User:Etienne Robillard/Notebook/chim trills notebook/Research

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Research topics

Translocation and internalization of metallic nanoparticles


Translocation of aluminium oxide in the microglia

Nanotoxicity and genotoxicity of long-term PM2.5 exposure


  • The immunological nanotoxicity and genotoxicity of fine/ultra-fine particulate matter (PM size < 2.5µm) is under investigation.
  • The chemical clumping (aerosol aggregation) behavior of PM2.5 may require a ultrasonic atomization device.
  • The synthetic nature and chemistry of PM2.5 may require further research.

Characterization of the Gulf War Syndrome (Unknown variant)

The phenotype of the Gulf War Syndrome (Unknown variant) is not well understood.

Epidemiological evidences of PM2.5-mediated damage to the neuroimmune system includes:

  • Alteration of cytokines and ROS production
  • Stress-induced neuroinflammation (GSK3, AKT, TLR4)[1][2]
  • Mitochondrial DNA (mtDNA) oxidative stress (Aluminium oxide?, silica)
  • Microglial activation markers? (MAC1, Glutaminase, TLR2, TLR4)[3]
  • Decrease in neurotrophin expression (BDNF)
  • Modulation of neuroendocrine response
  • Alteration of miRNA expression (miR-15, miR-146a, miR-222, miR-337-5p)
  • Glutamatergic NMDA dysregulation?
  • TLR4-mediated psychosis?

Nanotoxicity of metal oxides:

  • Aluminium oxide may induce proinflammatory cellular response and oxidative stress.

See also:

Nanoparticle-based drug delivery

Translocation and internalization of NPs:

Aerosolized drug carriers:

  • Photoactivated drug delivery vectors
  • Condensation (Monodisperse?) aerosols
  • Functionalized nanodiamonds (ND)
    • Diamond nanowire
  • Calcium carbonate
  • Gold nanoparticles (AuNP) (non-cytotoxic)
  • Mesoporous silica nanoparticles

Research projects

Differential effects of PM2.5 exposure on the neuroimmune system and microglial cells

I aim to understand the nanotoxicity and genotoxicity of long-term PM2.5 exposure on physiological and neurological processes:

  • In specific, I'm interested to understand the effects of PM2.5 exposure on chronic pulmonary diseases (COPD), miRNA expression (psychosis biomarker) and TLR signaling.
  • The differential effects of PM2.5 exposure on stress-induced neuroinflammation and microglial activation require further research.
  • Silica-mediated TLR4 signaling is poorly understood/documented.

Keywords: metal oxides, silica nanoparticles, gold nanoparticles, bioaerosol, drug delivery, CNS, microglia, PM2.5, TLR4, stress-induced neuroinflammation

Knowledge is power: Psychology of modern neurocognitive warfare

Clandestine geoengineering activity is a controversial issue. The aim of this research project is to understand how artificial intelligence is used to deter scientific research on solar geoengineering.

Research subtopics:

Keywords: psychology, consciousness, science, deception, media blackout, cognitive dissonance, disinformation, cognitive infiltration, education, research, PM2.5, neuropolitics


  1. [Paper1]
    Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior.
  2. [Paper4]
    The role of TLR4-mediated PTEN/PI3K/AKT/NF-κB signaling pathway in neuroinflammation in hippocampal neurons.
  3. [Paper2]
    Involvement of TLR2 and TLR4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter.
  4. [Paper3]
    Autoimmune limbic encephalitis presenting as relapsing psychosis.
  5. [Paper5]
    Enhanced peripheral toll-like receptor responses in psychosis: further evidence of a pro-inflammatory phenotype.
  6. [Paper6]
    Nanodiamonds act as Trojan horse for intracellular delivery of metal ions to trigger cytotoxicity.
  7. [Paper7]
    Evidence of activation of the Toll-like receptor-4 proinflammatory pathway in patients with schizophrenia.
  8. [Paper8]
    Silica-based nanoparticle uptake and cellular response by primary microglia.

See also