PHOTOBIOTREATMENT: INFLUENCE OF NITROGEN AND PHOSPHORUS RATIO IN WASTEWATER ON GROWTH KINETICS OF SCENEDESMUS OBLIQUUS

Nitrogen and phosphorus concentration in the effluent of a wastewater treatment plant can vary significantly, which could affect the growth kinetic and chemical composition of microalgae when cultivated in this medium. The aim of this work was to study the rate of growth, nutrient removal and carbon dioxide biofixation as well as biomass composition of Scenedesmus obliquus (S. obliquus) when it is cultivated in wastewater at different nitrogen and phosphorus ratio, from 1:1 to 35:1. A more homogeneous method for calculating productivities in batch reactors was proposed. The proper N:P ratio for achieving optimum batch biomass productivity ranged between 9 and 13 (263 and 322 mg L^?1 d^?1 respectively). This was also the ratio range for achieving a total N and P removal. Above and below this range (9–13) the maximum biomass concentration changed, instead of the specific growth rate.The maximum carbon dioxide biofixation rate was achieved at N:P ratio between 13 and 22 (553 and 557 mg CO2 L^?1 d^?1 respectively). Lipid and crude protein content, both depend on the aging culture, reaching the maximum lipid content (34%) at the lowest N:P (1:1) and the maximum crude protein content (34.2%) at the highest N:P (35:1).     

First Report of Peronospora belbahrii on Sweet Basil in Baja California Sur,México

In Baja California Sur, Mexico, a foliar disease occurred on sweet basil which seriously affected its quality and yield. The most common symptoms were yellowing and necrosis on leaves, caused by a downy mycelium growth on the lower leaf surface. Symptomatic leaves from two sampling sites were collected for morphological studies and molecular analysis of pathogen DNA. Based on morphological characteristics (sporangiophore size of 240–530 × 7–11 μm, branches of 5–8 order and a sporangia size of 27–31 × 21–25 μm) and molecular analysis (the GenBank blast of the PCR assays showed unique rDNA sequence data with 99% similarity to P. belbahrii), the pathogen was identified as Peronospora belbahrii, the causal agent of basil downy mildew. This is the first report of P. belbahrii affecting sweet basil in Mexico.     

Localized recrudescence of Toxoplasma infections in the central nervous system of immunocompromised mice assessed by in vivo bioluminescence imaging

Reactivation of infection in the central nervous system (CNS) with the opportunistic parasite Toxoplasma gondii is a major concern in chronically infected immunocompromised individuals. Yet, the pathophysiology associated with recrudescence of infection remains poorly characterized. The onset of acute reactivated Toxoplasma encephalitis in the murine model was assessed using bioluminescence imaging as a spatio-temporal indicator. An uneven distribution of recrudescence of infection in the CNS was found. Foci of recrudescence after immunosuppression were most commonly located in frontal and parietal cortex, whereas little infection was found in the cerebellum. Recrudescence was also more common in grey matter than in white matter. Pathology was exacerbated in mice deficient in interferon gamma receptors (IFN gamma R(-/-)) corroborating the importance of interferon gamma (IFN gamma) for control of CNS infection. Analysis of parasitic foci identified abundant leukocyte infiltration (CD45+, CD4+, CD8+, F4/80+ cells) in the vicinity of replicating parasites and microvasculature. This is the first report that addresses the suborganic localization of acute Toxoplasma encephalitis in the murine model. Collectively, the findings suggest that the localization of reactivation foci in the CNS, in conjunction with immune responses, influences the outcome of acute reactivated Toxoplasma encephalitis.     

Mek1/2 MAPK kinases are essential for Mammalian development, homeostasis, and Raf-induced hyperplasia

The p42/p44 mitogen-activated protein kinase (MAPK) cascade includes Ras, Raf, Mek, and Erk MAPK. To determine the effect of a full knockout at a single level of this signaling pathway in mammals, and to investigate functional redundancy between Mek1 and Mek2, we disrupted these genes in murine and human epidermis. Loss of either protein alone produced no phenotype, whereas combined Mek1/2 deletion in development or adulthood abolished Erk1/2 phosphorylation and led to hypoproliferation, apoptosis, skin barrier defects, and death. Conversely, a single copy of either allele was sufficient for normal development. Combined Mek1/2 loss also abolished Raf-induced hyperproliferation. Human tissue deficient in either Mek isoform was normal, whereas loss of both proteins led to hypoplasia, which was rescued by active Erk2 expression. These data indicate that Mek1/2 are functionally redundant in the epidermis, where they act as a linear relay in the MAPK pathway to mediate development and homeostasis.     

Two new species of Ginkgoales from the Middle Jurassic of Mexico

This paper reports two new species of Ginkgoales collected from the Cañada Alejandro and Río Ñumi (Zorrillo and Zorrillo–Taberna Undifferentiated Formations, Middle Jurassic). Thirty-one fossils were selected and compared with 14 species from different localities. A numerical taxonomy analysis was performed through a data matrix formed by 15 characters. Results indicate an important speciation process of the Ginkgoales during the Jurassic in the southeast of Mexico. New evidence suggests the existence of eight species from the Ginkgoidium Yokoyama, 1889 and Sphenobaiera (Florin) Harris and Millington, 1974 genera and two new species Ginkgoidiumnundichii Velasco-de León, Lozano-Carmona, Flores, Martínez and Silva and Sphenobaieramixteca Velasco-de León, Lozano-Carmona, Flores, Martínez and Silva     

Induction of dendritic cell migration upon Toxoplasma gondii infection potentiates parasite dissemination

