And once the mechanism has been found, we can start looking for ways to help these people. And these poor babies whose parents thought they were saving them from disease...
So necessary, but so hard to read. Just came from a wake for a 39 year old; 10 weeks from cancer diagnosis to death, leaving behind an 11 and 15 year old. Not to mention my husband’s aunt being found dead in her shower and his mom being found unconscious and dying 2 days later in hospital; both in March 22. No one will listen. Connect the dots, or be a dot. Wake. Up. Wake. Up.
The above data demonstrate that sequences within PrP mRNA have the propensity to switch between hairpin structures and G-quadruplexes depending on environmental conditions.
G-Quadruplexes in RNA Biology: Recent Advances and Future Directions
Other indirect but promising pieces of evidence support that RG4s might be part of the structural ‘switch’ induced by the pseudouridylation of tRNA-derived fragments important for translation initiation impacting stem cell commitment during key developmental processes.
Walter - you have been right all along about the pathogenesis and have helped greatly to develop the UVB/Ozone hypothesis - or, put more simply - a loss of energy due to chronic stress - a stress that is ultimately felt by the mitochondria inside the cell.
I covered amyloidosis and fibrosis in this presentation @ 23m 33s
I would contend that the immune aspects are connected to IFN-1 and cGAS-STING, which plays a major part in the cells stress response, and the gateway between autoimmune disease and cancer.
How - via the Keap1-Nrf2 Stress Response Pathway which promotes Mitochondrial Hyperfusion through Degradation of the Mitochondrial Fission Protein Drp1
It’s a balance between mitochondrial fission and fusion, between stress and relaxation, between oxidation and reduction, between loss and gain of electrons, between loss and gain of Energy!
I do wonder about a spill over effect among the FOUR HORSEMEN.
https://www.nature.com/articles/s41467-022-30932-1Published: 13 June 2022 Neurotoxic amyloidogenic peptides in the proteome of SARS-COV2: potential implications for neurological symptoms in COVID-19Mirren Charnley, Saba Islam, Guneet K. Bindra, Jeremy Engwirda, Julian Ratcliffe, Jiangtao Zhou, Raffaele Mezzenga, Mark D. Hulett, Kyunghoon Han, Joshua T. Berryman & Nicholas P. Reynolds COVID-19 is primarily known as a respiratory disease caused by SARS-CoV-2. However, neurological symptoms such as memory loss, sensory confusion, severe headaches, and even stroke are reported in up to 30% of cases and can persist even after the infection is over (long COVID). These neurological symptoms are thought to be produced by the virus infecting the central nervous system, however we don’t understand the molecular mechanisms triggering them. The neurological effects of COVID-19 share similarities to neurodegenerative diseases in which the presence of cytotoxic aggregated amyloid protein or peptides is a common feature. Following the hypothesis that some neurological symptoms of COVID-19 may also follow an amyloid etiology we identified two peptides from the SARS-CoV-2 proteome that self-assemble into amyloid assemblies. Furthermore, these amyloids were shown to be highly toxic to neuronal cells. We suggest that cytotoxic aggregates of SARS-CoV-2 proteins may trigger neurological symptoms in COVID-19.
And once the mechanism has been found, we can start looking for ways to help these people. And these poor babies whose parents thought they were saving them from disease...
Thank you and blessings to you, as well!!
So necessary, but so hard to read. Just came from a wake for a 39 year old; 10 weeks from cancer diagnosis to death, leaving behind an 11 and 15 year old. Not to mention my husband’s aunt being found dead in her shower and his mom being found unconscious and dying 2 days later in hospital; both in March 22. No one will listen. Connect the dots, or be a dot. Wake. Up. Wake. Up.
The image reminds me of a rifle scope crosshairs, focused on an amyloid formation. The quadrants name the consequences. Well done, Walter!
💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕Walter M Chesnut 💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕💕
Absolutely brilliant! Looking forward to your summary post...
Blessings to you as well. We all need them and a bit of luck
As your diagram accurately portrays, the spike unites them and one of the uniting mechanisms is Treg perturbation.
Love the title!
MPV and RNA G-quadruplex structures:
https://www.biorxiv.org/content/10.1101/2022.06.18.496696v1
We are being told that MPV (and poxviridae) is a "DNA virus". Yet, poxviridae is also a mycobacterium, a variant of M. leprae:
https://archive.org/details/b30503036/page/n34/mode/1up (pg 16-18)
The Sars-Cov-2 genome has amino acid sequences from M. leprae:
https://www.sciencedirect.com/science/article/pii/S0171298521000395
Non-coding RNA and M. tuberculosis:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3384566/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8628891/
https://www.frontiersin.org/articles/10.3389/fcimb.2014.00096/full
Non-coding RNA and prions:
https://www.researchgate.net/publication/326183713_Interrelation_of_prions_with_non-coDing_RNAs
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7333576/
https://pubmed.ncbi.nlm.nih.gov/34209482/
https://rupress.org/jcb/article/210/4/529/38290/Prion-like-domains-in-RNA-binding-proteins-are
G-quadruplexes and prions:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4132711/
The above data demonstrate that sequences within PrP mRNA have the propensity to switch between hairpin structures and G-quadruplexes depending on environmental conditions.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7314185/
https://www.cell.com/trends/biochemical-sciences/fulltext/S0968-0004(20)30272-3
G-Quadruplexes in RNA Biology: Recent Advances and Future Directions
Other indirect but promising pieces of evidence support that RG4s might be part of the structural ‘switch’ induced by the pseudouridylation of tRNA-derived fragments important for translation initiation impacting stem cell commitment during key developmental processes.
