Reporter's review: The pictures show that Spike + fibrin + thrombin - plasmin protein. Strong reaction under the purple light. Basic knowledge: Health prosecutors carry purple light flashlights and illumination inspections, dirty food or utensils that cannot be seen in the eyes. …After the dark pandemic, questioning and refusing injections and protecting the body for cleaning is a wise move! … The crown vaccine destroys endothelial cells, however! Vitamin D3 and various vitamins protect endothelial cells, wishing you good health! / France: Free health human rights reporter: Han Rongli
A Curious Matter of Timing: How Annual COVID mRNA May Enable Constant Endothelial Inflammation/Microclotting (SPED) As soon as the Spike Protein factories that mRNA induces begin to shut down, they are given a “booster” to keep production going. WALTER M CHESNUT JUL 21
Representative confocal microscopy images for qualitative analysis of co-localization of fluorescein labeled fibrin(ogen) and Cy5 labeled Spike amyloid. Top panels illustrate samples where fibrinogen has been co-incubated with Spike amyloid prior to plasmin degradation. Lower panel illustrate the degree of co-localization between Spike amyloid fibrils and thrombin induced fibrin.
It has been almost five years since I predicted that the Spike Protein of SARS-CoV-2 would induce what I eventually called SPED (Spike Protein Endothelial Disease). In December of last year, this was described almost precisely as I envisioned in a research article.
In this study, we investigated the scope of the vascular inflammatory effect of SARS-CoV-2 spike protein on phenotypic, functional, and transcriptional levels in both lung microvascular and aortic ECs. To provide a more comprehensive insight into the profile of vascular inflammation, we included a comparison with the inflammatory cytokine TNF-α, which is known to induce prolonged activation of ECs [47, 48]. Consistent with previous findings, our study revealed that SARS-CoV-2 spike protein triggered prolonged cell adhesion marker expression and cytokine/chemokine releases, along with increased immune cell binding and formation of a procoagulant state of the ECs [20, 22, 46, 49,50,51]. We observed a similar degree of vascular inflammation by SARS-CoV-2 spike protein to that with TNF-α. However, distinct gene activation profiles were found for the viral spike protein. We also showed that on the transcriptome level, SARS-CoV-2 spike resulted in sustained inflammation, changes in antigen presentation, and coagulation state of the endothelium. The observed prolonged effects beyond the presence of the spike protein suggests possible long-term consequences of SARS-CoV-2 on the endothelium.
I also predicted that this would result in damage to the microvasculature via microclotting, which would in turn damage organs and tissues. This was shown to be the case in a paper published July 1st.
An association between the amyloidogenic Spike protein of SARS-CoV-2 and impaired fibrinolysis has previously been made when it was observed that fibrin clots formed in the presence of a mixture of amyloid fibrils from the spike protein displayed a resistance to plasmin-mediated lysis. Here we investigated the molecular processes of impaired fibrinolysis using seven amyloidogenic SARS-COV-2 Spike peptides. Five out of seven Spike amyloid fibrils appeared not to substantially interfere with the fibrinogen-fibrin-fibrinolysis process in vitro, while two spike fibrils were active in different ways. Spike601 amyloid fibrils (sequence 601-620) impaired thrombin mediated fibrin formation by binding and sequestering fibrinogen but did not affect fibrinolysis. On contrary fibrin clots formed in the presence of Spike685 amyloid fibrils (sequence 685-701) exhibited a marked resistance to plasmin mediated fibrinolysis. We conclude that Spike685 amyloid fibrils can induce dense fibrin clot networks, as well as incorporate fibrin into aggregated structures that resist fibrinolysis. These results demonstrate how the Spike protein of SARS-CoV-2 could contribute to the formation fibrinolysis-resistant microclots observed in long COVID.
So, we know for certain now that the Spike Protein damages the endothelium and then that damage denies oxygen and nutrients to organs and tissues which, in turn, damages them. Clearly, the presence of the Spike Protein in the body is something which should be avoided.
We were told that the COVID vaccine mRNA, which produces the Spike Protein, was only localized and would not spread beyond the site of injection. I knew – and I am certain you did, too – that this was pure and absolute hogwash. Indeed, within a few years researchers began discovering that the mRNA was everywhere – and doing immense damage, even lethal damage.
