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    ABSTRACT: The life cycle of four Steinernema species was observed in 4 insect micro-insect host species (less than 5mm long). Several parameters were measured: sex ratio of invading nematodes, percentages of host infection and offspring production, penetration rate of infective juveniles per insect and number of new generation of infective juveniles. All parameters varied among nematode species, micro-host species and application rates. All Steinernema species were capable to invade micro-insect hosts, however, invasion decreased as insect size decreased and as nematode species size increased. None of the nematode species achieved 100% mortality in the micro-hosts. Due to size differences in the nematode species, Steinernema glaseri was less capable of completing its life cycle and unable to invade smaller hosts whereas S. riobrave completed its life cycle in smaller hosts more frequently. The number of invading nematodes and the number of offspring produced had the same levels regardless of the nematode application rates, those results showed a maximum top in the number of individuals per micro-insect host. The offspring production in thrips species was only possible by endotokia matricida in S. riobrave. The sex of the invader nematodes also impeded the life cycle of S. affine because males colonized the entire body of the micro-insect host leaving no room for female invasion. The size of the host plays an irrefutable role in limiting the development of nematodes and it appears improbable that an entomopathogenic nematode population can persist in the soil without the presence of bigger insects.
    No preview · Article · Jul 2014 · Journal of Invertebrate Pathology
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    ABSTRACT: Anti-T. discrepans F(ab')2 ELISA recognition of T. discrepans toxins was measured with regression analysis and its slope called ELISA recognition value (ERv). Fractions containing toxins affecting mammal macrophages or Na(+)-channels have Ervs > 19. Toxins affecting potassium channels or insect NaV channels have ERvs <10. Fractions including curarizing or antineoplasic peptides had ERvs < 1. Erv increases in proportion to mammalian toxin toxicity rather than to toxin molecular mass.
    Full-text · Article · Jun 2014 · Toxicon
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    ABSTRACT: Liver sinusoid endothelial cells (LSEC) constitute an in vitro and in vivo microenvironment for the proliferation and differentiation of hematopoietic stem cells (HSC). Previously, we have shown that LSEC support the survival and growth of murine embryonic stem cells (ESC). In this study, we investigated the capacity of LSEC to promote hematopoietic differentiation from the murine ESC cell line, CGR8. Undifferentiated ESC were cultured on LSEC monolayers in the absence of exogenous cytokines. After 10 and 20 days, cells were harvested and examined by their morphology, phenotype and capacity of hematopoietic colony formation. Microscopic observation of LSEC/ESC cocultures showed the presence of cobblestone areas formation, which indicates active hematopoiesis. Morphological analysis of cell from these foci showed the presence of hematopoietic cells at different stages of differentiation. Cells expressing B lymphoid markers (B220 and CD19) were detected by flow cytometry, and clonogenic assays showed the formation of CFU-pre B colonies. Similar results were observed when ESC were cultured with LSEC conditioned media. Myeloid precursors were also detected by the presence of CFU-GM colonies and cells expressing myeloid markers. These results indicate that LSEC provided an in vitro microenvironment mainly for B cell development, but also myeloid differentiation from ESC. Coculture of ESC with LSEC may constitute a very powerful tool to study the mechanisms involved in B cell generation from ESC.
    Full-text · Article · May 2014 · Immunology Letters


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    Carretera Panamericana Kilómetro 11, 01204, Caracas, Miranda, Venezuela
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    Eloy Sira
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Top publications last week by reads

Rol del estrés oxidativo en la enfermedad, Investigación Clínica; 04/2015
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Journal of Molecular Biology 02/2016; DOI:10.1016/j.jmb.2016.01.027
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