gene based COVID injection? Makis again points to Social Media Influencers on Youtube, Instagram, TikTok etc.getting Turbo Cancers - 20 Social Media stars with a combined 60+million subscribers; dying
Shocking..unbeleivable...where is the awareness that this is Not Normal? The stuff going on now...and most people remain so totally unaware...and tptb are working hard to make sure they remain this way. I'm in a nighmare...WE are in a nightmare so big and so evil...it is hard to grasp
It is a nightmare an, d will continue to manifest its ugly tenticles into our lives yet once again. With all the chatter of mask mandates on the near horizon, the push for more vaccines..whats that now "7" - We have to come along side each other, stand strong in our faith, arm ourselves up with the armor of God, and just say NO...Not this time!
It’s now “normal” to see young, healthy, beautiful girls and boys chronicle their cancer journeys on video. It’s bizarre and so unreal that almost 100% of them make no connection to the injections. Just wow.
Oxidative damage is the cause of these adverse effects, including cancer.
Actually, oxidative processes are involved in all disease states, but have nothing to do specifically with oxygen. Regarding cancer, low cellular oxygen makes it much easier to survive. A cancerous cell should be nothing to a healthy body, the cell will either repair or self destruct. Either way, the cancer is gone. Problem is, when the cell cannot create enough energy to do that, in which case it starts to divide (or should that be multiply?:-)). The cell can't create the required energy if, either its mitochondria are not working optimally, else the cell is expending large amounts of energy such as when removing sodium (one reason why salt is bad).
Of course, the effin' injections 'create' trillions of spikes which damage mitochondria, and possibly hello cancer. The immune system is the last line of cancer defence, if the cell cannot deal with it. And, again of course, the effin' injections suppress immune responses to cancer, such as taking down some of the toll-like receptors, or if mRNA directly infects T-cells.
The mechanisms are likely endless, which is why (imho) a cancerpocalypse is coming.
Background: Cancer is considered a major cause of death worldwide. The etiology of cancer is linked to environmental and genetic inheritance causes. Approximately 90 percent of all human cancers have an environmental cause (non-genetic inheritance) predominantly through lifestyle choices (smoking, diet, UV radiation) while the remaining due to infections and chemical exposure. Cancer is a multistage process that involves mutational changes and uncontrolled cell proliferation. Research has firmly established a causal and contributory role of oxidative stress and oxidative damage in cancer initiation and progression.
Methods: The purpose of this article is to review the role that oxidative stress and reactive oxygen species play in the development of cancer. Both endogenous and exogenous sources of reactive oxygen species result in increased oxidative stress in the cell. Excess reactive oxygen fumed can result in damage to and modification of cellular macromolecules most importantly genomic DNA that can produce mutations. In addition, oxidative stress modulates gene expression of downstream targets involved in DNA repair, cell proliferation and antioxidants. The modulation of gene expression by oxidative stress occurs in part through activation or inhibition of transcription factors and second messengers. The role of single nuclear polymorphism for oxidative DNA repair and enzymatic antioxidants is important in determining the potential human cancer risk.
Conclusion: oxidative stress and the resulting oxidative damage are important contributors to the formation and progression of cancer.
Mitochondrial oxidation-induced cell death, a physiological process triggered by various cancer therapeutics to induce oxidative stress on tumours, has been challenging to investigate owing to the difficulties in generating mitochondria-specific oxidative stress and monitoring mitochondrial responses simultaneously. Accordingly, to the best of our knowledge, the relationship between mitochondrial protein oxidation via oxidative stress and the subsequent cell death-related biological phenomena has not been defined. Here, we developed a multifunctional iridium(III) photosensitiser, Ir-OA, capable of inducing substantial mitochondrial oxidative stress and monitoring the corresponding change in viscosity, polarity, and morphology. Photoactivation of Ir-OA triggers chemical modifications in mitochondrial protein-crosslinking and oxidation (i.e., oxidative phosphorylation complexes and channel and translocase proteins), leading to microenvironment changes, such as increased microviscosity and depolarisation. These changes are strongly related to cell death by inducing mitochondrial swelling with excessive fission and fusion. We suggest a potential mechanism from mitochondrial oxidative stress to cell death based on proteomic analyses and phenomenological observations.