The distribution and duration of SARS-CoV-2 mRNA vaccine persistence in human tissues is unclear. Here, we developed specific RT-qPCR-based assays to detect each mRNA vaccine and screened lymph nodes, liver, spleen, and myocardium from recently vaccinated deceased patients. Vaccine was detected in the axillary lymph nodes in the majority of patients dying within 30 days of vaccination, but not in patients dying more than 30 days from vaccination. Vaccine was not detected in the mediastinal lymph nodes, spleen, or liver. Vaccine was detected in the myocardium in a subset of patients vaccinated within 30 days of death. Cardiac ventricles in which vaccine was detected had healing myocardial injury at the time of vaccination and had more myocardial macrophages than the cardiac ventricles in which vaccine was not detected. These results suggest that SARS-CoV-2 mRNA vaccines routinely persist up to 30 days from vaccination and can be detected in the heart.
Duration of SARS-CoV-2 mRNA vaccine persistence and factors associated with cardiac involvement in recently vaccinated patients https://pubmed.ncbi.nlm.nih.gov/37758751/
So, we then knew the mRNA could persist for up to 30 days. But was this the limit? We were told it would be disintegrated by the body within days, but thirty? Turns out, it can go on for longer. Far, far longer. On April 3rd of this year, we learned it can persist for as long as 17 MONTHS.
Spike protein expression was detected in 43.8 % of vaccinated patients, predominantly localized to the intima of cerebral arteries, even up to 17 months post-vaccination. While no active inflammatory changes were identified, infiltration of CD4-, CD8- and CD68- positive cells was observed in the spike protein positive vessels. In situ hybridization confirmed the presence of both vaccine-derived mRNA and SARS-CoV-2 virus-derived mRNA, which encode the spike protein, in select cases. Notably, spike protein positivity was observed exclusively in female patients (P = 0.015). None of the cases showed nucleocapsid protein positivity, supporting the absence of active viral infection.
Why is this important? Because both vaccine-derived mRNA and virus-derived mRNA were found in the cerebral arteries. If the mRNA is persisting for up to 17 months, then there is the potential for endothelial damage and inflammation to continue and never cease. How? Recurring infections and – boosters. It would seem to be madness to keep reintroducing a protein into the which causes such widespread damage and inflammation on a yearly basis. Espceially when it can persist for almost a year and a half. I don’t wish to cast aspersions, but, if you wanted to push the elderly (or any of us) towards a quicker end, recommending hyperaccelerated inflammaging and vascular damage every year would certainly do the trick.
The insanity must end.
I will continue to work towards understanding and healing. Thank you, as always, for your continued support, dialogue and readership. Please have a blessed week and be hopeful.
Reporter's review: The pictures show that Spike + fibrin + thrombin - plasmin protein. Strong reaction under the purple light. Basic knowledge: Health prosecutors carry purple light flashlights and illumination inspections, dirty food or utensils that cannot be seen in the eyes. …After the dark pandemic, questioning and refusing injections and protecting the body for cleaning is a wise move!
… The crown vaccine destroys endothelial cells, however! Vitamin D3 and various vitamins protect endothelial cells, wishing you good health!
/ France: Free health human rights reporter: Han Rongli
记者综述：图片显示，Spike +纤维蛋白 +凝血酶 - 质蛋白。在紫光的下的强烈反应。基本知识，卫生检察官随身携带紫光灯手电、照射检查，眼睛看不到的紫光反射的肮脏食品或器具。…黑暗疫情大流行后、质疑并拒绝注射、保护身体清洁是明智之举！…新冠疫苗破坏内皮细胞，然而！维生素D3、及各种维生素保护内皮细胞，祝你健康！/ 法国：自由健康人权记者：韩荣利
好奇的时机问题：年度COVID mRNA疫苗如何可能导致持续的内皮炎症/微血栓（SPED）
一旦由mRNA诱导产生的刺突蛋白“工厂”开始关闭，它们就会被“加强针”重新启动，以维持蛋白的持续生产。
沃尔特·M·切斯纳特
2025年7月21日
A Curious Matter of Timing: How Annual COVID mRNA May Enable Constant Endothelial Inflammation/Microclotting (SPED)
As soon as the Spike Protein factories that mRNA induces begin to shut down, they are given a “booster” to keep production going.
WALTER M CHESNUT
JUL 21
https://open.substack.com/pub/wmcresearch/p/a-curious-matter-of-timing-how-annual
READ IN APP
Representative confocal microscopy images for qualitative analysis of co-localization of fluorescein labeled fibrin(ogen) and Cy5 labeled Spike amyloid. Top panels illustrate samples where fibrinogen has been co-incubated with Spike amyloid prior to plasmin degradation. Lower panel illustrate the degree of co-localization between Spike amyloid fibrils and thrombin induced fibrin.
