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World-renowned biomedical scientist: COVID-19 vaccine damages DNA to accelerate aging and disease
invite response
2025 Jul 16, 1:43pm 59 views 1 comment
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HANrongli
2025 Jul 16, 10:12pm
这个SARS-SPIKE的东西他们制造了废墟大脑培养了一项新的研究表明，在人脑的特定领域中表现出脾剧（减少的葡萄糖摄取） - 思考脑雾/ 杰西卡
This SARS-spike thing they made ruins brains
A new study demonstrates hypometabolism (reduced glucose uptake) in specific areas of the human brain - think reason for brain fog
JESSICA ROSE
JUL 15
READ IN APP
A new study has been published in Scientific Reports entitled: “Mapping brain changes in post-COVID-19 cognitive decline via FDG PET hypometabolism and EEG slowing”,¹ and it lays out a mechanism of action for brain fog/neurodegeneration/cognitive decline and other forms of brain deterioration seen in hundreds of millions of people from being subjected to SARS-2, and I might add, inevitably, from the COVID-19 shots encoding spike protein as well. The reason I say this is that there is no doubt in my mind at this point that the culprit of neuroinflammation and brain pathologies is the spike protein.
Our study aimed to investigate brain functional alterations and the underlying mechanisms using PET and EEG in post-COVID-19 subjects with subjective cognitive decline following mild SARS-CoV-2 infection, compared to healthy controls.
So they found brain functional alterations in people with what they refer to as “mild SARS-CoV-2 infection”.
Fluorodeoxyglucose positron emission tomography (FDG PET) measures brain glucose metabolism to assess function and disease, while electroencephalography (EEG) records electrical brain activity to evaluate neurological conditions. They used both techniques to paint a better picture of the connection between brain electrical activity and cerebral glucose metabolism in the context of brain functional dysfunction.
What they found in the 28 people with cognitive decline (defined as memory deficits, reduced attention, and executive function impairments, as well as fatigue) from SARS-CoV-2 (ahem: spike protein) in comparison with controls (28 people who’d had EEGs prior to the COVID-era with no recorded history of cognitive impairment or any other neurological disorders), was that the test group exhibited significant hypometabolism in particular locations in the brain. They found the largest hypometabolic cluster in the right frontal lobes of test subjects.
figure 1
Fig.1 from article https://www.nature.com/articles/s41598-025-04815-6/figures/1 - hypometabolic clusters (highlighted) found in text subjects
The right frontal lobe plays a key role in various human activities and behaviors, primarily those involving executive functions, emotional regulation, and social cognition. So if its damaged, it can lead to impulsivity, poor social judgment, emotional dysregulation, or reduced insight into one's behavior. Interesting.
The left frontal lobes, the temporal lobes and the parietal lobes were also found to exhibit hypometabolism. Wherever you find reduced glucose uptake, you’ll find impaired brain function.
Our study identified a shift in EEG rhythms from higher frequencies, such as alpha, to lower frequencies like theta and delta, particularly in anterior regions, which aligned with the observed hypometabolism clusters.
The shift from alpha to theta/delta EEG rhythms in anterior regions, characterized concurrently with hypometabolism in the frontal, temporal, parietal, and left occipital lobes, suggests neurodegenerative or pathological processes causing cognitive, behavioral, and perceptual deficits.
Sounds a lot like Alzheimer’s (dementia) to me.
The authors also point out this critical point in the Discussion.
Notably, the neurochemical basis of these findings may be linked to disrupted neurotransmitter systems, particularly involving GABAergic and glutamatergic pathways.
Yes. It could be. I believe the mechanism of action here is spike-induced neuroinflammation and vascular damage. On its own, hypometabolism reflects reduced neuronal glucose uptake due to dysfunction or inflammation. The spike protein's inflammatory and immunomodulatory effects are certainly contributing to hypometabolism in these brain regions by disrupting neuronal function and energy metabolism through microglial activation and cytokine release. Among other things.
