Production of asphalt mixes with copper industry wastes: Use of copper slag as raw material replacement.

Copper slag is a waste obtained from copper production and it has a limited use, being mainly accumulated in landfills on a massive scale. This material presents a high hardness and it has hydrophobic properties, so it can be used as aggregate replacement in the production of asphalt mixtures. However, each size of copper slag behaves differently when used in asphalt mixes, especially under changing conditions of moisture or temperature. Precisely these climatic factors directly affect the service life of asphalt pavements. In this research, semi-dense graded asphalt mixtures were produced with copper slag as replacement of aggregates, varying the particle sizes used in the range from 2.5 to 0.08 mm to determine the size of copper slag with the best performance. Indirect tensile strength tests were used to analyze samples subjected to different moisture and temperature conditions and ageing degrees. The results show that copper slag can be used as aggregate replacement in asphalt mixes when the proper size is selected. The strength of the asphalt mixture increased as the size of the copper slag increased, especially under variable moisture and ageing conditions. Superior behaviour compared to a reference mixture was obtained when replacing the size of aggregate No. 8 with copper slag, increasing its indirect tensile strength and retained strength, reducing its stiffness under all the ageing periods, and being equally effective at the different temperatures, which results in mixtures with improved durability and delayed cracking. Furthermore, it would help to reduce between 15 and 20% of the virgin aggregate needed to produce asphalt mixes and it would also allow reducing the accumulated volume of this waste, decreasing the environmental impact of both industries.

Identification of novel monocistronic HTLV-1 mRNAs encoding functional Rex isoforms.

BACKGROUND: Human T cell leukemia virus type 1 (HTLV-1) gene expression is controlled by the key regulatory proteins Tax and Rex. The concerted action of these proteins results in a two-phase kinetics of viral expression that depends on a time delay between their action. However, it is difficult to explain this delay, as Tax and Rex are produced from the same mRNA. In the present study we investigated whether HTLV-1 may produce novel mRNA species capable of expressing Rex and Tax independently. FINDINGS: Results revealed the expression of three alternatively spliced transcripts coding for novel Rex isoforms in infected cell lines and in primary samples from infected patients. One mRNA coded for a Tax isoform and a Rex isoform, and two mRNAs coded for Rex isoforms but not Tax. Functional assays showed that these Rex isoforms exhibit activity comparable to canonic Rex. An analysis of the temporal expression of these transcripts upon ex vivo culture of cells from infected patients and cell lines transfected with a molecular clone of HTLV-1 revealed early expression of the dicistronic tax/rex mRNAs followed by the monocistronic mRNAs coding for Rex isoforms. CONCLUSION: The production of monocistronic HTLV-1 mRNAs encoding Rex isoforms with comparable activity to canonical Rex, but with distinct timing, would support a prolonged duration of Rex function with gradual loss of Tax, and is consistent with the two-phase expression kinetics. A thorough understanding of these regulatory circuits will shed light on the basis of viral latency and provide groundwork to develop strategies for eradicating persistent infections.

Water quality and quantity assessment of pervious pavements performance in experimental car park areas.

Pervious pavements have become one of the most used sustainable urban drainage system (SUDS) techniques in car parks. This research paper presents the results of monitoring water quality from several experimental car park areas designed and constructed in Spain with bays made of interlocking concrete block pavement, porous asphalt, polymer-modified porous concrete and reinforced grass with plastic and concrete cells. Moreover, two different sub-base materials were used (limestone aggregates and basic oxygen furnace slag). This study therefore encompasses the majority of the materials used as permeable surfaces and sub-base layers all over the world. Effluent from the test bays was monitored for dissolved oxygen, pH, electric conductivity, total suspended solids, turbidity and total petroleum hydrocarbons in order to analyze the behaviour shown by each combination of surface and sub-base materials. In addition, permeability tests were undertaken in all car parks using the 'Laboratorio Caminos Santander' permeameter and the Cantabrian Portable Infiltrometer. All results are presented together with the influence of surface and sub-base materials on water quality indicators using bivariate correlation statistical analysis at a confidence level of 95%. The polymer-modified porous concrete surface course in combination with limestone aggregate sub-base presented the best performance.

Suppression of HTLV-1 replication by Tax-mediated rerouting of the p13 viral protein to nuclear speckles.

Disease development in human T-cell leukemia virus type 1 (HTLV-1)-infected individuals is positively correlated with the level of integrated viral DNA in T cells. HTLV-1 replication is positively regulated by Tax and Rex and negatively regulated by the p30 and HBZ proteins. In the present study, we demonstrate that HTLV-1 encodes another negative regulator of virus expression, the p13 protein. Expressed separately, p13 localizes to the mitochondria, whereas in the presence of Tax, part of it is ubiquitinated, stabilized, and rerouted to the nuclear speckles. The p13 protein directly binds Tax, decreases Tax binding to the CBP/p300 transcriptional coactivator, and, by reducing Tax transcriptional activity, suppresses viral expression. Because Tax stabilizes its own repressor, these findings suggest that HTLV-1 has evolved a complex mechanism to control its own replication. Further, these results highlight the importance of studying the function of the HTLV-1 viral proteins, not only in isolation, but also in the context of full viral replication.