It has been almost five years since I predicted that the Spike Protein of SARS-CoV-2 would induce what I eventually called SPED (Spike Protein Endothelial Disease). In December of last year, this was described almost precisely as I envisioned in a research article.
In this study, we investigated the scope of the vascular inflammatory effect of SARS-CoV-2 spike protein on phenotypic, functional, and transcriptional levels in both lung microvascular and aortic ECs. To provide a more comprehensive insight into the profile of vascular inflammation, we included a comparison with the inflammatory cytokine TNF-α, which is known to induce prolonged activation of ECs [47, 48]. Consistent with previous findings, our study revealed that SARS-CoV-2 spike protein triggered prolonged cell adhesion marker expression and cytokine/chemokine releases, along with increased immune cell binding and formation of a procoagulant state of the ECs [20, 22, 46, 49,50,51]. We observed a similar degree of vascular inflammation by SARS-CoV-2 spike protein to that with TNF-α. However, distinct gene activation profiles were found for the viral spike protein. We also showed that on the transcriptome level, SARS-CoV-2 spike resulted in sustained inflammation, changes in antigen presentation, and coagulation state of the endothelium. The observed prolonged effects beyond the presence of the spike protein suggests possible long-term consequences of SARS-CoV-2 on the endothelium.
Sustained Vascular Inflammatory Effects of SARS-CoV-2 Spike Protein on Human Endothelial Cells
https://link.springer.com/article/10.1007/s10753-024-02208-x#Sec20
I also predicted that this would result in damage to the microvasculature via microclotting, which would in turn damage organs and tissues. This was shown to be the case in a paper published July 1st.
An association between the amyloidogenic Spike protein of SARS-CoV-2 and impaired fibrinolysis has previously been made when it was observed that fibrin clots formed in the presence of a mixture of amyloid fibrils from the spike protein displayed a resistance to plasmin-mediated lysis. Here we investigated the molecular processes of impaired fibrinolysis using seven amyloidogenic SARS-COV-2 Spike peptides. Five out of seven Spike amyloid fibrils appeared not to substantially interfere with the fibrinogen-fibrin-fibrinolysis process in vitro, while two spike fibrils were active in different ways. Spike601 amyloid fibrils (sequence 601-620) impaired thrombin mediated fibrin formation by binding and sequestering fibrinogen but did not affect fibrinolysis. On contrary fibrin clots formed in the presence of Spike685 amyloid fibrils (sequence 685-701) exhibited a marked resistance to plasmin mediated fibrinolysis. We conclude that Spike685 amyloid fibrils can induce dense fibrin clot networks, as well as incorporate fibrin into aggregated structures that resist fibrinolysis. These results demonstrate how the Spike protein of SARS-CoV-2 could contribute to the formation fibrinolysis-resistant microclots observed in long COVID.
SARS-CoV-2 spike protein amyloid fibrils impair fibrin formation and fibrinolysis
https://www.biorxiv.org/content/10.1101/2025.06.30.661938v1.full
So, we know for certain now that the Spike Protein damages the endothelium and then that damage denies oxygen and nutrients to organs and tissues which, in turn, damages them. Clearly, the presence of the Spike Protein in the body is something which should be avoided.
We were told that the COVID vaccine mRNA, which produces the Spike Protein, was only localized and would not spread beyond the site of injection. I knew – and I am certain you did, too – that this was pure and absolute hogwash. Indeed, within a few years researchers began discovering that the mRNA was everywhere – and doing immense damage, even lethal damage.
The distribution and duration of SARS-CoV-2 mRNA vaccine persistence in human tissues is unclear. Here, we developed specific RT-qPCR-based assays to detect each mRNA vaccine and screened lymph nodes, liver, spleen, and myocardium from recently vaccinated deceased patients. Vaccine was detected in the axillary lymph nodes in the majority of patients dying within 30 days of vaccination, but not in patients dying more than 30 days from vaccination. Vaccine was not detected in the mediastinal lymph nodes, spleen, or liver. Vaccine was detected in the myocardium in a subset of patients vaccinated within 30 days of death. Cardiac ventricles in which vaccine was detected had healing myocardial injury at the time of vaccination and had more myocardial macrophages than the cardiac ventricles in which vaccine was not detected. These results suggest that SARS-CoV-2 mRNA vaccines routinely persist up to 30 days from vaccination and can be detected in the heart.