The processes leading to systemic dissemination of the obligate intracellular parasite Toxoplasma gondii remain unelucidated. In vitro studies on human and murine dendritic cells (DC) revealed that active invasion of DC by Toxoplasma induces a state of hypermotility in DC, enabling transmigration of infected DC across endothelial cell monolayers in the absence of chemotactic stimuli. Infected DC exhibited upregulation of maturation markers and co-stimulatory molecules. While modulation of cell adhesion molecules CD11/CD18 was similar for Toxoplasma-infected DC and lipopolysaccharide (LPS)-matured DC, Toxoplasma-infected DC did not exhibit upregulation of CD54/ICAM-1. Induction of host cell migration in vitro required live intracellular parasite(s) and was inhibited by uncoupling the Gi-protein signalling pathway with pertussis toxin, but did not depend on CCR5, CCR7 or Toll/interleukin-1 receptor signalling. When migration of Toxoplasma-infected DC was compared with migration of LPS-stimulated DC in vivo, similar or higher numbers of Toxoplasma-infected DC reached the mesenteric lymph nodes and spleen respectively. Adoptive transfer of Toxoplasma-infected DC resulted in more rapid dissemination of parasites to distant organs and in exacerbation of infection compared with inoculation with free parasites. Altogether, these findings show that Toxoplasma is able to subvert the regulation of host cell motility and likely exploits the host's natural pathways of cellular migration for parasite dissemination.     

Pig melatonin receptor 1a (MTNR1A) genotype is associated with seasonal variation of sow litter size

The duration of nocturnal melatonin secretion reaches its minimum in summer, a physiological event that is likely related with the diminished sow fertility and delayed puberty typically observed in this season. Melatonin exerts its function by binding two different receptors named as MTNR1A and MTNR1B. Interestingly, the MTNR1A gene is located on a chromosome SSC17 region where QTL for prolificacy traits have been detected in previous studies. In this work, we have found a synonymous T162C polymorphism at exon 2 of the pig MTNR1A gene. An association analysis between this polymorphism and sow prolificacy in an Iberian ×  Meishan intercross was performed. The utilization of four statistical models of increasing complexity demonstrated that the MTNR1A gene has both additive and dominant effects on total number of born piglets (TNB) and number of piglets born alive (NBA). Additive effects were significant in summer (TNB, P < 0.01; NBA, P < 0.001), whereas dominant effects reached significance both in fall (TNB, P < 0.01; NBA, P < 0.05) and in winter (TNB, P < 0.001; NBA, P < 0.05). The seasonal variation observed for MTNR1A additive and dominant effects might be produced by the influence of photoperiod on the pattern and duration of melatonin secretion. These results illustrate that the complex interaction between genotype and environment can be an important source of phenotypic variation of reproductive traits.     

The unicellular eukaryotic parasite Toxoplasma gondii hijacks the migration machinery of mononuclear phagocytes to promote its dissemination

Toxoplasma gondii is an obligate intracellular protozoan with the ability to infect virtually any type of nucleated cell in warm-blooded vertebrates including humans. Toxoplasma gondii invades immune cells, which the parasite employs as shuttles for dissemination by a Trojan horse mechanism. Recent findings are starting to unveil how this parasite orchestrates the subversion of the migratory functions of parasitised mononuclear phagocytes, especially dendritic cells (DCs) and monocytes. Here, we focus on how T. gondii impacts host cell signalling that regulates leukocyte motility and systemic migration in tissues. Shortly after active parasite invasion, DCs undergo mesenchymal-to-amoeboid transition and adopt a high-speed amoeboid mode of motility. To trigger migratory activation – termed hypermigratory phenotype – T. gondii induces GABAergic signalling, which results in calcium fluxes mediated by voltage-gated calcium channels in parasitised DCs and brain microglia. Additionally, a TIMP-1-CD63-ITGB1-FAK signalling axis and signalling via the receptor tyrosine kinase MET promotes sustained hypermigration of parasitised DCs. Recent reports show that the activated signalling pathways converge on the small GTPase Ras to activate the MAPK Erk signalling cascade, a central regulator of cell motility. To date, three T. gondii-derived putative effector molecules have been linked to hypermigration: Tg14-3-3, TgWIP and ROP17. Here, we discuss their impact on the hypermigratory phenotype of phagocytes. Altogether, the emerging concept suggests that T. gondii induces metastasis-like migratory properties in parasitised mononuclear phagocytes to promote infection-related dissemination.     

Transepithelial migration of Toxoplasma gondii involves an interaction of intercellular adhesion molecule 1 (ICAM-1) with the parasite adhesin MIC2

Toxoplasma gondii crosses non-permissive biological barriers such as the intestine, the blood-brain barrier and the placenta thereby gaining access to tissues where it most commonly causes severe pathology. Herein we show that in the process of migration Toxoplasma initially concentrates around intercellular junctions and probably uses a paracellular pathway to transmigrate across biological barriers. Parasite transmigration required viable and actively motile parasites. Interestingly, the integrity of host cell barriers was not altered during parasite transmigration. As intercellular adhesion molecule 1 (ICAM-1) is upregulated on cellular barriers during Toxoplasma infection, we investigated the role of this receptor in parasite transmigration. Soluble human ICAM-1 and ICAM-1 antibodies inhibited transmigration of parasites across cellular barriers implicating this receptor in the process of transmigration. Furthermore, human ICAM-1 immunoprecipitated the mature form of the parasite adhesin MIC2 present on the parasite surface, indicating that this interaction may contribute to cellular migration. These findings reveal that Toxoplasma exploits the natural cell trafficking pathways in the host to cross cellular barriers and disseminate to deep tissues.