constructed by combining the simulation with experimental data from φ value analysis and NMR.

Excitation transfer spectroscopy with two metastable 138Ba+ ions in same trap.

In the absence of lasers approaching trapped ion clock transitions in sharpness we propose to replace the 12.49 m laser field exciting the D3/2-D5/2 transition of the single Ba+ ion A in D3/2 with the near-field of a close by identical ion B in the excited D5/2 state. We tune the frequency of the near-field by the differential Stark shift generated when the center of mass of the tuned ions is slightly moved out of the trap center by a small bias voltage. We demonstrate that the resultant resonant energy exchange can be made considerably faster than the natural lifetime of either metastable level and show how it might be detected.

Irreversible inactivation of interleukin 2 in a pump-based delivery environment.

The physical stability of pharmaceutical proteins in delivery environments is a critical determinant of biological potency and treatment efficacy, and yet it is often taken for granted. We studied both the bioactivity and physical stability of interleukin 2 upon delivery via continuous infusion. We found that the biological activity of the delivered protein was dramatically reduced by approximately 90% after a 24-hr infusion program. Only a portion of these losses could be attributed to direct protein deposition on the delivery surfaces. Analysis of delivered protein by size exclusion chromatography gave no indication of insulin-like, surface-induced aggregation phenomena. Examination of the secondary and tertiary structure of both adsorbed and delivered protein via Fourier-transform infrared spectroscopy, circular dichroism, and fluorescence spectroscopy indicated that transient surface association of interleukin 2 with the catheter tubing resulted in profound, irreversible structural changes that were responsible for the majority of the biological activity losses.

The N-terminal region (A/B) of rat thyroid hormone receptors alpha 1, beta 1, but not beta 2 contains a strong thyroid hormone-dependent transactivation function.

In this study we have investigated the role of the N-terminal region of thyroid hormone receptors (TRs) in thyroid hormone (TH)-dependent transactivation of a thymidine kinase promoter containing TH response elements composed either of a direct repeat or an inverted palindrome. Comparison of rat TR beta 1 with TR beta 2 provides an excellent model since they share identical sequences except for their N termini. Our results show that TR beta 2 is an inefficient TH-dependent transcriptional activator. The degree of transactivation corresponds to that observed for the mutant TR delta N beta 1/2, which contains only those sequences common to TR beta 1 and TR beta 2. Thus, TH-dependent activation appears to be associated with two separate domains. The more important region, however, is embedded in the N-terminal domain. Furthermore, the transactivating property of TR alpha 1 was also localized to the N-terminal domain between amino acids 19 and 30. Using a coimmunoprecipitation assay, we show that the differential interaction of the N terminus of TR beta 1 and TR beta 2 with transcription factor IIB correlates with the TR beta 1 activation function. Hence, our results underscore the importance of the N-terminal region of TRs in TH-dependent transactivation and suggest that a transactivating signal is transmitted to the general transcriptional machinery via a direct interaction of the receptor N-terminal region with transcription factor IIB.

Red supergiants around the obscured open cluster Stephenson 2

Context. Several clusters of red supergiants have been discovered in a small region of the Milky Way close to the base of the Scutum-Crux Arm and the tip of the Long Bar. Population synthesis models indicate that they must be very massive to harbour so many supergiants. Amongst these clusters, Stephenson 2, with a core grouping of 26 red supergiants, is a strong candidate to be the most massive young cluster in the Galaxy. Aims. Stephenson 2 is located close to a region where a strong over-density of red supergiants had been found. We explore the actual cluster size and its possible connection to this over-density. Methods. Taking advantage of Virtual Observatory tools, we have performed a cross-match between the DENIS, USNO-B1 and 2MASS catalogues to identify candidate obscured luminous red stars around Stephenson 2, and in a control nearby region. More than 600 infrared bright stars fulfill our colour criteria, with the vast majority having a counterpart in the I band and >400 being sufficiently bright in I to allow observation with a 4-m class telescope. We observed a subsample of ~250 stars, using the multi-object, wide-field, fibre spectrograph AF2 on the WHT telescope in La Palma, obtaining intermediate-resolution spectroscopy in the 7500–9000 Å range. We derived spectral types and luminosity classes for all these objects and measured their radial velocities. Results. Our targets turned out to be G and K supergiants, late (≥ M4) M giants, and M-type bright giants (luminosity class II) and supergiants. We found ~35 red supergiants with radial velocities similar to Stephenson 2 members, spread over the two areas surveyed. In addition, we found ~40 red supergiants with radial velocities incompatible in principle with a physical association. Conclusions. Our results show that Stephenson 2 is not an isolated cluster, but part of a huge structure likely containing hundreds of red supergiants, with radial velocities compatible with the terminal velocity at this Galactic longitude (and a distance ~6 kpc). In addition, we found evidence of several populations of massive stars at different distances along this line of sight.

