My father, 2 injections for sure, has been stating that his balabce is extremely off. I witnessed it. I asked about it. He said "my legs, they just don't seem to be working." The first thing that came to my mind was MS and I said to him "do you think it could be MS?" The words just came out of me from an Unknown Place where many answers and information have been coming from over the last 2+ years. Something is working through me. I've been spot on and ahead of the game this whole time. What do I do for him? This happened yesterday. Your article today appears to have provided me with the answer. I do not find it a coincidence.
miR-223-3p also increases the production of type 1 IFN via directly targeting FOXO3. Moreover, type 1 IFN raises the expression of miR-223-3p in a positive feedback loop
However, the Spike protein inhibits IFN1 therefore reduces miR-223 which increases FBXW7 which reduces myelination and it also reduces STAT2 because of the inverse relationship of FBXW7 and STAT2, thereby making you more vulnerable to viral infection and demyelination
Good Morning from “over the puddle” Walter - yet another outstanding hypothesis! I am fascinated and equally alarmed at Amyloidosis .. where does it begin? In layman’s terms if possible. I do have a Masters Degree in Psychology but not much good here! I wanted also to mention that having spent quite a long time outside recently - walking along a river and through fields (it was exceptionally “cloudy”) when l arrived home and blew my nose the most horrifying but fascinating mucus was expelled .. lt was made up of thousands of strands of a black substance .. you really need to see photo. - not the greatest subject if you are eating or about to eat! I live in the county of Suffolk which is heavily farmed .. l was wondering whether Graphene was involved? Can you shed any light?
Syncytin-1/HERV-W envelope is an early activation marker of leukocytes and is upregulated in multiple sclerosis patients "In addition, syncytin-1 transgenic mice expressing this protein in astrocytes under the glial fibrillary acidic protein promoter exhibit neuroinflammation and diminished levels of myelin proteins in the corpus callosum, together with neurobehavioral abnormalities "
Graphene has been used EVERYWHERE lately - ALL masks INHALATION !!!, PCR "tests" inserted close to the brain instead closer to the lungs! "vaccines", chemtrails, food, drugs, nano tech has been even found in e-cigarettes...
Few epidemiological studies focused on human exposure to GO particularly for the highly exposed population. For the in-vivo models including rats, mice, zebra fish, nematodes, and daphnia, the animals could induce nanotoxicity including acute, developmental, neurological, reproductive, immunological, and neurobehavioral toxicity as well as shortened longevity after they were exposed to GO NPs (Sanchez et al., 2012; Patlolla et al., 2017; Qu et al., 2017; Souza et al., 2017; Kim et al., 2018; Qu et al., 2019; Kim et al., 2020). In the past years, in vivo and in vitro GO NPs toxic effects, including immunotoxicity, activation of inflammation, induction of reactive oxygen species (ROS), generation of oxidative stress, apoptosis, and potential GO exposure mechanisms have been investigated (Guo and Mei, 2014; Bengtson et al., 2017; Pelin et al., 2018; Tang et al., 2018). The accumulation of GO in the cytoplasm causes dramatic morphological alterations and reduces the ability of toll-like receptor 4 (TLR4) for phagocytosis (Qu et al., 2013a). However, an increase in intracellular ROS contributes to necrotic cell death in macrophages (Qu et al., 2013a). Previous studies have also reported that GO promotes cell growth inhibition, hatching delay, ROS generation, and damages the circulatory system of zebrafish embryos (Liu et al., 2014; Chen et al., 2016; Souza et al., 2017). In mice, GO can accumulate in organs such as the liver, lungs, spleen, and kidneys, which may induce organismal toxicity through intracellular oxidative stress caused by the accumulation of ROS (Qu et al., 2013b; Yang et al., 2013). GO can enter the human body through inhalation and may be deposited in regions of the respiratory tract. When deposited in alveolar regions, it may impair clearance, form granulomas, and possibly produce fibrosis (Sanchez et al., 2012).
