User:Tkadm30/Notebook/chim trills notebook/Research: Difference between revisions
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'''This page has moved [https://www.isotoperesearch.ca/wiki/index.php?title=Geoengineering/Research here]''' | |||
__TOC__ | __TOC__ | ||
== Research topics == | == Research topics == | ||
===Translocation and internalization of | ===Translocation and internalization of metallic nanoparticles=== | ||
Review: | |||
* [http://www.ncbi.nlm.nih.gov/pubmed/11696403 Aluminium-induced neurotoxicity] and chronic neuroinflammation in the microglia | * [http://www.ncbi.nlm.nih.gov/pubmed/11696403 Aluminium-induced neurotoxicity] and chronic neuroinflammation in the microglia | ||
* [http://www.ncbi.nlm.nih.gov/pubmed/15204759 Translocation of PM2.5 to the brain]. | * [http://www.ncbi.nlm.nih.gov/pubmed/15204759 Translocation of PM2.5 to the brain]. | ||
* [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759935/ The Effects of Nanomaterials as Endocrine Disruptors]. | * [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759935/ The Effects of Nanomaterials as Endocrine Disruptors]. | ||
====Translocation of aluminium oxide | ====Translocation of aluminium oxide in the microglia==== | ||
* [http://www.ncbi.nlm.nih.gov/pubmed/19523415 Glia activation induced by peripheral administration of aluminum oxide nanoparticles in rat brains] | * [http://www.ncbi.nlm.nih.gov/pubmed/19523415 Glia activation induced by peripheral administration of aluminum oxide nanoparticles in rat brains] | ||
===Nanotoxicity of | ===Nanotoxicity and genotoxicity of long-term PM2.5 exposure=== | ||
[[Image:Chemtrails-on-and-off-exhibits.jpg]] | [[Image:Chemtrails-on-and-off-exhibits.jpg]] | ||
* The chemical clumping behavior of PM2.5 require a | * 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 of PM2.5 require further research. | * The synthetic nature and chemistry of PM2.5 may require further research. | ||
===Characterization of the Gulf War Syndrome=== | ===Characterization of the Gulf War Syndrome (Unknown variant)=== | ||
The | The phenotype of the Gulf War Syndrome (Unknown variant) is not well understood. | ||
Epidemiological evidences of PM2.5 damage to ''' | Epidemiological evidences of PM2.5-mediated damage to the '''neuroimmune''' system | ||
* Alteration of cytokines production | includes: | ||
* | * Alteration of cytokines and ROS production | ||
* | * Stress-induced neuroinflammation (GSK3, AKT, '''TLR4''')<cite>Paper1</cite><cite>Paper4</cite> | ||
* Microglial activation? | * Mitochondrial DNA (mtDNA) oxidative stress (Aluminium oxide?, silica) | ||
* Decrease in neurotrophin expression | * Microglial activation markers? (MAC1, Glutaminase, TLR2, TLR4)<cite>Paper2</cite> | ||
* Modulation of neuroendocrine response | * 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 | Nanotoxicity of metal oxides: | ||
* Aluminium oxide | * Aluminium oxide may induce proinflammatory cellular response and [http://www.ncbi.nlm.nih.gov/pubmed/25875951 oxidative stress]. | ||
See also: | |||
* [https://www.ncbi.nlm.nih.gov/pubmed/12700181 The neuroendocrinology of chronic fatigue syndrome.] | * [https://www.ncbi.nlm.nih.gov/pubmed/12700181 The neuroendocrinology of chronic fatigue syndrome.] | ||
* [https://www.ncbi.nlm.nih.gov/pubmed/23046173 Aluminium oxide nanoparticles induce mitochondrial-mediated oxidative stress and alter the expression of antioxidant enzymes in human mesenchymal stem cells.] | |||
* [https://en.wikipedia.org/wiki/Limbic_encephalitis Limbic encephalitis] | |||
* [http://nnjournal.net/article/view/1125 Topic: Neurovascular and neuroinflammation mechanisms associated with bipolar disorder] | |||
===Nanoparticle-based drug delivery=== | ===Nanoparticle-based drug delivery systems=== | ||
Translocation and internalization of NPs: | Translocation and internalization of NPs: | ||
* [https://www.ncbi.nlm.nih.gov/pubmed/25658858 Synthetic nucleic acid delivery systems] | * [https://www.ncbi.nlm.nih.gov/pubmed/25658858 Synthetic nucleic acid delivery systems] | ||
* [https://www.ncbi.nlm.nih.gov/pubmed/27429164 Engineered nanoparticles] can be developed to enter blood-brain barrier through intracellular (siRNA) delivery. | * [https://www.ncbi.nlm.nih.gov/pubmed/27429164 Engineered nanoparticles] can be developed to enter blood-brain barrier through intracellular (siRNA) delivery. | ||
* [https://www.ncbi.nlm.nih.gov/pubmed/23546675 Cellular internalization of quantum dots.] | * [https://www.ncbi.nlm.nih.gov/pubmed/23546675 Cellular internalization of quantum dots.] | ||
Aerosolized | 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 | |||
* Microfluidics (MEMS) | |||
== Research projects == | == Research projects == | ||
===Differential effects of | ===Project SOUR DIESEL: Differential effects of PM2.5 exposure on the neuroimmune system and microglial cells=== | ||
I aim to understand the nanotoxicity of | I aim to understand the nanotoxicity and genotoxicity of long-term PM2.5 and aerosolized nanoparticles 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 TLR4 signaling. | |||