Population synthesis of isolated neutron stars with magneto-rotational evolution

We revisit the population synthesis of isolated radio-pulsars incorporating recent advances on the evolution of the magnetic field and the angle between the magnetic and rotational axes from new simulations of the magneto-thermal evolution and magnetosphere models, respectively. An interesting novelty in our approach is that we do not assume the existence of a death line. We discuss regions in parameter space that are more consistent with the observational data. In particular, we find that any broad distribution of birth spin periods with P0 ≲ 0.5 s can fit the data, and that if the alignment angle is allowed to vary consistently with the torque model, realistic magnetospheric models are favoured compared to models with classical magneto-dipolar radiation losses. Assuming that the initial magnetic field is given by a lognormal distribution, our optimal model has mean strength 〈log B0[G]〉 ≈ 13.0–13.2 with width σ(log B0) = 0.6–0.7. However, there are strong correlations between parameters. This degeneracy in the parameter space can be broken by an independent estimate of the pulsar birth rate or by future studies correlating this information with the population in other observational bands (X-rays and γ-rays).

Potentiostatic Reversible Photoelectrochromism: An Effect Appearing in Nanoporous TiO2/Ni(OH)2 Thin Films

In the field of energy saving, finding composite materials with the ability of coloring upon both illumination and change of the applied electrode potential keeps on being an important goal. In this context, chemical bath deposition of Ni(OH)2 into nanoporous TiO2 thin films supported on conducting glass leads to electrodes showing both conventional electrochromic behavior (from colorless to dark brown and vice versa) together with photochromism at constant applied potential. The latter phenomenon, reported here for the first time, is characterized by fast and reversible coloration upon UV illumination. The bleaching kinetics shows first order behavior with respect to the NiIII centers in the film, and an order 1.2 with respect to electrons in the TiO2 film. From a more applied point of view, this study opens up the possibility of having two-mode smart windows showing not only conventional electrochromism but also reversible darkening upon illumination.

Synthesis of xanthone-1,2,3-triazole dyads

Xanthones and 1,2,3-triazoles are known to exhibit several biological, pharmacological and biocidal properties[1]. The potential applications of these two classes of heterocycles led us to develop new strategies to synthesize xanthone-1,2,3-triazole dyads, aiming to get potentially improved therapeutic agents[2]. With this rational in mind we designed and synthesized novel chromone derivatives 1a-d to be used as building motifs and to explore the reactivity of the two unsaturated systems (the diene and the alkyne). In the present communication we will present a new synthetic route towards the synthesis of xanthone-1,2,3-triazole dyads 7a-d using consecutively the azide-alkyne Huisgen 1,3-dipolar cycloaddition and Diels-Alder reaction. Our approach involves the synthesis chromone-triazole derivatives 2a-d using the reaction of 1a-d with sodium azide, followed by the methylation of the NH of the triazole moiety. The methylation afforded three isomers 3a-d, 4a-d and 5a-d, as expected. The major isomers 3a-d were used in the Diels-Alder reaction with N-methylmaleimide, and the adducts obtained 6a-d were oxidized to afford the xanthone-1,2,3-triazole dyads 7a-d. All the synthetic details as well as the structural characterization (by 1D and 2D NMR studies) of the new synthesised compounds will be presented and discussed.

Genetic association of CD247 (CD3ζ) with SLE in a large-scale multiethnic study

A classic T-cell phenotype in systemic lupus erythematosus (SLE) is the downregulation and replacement of the CD3ζ chain that alters T-cell receptor signaling. However, genetic associations with SLE in the human CD247 locus that encodes CD3ζ are not well established and require replication in independent cohorts. Our aim was therefore to examine, localize and validate CD247-SLE association in a large multiethnic population. We typed 44 contiguous CD247 single-nucleotide polymorphisms (SNPs) in 8922 SLE patients and 8077 controls from four ethnically distinct populations. The strongest associations were found in the Asian population (11 SNPs in intron 1, 4.99 × 10(-4) < P < 4.15 × 10(-2)), where we further identified a five-marker haplotype (rs12141731-rs2949655-rs16859085-rs12144621-rs858554; G-G-A-G-A; P(hap) = 2.12 × 10(-5)) that exceeded the most associated single SNP rs858554 (minor allele frequency in controls = 13%; P = 4.99 × 10(-4), odds ratio = 1.32) in significance. Imputation and subsequent association analysis showed evidence of association (P < 0.05) at 27 additional SNPs within intron 1. Cross-ethnic meta-analysis, assuming an additive genetic model adjusted for population proportions, showed five SNPs with significant P-values (1.40 × 10(-3) < P< 3.97 × 10(-2)), with one (rs704848) remaining significant after Bonferroni correction (P(meta) = 2.66 × 10(-2)). Our study independently confirms and extends the association of SLE with CD247, which is shared by various autoimmune disorders and supports a common T-cell-mediated mechanism.