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🔬🧂SPED (Spike Protein Endothelial Disease) is Real. The Finding that Spike Mimics TNFa May be a Clue to Rising Cancer Rates SPED（尖峰蛋白内皮疾病）是真实存在的。 Spike 模仿 TNFa 的发现可能是癌症发病率上升的线索

Published NYE, Gultom, et al., Show that SPED (Spike Protein Endothelial Disease) is Real. The Finding that Spike Mimics TNFa May be a Clue to Rising Cancer Rates
The Spike also increases ICAM-1 expression, another immunosuppressive, tumor promoting molecule.生物医学家破解mRNA新冠疫苗
WALTER M CHESNUT
JAN 6

纽约，Gultom，等，表明，Sped（穗蛋白内皮疾病）是真实的。 Spike Mimics TNFA的发现可能是癌症率上升的线索，尖峰也增加了ICAM-1表达，另一种免疫抑制肿瘤促进分子。 沃尔特M Chesnut

（Reporter's summary: Support the respected and respected Mr. WALTER M CHESNUT, who is the world's top genius biomedical scientist. He has cracked the mRNA COVID-19 vaccine with a heart of philanthropy. He has persevered and worked hard and published a large number of papers to help those injured by the vaccine. / France🇫🇷Freelance health reporter: Han Rongli记者综述：声援德高望重的WALTER M CHESNUT 先生是世界顶级天才生物医学家，秉持博爱之心破解mRNA新冠疫苗，持之以恒、兢兢业业，大量论文救助疫苗受伤者。/ 法国🇫🇷自由健康记者：韩荣利 ）

https://open.substack.com/pub/wmcresearch/p/published-nye-gultom-et-al-show-that

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SARS-CoV-2 spike protein-activated endothelial cells exhibit prolonged ICAM1 expression. Human pulmonary microvascular endothelial cells (HPMC) and human aortic endothelial cells (HAoEC) grown under flow conditions (10 dyne/cm2) and treated with 1 μg/ml SARS-CoV-2 spike protein, 1 ng/ml TNF-α, or remained untreated for 24 h. The cells were washed after the activation and further cultured for a total of 96 h post-activation. At the indicated time point, cells were fixed and stained for ICAM1 (green), E-Selectin (yellow), VE-Cadherin (white), and nuclei (blue) (a). Figures depict representative images. Quantification of the coverage of ICAM1 (b, c) as well as E-Selectin (d, e) at 24 h and 96 h post-treatment, respectively, were obtained from at least three biological replicates. Statistical analysis was done using one-way ANOVA with multiple comparisons.

A preprint I reviewed in October of last year was published in peer-reviewed form NYE. I revisited the article and read two very interesting findings about the Spike Protein and the Endothelium. As readers of this Substack know, I have long hypothesized that the Endothelium was the gateway through which the Spike protein would damage organs and induce myriad diseases, such as cancer and neurodegenerative diseases. Two findings I read about provide a solid explanation for rising cancer rates.

The first finding that caught my eye was how the Spike Protein mimics TNFa’s induction of cytokines and chemokines. In some cases, the Spike induced considerably higher levels.

To see the profile of the cytokine and chemokine releases by human ECs due to SARS-CoV-2 spike protein treatment, we measured the level of cytokines and chemokines in the perfusion media 24 h and 96 h after treatment using a Luminex-type assay. For HPMC (Fig. 2a) and HAoEC (Fig. 2b), we observed cytokine and chemokine changes due to treatment with SARS-CoV-2 spike protein or TNF-α at both time points. At 24 h, most cytokines and chemokines were upregulated to various degrees. For both HPMC and HAoEC, several cytokine and chemokine levels in SARS-CoV-2 spike-treated ECs were increased to a comparable level as with TNF-α (Figs. 2a, b). Some cell type- and treatment-specific changes were also observed. Notably, cytokines and chemokines associated with microbial infection, such as CXCL1 and CXCL2, and proinflammatory cytokine IL-6 were expressed at a considerably higher level with SARS-CoV-2 spike than with TNF-α at 24 h (Figs. 2a, b).

Sustained Vascular Inflammatory Effects of SARS-CoV-2 Spike Protein on Human Endothelial Cells

What piqued my interest in these elevated chemokine/cytokine levels is that the types of cancers we are seeing a rapid increase in are those associated with TNFa and its expression.