Introduction
Elucidating the process of mitochondrial oxidation-induced cell death is essential to understanding and improving cancer therapeutics based on oxidative damage to tumours1,2,3,4. To this end, various mitochondria-targeted photosensitisers that can produce reactive oxygen species (ROS) have been utilised to understand the underlying chemical effect of mitochondrial oxidation5,6.
Oxidative stress induced by photosensitisers causes chemical modifications of biomolecules including proteins7,8,9, unsaturated lipids10,11, and DNA12,13. Notably, protein modifications occurring via methionine oxidation and dityrosine crosslinking are clearly described chemical modifications for mitochondrial oxidation-induced cell death9,14. However, the connection between the chemical modifications of mitochondrial proteins and the biological response in cell death remains elusive due to the absence of a chemical tool to analyse the biological phenomena (i.e., environmental changes in mitochondrial surroundings in terms of viscosity, polarity, morphology, pH, and temperature) that occur in mitochondria in response to oxidative stress. Therefore, photosensitisers that efficiently oxidise proteins and subsequently monitor the consequent protein dysfunction-related mitochondrial responses are needed15,16,17. To address this, we employed organometallic iridium(III) complexes because of their notable ROS generation efficiency, lifetime sensitivity to microviscosity, straightforward ligand tuning, cell permeability, and photostability16,18,19.
In this work, our designed iridium(III) complex, Ir-OA, showed accelerated ROS production and micropolarity-dependent ratiometric emission properties owing to intramolecular energy transfer system. With these characteristics, we successfully employed Ir-OA to (i) induce cell death by producing ROS in the mitochondria, (ii) monitor changes in the mitochondrial microenvironment (i.e., viscosity, polarity, and morphology) using various techniques including lifetime and ratiometric imaging, and (iii) identify the mode of action for microenvironment changes by profiling the modified proteins (i.e., crosslinked and oxidised proteins) through oxidative stress. Collectively, we suggest a promising mechanism that describes how oxidative stress affects the mitochondria and induces cell death, corroborating the correlation between mitochondrial microenvironment changes and the oxidised proteome. The proposed mechanism may aid the understanding of how some cancer therapeutics can induce mitochondrial oxidative stress.
Reactive oxygen species (ROS) can damage lipids, nucleic acids, and proteins, thereby altering their functions. When a balance between production of ROS and antioxidative defense is disturbed, state of oxidative stress occurs. Oxidative stress leads to many diseases. There are few biomarkers that are used for better understanding how oxidative stress is involved in cancer pathophysiology. This review focuses on 8-hidroxy-2-deoxyguanosine (8-OHdG) and antioxidative enzymes as biomarkers for measurement of oxidative stress in different types of cancer. This review also deals with the product of lipid peroxidation, malondialdehyde (MDA), and across a variety of cancers. To address this aim, analysis of studies of breast, prostate, lung, colon, cervical, ovarian, brain, bladder, renal, thyroid cancer, and chronic lymphocytic leukemia has been conducted. In general, levels of antioxidative enzymes are mostly lower in cancer patients, while 8-OHdG and MDA are higher. Further research is needed, with focus on correlation levels of these biomarkers and advancement of the disease. Moreover, all studies explored the idea of those biomarkers as a useful tool in determining the levels of oxidative stress. Some of the studies proposed their potential in defining the stage of tumor progression.