Great work !! no wonder the "Twitts" canned him...right over the proverbial target
it cant be a more appropriate title ... tumultuous times.
thank you again for all you do for humanity and God bless you!!
Walter - you have been right all along about the pathogenesis and have helped greatly to develop the UVB/Ozone hypothesis - or, put more simply - a loss of energy due to chronic stress - a stress that is ultimately felt by the mitochondria inside the cell.
I covered amyloidosis and fibrosis in this presentation @ 23m 33s
https://www.bitchute.com/video/7ISiQ7P8GxAN/
I would contend that the immune aspects are connected to IFN-1 and cGAS-STING, which plays a major part in the cells stress response, and the gateway between autoimmune disease and cancer.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8634458/
UVB activates both IFN-1 and the cGAS-STING pathway - setting up the environment for both immunosuppression and autoimmunity.
https://www.nature.com/articles/s41598-020-64865-w
https://pubmed.ncbi.nlm.nih.gov/33423764/
However, inside the cell it is the mitochondrial stress that mediates the cGAS-STING pathway via DRP1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8867650/
“Drp1 overexpression induces mitochondrial dysfunction and cytosolic mtDNA stress, which subsequently activates the cGAS-STING pathway”
and the cGAS–STING pathway is thought to drive type I IFN immunopathology in COVID-19
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8891013/
As well as COVID-19 infection being associated with prolonged cGAS-STING pathway activation in leucocytes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8349977/
DRP1 is relevant because it is involved in mitochondria fission and there is bioinformatics connecting it to Covid.
https://twitter.com/teamsforlife/status/1493281550909284357?s=21&t=2BxTJMBgaU9nf_VPiarRGg
And DRP1 just happens to be strongly regulated by UVB in a dose dependent manner.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5059735/
And also Ozone
https://discovery.researcher.life/article/chronic-exposure-to-ozone-induces-cardiac-antioxidant-response-and-overexpression-of-either-mitochondrial-fision-protein-drp1-and-hipertrophyc-related-proteins/18d4a74bbd2231879bf87518b20764ea
The Oxidative and electrophilic stresses associated with uvb and ozone trigger the NRF2 stress response
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1317630/
NRF2 negatively regulates cGAS-STING
https://www.frontiersin.org/articles/10.3389/fimmu.2019.02101/full
How - via the Keap1-Nrf2 Stress Response Pathway which promotes Mitochondrial Hyperfusion through Degradation of the Mitochondrial Fission Protein Drp1
https://pubmed.ncbi.nlm.nih.gov/28494652/
It’s a balance between mitochondrial fission and fusion, between stress and relaxation, between oxidation and reduction, between loss and gain of electrons, between loss and gain of Energy!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6324937/
Thank you, Wondrous Walter!
Brilliant theory!
I do wonder about a spill over effect among the FOUR HORSEMEN.
https://www.nature.com/articles/s41467-022-30932-1Published: 13 June 2022 Neurotoxic amyloidogenic peptides in the proteome of SARS-COV2: potential implications for neurological symptoms in COVID-19Mirren Charnley, Saba Islam, Guneet K. Bindra, Jeremy Engwirda, Julian Ratcliffe, Jiangtao Zhou, Raffaele Mezzenga, Mark D. Hulett, Kyunghoon Han, Joshua T. Berryman & Nicholas P. Reynolds COVID-19 is primarily known as a respiratory disease caused by SARS-CoV-2. However, neurological symptoms such as memory loss, sensory confusion, severe headaches, and even stroke are reported in up to 30% of cases and can persist even after the infection is over (long COVID). These neurological symptoms are thought to be produced by the virus infecting the central nervous system, however we don’t understand the molecular mechanisms triggering them. The neurological effects of COVID-19 share similarities to neurodegenerative diseases in which the presence of cytotoxic aggregated amyloid protein or peptides is a common feature. Following the hypothesis that some neurological symptoms of COVID-19 may also follow an amyloid etiology we identified two peptides from the SARS-CoV-2 proteome that self-assemble into amyloid assemblies. Furthermore, these amyloids were shown to be highly toxic to neuronal cells. We suggest that cytotoxic aggregates of SARS-CoV-2 proteins may trigger neurological symptoms in COVID-19.
You don’t muck around - your right onto it!
I'd go for THE 4 SPIKEMEN OF APOCALYPSE, each driving a different version of the same animal.
edit a different *manifestation* of the same animal:
=> I'd go for THE 4 SPIKEMEN OF APOCALYPSE, each driving a different manifestation of the same animal.