There has been a large amount of evidence linking pro-inflammatory cytokines to cancer and the association with poor prognosis (reviewed by Mantovani) [59]. TNFα is one of the major pro-inflammatory cytokines of the immune system and has been found in several human cancers, such as breast [60], gastric [61], pancreatic [62], ovarian [63,64], endometrial [65], prostate [45], bladder [66], colorectal [67], oral [68], and liver [69]. It has also been detected in leukemias and lymphomas. Even so, there has been disagreement in considering TNFα expression as a biomarker, since the cytokine is increased in numerous other pathologies as well.

Harnessing Tumor Necrosis Factor Alpha to Achieve Effective Cancer Immunotherapy

The second finding, also associated with tumor promotion, is that the Spike also increases the expression of ICAM1.

We saw that treatment of both HPMC and HAoEC with SARS-CoV-2 spike led to the expression of the cellular adhesion molecules ICAM1 and E-Selectin. We observed a significant induction of ICAM1 (p-value = 0.0001 for HMPC, < 0.0001 for HAoEC) and E-Selectin (p-value = 0.0069 for HPMC, 0.01 for HAoEC) expression at 24 h and post-activation with SARS-CoV-2 spike compared to untreated controls (Figs. 1a, b, and d). At 96 h post-treatment, we saw that a significant ICAM1 expression can still be detected on both HPMC and HAoEC (p-value = 0.03 and 0.0026, respectively, Figs. 1a, c). The expression of E-Selectin, however, was not detectable anymore at 96 h post-treatment (Figs. 1a, e). Treatment with TNF-α had a similar effect as SARS-CoV-2 spike on ICAM1 expression after 24 h (Fig. 1b) and E-Selectin expression after 24 h and 96 h (Figs. 1d, e).

Sustained Vascular Inflammatory Effects of SARS-CoV-2 Spike Protein on Human Endothelial Cells

This adhesion molecule is necessary to induce tumor promoting immunosuppression.

Infusion of purified exosomes derived from MC38 cells promoted the growth of tumors, while exosomes pre-treated with anti-ICAM-1 antibodies attenuated this effect (Figure S8G). The infiltration and activation of CD8+ T cells in tumor microenvironment were analyzed 22 days post-implantation of tumors. Immunohistochemistry (IHC) staining showed CD8+ TILs was decreased after the injection of exosomes pre-treated with the IgG isotype antibodies, but not the exosomes pre-treated anti-ICAM-1 antibodies (Figure S8H and S8I). Flow cytometry analysis also showed the decreased CD8+ TILs after the injection of exosomes pre-treated with IgG isotype; pre-treating exosomes anti-ICAM-1 antibodies showed less inhibitory effect (Figure S8J).

ICAM-1-mediated Adhesion is a Prerequisite for Exosome-induced T Cell Suppression

So, we now have a mechanism which can explain how the Spike Protein may be implicated in the dramatic rise of certain cancers. I will be researching if there are analogous mechanisms for other diseases which may be induced by the Spike Protein.

If there is a silver lining in all of this, it is that we have understood the Spike Protein induces SPED, and that the therapeutics we have been discovering are therefore more likely to be effective. Understanding the cause is the only way to find the cure. I will continue to forge the path towards full understanding of this virus and its proteins. We can leave no stone unturned.