Now. Think COVID-19 shots. What was the template they insisted on using to encode which protein now to be non-stop produced by people’s own cells? Hmm. Was it something like… spike protein? Or something?
I will leave you guys with a VAERS query of neuroinflammation-related reports. I included some of the symptoms reported in the study above including dizziness and headache.
In addition to cognitive decline, post-COVID-19 symptoms at the time of evaluation included asthenia (46.4%), persistent dyspnea (35.7%), hyposmia (28.6%), headache (25.0%), myalgia/arthralgia (17.9%), hypogeusia (17.9%), dizziness/gait instability (17.9%), palpitations/tachycardia (10.7%), and gastrointestinal distress (10.7%).
The chart below shows only VAERS ‘neuro’ reports (absolute counts by age group) that got to the front-end system. This is the tip of the iceberg - a representation of the 467,754 neuro reports in VAERS - based on those with age-data, and those reports that ‘got in’ and not subsequently removed. And this is ONLY in the COVID-19 shot context.
What do you think? Is spike ruining our brains? I think it is. It’s doing more than that though, don’t forget, but the brain is kind of important.
1
Manganotti, P., Iscra, K., Furlanis, G. et al. Mapping brain changes in post-COVID-19 cognitive decline via FDG PET hypometabolism and EEG slowing. Sci Rep 15, 23141 (2025). https://doi.org/10.1038/s41598-025-04815-6 这个SARS-SPIKE的东西他们制造了废墟大脑培养了一项新的研究表明，在人脑的特定领域中表现出脾剧（减少的葡萄糖摄取） - 思考脑雾杰西卡的原因在APP中阅读了一个新的研究，该研究已经出版了一个新的学习，题为题为 我说的原因是我脑子里毫无疑问，这一点是神经引发和脑病理的罪魁祸首是穗蛋白。 我们的研究旨在调查脑功能改变和使用宠物和脑电图的潜在的潜在机制，在Covid-19受试者中具有主观认知下降，与健康对照组相比。 因此，他们发现人们称为“轻度SARS-COV-2感染”的人的脑功能改变。 氟脱氧葡萄糖正电子发射断层扫描（FDG PET）测量脑葡萄糖代谢以评估功能和疾病，而脑电图（EEG）记录电脑活动以评估神经病症。 他们使用两种技术来绘制在脑功能功能障碍的背景下脑电活动和脑葡萄糖代谢之间的更好图像。 与对照组相比，他们在28人中发现了28人认知下降（定义为记忆赤字，减少注意力和执行函数损伤以及疲劳）（之前的28人） 他们发现了测试对象的右前瓣中最大的抑制粒子。 图1图1从文章https://www.nature.com/articles/s41598-025-04815-6/5/5/11 - 低音olted）在文本主题中发现的右前叶扮演一个 因此，如果其损坏，它可能会导致冲动，社会判断，情绪化失调，或减少对一个人的行为的洞察力。 有趣。 还发现左前瓣，颞叶和顶叶裂片表现出抑郁症。 无论您发现降低葡萄糖摄取，您都会发现大脑功能受损。 我们的研究确定了从较高频率的EEG节奏的转变，例如α，较低的频率，如θ和三角洲，特别是在与观察到的抑郁型簇相对的前区域。 从α到θ/ delta eeg节奏的α转移在前部区域，在正面，颞叶和左侧枕叶中同时表现为衰减亢进，表明神经变性或病理过程 听起来很像Alzheimer（痴呆症）给我。 作者还指出了讨论中的这一关键点。 值得注意的是，这些发现的神经化学基础可以与破坏的神经递质系统相关联，特别是涉及加巴能和谷氨酸宫的途径。 是。 它可能是。 我相信这里的作用机制是穗状体炎症的神经炎和血管损伤。 在其自身的情况下，抑郁率异常反映由于功能障碍或炎症引起的神经元葡萄糖摄取。 通过显微胶质激活和细胞因子释放破坏神经元函数和能量代谢，穗蛋白的炎症和免疫调节效果肯定会导致这些脑区中的衰减溶解。 在其他事情之外。 现在。 认为covid-19镜头。 他们坚持用来编码哪种蛋白质的模板是什么，该蛋白质由人类自己的细胞产生不间断？ 嗯。 它是类似的...刺蛋白吗？ 还是什么？ 我会把伙计们留下vaers查询神经炎症相关的报告。 我包括上述研究中报告的一些症状，包括头晕和头痛。 除认知下降外，评估后的Covid-19症状包括哮喘（46.4％），持续的呼吸困难（35.7％），Hyposmia（28.6％），头痛（25.0％）， 下图仅显示了转到前端系统的VAERS'NEURO'报告（由年龄组的绝对计数）。 这是冰山一角 - 基于随着年龄数据的人的狂热中的467,754个神经报告的代表性，以及“进入”并未删除的那些报告。 这仅在Covid-19拍摄背景下。 你觉得怎么样？ 尖峰毁了我们的大脑吗？ 我想是。 它的做法不仅仅是那个，别忘了，但大脑是重要的。 1 Manganotti，P.，Iscra，K。，Furlanis，G.等人。 通过FDG宠物抑制和EEG减速，Covid-19认知衰退的映射脑改变。 SCI REP 15,23141（2025）。 https://doi.org/10.1038/s41598-025-04815-6
这个SARS-SPIKE的东西他们制造了废墟大脑培养了一项新的研究表明，在人脑的特定领域中表现出脾剧（减少的葡萄糖摄取） - 思考脑雾/ 杰西卡