3.3. GO NP Exposure Affects Locomotive Behavior
Locomotive behavior assays are well-established methods for studying nematode neurotoxicity. After prolonged exposure, GO induced obvious decreases in both head thrashing and body bending in nematodes (Fig. 3). In the head thrash examination, 0.0100, 0.100 and, 1.00 µg L–1 concentrations of GO NPs significantly decreased head thrashing by 12.0, 5.41, and 19.8%, respectively, compared to the untreated control. Furthermore, body bending was significantly reduced at 0.00100, 0.0100, 0.100 and 1.00 µg L–1 GO NPs by 8.78, 21.2, 31.5, and 40.8%, respectively, in comparison with the control groups. Our results were consistent with those in most published articles, implying that GO NP exposure damages the neurological functions and negatively disrupts head thrashing and body bending behavior (Wu et al., 2013, 2014; Zhao et al., 2015, 2016c; Chen et al., 2017; Li et al., 2017; Qu et al., 2017; Kim et al., 2018; Rive et al., 2019; Zhao et al., 2020). In Wu’s report (Wu et al., 2014), head thrash and body bend locomotion was significantly reduced at 0.0100, 0.100, and 1.00 mg L–1 levels compared with an untreated control. Li et al. (2017) indicated that prolonged exposure to GO NPs (5.00–100 mg L–1) significantly reduced body bending, head thrashing, pharynx pumping frequency, mean speed, bending angle-frequency, and the wavelength of the crawling movement of nematodes. GO NPs also induced damage to dopaminergic and glutamatergic neurons in nematodes (Li et al., 2017). Kim et al. (2020) also proposed that GO significantly accumulated in the head regions, generated ROS induction, reduced neurotransmitter substances in dopaminergic and glutamatergic neurons, and damaged AFD neurons, which are the main thermosensors in C. elegans, after the nematodes were exposed to GO NPs (10 mg L–1). In a Korean study, Kim et al. (2018) also found that neurotransmitters, such as dopamine, γ-Aminobutyric acid (GABA), tyramine, tryptophan, and tyrosine, were reduced in nematodes exposed to GO NPs. According to the current data, including the present study (Wu et al., 2013, 2014; Zhao et al., 2015, 2016a; Chen et al., 2017; Li et al., 2017; Qu et al., 2017; Kim et al., 2018; Rive et al., 2019; Zhao et al., 2020), it has been concluded that GO NPs exposure causes adverse effects on the neurological system of C. elegans particularly in terms of damage to neurons, influences on neurotransmitter neurodisruptions, and delays in neurobehavioral development. In the present study, environmental levels (0.0100–1.00 µg L–1) of GO NP doses were used to treat the nematodes to determine the negative impact on their locomotion behavior.
Oxidative stress is increasingly implicated as a co-factor of tissue injury in inflammatory/demyelinating disorders of the central nervous system (CNS), such as multiple sclerosis (MS).
I wonder if this would explain the fainting out of nowhere as well. My DIL had one of these fainting episodes (that led to stitches in her face from hitting a table) shortly after she was (relentlessly) pressured into the jab from her employer. I have heard of several people that experienced the after jab fainting. I have been wondering if the fainting in these cases indicated some sort of an attack on the brain. I thought maybe it was the micro clotting hitting something in the brain, but this is another possible explanation as well.
This makes sense with all the POTs like symptoms (and GBS) occurring from the jabs too. It is possible to recreate the myelin sheaths as people do recover from GBS (a relative of mine is an example - though it took them about a year to fully recover from GBS-MFS but they had IVIG initially to stop the progression and then they had to work at using their eyes and fingers again - like a little kid learning to use their limbs and digits).
This graphene/cobalt (Co), iron (Fe), chromium (Cr), titanium (Ti)), rare earth metals such as cerium (Ce) and gadolinium (Gd), barium (Ba), cesium (Cs), aluminum (Al), silicon (Si), sulfur (S), potassium (K) and calcium (Ca) injections ARE NOT ANY VIRAL. They are to establish nano network for communication - nano sensors, nano transmitters (for blockchain, telemedicine, control, "carbon footprint", Big Pharma monopoly, population control and other purposes very different than your HEALTH. So no, this is not a Spike protein issue. Mac address is NOT a question of Spike Protein but is about sending digital currency. Banks/corporations are behind your "vaccination ID" aka "Green certificate". This is WHY there is such a push for injections - even this substance does not stop any transmission.
I think we need to revisit what is causing the disease, how it is causing the disease and what the co-factors may be. People have a much better understanding of why the shots are dangerous.
