User:Tkadm30/Notebook/chim trills notebook/Research

Research topics

Translocation and internalization of metal oxide nanoparticles (PM2.5)

• Aluminium-induced neurotoxicity and chronic neuroinflammation in the microglia
• Translocation of PM2.5 to the brain.
• The Effects of Nanomaterials as Endocrine Disruptors.

Translocation of aluminium oxide nanoparticles in the microglia

• Glia activation induced by peripheral administration of aluminum oxide nanoparticles in rat brains

Nanotoxicity and genotoxicity of drug nanoparticles exposure

• The immunological nanotoxicity and genotoxicity of fine particulate matter (PM2.5) is under investigation.
• The chemical clumping behavior of PM2.5 nanoparticles may require a ultrasonic atomization delivery system.
• The synthetic nature of PM2.5 require further research.

Characterization of the Gulf War Syndrome/X variant

The phenotype of the Gulf War Syndrome/X variant (GWSX) is not well characterized. The immunotoxicity, neurotoxicity, and nanotoxicity of PM2.5 exposure require further research.

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

• Alteration of cytokines production
• Stress-induced neuroinflammation (GSK3, AKT, TLR4)[1][2]
• Mitochondrial DNA (mtDNA) oxidative stress (Aluminium oxide?)
• Microglial activation markers? (MAC1, Glutaminase, TLR2)[3]
• Decrease in neurotrophin expression
• Modulation of neuroendocrine response
• Alteration of miRNA expression (miR-15, miR-146a, miR-222)
• Autoimmune limbic encephalitis [4]

Nanotoxicity of metal oxides nanoparticles:

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

See also:

• The neuroendocrinology of chronic fatigue syndrome.
• Aluminium oxide nanoparticles induce mitochondrial-mediated oxidative stress and alter the expression of antioxidant enzymes in human mesenchymal stem cells.
• Limbic encephalitis
• Topic: Neurovascular and neuroinflammation mechanisms associated with bipolar disorder

Nanoparticle-based drug delivery

Translocation and internalization of NPs:

• Synthetic nucleic acid delivery systems
• Engineered nanoparticles can be developed to enter blood-brain barrier through intracellular (siRNA) delivery.
• Cellular internalization of quantum dots.

Aerosolized drug nanoparticles

• Photoactivated drug delivery vectors
• Monodisperse aerosols

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 summary, I'm interested to understand the effects of PM2.5 exposure on chronic pulmonary diseases (COPD), miRNA expression (synaptic plasticity) and TLR signaling.
• The differential effects of PM2.5 exposure on chronic neuroinflammation and microglial activation (reactive microgliosis) require further research.

Keywords: metal oxides, nanoparticles, bioaerosol, drug delivery, CNS, neuroinflammation, microglia, PM2.5, TLR-2

Knowledge is power: Psychology of modern psychochemical 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 PM2.5.

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

References

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783243/

   Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

2. https://www.ncbi.nlm.nih.gov/pubmed/24680857

   The role of TLR4-mediated PTEN/PI3K/AKT/NF-κB signaling pathway in neuroinflammation in hippocampal neurons.

3. https://www.ncbi.nlm.nih.gov/pubmed/19406832

   Involvement of TLR2 and TLR4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter.

4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762128/

   Autoimmune limbic encephalitis presenting as relapsing psychosis

5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309507/

   Enhanced peripheral toll-like receptor responses in psychosis: further evidence of a pro-inflammatory phenotype

See also

• Photographic evidences