Requirement of the human T-cell leukemia virus p12 and p30 products for infectivity of human dendritic cells and macaques but not rabbits.

The identification of the genes necessary for human T-cell leukemia virus (HTLV-1) persistence in humans may provide targets for therapeutic approaches. We demonstrate that ablation of the HTLV-1 genes encoding p12, p30, or the HBZ protein, does not affect viral infectivity in rabbits and in this species, only the absence of HBZ is associated with a consistent reduction in virus levels. We observed reversion of the HTLV-1 mutants to the HTLV-1 wild-type genotype in none of the inoculated rabbits. In contrast, in macaques, the absence of HBZ was associated with reversion of the mutant virus to the wild-type genotype in 3 of the 4 animals within weeks from infection. Similarly, reversion to the wild type was observed in 2 of the 4 macaque inoculated with the p30 mutant. The 4 macaques exposed to the p12 knock remained seronegative, and only 2 animals were positive at a single time point for viral DNA in tissues. Interestingly, we found that the p12 and the p30 mutants were also severely impaired in their ability to replicate in human dendritic cells. These data suggest that infection of dendritic cells may be required for the establishment and maintenance of HTLV-1 infection in primate species.

In vivo genetic mutations define predominant functions of the human T-cell leukemia/lymphoma virus p12I protein.

The human T-cell leukemia/lymphoma virus type 1 (HTLV-1) ORF-I encodes a 99-amino acid hydrophobic membrane protein, p12(I), that affects receptors in different cellular compartments. We report here that proteolytic cleavage dictates different cellular localization and functions of p12(I). The removal of a noncanonical endoplasmic reticulum (ER) retention/retrieval signal within the amino terminus of p12(I) is necessary for trafficking to the Golgi apparatus and generation of a completely cleaved 8-kDa protein. The 8-kDa protein in turn traffics to the cell surface, is recruited to the immunologic synapse following T-cell receptor (TCR) ligation, and down-regulates TCR proximal signaling. The uncleaved 12-kDa form of p12(I) resides in the ER and interacts with the beta and gamma(c) chains of the interleukin-2 receptor (IL-2R), the heavy chain of the major histocompatibility complex (MHC) class I, as well as calreticulin and calnexin. Genetic analysis of ORF-I from ex vivo samples of HTLV-1-infected patients reveals predominant amino acid substitutions within ORF-I that affect proteolytic cleavage, suggesting that ER-associated functions of p12(I) may contribute to the survival and proliferation of the infected T cells in the host.

Proposal of a New Porous Concrete Dosage Methodology for Pavements.

Although porous concrete pavement design methods are mainly focused on maintaining high permeability rates in order to improve their ability to manage stormwater runoff, the mixture strength is paramount for its durability and service life. This paper proposes a new mixture design method for porous concrete, named PCD (porous concrete design), derived from the ACI 522R-10 and ACI 211.3R-02 standards. The aim is to improve mechanical strength in porous concrete mixtures, while ensuring enough permeability for its use in urban roads. With PCD methodology it is possible to obtain mechanical strengths 30% higher than those produced with ACI methodologies, while maintaining permeability rates close to 2 cm/s, lower than those obtained with ACI methods but still enough to manage extreme storm events. Finally, with the analytical Hierarchy Process (AHP) multi-criteria decision-making methodology and also bearing in mind safety variables, the best porous concrete mixtures are the ones produced with PCD methodology.

Characterization of wash-off from urban impervious surfaces and SuDS design criteria for source control under semi-arid conditions.

Knowledge about pollutant wash-off from urban impervious surfaces is a key feature for developing effective management strategies. Accordingly, further information is required about urban areas under semi-arid climate conditions at the sub-catchment scale. This is important for designing source control systems for pollution. In this study, a characterization of pollutant wash-off has been performed over sixteen months, at the sub-catchment scale for urban roads as impervious surfaces. The study was conducted in Valencia, Spain, a city with a Mediterranean climate. The results show high event mean concentrations for suspended solids (98mg/l), organic matter (142mgCOD/l, 25mgBOD5/l), nutrients (3.7mgTN/l, 0.4mgTP/l), and metals (0.23, 0.32, 0.62 and 0.17mg/l for Cu, Ni, Pb, and Zn, respectively). The results of the runoff characterization highlight the need to control this pollution at its source, separately from wastewater because of their different characteristics. The wash-off, defined in terms of mobilized mass (g/m2) fits well with both process-based and statistical models, with the runoff volume and rainfall depth being the main explanatory variables. Based on these results and using information collected from hydrographs and pollutographs, an approach for sizing sustainable urban drainage systems (SuDS), focusing on water quality and quantity variables, has been proposed. By setting a concentration-based target (TSS discharged to receiving waters <35mg/l), the results indicate that for a SuDS type detention basin (DB), an off-line configuration performs better than an on-line configuration. The resulting design criterion, expressed as SuDS volume per unit catchment area, assuming a DB type SuDS, varies between 7 and 10l/m2.