This SARS-spike thing they made ruins brains
A new study demonstrates hypometabolism (reduced glucose uptake) in specific areas of the human brain - think reason for brain fog
JESSICA ROSE
JUL 15
READ IN APP
A new study has been published in Scientific Reports entitled: “Mapping brain changes in post-COVID-19 cognitive decline via FDG PET hypometabolism and EEG slowing”,¹ and it lays out a mechanism of action for brain fog/neurodegeneration/cognitive decline and other forms of brain deterioration seen in hundreds of millions of people from being subjected to SARS-2, and I might add, inevitably, from the COVID-19 shots encoding spike protein as well. The reason I say this is that there is no doubt in my mind at this point that the culprit of neuroinflammation and brain pathologies is the spike protein.
Our study aimed to investigate brain functional alterations and the underlying mechanisms using PET and EEG in post-COVID-19 subjects with subjective cognitive decline following mild SARS-CoV-2 infection, compared to healthy controls.
So they found brain functional alterations in people with what they refer to as “mild SARS-CoV-2 infection”.
Fluorodeoxyglucose positron emission tomography (FDG PET) measures brain glucose metabolism to assess function and disease, while electroencephalography (EEG) records electrical brain activity to evaluate neurological conditions. They used both techniques to paint a better picture of the connection between brain electrical activity and cerebral glucose metabolism in the context of brain functional dysfunction.
What they found in the 28 people with cognitive decline (defined as memory deficits, reduced attention, and executive function impairments, as well as fatigue) from SARS-CoV-2 (ahem: spike protein) in comparison with controls (28 people who’d had EEGs prior to the COVID-era with no recorded history of cognitive impairment or any other neurological disorders), was that the test group exhibited significant hypometabolism in particular locations in the brain. They found the largest hypometabolic cluster in the right frontal lobes of test subjects.
figure 1
Fig.1 from article https://www.nature.com/articles/s41598-025-04815-6/figures/1 - hypometabolic clusters (highlighted) found in text subjects
The right frontal lobe plays a key role in various human activities and behaviors, primarily those involving executive functions, emotional regulation, and social cognition. So if its damaged, it can lead to impulsivity, poor social judgment, emotional dysregulation, or reduced insight into one's behavior. Interesting.
The left frontal lobes, the temporal lobes and the parietal lobes were also found to exhibit hypometabolism. Wherever you find reduced glucose uptake, you’ll find impaired brain function.
Our study identified a shift in EEG rhythms from higher frequencies, such as alpha, to lower frequencies like theta and delta, particularly in anterior regions, which aligned with the observed hypometabolism clusters.
