Purification, characterization and application of laccase from Trametes versicolor for colour and phenolic removal of olive mill wastewater in the presence of 1- hydroxybenzotriazole

Laccase forms (L1 and L2) from Trametes versicolor CCT 4521 showed a molecular mass of 66 kDa and optimum temperature around 40oC. The optimum pH (4.0 and 5.0) and Km (28.6 and 5 ìM) values usingsyringaldazine as substrate were found for L1 and L2, respectively. The enzymes were able to oxidize several compounds and were strongly inhibited by sodium azide, L-cysteine and dithiothreitol. The 75%of the N-terminal sequences were identical in both forms and similarities around 40 - 60% of laccases from wood-degrading fungi were observed. The use of 1-hydroxybenzotriazole as a mediator increased the compounds oxidized by laccases in olive mill wastewater

Purification, characterization and application of laccase from Trametes versicolor for colour and phenolic removal of olive mill wastewater in the presence of 1-hydroxybenzotriazole

Laccase forms ( L1 and L2) from Trametes versicolor CCT 4521 showed a molecular mass of 66 kDa and optimum temperature around 40 degrees C. The optimum pH ( 4.0 and 5.0) and K-m ( 28.6 and 5 mu M) values using syringaldazine as substrate were found for L1 and L2, respectively. The enzymes were able to oxidize several compounds and were strongly inhibited by sodium azide, L-cysteine and dithiothreitol. The 75% of the N-terminal sequences were identical in both forms and similarities around 40-60% of laccases from wood-degrading fungi were observed. The use of 1-hydroxybenzotriazole as a mediator increased the compounds oxidized by laccases in olive mill wastewater.6101248125

Improving postpartum care delivery and uptake by implementing context-specific interventions in four countries in Africa: a realist evaluation of the Missed Opportunities in Maternal and Infant Health (MOMI) project.

Postpartum care (PPC) has remained relatively neglected in many interventions designed to improve maternal and neonatal health in sub-Saharan Africa. The Missed Opportunities in Maternal and Infant Health project developed and implemented a context-specific package of health system strengthening and demand generation in four African countries, aiming to improve access and quality of PPC. A realist evaluation was conducted to enable nuanced understanding of the influence of different contextual factors on both the implementation and impacts of the interventions. Mixed methods were used to collect data and test hypothesised context-mechanism-outcome configurations: 16 case studies (including interviews, observations, monitoring data on key healthcare processes and outcomes), monitoring data for all study health facilities and communities, document analysis and participatory evaluation workshops. After evaluation in individual countries, a cross-country analysis was conducted that led to the development of four middle-range theories. Community health workers (CHWs) were key assets in shifting demand for PPC by 'bridging' communities and facilities. Because they were chosen from the community they served, they gained trust from the community and an intrinsic sense of responsibility. Furthermore, if a critical mass of women seek postpartum healthcare as a result of the CHWs bridging function, a 'buzz' for change is created, leading eventually to the acceptability and perceived value of attending for PPC that outweighs the costs of attending the health facility. On the supply side, rigid vertical hierarchies and defined roles for health facility workers (HFWs) impede integration of maternal and infant health services. Additionally, HFWs fear being judged negatively which overrides the self-efficacy that could potentially be gained from PPC training. Instead the main driver of HFWs' motivation to provide comprehensive PPC is dependent on accountability systems for delivering PPC created by other programmes. The realist evaluation offers insights into some of the contextual factors that can be pivotal in enabling the community-level and service-level interventions to be effective

Creatine Transporter (CrT; Slc6a8) Knockout Mice as a Model of Human CrT Deficiency

Mutations in the creatine (Cr) transporter (CrT; Slc6a8) gene lead to absence of brain Cr and intellectual disabilities, loss of speech, and behavioral abnormalities. To date, no mouse model of CrT deficiency exists in which to understand and develop treatments for this condition. The purpose of this study was to generate a mouse model of human CrT deficiency. We created mice with exons 2–4 of Slc6a8 flanked by loxP sites and crossed these to Cre:CMV mice to create a line of ubiquitous CrT knockout expressing mice. Mice were tested for learning and memory deficits and assayed for Cr and neurotransmitter levels. Male CrT−/y (affected) mice lack Cr in the brain and muscle with significant reductions of Cr in other tissues including heart and testes. CrT−/y mice showed increased path length during acquisition and reversal learning in the Morris water maze. During probe trials, CrT−/y mice showed increased average distance from the platform site. CrT−/y mice showed reduced novel object recognition and conditioned fear memory compared to CrT+/y. CrT−/y mice had increased serotonin and 5-hydroxyindole acetic acid in the hippocampus and prefrontal cortex. Ubiquitous CrT knockout mice have learning and memory deficits resembling human CrT deficiency and this model should be useful in understanding this disorder

Dengue Virus Capsid Protein Usurps Lipid Droplets for Viral Particle Formation

Dengue virus is responsible for the highest rates of disease and mortality among the members of the Flavivirus genus. Dengue epidemics are still occurring around the world, indicating an urgent need of prophylactic vaccines and antivirals. In recent years, a great deal has been learned about the mechanisms of dengue virus genome amplification. However, little is known about the process by which the capsid protein recruits the viral genome during encapsidation. Here, we found that the mature capsid protein in the cytoplasm of dengue virus infected cells accumulates on the surface of ER-derived organelles named lipid droplets. Mutagenesis analysis using infectious dengue virus clones has identified specific hydrophobic amino acids, located in the center of the capsid protein, as key elements for lipid droplet association. Substitutions of amino acid L50 or L54 in the capsid protein disrupted lipid droplet targeting and impaired viral particle formation. We also report that dengue virus infection increases the number of lipid droplets per cell, suggesting a link between lipid droplet metabolism and viral replication. In this regard, we found that pharmacological manipulation of the amount of lipid droplets in the cell can be a means to control dengue virus replication. In addition, we developed a novel genetic system to dissociate cis-acting RNA replication elements from the capsid coding sequence. Using this system, we found that mislocalization of a mutated capsid protein decreased viral RNA amplification. We propose that lipid droplets play multiple roles during the viral life cycle; they could sequester the viral capsid protein early during infection and provide a scaffold for genome encapsidation