Abstract
In addition to the well-established role of the mitochondria in energy metabolism, regulation of cell death has recently emerged as a second major function of these organelles. This, in turn, seems to be intimately linked to their role as the major intracellular source of reactive oxygen species (ROS), which are mainly generated at Complex I and III of the respiratory chain. Excessive ROS production can lead to oxidation of macromolecules and has been implicated in mtDNA mutations, ageing, and cell death. Mitochondria-generated ROS play an important role in the release of cytochrome c and other pro-apoptotic proteins, which can trigger caspase activation and apoptosis. Cytochrome c release occurs by a two-step process that is initiated by the dissociation of the hemoprotein from its binding to cardiolipin, which anchors it to the inner mitochondrial membrane. Oxidation of cardiolipin reduces cytochrome c binding and results in an increased level of “free” cytochrome c in the intermembrane space. Conversely, mitochondrial antioxidant enzymes protect from apoptosis. Hence, there is accumulating evidence supporting a direct link between mitochondria, oxidative stress and cell death.
And that's the ones on TikTok. Countless others without millions of followers are suffering the same things. How many of us know people personally who are dealing with this (all jabbed) as well as other adverse effects? I know of at least 2 with breast cancer, 2 with lung cancer , diabetes, etc. and these are people I KNOW. Others chronically ill because their immune systems are shot. It's sad and maddening at the same time.
And now, they COULD make a brave choice. A just choice. They have the platforms...Dr. Alexander's post shows them something's up, and there's an issue that needs fulsome discussion and investigation.
Can I ask my fellow experts here if they have heard if Dr. Vanden Bosch is still standing behind his prediction, that this fall will be a massive amount of deaths for those people that were vaccinated? Thank you.
"I’m Dr. Mike Yeadon, it’s known I’m extremely dark about where I deduce this is going, and I expect the results will make Stalin, Hitler & Mao look like beginners. Depopulation under fear, controlled by VaxPass & accomplished using “variant vaccines”. It's perfect in it's evilness" ~ Dr. Michael Yeadon (former VP and Chief Scientist of Pfizer)
Common to whom? It's just that 'Sheep', to me anyway, implies a large percentage of the population. Maybe correct at the start of the roll-out, but not now. Even Canada only had 25% lining up for the last one, and the previous one was around 50%. If that holds for the next, only 12.5% will be stupid/alive enough to roll up their sleeves. No doubt, there is a basement - it will be interesting to see what that is. People obviously know (or sense) something is seriously, seriously wrong - they are just not sure what to do about it.
How the cabal runs everything. Compartmentalise, never let them see the dots connected, cumulative data, patterns, trends, EVIDENCE! Thanks for doing the opposite! My god this is a lot of pain and sorrow in one post.
Me: “Massive unintended consequences” - unintended? The US DOD and DARPA can't create Super Soldiers without intentionally changing their Genetic Codes, can they?
These people had their genetic codes fucked around with by Big Pharma on behalf of the US DOD and DARPA - see my article today - what else would you have expected?
Shocking..unbeleivable...where is the awareness that this is Not Normal? The stuff going on now...and most people remain so totally unaware...and tptb are working hard to make sure they remain this way. I'm in a nighmare...WE are in a nightmare so big and so evil...it is hard to grasp
At least we know it now.
They are trying to pass these deaths off as normal and they're pulling all sorts of nonsense rabbits out of their hat to do it. Here is the symptom:
http://tritorch.com/degradation/!MysteriousDiseaseKillHundredsInAustralia.png [image]
Here is the deflection:
http://tritorch.com/degradation/%21VastIncreaseInHeartAttacksBlamedOnPostPandemicStessDisorderAndNotVaccine.png [image]
Here are many many more: https://tritorch.com/newnormal
My heart just breaks. If it wasn't for my substack channels I'd have been clueless about the horrors going on. It makes me so damned angry.
It is a nightmare an, d will continue to manifest its ugly tenticles into our lives yet once again. With all the chatter of mask mandates on the near horizon, the push for more vaccines..whats that now "7" - We have to come along side each other, stand strong in our faith, arm ourselves up with the armor of God, and just say NO...Not this time!