Vaccine induced antibodies to the first variable loop of human immunodeficiency virus type 1 gp120, mediate antibody-dependent virus inhibition in macaques.

The role of antibodies directed against the hyper variable envelope region V1 of human immunodeficiency virus type 1 (HIV-1), has not been thoroughly studied. We show that a vaccine able to elicit strain-specific non-neutralizing antibodies to this region of gp120 is associated with control of highly pathogenic chimeric SHIV(89.6P) replication in rhesus macaques. The vaccinated animal that had the highest titers of antibodies to the amino terminus portion of V1, prior to challenge, had secondary antibody responses that mediated cell killing by antibody-dependent cellular cytotoxicity (ADCC), as early as 2 weeks after infection and inhibited viral replication by antibody-dependent cell-mediated virus inhibition (ADCVI), by 4 weeks after infection. There was a significant inverse correlation between virus level and binding antibody titers to the envelope protein, (R=-0.83, p=0.015), and ADCVI (R=-0.84 p=0.044). Genotyping of plasma virus demonstrated in vivo selection of three SHIV(89.6P) variants with changes in potential N-linked glycosylation sites in V1. We found a significant inverse correlation between virus levels and titers of antibodies that mediated ADCVI against all the identified V1 virus variants. A significant inverse correlation was also found between neutralizing antibody titers to SHIV(89.6) and virus levels (R=-0.72 p=0.0050). However, passive inoculation of purified immunoglobulin from animal M316, the macaque that best controlled virus, to a naïve macaque, resulted in a low serum neutralizing antibodies and low ADCVI activity that failed to protect from SHIV(89.6P) challenge. Collectively, while our data suggest that anti-envelope antibodies with neutralizing and non-neutralizing Fc(R-dependent activities may be important in the control of SHIV replication, they also demonstrate that low levels of these antibodies alone are not sufficient to protect from infection.

HAART reduces death ligand but not death receptors in lymphoid tissue of HIV-infected patients and simian immunodeficiency virus-infected macaques.

OBJECTIVE: To determine how antiretroviral therapy (ART) or HAART affects the expression of apoptotic ligands and their death receptors in the blood and lymphoid tissues of HIV-infected patients and simian immunodeficiency virus-infected macaques. METHODS: We analyzed the mRNA expression of death molecules [tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and FasL] and their receptors (DR5 and Fas) in blood and tonsils from HIV-infected patients (HIV positive), HIV-infected patients receiving HAART and HIV-uninfected (HIV negative) donors in a cross-sectional study. We comparatively analyzed mRNA expression of TRAIL and DR5 in blood and lymph nodes collected longitudinally from simian immunodeficiency virus-infected macaques before and after ART. RESULTS: Expression of TRAIL, FasL, DR5 and Fas was elevated in circulating CD4 T cells from a group of HIV-positive patients as compared with that from both HIV-negative donors and HAART patients. In a different study group, TRAIL, FasL, DR5 and Fas were increased in tonsils of HIV-positive patients as compared with HIV-negative donors and HAART patients. However, tonsils from HAART patients showed reduced expression of TRAIL and FasL but not DR5 and Fas as compared with HIV-positive patients. Similarly, data obtained in a longitudinal study of simian immunodeficiency virus-infected macaques showed that ART reduced both TRAIL and DR5 in peripheral blood but only TRAIL and not DR5 in lymph nodes from the same animals. CONCLUSION: These findings suggest that HAART or ART is ineffective in reducing the expression of apoptotic death receptors in lymphoid tissue. However, analysis limited to blood leukocytes may not reveal such a defect. Our results highlight the persistence of an underlying immunologic condition that may prevent therapy-induced restoration of CD4 T cells in lymphoid tissue.

Inhibition of T-cell receptor signal transduction and viral expression by the linker for activation of T cells-interacting p12(I) protein of human T-cell leukemia/lymphoma virus type 1.

The p12(I) protein of human T-cell leukemia/lymphoma virus type 1 (HTLV-1) is a small oncoprotein that increases calcium release following protein kinase C activation by phorbol myristate acetate, and importantly, this effect is linker for activation of T cells (LAT) independent. Here, we demonstrate that p12(I) inhibits the phosphorylation of LAT, Vav, and phospholipase C-gamma 1 and decreases NFAT (nuclear factor of activated T cells) activation upon engagement of the T-cell receptor (TCR) with anti-CD3 antibody. Furthermore, we demonstrate that p12(I) localizes to membrane lipid rafts and, upon engagement of the TCR, relocalizes to the interface between T cells and antigen-presenting cells, defined as the immunological synapse. A p12(I) knockout molecular clone of HTLV-1 expresses more virus upon antigen stimulation than the isogenic wild type, suggesting that, by decreasing T-cell responsiveness, p12(I) curtails viral expression. Thus, p12(I) has contrasting effects on TCR signaling: it down-regulates TCR in a LAT-dependent manner on one hand, and on the other, it increases calcium release in a LAT-independent manner. The negative regulation of T-cell activation by p12(I) may have evolved to minimize immune recognition of infected CD4(+) T cells, to impair the function of infected cytotoxic CD8(+) T cells, and to favor viral persistence in the infected host.