The shift from alpha to theta/delta EEG rhythms in anterior regions, characterized concurrently with hypometabolism in the frontal, temporal, parietal, and left occipital lobes, suggests neurodegenerative or pathological processes causing cognitive, behavioral, and perceptual deficits.
Sounds a lot like Alzheimer’s (dementia) to me.
The authors also point out this critical point in the Discussion.
Notably, the neurochemical basis of these findings may be linked to disrupted neurotransmitter systems, particularly involving GABAergic and glutamatergic pathways.
Yes. It could be. I believe the mechanism of action here is spike-induced neuroinflammation and vascular damage. On its own, hypometabolism reflects reduced neuronal glucose uptake due to dysfunction or inflammation. The spike protein's inflammatory and immunomodulatory effects are certainly contributing to hypometabolism in these brain regions by disrupting neuronal function and energy metabolism through microglial activation and cytokine release. Among other things.
Now. Think COVID-19 shots. What was the template they insisted on using to encode which protein now to be non-stop produced by people’s own cells? Hmm. Was it something like… spike protein? Or something?
I will leave you guys with a VAERS query of neuroinflammation-related reports. I included some of the symptoms reported in the study above including dizziness and headache.
In addition to cognitive decline, post-COVID-19 symptoms at the time of evaluation included asthenia (46.4%), persistent dyspnea (35.7%), hyposmia (28.6%), headache (25.0%), myalgia/arthralgia (17.9%), hypogeusia (17.9%), dizziness/gait instability (17.9%), palpitations/tachycardia (10.7%), and gastrointestinal distress (10.7%).
The chart below shows only VAERS ‘neuro’ reports (absolute counts by age group) that got to the front-end system. This is the tip of the iceberg - a representation of the 467,754 neuro reports in VAERS - based on those with age-data, and those reports that ‘got in’ and not subsequently removed. And this is ONLY in the COVID-19 shot context.
What do you think? Is spike ruining our brains? I think it is. It’s doing more than that though, don’t forget, but the brain is kind of important.
1
Manganotti, P., Iscra, K., Furlanis, G. et al. Mapping brain changes in post-COVID-19 cognitive decline via FDG PET hypometabolism and EEG slowing. Sci Rep 15, 23141 (2025). https://doi.org/10.1038/s41598-025-04815-6 这个SARS-SPIKE的东西他们制造了废墟大脑培养了一项新的研究表明，在人脑的特定领域中表现出脾剧（减少的葡萄糖摄取） - 思考脑雾杰西卡的原因在APP中阅读了一个新的研究，该研究已经出版了一个新的学习，题为题为 我说的原因是我脑子里毫无疑问，这一点是神经引发和脑病理的罪魁祸首是穗蛋白。 我们的研究旨在调查脑功能改变和使用宠物和脑电图的潜在的潜在机制，在Covid-19受试者中具有主观认知下降，与健康对照组相比。 因此，他们发现人们称为“轻度SARS-COV-2感染”的人的脑功能改变。 氟脱氧葡萄糖正电子发射断层扫描（FDG PET）测量脑葡萄糖代谢以评估功能和疾病，而脑电图（EEG）记录电脑活动以评估神经病症。 他们使用两种技术来绘制在脑功能功能障碍的背景下脑电活动和脑葡萄糖代谢之间的更好图像。 与对照组相比，他们在28人中发现了28人认知下降（定义为记忆赤字，减少注意力和执行函数损伤以及疲劳）（之前的28人） 他们发现了测试对象的右前瓣中最大的抑制粒子。 