Because all these folks got vaxxed ie; CV
I personally would NOT wish this on ANYONE!
It’s now “normal” to see young, healthy, beautiful girls and boys chronicle their cancer journeys on video. It’s bizarre and so unreal that almost 100% of them make no connection to the injections. Just wow.
NANOTECHNOLOGY DOESN'T CURE CANCER. IT CAUSES CANCER. IS TOXIC
Oxidative damage is the cause of these adverse effects, including cancer.
People need to take antioxidants or deliver oxygen to their cells in another way
Oxidative damage is the cause of these adverse effects, including cancer.
Actually, oxidative processes are involved in all disease states, but have nothing to do specifically with oxygen. Regarding cancer, low cellular oxygen makes it much easier to survive. A cancerous cell should be nothing to a healthy body, the cell will either repair or self destruct. Either way, the cancer is gone. Problem is, when the cell cannot create enough energy to do that, in which case it starts to divide (or should that be multiply?:-)). The cell can't create the required energy if, either its mitochondria are not working optimally, else the cell is expending large amounts of energy such as when removing sodium (one reason why salt is bad).
Of course, the effin' injections 'create' trillions of spikes which damage mitochondria, and possibly hello cancer. The immune system is the last line of cancer defence, if the cell cannot deal with it. And, again of course, the effin' injections suppress immune responses to cancer, such as taking down some of the toll-like receptors, or if mRNA directly infects T-cells.
The mechanisms are likely endless, which is why (imho) a cancerpocalypse is coming.
https://www.eurekaselect.com/article/96687
Background: Cancer is considered a major cause of death worldwide. The etiology of cancer is linked to environmental and genetic inheritance causes. Approximately 90 percent of all human cancers have an environmental cause (non-genetic inheritance) predominantly through lifestyle choices (smoking, diet, UV radiation) while the remaining due to infections and chemical exposure. Cancer is a multistage process that involves mutational changes and uncontrolled cell proliferation. Research has firmly established a causal and contributory role of oxidative stress and oxidative damage in cancer initiation and progression.
Methods: The purpose of this article is to review the role that oxidative stress and reactive oxygen species play in the development of cancer. Both endogenous and exogenous sources of reactive oxygen species result in increased oxidative stress in the cell. Excess reactive oxygen fumed can result in damage to and modification of cellular macromolecules most importantly genomic DNA that can produce mutations. In addition, oxidative stress modulates gene expression of downstream targets involved in DNA repair, cell proliferation and antioxidants. The modulation of gene expression by oxidative stress occurs in part through activation or inhibition of transcription factors and second messengers. The role of single nuclear polymorphism for oxidative DNA repair and enzymatic antioxidants is important in determining the potential human cancer risk.
Conclusion: oxidative stress and the resulting oxidative damage are important contributors to the formation and progression of cancer.
And so on...
https://www.nature.com/articles/s41467-020-20210-3
Abstract
Mitochondrial oxidation-induced cell death, a physiological process triggered by various cancer therapeutics to induce oxidative stress on tumours, has been challenging to investigate owing to the difficulties in generating mitochondria-specific oxidative stress and monitoring mitochondrial responses simultaneously. Accordingly, to the best of our knowledge, the relationship between mitochondrial protein oxidation via oxidative stress and the subsequent cell death-related biological phenomena has not been defined. Here, we developed a multifunctional iridium(III) photosensitiser, Ir-OA, capable of inducing substantial mitochondrial oxidative stress and monitoring the corresponding change in viscosity, polarity, and morphology. Photoactivation of Ir-OA triggers chemical modifications in mitochondrial protein-crosslinking and oxidation (i.e., oxidative phosphorylation complexes and channel and translocase proteins), leading to microenvironment changes, such as increased microviscosity and depolarisation. These changes are strongly related to cell death by inducing mitochondrial swelling with excessive fission and fusion. We suggest a potential mechanism from mitochondrial oxidative stress to cell death based on proteomic analyses and phenomenological observations.