My father, 2 injections for sure, has been stating that his balabce is extremely off. I witnessed it. I asked about it. He said "my legs, they just don't seem to be working." The first thing that came to my mind was MS and I said to him "do you think it could be MS?" The words just came out of me from an Unknown Place where many answers and information have been coming from over the last 2+ years. Something is working through me. I've been spot on and ahead of the game this whole time. What do I do for him? This happened yesterday. Your article today appears to have provided me with the answer. I do not find it a coincidence.
Thank you
Ultimately it is UVR that controls myelination!
Low UVB rather than low Vit D per se, is associated with the demyelination in MS.
“UV light suppression of EAE (a mouse model of multiple sclerosis) is independent of vitamin D and its receptor”
https://www.pnas.org/doi/10.1073/pnas.1913294116
“UV radiation suppresses experimental autoimmune
encephalomyelitis independent of vitamin D
production”
https://www.pnas.org/doi/pdf/10.1073/pnas.1001119107
And one of the control mechanisms is FBXW7, which limits Myelination by Inhibiting mTOR Signaling.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4635133/
FBXW7 is increased by UVB as part of a negative feedback loop
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8347623/
FBXW7 is also involved in immune regulation
https://www.frontiersin.org/articles/10.3389/fonc.2022.925041/full?amp;amp
And is therefore connected to Cancers, autoimmunity and infections as it modulates the cellular stress response
miR-223 negatively regulates FBXW7
https://pubmed.ncbi.nlm.nih.gov/34953047/
And miR-223 is also involved in protection from demyelination
“microRNA-223-3p were upregulated at sites of myelin injury within activated macrophages and microglia”.
https://pubmed.ncbi.nlm.nih.gov/35633501/
And is also involved in Covid pathology
“Contribution of Host miRNA-223-3p to SARS-CoV-Induced Lung Inflammatory Pathology”
https://pubmed.ncbi.nlm.nih.gov/35229638/
Moreover, MicroRNA analysis has identified FBXW7 as one of the most modified genes in Covid
https://www.sciencedirect.com/science/article/pii/S0009279721004154#tbl2
miR-223-3p also increases the production of type 1 IFN via directly targeting FOXO3. Moreover, type 1 IFN raises the expression of miR-223-3p in a positive feedback loop
However, the Spike protein inhibits IFN1 therefore reduces miR-223 which increases FBXW7 which reduces myelination and it also reduces STAT2 because of the inverse relationship of FBXW7 and STAT2, thereby making you more vulnerable to viral infection and demyelination
https://pubmed.ncbi.nlm.nih.gov/35229638/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6955312/
UVB increases miR-223!
https://www.spandidos-publications.com/10.3892/ol.2012.551
Walter - FBXW7 solved the puzzle of low AUF1 in an inflammatory environment - which is why I maintain UVR is the control not HIF1
This is because AUF1 is regulated by the VHL tumour suppressor gene and hypoxia.
mcr.aacrjournals.org/content/10/1/1…
And,
in hypoxia the VHL protein is downregulated, stops binding to HIF-1 and initiates the hypoxic response, which involves an increase in AUF1
AUF1 is reduced by FBXW7
Good Morning from “over the puddle” Walter - yet another outstanding hypothesis! I am fascinated and equally alarmed at Amyloidosis .. where does it begin? In layman’s terms if possible. I do have a Masters Degree in Psychology but not much good here! I wanted also to mention that having spent quite a long time outside recently - walking along a river and through fields (it was exceptionally “cloudy”) when l arrived home and blew my nose the most horrifying but fascinating mucus was expelled .. lt was made up of thousands of strands of a black substance .. you really need to see photo. - not the greatest subject if you are eating or about to eat! I live in the county of Suffolk which is heavily farmed .. l was wondering whether Graphene was involved? Can you shed any light?
Thank you, Wondrous Walter!
Thoughts about the role of syncytin
?https://pubmed.ncbi.nlm.nih.gov/32012247/
Syncytin-1/HERV-W envelope is an early activation marker of leukocytes and is upregulated in multiple sclerosis patients "In addition, syncytin-1 transgenic mice expressing this protein in astrocytes under the glial fibrillary acidic protein promoter exhibit neuroinflammation and diminished levels of myelin proteins in the corpus callosum, together with neurobehavioral abnormalities "
Graphene has been used EVERYWHERE lately - ALL masks INHALATION !!!, PCR "tests" inserted close to the brain instead closer to the lungs! "vaccines", chemtrails, food, drugs, nano tech has been even found in e-cigarettes...