图1图1从文章https://www.nature.com/articles/s41598-025-04815-6/5/5/11 - 低音olted）在文本主题中发现的右前叶扮演一个 因此，如果其损坏，它可能会导致冲动，社会判断，情绪化失调，或减少对一个人的行为的洞察力。 有趣。 还发现左前瓣，颞叶和顶叶裂片表现出抑郁症。 无论您发现降低葡萄糖摄取，您都会发现大脑功能受损。 我们的研究确定了从较高频率的EEG节奏的转变，例如α，较低的频率，如θ和三角洲，特别是在与观察到的抑郁型簇相对的前区域。 从α到θ/ delta eeg节奏的α转移在前部区域，在正面，颞叶和左侧枕叶中同时表现为衰减亢进，表明神经变性或病理过程 听起来很像Alzheimer（痴呆症）给我。 作者还指出了讨论中的这一关键点。 值得注意的是，这些发现的神经化学基础可以与破坏的神经递质系统相关联，特别是涉及加巴能和谷氨酸宫的途径。 是。 它可能是。 我相信这里的作用机制是穗状体炎症的神经炎和血管损伤。 在其自身的情况下，抑郁率异常反映由于功能障碍或炎症引起的神经元葡萄糖摄取。 通过显微胶质激活和细胞因子释放破坏神经元函数和能量代谢，穗蛋白的炎症和免疫调节效果肯定会导致这些脑区中的衰减溶解。 在其他事情之外。 现在。 认为covid-19镜头。 他们坚持用来编码哪种蛋白质的模板是什么，该蛋白质由人类自己的细胞产生不间断？ 嗯。 它是类似的...刺蛋白吗？ 还是什么？ 我会把伙计们留下vaers查询神经炎症相关的报告。 我包括上述研究中报告的一些症状，包括头晕和头痛。 除认知下降外，评估后的Covid-19症状包括哮喘（46.4％），持续的呼吸困难（35.7％），Hyposmia（28.6％），头痛（25.0％）， 下图仅显示了转到前端系统的VAERS'NEURO'报告（由年龄组的绝对计数）。 这是冰山一角 - 基于随着年龄数据的人的狂热中的467,754个神经报告的代表性，以及“进入”并未删除的那些报告。 这仅在Covid-19拍摄背景下。 你觉得怎么样？ 尖峰毁了我们的大脑吗？ 我想是。 它的做法不仅仅是那个，别忘了，但大脑是重要的。 1 Manganotti，P.，Iscra，K。，Furlanis，G.等人。 通过FDG宠物抑制和EEG减速，Covid-19认知衰退的映射脑改变。 SCI REP 15,23141（2025）。 https://doi.org/10.1038/s41598-025-04815-6
World-renowned biomedical scientist: COVID-19 vaccine damages DNA to accelerate aging and disease
世界著名生物医学家：新冠疫苗损伤DNA加速衰老与疾病
The Spike Protein Alone Activates All Major Pathways Involved in Chronic Disease
This is in addition to its ability to induce all Nine Hallmarks of Aging. We can age faster; we can get sick faster – and stay sick.
WALTER M CHESNUT
JUL 14
https://open.substack.com/pub/wmcresearch/p/the-spike-protein-alone-activates
READ IN APP
SARS-CoV-2 spike protein induces reactive oxygen species (ROS), and DNA double-strand breaks (measured by H2AX) in human lung cells. Single-cell suspension of freshly explanted normal human lung cells (A-B) were seeded at 104 cells per well into 96-well plates. Half of the culture wells were incubated with the antioxidant MMS350 (400 μM) one hour before addition of spike protein (0.50 μg/ml), 5 Gy irradiation or both spike protein plus 5 Gy. One hour later, cells were assayed for ROS (A) and DNA double-strand breaks (B). For the statistical analysis, analysis of variance followed by a Student’s t-test were used. ROS increased in human lung cells under all conditions and was reduced when cells were incubated in MMS350. DNA double-strand breaks in human lung samples (n=4) were increased under all treatments but were reduced when the cells were treated with MMS350. Significantly different at p<0.05 vs. *0 Gy, # MMS350.
Perhaps the singular most important reason for the recent emergence of what I shall call catastrophic chronic diseases, is the introduction of the Spike Protein into the human body. By catastrophic, I mean the sudden onset of turbocancers, T2D and other aggressive autoimmune/chronic diseases.
Years ago, I demonstrated that the Spike Protein of SARS_CoV-2 could, on its own, induce the canonical Nine Hallmarks of Aging.