Introduction
Elucidating the process of mitochondrial oxidation-induced cell death is essential to understanding and improving cancer therapeutics based on oxidative damage to tumours1,2,3,4. To this end, various mitochondria-targeted photosensitisers that can produce reactive oxygen species (ROS) have been utilised to understand the underlying chemical effect of mitochondrial oxidation5,6.
Oxidative stress induced by photosensitisers causes chemical modifications of biomolecules including proteins7,8,9, unsaturated lipids10,11, and DNA12,13. Notably, protein modifications occurring via methionine oxidation and dityrosine crosslinking are clearly described chemical modifications for mitochondrial oxidation-induced cell death9,14. However, the connection between the chemical modifications of mitochondrial proteins and the biological response in cell death remains elusive due to the absence of a chemical tool to analyse the biological phenomena (i.e., environmental changes in mitochondrial surroundings in terms of viscosity, polarity, morphology, pH, and temperature) that occur in mitochondria in response to oxidative stress. Therefore, photosensitisers that efficiently oxidise proteins and subsequently monitor the consequent protein dysfunction-related mitochondrial responses are needed15,16,17. To address this, we employed organometallic iridium(III) complexes because of their notable ROS generation efficiency, lifetime sensitivity to microviscosity, straightforward ligand tuning, cell permeability, and photostability16,18,19.
In this work, our designed iridium(III) complex, Ir-OA, showed accelerated ROS production and micropolarity-dependent ratiometric emission properties owing to intramolecular energy transfer system. With these characteristics, we successfully employed Ir-OA to (i) induce cell death by producing ROS in the mitochondria, (ii) monitor changes in the mitochondrial microenvironment (i.e., viscosity, polarity, and morphology) using various techniques including lifetime and ratiometric imaging, and (iii) identify the mode of action for microenvironment changes by profiling the modified proteins (i.e., crosslinked and oxidised proteins) through oxidative stress. Collectively, we suggest a promising mechanism that describes how oxidative stress affects the mitochondria and induces cell death, corroborating the correlation between mitochondrial microenvironment changes and the oxidised proteome. The proposed mechanism may aid the understanding of how some cancer therapeutics can induce mitochondrial oxidative stress.
https://pubmed.ncbi.nlm.nih.gov/33723127/
Abstract
Reactive oxygen species (ROS) can damage lipids, nucleic acids, and proteins, thereby altering their functions. When a balance between production of ROS and antioxidative defense is disturbed, state of oxidative stress occurs. Oxidative stress leads to many diseases. There are few biomarkers that are used for better understanding how oxidative stress is involved in cancer pathophysiology. This review focuses on 8-hidroxy-2-deoxyguanosine (8-OHdG) and antioxidative enzymes as biomarkers for measurement of oxidative stress in different types of cancer. This review also deals with the product of lipid peroxidation, malondialdehyde (MDA), and across a variety of cancers. To address this aim, analysis of studies of breast, prostate, lung, colon, cervical, ovarian, brain, bladder, renal, thyroid cancer, and chronic lymphocytic leukemia has been conducted. In general, levels of antioxidative enzymes are mostly lower in cancer patients, while 8-OHdG and MDA are higher. Further research is needed, with focus on correlation levels of these biomarkers and advancement of the disease. Moreover, all studies explored the idea of those biomarkers as a useful tool in determining the levels of oxidative stress. Some of the studies proposed their potential in defining the stage of tumor progression.