It is not Spike, it is graphene toxicity
https://aaqr.org/articles/aaqr-20-09-oa-0559
Few epidemiological studies focused on human exposure to GO particularly for the highly exposed population. For the in-vivo models including rats, mice, zebra fish, nematodes, and daphnia, the animals could induce nanotoxicity including acute, developmental, neurological, reproductive, immunological, and neurobehavioral toxicity as well as shortened longevity after they were exposed to GO NPs (Sanchez et al., 2012; Patlolla et al., 2017; Qu et al., 2017; Souza et al., 2017; Kim et al., 2018; Qu et al., 2019; Kim et al., 2020). In the past years, in vivo and in vitro GO NPs toxic effects, including immunotoxicity, activation of inflammation, induction of reactive oxygen species (ROS), generation of oxidative stress, apoptosis, and potential GO exposure mechanisms have been investigated (Guo and Mei, 2014; Bengtson et al., 2017; Pelin et al., 2018; Tang et al., 2018). The accumulation of GO in the cytoplasm causes dramatic morphological alterations and reduces the ability of toll-like receptor 4 (TLR4) for phagocytosis (Qu et al., 2013a). However, an increase in intracellular ROS contributes to necrotic cell death in macrophages (Qu et al., 2013a). Previous studies have also reported that GO promotes cell growth inhibition, hatching delay, ROS generation, and damages the circulatory system of zebrafish embryos (Liu et al., 2014; Chen et al., 2016; Souza et al., 2017). In mice, GO can accumulate in organs such as the liver, lungs, spleen, and kidneys, which may induce organismal toxicity through intracellular oxidative stress caused by the accumulation of ROS (Qu et al., 2013b; Yang et al., 2013). GO can enter the human body through inhalation and may be deposited in regions of the respiratory tract. When deposited in alveolar regions, it may impair clearance, form granulomas, and possibly produce fibrosis (Sanchez et al., 2012).
3.3. GO NP Exposure Affects Locomotive Behavior
Locomotive behavior assays are well-established methods for studying nematode neurotoxicity. After prolonged exposure, GO induced obvious decreases in both head thrashing and body bending in nematodes (Fig. 3). In the head thrash examination, 0.0100, 0.100 and, 1.00 µg L–1 concentrations of GO NPs significantly decreased head thrashing by 12.0, 5.41, and 19.8%, respectively, compared to the untreated control. Furthermore, body bending was significantly reduced at 0.00100, 0.0100, 0.100 and 1.00 µg L–1 GO NPs by 8.78, 21.2, 31.5, and 40.8%, respectively, in comparison with the control groups. Our results were consistent with those in most published articles, implying that GO NP exposure damages the neurological functions and negatively disrupts head thrashing and body bending behavior (Wu et al., 2013, 2014; Zhao et al., 2015, 2016c; Chen et al., 2017; Li et al., 2017; Qu et al., 2017; Kim et al., 2018; Rive et al., 2019; Zhao et al., 2020). In Wu’s report (Wu et al., 2014), head thrash and body bend locomotion was significantly reduced at 0.0100, 0.100, and 1.00 mg L–1 levels compared with an untreated control. Li et al. (2017) indicated that prolonged exposure to GO NPs (5.00–100 mg L–1) significantly reduced body bending, head thrashing, pharynx pumping frequency, mean speed, bending angle-frequency, and the wavelength of the crawling movement of nematodes. GO NPs also induced damage to dopaminergic and glutamatergic neurons in nematodes (Li et al., 2017). Kim et al. (2020) also proposed that GO significantly accumulated in the head regions, generated ROS induction, reduced neurotransmitter substances in dopaminergic and glutamatergic neurons, and damaged AFD neurons, which are the main thermosensors in C. elegans, after the nematodes were exposed to GO NPs (10 mg L–1). In a Korean study, Kim et al. (2018) also found that neurotransmitters, such as dopamine, γ-Aminobutyric acid (GABA), tyramine, tryptophan, and tyrosine, were reduced in nematodes exposed to GO NPs. According to the current data, including the present study (Wu et al., 2013, 2014; Zhao et al., 2015, 2016a; Chen et al., 2017; Li et al., 2017; Qu et al., 2017; Kim et al., 2018; Rive et al., 2019; Zhao et al., 2020), it has been concluded that GO NPs exposure causes adverse effects on the neurological system of C. elegans particularly in terms of damage to neurons, influences on neurotransmitter neurodisruptions, and delays in neurobehavioral development. In the present study, environmental levels (0.0100–1.00 µg L–1) of GO NP doses were used to treat the nematodes to determine the negative impact on their locomotion behavior.
https://pubmed.ncbi.nlm.nih.gov/29136024/
Abstract
Oxidative stress is increasingly implicated as a co-factor of tissue injury in inflammatory/demyelinating disorders of the central nervous system (CNS), such as multiple sclerosis (MS).