Those, of course, make us age faster. It has now also occurred to me that, in tandem with this acceleration in aging, there is also an acceleration in inducing diseases associated with aging. This is accomplished by the Spike Protein, on its own, as well. How? By activating all the major pathways associated with chronic disease; the diseases of aging.
First, let us take a look at the major pathways involved in chronic disease.
Chronic diseases are frequently linked to the activation and dysregulation of various cellular pathways, particularly those involved in inflammation.
Here are some key pathways and their involvement in chronic diseases:
NF-κB pathway: This protein complex regulates DNA transcription, cytokine production, and cell survival, playing a significant role in inflammatory and immune responses. Its dysregulation is linked to inflammatory, autoimmune, and metabolic diseases, as well as cancers.
MAPK pathways: Mitogen-activated protein kinases are involved in cellular responses to stimuli like inflammatory cytokines and stress. They regulate processes like proliferation, differentiation, and cell survival. Abnormal signaling in these pathways is implicated in inflammatory, autoimmune, and metabolic disorders, along with cancer.
JAK-STAT pathway: This pathway controls gene expression in response to extracellular factors like cytokines and growth factors. Dysregulation is associated with inflammatory, autoimmune, metabolic diseases, and various cancers.
Oxidative stress pathways: An imbalance between reactive oxygen species production and detoxification leads to oxidative stress. This can activate transcription factors, increasing the expression of genes promoting inflammation. Oxidative stress is linked to cardiovascular disease, cancer, diabetes, and aging.
Google AI, July 13, 2025
Inflammation is a biological response of the immune system that can be triggered by a variety of factors, including pathogens, damaged cells and toxic compounds. These factors may induce acute and/or chronic inflammatory responses in the heart, pancreas, liver, kidney, lung, brain, intestinal tract and reproductive system, potentially leading to tissue damage or disease. Both infectious and non-infectious agents and cell damage activate inflammatory cells and trigger inflammatory signaling pathways, most commonly the NF-κB, MAPK, and JAK-STAT pathways.
Inflammatory responses and inflammation-associated diseases in organs
https://pmc.ncbi.nlm.nih.gov/articles/PMC5805548/
One-by-one, we see that the Spike Protein, alone, activates these pathways.
NF-kB
When stimulated with extracellular S protein, human and mouse lung epithelial cells also produced inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein intracellularly were non-inflammatory, but elicited an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-κB pathway in a MyD88-dependent manner.
SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway
https://pmc.ncbi.nlm.nih.gov/articles/PMC8709575/
MAPK
Please also note the activation of monocytes and microglia, which I have previously discussed.
A growing number of studies (in multiple cell types) demonstrated that treatment of cells with the S1 spike protein changes cell signaling, especially the activation of MAPK ERK1/2, and promotes pro-inflammatory cytokine production [18,19,43,61]. These largely lung cell types also include direct activation of monocytes and microglia by S1 spike [62,63].
The SARS-CoV-2 S1 Spike Protein Promotes MAPK and NF-kB Activation in Human Lung Cells and Inflammatory Cytokine Production in Human Lung and Intestinal Epithelial Cells
https://pmc.ncbi.nlm.nih.gov/articles/PMC9607240/
JAK-STAT
To investigate the mechanism underlying the synergistic effect of IL-2 and spike protein in inducing CRS, transcriptomic analysis was conducted on PBMCs treated with PBS, spike protein, IL-2, or a combination of spike protein and IL-2. Our analysis revealed that stimulation with spike protein activated multiple signaling pathways, including NF-κB, TNF, and Janus kinase-signal transducer and activator of transcription (JAK-STAT) in PBMCs (Supplementary Figures S4A–C).
SARS-CoV-2 spike protein induces the cytokine release syndrome by stimulating T cells to produce more IL-2
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1444643/full
OXIDATIVE STRESS
Also, please note the observed similarities between Spike Protein exposure and radiation. A finding I predicted years ago. Please see wmcresearch.org for the post.
