User:Tkadm30/Notebook/chim trills notebook/Research: Difference between revisions
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<biblio> | <biblio> | ||
#Paper1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783243/ | #Paper1 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 | //Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior. | ||
#Paper2 https://www.ncbi.nlm.nih.gov/pubmed/19406832 | #Paper2 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. | //Involvement of TLR2 and TLR4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter. | ||
#Paper3 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762128/ | #Paper3 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762128/ | ||
//<font color="red">Autoimmune limbic encephalitis presenting as relapsing psychosis</font> | //<font color="red">Autoimmune limbic encephalitis presenting as relapsing psychosis.</font> | ||
#Paper4 https://www.ncbi.nlm.nih.gov/pubmed/24680857 | #Paper4 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. | //The role of TLR4-mediated PTEN/PI3K/AKT/NF-κB signaling pathway in neuroinflammation in hippocampal neurons. | ||
#Paper5 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309507/ | #Paper5 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309507/ | ||
//Enhanced peripheral toll-like receptor responses in psychosis: further evidence of a pro-inflammatory phenotype | //Enhanced peripheral toll-like receptor responses in psychosis: further evidence of a pro-inflammatory phenotype. | ||
#Paper6 http://particleandfibretoxicology.biomedcentral.com/articles/10.1186/s12989-014-0075-z | |||
//Nanodiamonds act as Trojan horse for intracellular delivery of metal ions to trigger cytotoxicity. | |||
</biblio> | </biblio> | ||
Revision as of 03:19, 29 March 2017
Research topics
Translocation and internalization of metal oxide particulate matter (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 in the microglia
Nanotoxicity and genotoxicity of long-term PM2.5 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, miR-337-5p)
- Autoimmune limbic encephalitis [4]
Nanotoxicity of metal oxides:
- Aluminium oxide 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
- Nanodiamonds
- Calcium carbonate
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
-
Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior.
-
The role of TLR4-mediated PTEN/PI3K/AKT/NF-κB signaling pathway in neuroinflammation in hippocampal neurons.
-
Involvement of TLR2 and TLR4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter.
-
Autoimmune limbic encephalitis presenting as relapsing psychosis.
-
Enhanced peripheral toll-like receptor responses in psychosis: further evidence of a pro-inflammatory phenotype.
-
Nanodiamonds act as Trojan horse for intracellular delivery of metal ions to trigger cytotoxicity.