Eileah Loda

Rush University Medical Center, Chicago, IL, United States

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Publications (3)10.67 Total impact

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    ABSTRACT: This series of experiments evaluates the nature of the representation that mediates human (Homo sapiens) and rat (Rattus norvegicus) movement characteristics on analogous spatial learning tasks. The results of Experiment 1 demonstrated that self-movement cues were sufficient to guide the performance of human participants during place training and matching-to-place testing tasks adapted to tabletop or manipulatory scale. Experiment 2 investigated the effect of manipulating access to environmental cues during place training on the nature of the representation used to guide performance. Blindfolded human participants appeared to encode the absolute location of the goal, whereas participants with access to environmental cues appeared to encode the relative location of the goal. The results of Experiment 3 demonstrated that human participants with access to environmental cues exhibited a similar response tendency (as observed in Experiment 2) after half as many trials of place training. During Experiment 4, rats exhibited movement characteristics in the water maze that were similar to movement characteristics observed in human participants who were provided access to environmental cues. These observations provide evidence that direction and distance estimation processes mediate performance on spatial tasks that are conserved across humans and rats. (PsycINFO Database Record (c) 2012 APA, all rights reserved).
    Journal of Comparative Psychology 10/2012; · 1.89 Impact Factor
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    ABSTRACT: Neuromyelitis optica (NMO) is a chronic inflammatory disease of the CNS that is mediated, in part, by a self-reactive Ab against the astrocyte aquaporin-4 protein. In the current study, we examined the possibility and the biological significance of cross-immunoreactivity between bacterial aquaporin-Z and human aquaporin-4 proteins. Sequence-alignment analysis of these proteins revealed several regions of significant structural homology. Some of the homologous regions were also found to overlap with important immune and disease-relevant epitopes. Cross-immunoreactivity between aquaporin-Z and aquaporin-4 was investigated and ascertained in multiple immune-based assays using sera from patients with neuromyelitis optica, immune mouse serum, and Abs raised against aquaporin-Z. The biological significance of this phenomenon was established in series of experiments demonstrating that induction of an immune response against aquaporin-Z or its homologous regions can also trigger an autoimmune reaction against aquaporin-4 and inflammation of the CNS. Our study indicates that the autoimmune response against aquaporin-4 in neuromyelitis optica may be triggered by infection-induced cross-immunoreactivity and presents a new perspective on the pathogenesis of this disease.
    The Journal of Immunology 09/2012; 189(9):4602-11. · 5.52 Impact Factor
  • Eileah Loda, Roumen Balabanov
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    ABSTRACT: Oligodendrocyte injury and inflammatory demyelination are key pathological abnormalities of multiple sclerosis (MS), and its animal model, i.e., the experimental autoimmune encephalomyelitis (EAE). Traditionally, they are viewed as destructive processes secondary to a dysregulated autoimmune reaction. New evidence emerged over the last decade indicating that oligodendrocytes are not merely immune targets but rather active participants in the neuroimmune network and, in fact, can regulate the events leading to inflammatory demyelination. In this review, we are discussing the role of interferon regulatory factor 1 (IRF-1) as a master transcription factor orchestrating oligodendrocyte injury and inflammatory demyelination in MS and EAE. We are also discussing the significance of IRF-1 signaling in the induction of oligodendrocyte pyroptosis, a Caspase 1-dependent pro-inflammatory cell death, as a disease-enhancing mechanism. Finally, we are drawing attention to IRF-1 as a potential therapeutic target in MS and to the importance of investigating other oligodendrocyte-dependent disease mechanisms.
    Reviews in the neurosciences 01/2012; 23(2):145-52. · 3.26 Impact Factor