SARS-CoV-2 spike protein induced reactive oxygen species, DNA double-strand breaks, transforming growth factor-β signaling pathways, and senescence, which were exacerbated by prior or subsequent ionizing irradiation. The water-soluble radiation countermeasure, MMS350, reduced spike protein-induced changes. Conclusion: In both the SARS-Co-2 and the irradiation mouse models, similar responses were seen indicating that irradiation or exposure to SARS-CoV-2 virus may lead to similar lung diseases such as pulmonary fibrosis.
SARS-CoV-2 Spike Protein Induces Oxidative Stress and Senescence in Mouse and Human Lung
https://iv.iiarjournals.org/content/38/4/1546.long
So, what we have here is a pathogenic protein which not only accelerates aging but also induces an environment in which the diseases of aging can much more easily take root and rapidly accelerate themselves. It is almost like a conveyer belt. Wherever you are on the spectrum of biological age, the Spike Protein hurries the body’s trajectory along that belt towards the inevitable decline into the maladies of old age. It also makes it far more likely that one of the fatal diseases of old age will develop – and kill far more quickly. I simply find it difficult to believe that such a protein occurred naturally.
Fortunately, these pathways of chronic disease can be attenuated, and biological age can be slowed down. The more we understand, the more we can heal. I will continue to battle on both fronts. Thank you, as always, for your readership, dialogue and support. I am extremely grateful that another individual made a generous direct donation over the weekend, and we gained another paid subscriber. You keep me going. Please have a blessed week. 单独的穗蛋白激活所有患有慢性疾病所涉及的主要途径，这是诱导所有九个衰老标志的能力。 我们可以增长更快; 我们可以更快地生病 - 并保持生病。 沃尔特M Chesnut 7月14日在APP SARS-COV-2尖峰蛋白中读取了人肺细胞中的反应性氧物质（ROS）和DNA双链断裂（通过H2AX测量）。 将新鲜脱盐的正常人肺细胞（A-B）的单细胞悬浮液以每孔104个细胞接种成96孔板。 在加入穗蛋白（0.50μg/ ml），5GY辐射或尖峰蛋白加5Gy之前，将一半的培养孔与抗氧化MMS350（400μm）孵育一小时。 一小时后，测定细胞用于ROS（a）和DNA双链断裂（b）。 对于统计分析，使用了学生T检验的方差分析。 在所有条件下，人肺细胞中的ROS增加，当在MMS350中孵育细胞时，减少。 