Duration of SARS-CoV-2 mRNA vaccine persistence and factors associated with cardiac involvement in recently vaccinated patients
https://pubmed.ncbi.nlm.nih.gov/37758751/
So, we then knew the mRNA could persist for up to 30 days. But was this the limit? We were told it would be disintegrated by the body within days, but thirty? Turns out, it can go on for longer. Far, far longer. On April 3rd of this year, we learned it can persist for as long as 17 MONTHS.
Spike protein expression was detected in 43.8 % of vaccinated patients, predominantly localized to the intima of cerebral arteries, even up to 17 months post-vaccination. While no active inflammatory changes were identified, infiltration of CD4-, CD8- and CD68- positive cells was observed in the spike protein positive vessels. In situ hybridization confirmed the presence of both vaccine-derived mRNA and SARS-CoV-2 virus-derived mRNA, which encode the spike protein, in select cases. Notably, spike protein positivity was observed exclusively in female patients (P = 0.015). None of the cases showed nucleocapsid protein positivity, supporting the absence of active viral infection.
Expression of SARS-CoV-2 spike protein in cerebral Arteries: Implications for hemorrhagic stroke Post-mRNA vaccination
https://pubmed.ncbi.nlm.nih.gov/40184822/
Why is this important? Because both vaccine-derived mRNA and virus-derived mRNA were found in the cerebral arteries. If the mRNA is persisting for up to 17 months, then there is the potential for endothelial damage and inflammation to continue and never cease. How? Recurring infections and – boosters. It would seem to be madness to keep reintroducing a protein into the which causes such widespread damage and inflammation on a yearly basis. Espceially when it can persist for almost a year and a half. I don’t wish to cast aspersions, but, if you wanted to push the elderly (or any of us) towards a quicker end, recommending hyperaccelerated inflammaging and vascular damage every year would certainly do the trick.
The insanity must end.
I will continue to work towards understanding and healing. Thank you, as always, for your continued support, dialogue and readership. Please have a blessed week and be hopeful.