Abstract
In addition to the well-established role of the mitochondria in energy metabolism, regulation of cell death has recently emerged as a second major function of these organelles. This, in turn, seems to be intimately linked to their role as the major intracellular source of reactive oxygen species (ROS), which are mainly generated at Complex I and III of the respiratory chain. Excessive ROS production can lead to oxidation of macromolecules and has been implicated in mtDNA mutations, ageing, and cell death. Mitochondria-generated ROS play an important role in the release of cytochrome c and other pro-apoptotic proteins, which can trigger caspase activation and apoptosis. Cytochrome c release occurs by a two-step process that is initiated by the dissociation of the hemoprotein from its binding to cardiolipin, which anchors it to the inner mitochondrial membrane. Oxidation of cardiolipin reduces cytochrome c binding and results in an increased level of “free” cytochrome c in the intermembrane space. Conversely, mitochondrial antioxidant enzymes protect from apoptosis. Hence, there is accumulating evidence supporting a direct link between mitochondria, oxidative stress and cell death.
https://link.springer.com/article/10.1007/s10495-007-0756-2
And that's the ones on TikTok. Countless others without millions of followers are suffering the same things. How many of us know people personally who are dealing with this (all jabbed) as well as other adverse effects? I know of at least 2 with breast cancer, 2 with lung cancer , diabetes, etc. and these are people I KNOW. Others chronically ill because their immune systems are shot. It's sad and maddening at the same time.
Like me. Give me attention. Look at me. I’ll tell you what you should do.
Go see your doctor. Get vaxxed. Be a follower!!
Is it unadulterated narcissism? Unacknowledged arrogance? It sure isnt influencing people to think for themselves and think critically.
Its fear. Fear masquerading as love. Its self over value.
They made their choice.
And now, they COULD make a brave choice. A just choice. They have the platforms...Dr. Alexander's post shows them something's up, and there's an issue that needs fulsome discussion and investigation.
The Actors, and performers guilds, insisted on the Covid Vax, or no performances, why else, the cancellations and sudden "illnesses?
Can I ask my fellow experts here if they have heard if Dr. Vanden Bosch is still standing behind his prediction, that this fall will be a massive amount of deaths for those people that were vaccinated? Thank you.
https://thehighwire.com/ark-videos/inescapable/
Yes, he definitely is still standing behind There will be a very bad winter coming ahead.
THE MRNA whackadoodle mumbo jumbo scary AF injections killed EVERY SINGLE one of the lab animals it was tested on.
WHO <==[double entendre] GREEN LIGHTS genocide on a global scale?????
"I’m Dr. Mike Yeadon, it’s known I’m extremely dark about where I deduce this is going, and I expect the results will make Stalin, Hitler & Mao look like beginners. Depopulation under fear, controlled by VaxPass & accomplished using “variant vaccines”. It's perfect in it's evilness" ~ Dr. Michael Yeadon (former VP and Chief Scientist of Pfizer)
Commonality? The "Sheep", believing the Fear Mongers, getting the Covid Vax, and maybe Boosters.....
Common to whom? It's just that 'Sheep', to me anyway, implies a large percentage of the population. Maybe correct at the start of the roll-out, but not now. Even Canada only had 25% lining up for the last one, and the previous one was around 50%. If that holds for the next, only 12.5% will be stupid/alive enough to roll up their sleeves. No doubt, there is a basement - it will be interesting to see what that is. People obviously know (or sense) something is seriously, seriously wrong - they are just not sure what to do about it.
Makes me want to throw up
We’re 2 1/2 years into this nightmare of the deathVAX , and it’s getting worse and worse
How the cabal runs everything. Compartmentalise, never let them see the dots connected, cumulative data, patterns, trends, EVIDENCE! Thanks for doing the opposite! My god this is a lot of pain and sorrow in one post.
This shows you exactly how heartless the system is.
Me: “Massive unintended consequences” - unintended? The US DOD and DARPA can't create Super Soldiers without intentionally changing their Genetic Codes, can they?
These people had their genetic codes fucked around with by Big Pharma on behalf of the US DOD and DARPA - see my article today - what else would you have expected?
I’m so not surprised any more.
Maybe they were all bitten.