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Function of RSKS-1-AAK-2-DAF-16 signaling cascade in enhancing toxicity of multi-walled carbon nanotubes can be suppressed by mir-259 activation in Caenorhabditis elegansMetallothioneins are required for formation of cross-adaptation response to neurobehavioral toxicity from lead and mercury exposure in nematodes.Evaluation of environmental safety concentrations of DMSA Coated Fe2O3-NPs using different assay systems in nematode Caenorhabditis elegans.Molecular control of TiO₂-NPs toxicity formation at predicted environmental relevant concentrations by Mn-SODs proteins.High concentration of vitamin E decreases thermosensation and thermotaxis learning and the underlying mechanisms in the nematode Caenorhabditis elegans.Beneficial effects of wheat gluten hydrolysate to extend lifespan and induce stress resistance in nematode Caenorhabditis elegans.Full toxicity assessment of Genkwa Flos and the underlying mechanism in nematode Caenorhabditis elegans.Genetic Screen Reveals Link between the Maternal Effect Sterile Gene mes-1 and Pseudomonas aeruginosa-induced Neurodegeneration in Caenorhabditis elegans.Adverse effects from clenbuterol and ractopamine on nematode Caenorhabditis elegans and the underlying mechanism.microRNAs control of in vivo toxicity from graphene oxide in Caenorhabditis elegans.Response of microRNAs to in vitro treatment with graphene oxide.In vivo translocation and toxicity of multi-walled carbon nanotubes are regulated by microRNAs.Crucial role of the biological barrier at the primary targeted organs in controlling the translocation and toxicity of multi-walled carbon nanotubes in the nematode Caenorhabditis elegans.NPR-9 regulates the innate immune response in Caenorhabditis elegans by antagonizing the activity of AIB interneurons.Exposure to mercury causes formation of male-specific structural deficits by inducing oxidative damage in nematodes.Association of oxidative stress with the formation of reproductive toxicity from mercury exposure on hermaphrodite nematode Caenorhabditis elegans.Immune response is required for the control of in vivo translocation and chronic toxicity of graphene oxide.Molecular signals regulating translocation and toxicity of graphene oxide in the nematode Caenorhabditis elegans.Quantum dots increased fat storage in intestine of Caenorhabditis elegans by influencing molecular basis for fatty acid metabolism.The in vivo underlying mechanism for recovery response formation in nano-titanium dioxide exposed Caenorhabditis elegans after transfer to the normal condition.Contributions of altered permeability of intestinal barrier and defecation behavior to toxicity formation from graphene oxide in nematode Caenorhabditis elegans.Transmissions of serotonin, dopamine, and glutamate are required for the formation of neurotoxicity from Al2O3-NPs in nematode Caenorhabditis elegans.Biosafety assessment of titanium dioxide nanoparticles in acutely exposed nematode Caenorhabditis elegans with mutations of genes required for oxidative stress or stress response.Carboxylic acid functionalization prevents the translocation of multi-walled carbon nanotubes at predicted environmentally relevant concentrations into targeted organs of nematode Caenorhabditis elegans.Susceptible genes regulate the adverse effects of TiO2-NPs at predicted environmental relevant concentrations on nematode Caenorhabditis elegans.Neuronal ERK signaling in response to graphene oxide in nematode Caenorhabditis elegans.p38 MAPK-SKN-1/Nrf signaling cascade is required for intestinal barrier against graphene oxide toxicity in Caenorhabditis elegans.Genome-wide identification and functional analysis of long noncoding RNAs involved in the response to graphene oxide.An epigenetic signal encoded protection mechanism is activated by graphene oxide to inhibit its induced reproductive toxicity in Caenorhabditis elegans.Dysregulation of let-7 by PEG modified graphene oxide in nematodes with deficit in epidermal barrierClose association of intestinal autofluorescence with the formation of severe oxidative damage in intestine of nematodes chronically exposed to Al(2)O(3)-nanoparticleInhibition of ROS elevation and damage to mitochondrial function prevents lead-induced neurotoxic effects on structures and functions of AFD neurons in Caenorhabditis elegans
P50
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P50
name
Qiuli Wu
@en
type
label
Qiuli Wu
@en
prefLabel
Qiuli Wu
@en