一旦MRNA诱导开始关闭的尖峰蛋白质工厂，每年Covid mRNA可以使年度CoVID mRNA能够实现恒定内皮炎症/微卷曲（加速），以便保持生产的“助推器”。 沃尔特M Chesnut 7月21日在App代表性共聚焦显微镜图像中阅读，用于荧光素纤维蛋白（ELOGEN）和CY5标记钉淀粉样蛋白的荧光素的共定位定位的定期分析。 顶面板说明在纤溶酶降解之前用穗淀粉样蛋白共孵育纤维蛋白原的样品。 下面的面板说明了穗淀粉样蛋白原纤维和凝血酶诱导的纤维蛋白之间的共同定位程度。 已经近五年了，因为我预测SARS-COV-2的尖峰蛋白会诱导我最终被称为SPED（穗蛋白内皮疾病）。 去年12月，正如我在研究文章中所设想的那样，这是恰恰恰恰相下的。 在这项研究中，我们研究了SARS-COV-2穗蛋白对肺部微血管和主动脉ECS的表型，功能性和转录水平的血管炎症作用的范围。 为了提供更全面的洞察血管炎症的型材，我们包括与炎症细胞因子TNF-α的比较，已知诱导ECS的长时间激活[47,48]。 我们的研究一致，我们的研究表明，SARS-COV-2尖峰蛋白触发的延长细胞粘附标记表达和细胞因子/趋化因子释放，以及ECS的促凝聚状态的免疫细胞结合和形成增加[20 我们观察到SARS-COV-2穗蛋白与TNF-α相似程度的血管炎症。 然而，发现了病毒穗蛋白的不同基因活化谱。 我们还表明，在转录组水平上，SARS-COV-2飙升导致持续炎症，抗原呈递变化，内皮的凝固状态。 观察到的长期效应超出了穗蛋白的存在，表明SARS-COV-2在内皮上可能的长期后果。 SARS-COV-2穗蛋白对人内皮细胞的持续血管炎症作用HTTPS://link.springer.com/article/10.1007/S10753-024-02208-X#SEC20 这是7月1日公布的文件中的情况。 在观察到在来自尖刺蛋白的淀粉样蛋白原纤维的混合物存在下形成的抗纤溶酶的抗性的情况下，先前已经进行了SARS-COV-2的淀粉样蛋白刺激蛋白和纤维蛋白溶解的纤维蛋白溶解的纤维蛋白蛋白质之间的关联。 在这里，我们研究了使用七个淀粉样蛋白SARS-COV-2穗肽的纤维蛋白溶解的分子过程。 七个穗淀粉样蛋白原纤维中的五种似乎没有基本上干扰纤维蛋白原 - 纤维蛋白纤维蛋白溶解过程，而两种尖峰原纤维以不同的方式活性。 Spike601淀粉样蛋白原纤维（序列601-620）通过结合和螯合纤维蛋白原而介导凝血酶介导的纤维蛋白形成，但不影响纤维蛋白原。 相反，在尖峰685淀粉样蛋白原纤维（序列685-701）存在下形成的相反纤维蛋白凝块表现出对纤溶酶介导的纤维蛋白溶解的显着抗性。 我们得出结论，Spike685淀粉样蛋白原纤维可以诱导致密纤维蛋白凝块网络，以及将纤维蛋白掺入抗纤维蛋白溶解的聚集结构中。 这些结果表明了SARS-COV-2的尖峰蛋白是如何促进长COVID中观察到的形成纤维蛋白溶解的微生物。 SARS-COV-2穗蛋白淀粉样蛋白蛋白蛋白抗纤维蛋白形成和纤维蛋白溶解HTTPS://www.biorxiv.org/content/10.1101 / 201525.06.30.661938v1。 显然，身体中穗蛋白的存在是应该避免的东西。 我们被告知，生成尖峰蛋白的Covid疫苗mRNA只是局部化，不会超过注射部位。 我知道 - 我也是你做的 - 这是纯粹的，绝对的热水。 实际上，在几年内，研究人员开始发现mRNA无处不在 - 并且造成巨大的伤害，甚至致命损害。 人体组织中SARS-COV-2 mRNA疫苗持久性的分布和持续时间尚不清楚。 在这里，我们开发了特定的RT-QPCR基测定，以检测来自最近疫苗的已故患者的每个mRNA疫苗和筛查的淋巴结，肝，脾和心肌。 在大多数患者疫苗接种后的大多数患者中，在大多数患者中检测到疫苗，但在疫苗接种疫苗的患者中没有患者不超过30天。 在纵隔淋巴结，脾脏或肝脏中未检测到疫苗。 在死亡后30天内接种患者的患者的心肌中检测到疫苗。 在疫苗接种时检测到疫苗的心脏脑室在疫苗接种时愈合心肌损伤，并且具有比未检测到疫苗的心室的心肌巨噬细胞。 这些结果表明，SARS-COV-2 mRNA疫苗在疫苗接种中常常持续到30天，并且可以在心脏中检测到。 SARS-COV-2 mRNA疫苗持续存在的持续时间和与心脏受累相关的因素在最近疫苗的患者HTTPS://pubmed.ncbi.nlm.nih.gov/37758751 /我们 但这是限制吗？ 我们被告知它会在几天内崩解，但三十岁？ 事实证明，它可以更长的时间。 远远较长。 今年4月3日，我们了解到它可以坚持为17个月。 在43.8％的疫苗患者中检测到穗蛋白表达，主要是脑动脉内部的疫苗，甚至疫苗接种后最多17个月。 虽然未发现有源炎症变化，但在尖峰蛋白阳性血管中观察到CD4-，CD8和CD68阳性细胞的渗透。 原位杂交证实在选择病例中证实了编码刺蛋白的疫苗衍生的mRNA和SARS-COV-2病毒衍生的mRNA。 值得注意的是，在女性患者中仅观察到穗蛋白阳性（P = 0.015）。 没有一个病例显示核衣壳蛋白阳性，支持不存在活性病毒感染。 SARS-COV-2穗蛋白在脑动脉中的表达：出血性脑卒中后MRNA疫苗接种的影响HTTPS://pubmed.ncbi.nlm.nih.gov/40184822/11 因为在脑动脉中发现疫苗衍生的mRNA和病毒衍生的mRNA。 如果mRNA持续到最多17个月，那么内皮损伤和炎症的潜力将继续，永不停止。 怎么样？ 经常感染和 - 助推器。 似乎渴望将蛋白质重新引入蛋白质，每年都会导致如此广泛的损伤和炎症。 当它持续近一年半的时候。 我不希望投入aspersions，但是，如果你想把老人（或任何人在我们中的任何人推向更快的目的，每年都会推荐高燃烧的炎炎和血管伤害肯定会做诀窍。 疯狂必须结束。 我将继续努力了解和治愈。 衷心感谢您继续支持，对话和读者。 请有一个幸福的一周，充满希望。