The symptoms of Antiphospholipid Syndrome do seem to coincide with the Covid vaccine adverse events.
Small Fiber Neuropathy may be involved: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5912271/
'All this occurred without the virus infecting the brain itself.'
So then what causes harm in the brain?
Cytokines released? The spike protein circulating in the blood? Autoantibodies?
I wonder if this would explain the fainting out of nowhere as well. My DIL had one of these fainting episodes (that led to stitches in her face from hitting a table) shortly after she was (relentlessly) pressured into the jab from her employer. I have heard of several people that experienced the after jab fainting. I have been wondering if the fainting in these cases indicated some sort of an attack on the brain. I thought maybe it was the micro clotting hitting something in the brain, but this is another possible explanation as well.
A must read paper about the deaths of US children post vaxx. Please read and pass on.
https://substack.com/redirect/2/eyJlIjoiaHR0cHM6Ly9tZXRhdHJvbi5zdWJzdGFjay5jb20vcC9jb3ZpZC12YWNjaW5lLWRlYXRocy1vZi1jaGlsZHJlbj90b2tlbj1leUoxYzJWeVgybGtJam8xTmpRMU5UQXdOU3dpY0c5emRGOXBaQ0k2TmpZMk9Ea3hNRGtzSW1saGRDSTZNVFkxT1RVd05qUTVNU3dpYVhOeklqb2ljSFZpTFRVM09UQTROU0lzSW5OMVlpSTZJbkJ2YzNRdGNtVmhZM1JwYjI0aWZRLm9QcHJaOHdia2NVdHl3blZEdzRkeWpXMTZZZlZHQjJTMVNFLUdWMWZVY2MiLCJwIjo2NjY4OTEwOSwicyI6NTc5MDg1LCJmIjpmYWxzZSwidSI6NTY0NTUwMDUsImlhdCI6MTY1OTUwNjQ5MSwiaXNzIjoicHViLTAiLCJzdWIiOiJsaW5rLXJlZGlyZWN0In0.bUiEHIcoYXGmh76B4H5180PCmJAh7LbayxlpsJj8V60?
This makes sense with all the POTs like symptoms (and GBS) occurring from the jabs too. It is possible to recreate the myelin sheaths as people do recover from GBS (a relative of mine is an example - though it took them about a year to fully recover from GBS-MFS but they had IVIG initially to stop the progression and then they had to work at using their eyes and fingers again - like a little kid learning to use their limbs and digits).
I wonder if the nicotinic receptor in the brain stem, locked in by the spike protein.....
might have a role...
This graphene/cobalt (Co), iron (Fe), chromium (Cr), titanium (Ti)), rare earth metals such as cerium (Ce) and gadolinium (Gd), barium (Ba), cesium (Cs), aluminum (Al), silicon (Si), sulfur (S), potassium (K) and calcium (Ca) injections ARE NOT ANY VIRAL. They are to establish nano network for communication - nano sensors, nano transmitters (for blockchain, telemedicine, control, "carbon footprint", Big Pharma monopoly, population control and other purposes very different than your HEALTH. So no, this is not a Spike protein issue. Mac address is NOT a question of Spike Protein but is about sending digital currency. Banks/corporations are behind your "vaccination ID" aka "Green certificate". This is WHY there is such a push for injections - even this substance does not stop any transmission.
https://link.springer.com/chapter/10.1007/978-3-030-58861-8_2 https://ieeexplore.ieee.org/document/9298084 DCCORONA
https://projects.ics.forth.gr/_publications/CORONA2015.pdf CORONA
I think we need to revisit what is causing the disease, how it is causing the disease and what the co-factors may be. People have a much better understanding of why the shots are dangerous.