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  • Book
    edited by Christopher Peacock, University of Western Australia, Nedlands, WA, Australia.
    Contents:
    The eukaryotic pathogen databases : a functional genomic resource integrating data from human and veterinary parasites
    From sequence mapping to genome assemblies
    Sequencing and annotation of mitochondrial genomes from individual parasitic helminths
    A beginners guide to estimating the non-synonymous to synonymous rate ratio of all protein-coding genes in a genome
    Exploiting genetic variation to discover genes involved in important disease phenotypes
    Identification and analysis of ingi-related retroposons in the trypanosomatid genomes
    Approaches for studying mRNA decay mediated by SIDER2 retroposons in Leishmania
    Gene suppression in schistosomes using RNAi
    Construction of Trypanosoma brucei illumina RNA-seq libraries enriched for transcript ends
    Techniques to study epigenetic control and the epigenome in parasites
    The genome-wide identification of promotor regions in Toxoplasma gondii
    RNA-seq approaches for determining mRNA abundance in Leishmania
    Protein microarrays for parasite antigen discovery
    A transposon-based tool for transformation and mutagenesis in Trypanosomatid protozoa
    Separation of basic proteins from Leishmania using a combination of free flow electrophoresis (FFE) and 2D electrophoresis (2-DE) under basic conditions
    Proteomic analysis of posttranslational modifications using iTRAQ in Leishmania
    Large-scale differential proteome analysis in Plamsmodium falciparum under drug treatment
    Use of ¹³C stable isotope labelling for pathway and metabolic flux analysis in Leishmania parasites
    Molecular genotyping of Trypanosoma cruzi for lineage assignment and population genetics
    Screening Leishmania donovani complex-specific genes required for visceral disease.
    Digital Access Springer 2015
  • Article
    Lázár G.
    Acta Biol Acad Sci Hung. 1979;30(3):245-55.
    One optic nerve in several frogs was filled with cobaltous-lysine complex, and the animals were left to survive from 1 day to 52 days. Degenerated cobalt-filled retinal fibres were phagocytosed by ependymo-glial, and microglial cells. The cobalt appeared in the ependymo-glial cells in the 4th postoperative day, and its amount was greatly reduced by the 52nd day. Within 12 days the labelled axons were replaced by cobalt-loaded microglial cells in the termination sites of optic fibres. By the end of the experimental period, the number of labelled cells increased in the periventricular layers, and decreased in places where retinal fibres had terminated. These processes were accompanied by the appearance of cobalt in the choroid plexus. It is supposed that glial cells dischargd the cobalt into brain ventricles, and the metal left the nervous tissue via the cerebrospinal fluid.
    Digital Access Access Options