在所有治疗中增加人肺样品（n = 4）的DNA双链断裂，但用MMS350处理细胞时减少。 P <0.05 Vs. * 0 GY，#mms350显着不同。 也许是最近出现的奇异最重要的原因是呼叫灾难性的慢性病的兴趣，是将穗蛋白引入人体。 通过灾难性，我的意思是涡轮癌，T2D和其他侵略性自身免疫/慢性病的突然发作。 几年前，我证明SARS_COV-2的尖峰蛋白可以自行诱导衰老的规范九个标志。 当然，那些让我们年龄更快。 它现在也发生在我身上，在随着衰老的这种加速度串联中，诱导与老化相关的疾病也有加速。 这是由穗蛋白质的，同时也是如此。 怎么样？ 通过激活与慢性疾病相关的所有主要途径; 老龄化的疾病。 首先，让我们看看患有慢性疾病的主要途径。 慢性疾病经常与各种细胞途径的活化和失调相关，特别是参与炎症的疾病。 以下是一些关键途径及其参与慢性病：NF-κB途径：该蛋白质复合物调节DNA转录，细胞因子生产和细胞存活，在炎症和免疫应答中发挥着重要作用。 其呼吸困难与炎症，自身免疫和代谢疾病以及癌症相关联。 MAPK途径：丝裂剂激活的蛋白激酶参与细胞反应与炎症细胞因子和胁迫等刺激。 它们调节增殖，分化和细胞存活等方法。 这些途径中的异常信号传导涉及炎症，自身免疫和代谢障碍以及癌症。 JAK-STAT途径：该途径控制基因表达，以应对细胞因子等细胞内因子和生长因子。 失呼率与炎症，自身免疫，代谢疾病和各种癌症有关。 氧化应激途径：反应性氧物种生产和排毒之间的不平衡导致氧化应激。 这可以激活转录因子，增加促进炎症的基因的表达。 氧化应激与心血管疾病，癌症，糖尿病和老化有关。 谷歌AI，7月13日，2025年炎症是免疫系统的生物反应，可通过各种因素引发，包括病原体，受损细胞和有毒化合物。 这些因素可以诱导心脏，胰腺，肝，肾，肺，脑，肠道和生殖系统中的急性和/或慢性炎症反应，可能导致组织损伤或疾病。 传染性和非传染性药物和细胞损伤激活炎症细胞，触发炎症信号通路，最常见的是NF-κB，MAPK和JAK-STAT途径。 炎症反应和炎症相关疾病在器官https://pmc.ncbi.nlm.nih.gov/articles/pmc5805548/一对一，我们看到穗蛋白，单独， 用细胞外的S蛋白刺激时，NF-KB，人和小鼠肺上皮细胞也产生炎症细胞因子和趋化因子。 有趣的是，表达蛋白质细胞内的上皮细胞是非炎症，但在共同培养时引发巨噬细胞的炎症反应。 生物化学研究表明，S蛋白通过以MyD88依赖性的方式激活NF-κB途径触发炎症。 SARS-COV-2穗蛋白通过TLR2依赖性活化的NF-κB途径HTTPS://pmc.ncbi.nlm.nih.gov/articles/pmc870957 越来越多的研究（多种细胞类型）证明了用S1穗蛋白的细胞处理细胞信号传导，尤其是MAPK ERK1 / 2的活化，并促进促炎细胞因子产生[18,19,43,61]。 这些主要是肺细胞类型还包括通过S1穗直接激活单核细胞和微胶质[62,63]。 SARS-COV-2 S1尖峰蛋白促进了人肺细胞中的MAPK和NF-KB活化，在人肺和肠上皮细胞HTTPS://pmc.ncbi.nlm中促进人肺细胞和炎性细胞因子产生。 我们的分析表明，用尖峰蛋白激活多个信号通路的刺激，包括PBMC的NF-κB，TNF和Janus激酶 - 信号传感器和转录（JAK-STAT）的活化剂（补充数据S4a- SARS-COV-2尖峰蛋白通过刺激T细胞产生细胞因子释放综合征，以产生更多IL-2 HTTPS://www.frontiersin.org/Journals/immunology/Articles/10.3389/fimm 我估计几年前的发现。 请参阅帖子的wmcresearch.org。 SARS-COV-2穗蛋白诱导的活性氧物质，DNA双链断裂，转化生长因子-β信号传导途径和衰老，通过预先或随后的电离照射加剧。 水溶性辐射对策，MMS350减少了尖峰蛋白质诱导的变化。 结论：在SARS-CO-2和辐照小鼠模型中，看到类似的反应表明，SARS-COV-2病毒的照射或暴露可能导致肺纤维化如类似的肺病。 SARS-COV-2穗蛋白诱导小鼠和人肺HTTPS://IV.IIARJOURNALS.ORG/Content/38/4/1546.1的氧化胁迫和衰老。所以，我们在这是一种致病蛋白质 它几乎就像一个传送带。 无论您在生物年龄的频谱上，尖峰蛋白都赶紧沿着身体的轨迹，朝着腰带朝着年龄的疾病的不可避免的下降。 它还使得老年的致命疾病之一更有可能发展 - 并更快地杀死。 我只是难以相信这种蛋白质自然发生。 幸运的是，这些慢性疾病的途径可以减弱，生物年龄可以减慢。 我们越多，我们就越能愈合。 我将继续在两端战斗。 衷心感谢您的读者，对话和支持。 我非常感谢另一个人在周末慷慨直接捐赠，我们获得了另一个付费订户。 你让我继续前进。 请有一个幸福的一周。