scholarly journals Animal Models for Salmonella Pathogenesis: Studies on the Virulence Properties Using Caenorhabditis elegans as a Model Host

10.5772/31058 ◽  
2012 ◽  
Author(s):  
Jeong Hoon ◽  
Jaya Bandyopadhyay
Keyword(s):  
Caenorhabditis Elegans ◽  
Animal Models ◽  
Virulence Properties

scholarly journals Correction: Identification of Virulence Properties in Salmonella Typhimurium DT104 Using Caenorhabditis elegans

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
Author(s):  
Surasri N. Sahu ◽  
Yuda Anriany ◽  
Christopher J. Grim ◽  
Sungji Kim ◽  
Zenas Chang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Salmonella Typhimurium ◽  
Virulence Properties

scholarly journals Cellular clearance of circulating transthyretin decreases cell-nonautonomous proteotoxicity in Caenorhabditis elegans

2018 ◽  
Vol 115 (33) ◽  
pp. E7710-E7719 ◽  
Author(s):  
Kayalvizhi Madhivanan ◽  
Erin R. Greiner ◽  
Miguel Alves-Ferreira ◽  
David Soriano-Castell ◽  
Nirvan Rouzbeh ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Animal Models ◽  
Sensory Neurons ◽  
Critical Role ◽  
Neuronal Dysfunction ◽  
Protein Aggregate ◽  
Tissue Degeneration ◽  
Neuronal Toxicity ◽  
Parkinson’S Diseases ◽  
In Trans

Cell-autonomous and cell-nonautonomous mechanisms of neurodegeneration appear to occur in the proteinopathies, including Alzheimer’s and Parkinson’s diseases. However, how neuronal toxicity is generated from misfolding-prone proteins secreted by nonneuronal tissues and whether modulating protein aggregate levels at distal locales affects the degeneration of postmitotic neurons remains unknown. We generated and characterized animal models of the transthyretin (TTR) amyloidoses that faithfully recapitulate cell-nonautonomous neuronal proteotoxicity by expressing human TTR in the Caenorhabditis elegans muscle. We identified sensory neurons with affected morphological and behavioral nociception-sensing impairments. Nonnative TTR oligomer load and neurotoxicity increased following inhibition of TTR degradation in distal macrophage-like nonaffected cells. Moreover, reducing TTR levels by RNAi or by kinetically stabilizing natively folded TTR pharmacologically decreased TTR aggregate load and attenuated neuronal dysfunction. These findings reveal a critical role for in trans modulation of aggregation-prone degradation that directly affects postmitotic tissue degeneration observed in the proteinopathies.

scholarly journals Use of Caenorhabditis Elegans and Zebrafish Embryo as an Alternative Model for Biocompatibility Assessment of Natural Latex Biocomposite

2021 ◽  
Author(s):  
Matheus Carlos Romeiro Miranda ◽  
Felipe Azevedo Borges ◽  
Natan Roberto Barros ◽  
Marina Paganine Marques ◽  
Mariana Cristina Galeane ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Animal Models ◽  
Cellular Proliferation ◽  
Calcium Phosphates ◽  
Sol Gel ◽  
Natural Rubber Latex ◽  
Morphological Alterations ◽  
Show Evidence

Abstract The number of animals killed used for research purposes has increased significantly in recent years. For this reason, several alternatives of animal models are widely used. In this study, two phases of calcium phosphates synthesized by the sol-gel method were added by precipitation to the surface of the natural rubber latex membranes for bone applications. Membranes cytotoxicity and toxicity was evaluated by in vitro and in vivo methods. Hemolysis levels were less than 3%, which indicates that there was no significant hemolytic activity. It was demonstrated that latex presents enzymes that can dissociate osteoblasts MC3T3, so it was necessary to eliminate these enzymes to obtain a good adhesion and cellular proliferation without morphological alterations. The in vivo toxicity test with Caenorhabditis elegans worms did not show evidence of toxicity with a sample of hydroxyapatite incubated for 5 days, exhibiting the lowest survival rate of the worms. In the Zebrafish embryotoxicity assay, 60% of embryos survived and there was no evidence of embryos with malformation or developmental delay. In summary, alternative animal models, which are not commonly used to assess biocompatibility, have provided reliable in vivo results that allow suggesting the use of these membranes in the bone biomedical.

scholarly journals Identification of Virulence Properties in Salmonella Typhimurium DT104 Using Caenorhabditis elegans

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e76673 ◽  
Author(s):  
Surasri N. Sahu ◽  
Yuda Anriany ◽  
Christopher J. Grim ◽  
Sungji Kim ◽  
Zenas Chang ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Salmonella Typhimurium ◽  
Virulence Properties

Reductionist thinking and animal models in neuropsychiatric research

2019 ◽  
Vol 42 ◽  
Author(s):  
Nicole M. Baran
Keyword(s):  
Animal Models ◽  
Mental Disorders ◽  
Environmental Factors ◽  
Neuropsychiatric Disorders ◽  
Model Organisms ◽  
Developmental Genetic ◽  
Term Study ◽  
Genetic And Environmental Factors ◽  
Mechanisms Of Plasticity

AbstractReductionist thinking in neuroscience is manifest in the widespread use of animal models of neuropsychiatric disorders. Broader investigations of diverse behaviors in non-model organisms and longer-term study of the mechanisms of plasticity will yield fundamental insights into the neurobiological, developmental, genetic, and environmental factors contributing to the “massively multifactorial system networks” which go awry in mental disorders.

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

Inflammational Animal Models for Schizophrenia

2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel
Keyword(s):  
Animal Model ◽  
Animal Models ◽  
Immune Activation ◽  
Microglial Activation ◽  
Treatment Options ◽  
Early Adulthood ◽  
Brain Regions ◽  
Synaptic Connections ◽  
Preventive Interventions ◽  
Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

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