* The differential effects of | |||
Research highlights: | |||
* The differential effects of PM2.5 exposure on stress-induced neuroinflammation and microglial activation require further research. | |||
* PM2.5-mediated TLR4 signaling is poorly understood/documented. | |||
Research subtopics: | |||
* Microglia/Brain | |||
* Toll-like receptor 4/miRNA | |||
* Drug delivery systems/Central nervous system | |||
* Psychosis/Aggression | |||
* Nanoparticles/MEMS | |||
* Drug addiction/Opioids | |||
Keywords: metal oxides, nanoparticles, microfluidics, bioaerosol, drug delivery, CNS, microglia, PM2.5, TLR4, stress-induced neuroinflammation | |||
===Project HONEY TRAP: Neuropsychology of modern cognitive warfare=== | |||
Clandestine/solar geoengineering activity is a controversial issue. The aim of this research project is to understand how artificial intelligence is used to deter public disclosure on solar geoengineering. | |||
Research subtopics: | |||
* Neuropolitics/Artificial intelligence | |||
* Ultrasonic neuromodulation/Brain-computer interfaces | |||
* Human behavior/Psychology | |||
* Psychocomputational energetics/Hypercomputation | |||
* Alzheimer | |||
External links: | |||
* [https://www.thenakedscientists.com/forum/index.php?topic=71349.0 The social neuropolitics of climate change] | |||
* [https://www.projectstreetwise.org Project STREET WISE] | |||
Keywords: psychology, consciousness, science, deception, media blackout, cognitive dissonance, disinformation, cognitive infiltration, education, research, PM2.5, neuropolitics, neuromodulation, behavior, humans, cognition | |||
==References== | |||
<biblio> | |||
#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. | |||
#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. | |||
#Paper3 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762128/ | |||
//Autoimmune limbic encephalitis presenting as relapsing psychosis. | |||
#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. | |||
#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. | |||
#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. | |||
#Paper7 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4853215/ | |||
//Evidence of activation of the Toll-like receptor-4 proinflammatory pathway in patients with schizophrenia. | |||
#Paper8 https://www.ncbi.nlm.nih.gov/pubmed/20439179 | |||
//Silica-based nanoparticle uptake and cellular response by primary microglia. | |||
</biblio> | |||
== | ==See also== | ||
* [https://openwetware.org/wiki/User:Etienne_Robillard/Notebook/Photographic_evidences Photographic evidences Notebook] | |||
* [https://openwetware.org/wiki/User:Etienne_Robillard/Notebook/miRNA MicroRNA Notebook] | |||
* [https://openwetware.org/wiki/User:Etienne_Robillard/Notebook/TLR TLR Notebook] |
Latest revision as of 14:58, 2 October 2018
This page has moved here
Research topics
Translocation and internalization of metallic nanoparticles
Review:
- 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/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:
- 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 systems
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 carriers:
- Photoactivated drug delivery vectors
- Condensation (Monodisperse?) aerosols
- Functionalized nanodiamonds (ND)
- Diamond nanowire
- Calcium carbonate
- Gold nanoparticles (AuNP) (non-cytotoxic)
- Mesoporous silica nanoparticles
- Microfluidics (MEMS)
Research projects
Project SOUR DIESEL: 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 and aerosolized nanoparticles 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 TLR4 signaling.
Research highlights:
- The differential effects of PM2.5 exposure on stress-induced neuroinflammation and microglial activation require further research.
- PM2.5-mediated TLR4 signaling is poorly understood/documented.
Research subtopics:
- Microglia/Brain
- Toll-like receptor 4/miRNA
- Drug delivery systems/Central nervous system
- Psychosis/Aggression
- Nanoparticles/MEMS
- Drug addiction/Opioids
Keywords: metal oxides, nanoparticles, microfluidics, bioaerosol, drug delivery, CNS, microglia, PM2.5, TLR4, stress-induced neuroinflammation
Project HONEY TRAP: Neuropsychology of modern cognitive warfare
Clandestine/solar geoengineering activity is a controversial issue. The aim of this research project is to understand how artificial intelligence is used to deter public disclosure on solar geoengineering.
Research subtopics:
- Neuropolitics/Artificial intelligence
- Ultrasonic neuromodulation/Brain-computer interfaces
- Human behavior/Psychology
- Psychocomputational energetics/Hypercomputation
- Alzheimer
External links:
Keywords: psychology, consciousness, science, deception, media blackout, cognitive dissonance, disinformation, cognitive infiltration, education, research, PM2.5, neuropolitics, neuromodulation, behavior, humans, cognition
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.
-
Evidence of activation of the Toll-like receptor-4 proinflammatory pathway in patients with schizophrenia.
-
Silica-based nanoparticle uptake and cellular response by primary microglia.