Happy New Year to all! I hope your holidays were pleasant and filled with peace, joy, hope and love. We have much to discover, and many to help heal. 纽约，Gultom，等，表明，Sped（穗蛋白内皮疾病）是真实的。 Spike Mimics TNFA的发现可能是癌症率上升的线索，尖峰也增加了ICAM-1表达，另一种免疫抑制肿瘤促进分子。 沃尔特M Chesnut Jan 6在App SARS-COV-2穗蛋白激活内皮细胞中阅读延长ICAM1表达。 在流动条件下生长的人肺微血管内皮细胞（HPMC）和人主动脉内皮细胞（HAOEC）和用1μg/ mL SARS-COV-2穗蛋白处理，1ng / 在活化后洗涤细胞，并在活化后进一步培养96小时。 在指示的时间点，将细胞固定并染色ICAM1（绿色），E-SELETIN（黄色），Ve-Cadherin（白色）和核（蓝色）（A）。 图描绘了代表性的图像。 从至少三种生物学重复，分别在24小时和96小时中定量ICAM1（B，C）以及E-选择素（D，E）的覆盖率。 使用单向ANOVA进行统计分析，具有多种比较。 我在去年10月审查的预印文出版于同行评审表格纽约州。 我重新审视了这篇文章，并阅读了关于穗蛋白和内皮的两个非常有趣的结果。 随着这种读者的读者知道，我已经长期假设内皮是内皮，尖峰蛋白质会损伤器官，诱发癌症和神经退行性疾病的患者。 我读过的两个发现，为癌症率上升提供了坚实的解释。 第一个发现我注意的发现是穗蛋白质模拟TNFA的细胞因子和趋化因子的诱导方式。 在某些情况下，尖峰诱导得多水平。 为了通过SARS-COV-2尖峰蛋白处理，通过人ECS进行细胞因子和趋化因子释放的概况，我们使用LuminX型测定在治疗后测量灌注介质24h和96h中的细胞因子和趋化因子水平。 对于HPMC（图2A）和HAOEC（图2B），我们观察了由于在两个时间点的SARS-COV-2穗蛋白或TNF-α处理而导致的细胞因子和趋化因子变化。 在24小时，大多数细胞因子和趋化因子被上调到各种程度。 对于HPMC和HAOEC，SARS-COV-2穗状体处理的几种细胞因子和趋化因子水平随着TNF-α的比较水平而增加（图2A，B）。 还观察到一些细胞类型和治疗的变化。 值得注意的是，与微生物感染的细胞因子和趋化因子，例如cxcl1和cxcl2，以及促炎细胞因子IL-6的用SARS-COV-2峰值比TNF-in表达得多。 SARS-COV-2穗蛋白对人内皮细胞HTTPS://link.springer.com/Article/10.1007/S10753-024-02208- X的持续血管炎症作用 已经有大量证据将促炎细胞因子联系在癌症和与预后差的关联（Mantovani审查）[59]。 TNFα是免疫系统的主要炎症细胞因子之一，已在几种人类癌症中发现，例如乳腺[60]，胃[61]，胰腺[62]，卵巢[63,64]，子宫内膜[ 它也已在白血病和淋巴瘤中检测到。 即便如此，考虑到TNFα表达作为生物标志物，由于细胞因子也增加了许多其他病理学。 利用肿瘤坏死因子α实现有效的癌症免疫疗法，也与肿瘤促进有关，是 我们看到HPMC和HAOEC的治疗与SARS-COV-2峰值导致了蜂窝粘附分子ICAM1和E-SELIENIN的表达。 我们观察到ICAM1的显着诱导（P值= 0.0001的HMPC，<0.0001的HMOEC）和E-SELECTIN（对于HPMC的P值= 0.0069，0.01的HPMC，0.01的HAOEC）表达，并与S后激活 在治疗后96小时，我们看到，仍然可以在HPMC和HAOEC（P值= 0.03和0.0026上，仍然可以检测到显着的ICAM1表达。1A，C）。 然而，E-SELETIN的表达在治疗后96小时内不再可检测到（图1A，e）。 用TNF-α治疗在24小时后ICAM1表达上的SARS-COV-2尖峰与SARS-COV-2刺有类似的效果（图1B）和96小时后E-SELECTIN表达（图1D，e）。 SARS-COV-2穗蛋白对人内皮细胞的持续血管炎症作用，衍生自MC38细胞衍生的纯化外来的输注促进了肿瘤的生长，而用抗ICAM-1抗体预处理的外索体抑制了这种效果（图S8G）。 分析肿瘤微环境中CD8 + T细胞的渗透和活化22天植入肿瘤后22天。 用IgG同种型抗体预处理的外来体液注射外来的免疫组织化学（IHC）染色表现出CD8 + TILs，但未治疗预处理的抗ICAM-1抗体（图S8 流式细胞术分析还显示出在用IgG同种型预处理的外泌体后降低的CD8 +直至; 预治疗外来抗-ICAM-1抗体显示出较少的抑制作用（图S8J）。 ICAM-1介导的粘附是外泌体诱导的T细胞抑制HTTPS://pmc.ncbi.nlm.nih.gov/articles/pmc8881799/的先决条件，我们现在有一个机制 我将研究是否存在类似于穗蛋白诱导的其他疾病的机制。 如果所有这一切都有一线希望，我们已经理解了穗蛋白诱导加速，因此我们发现的治疗方法更可能是有效的。 了解原因是找到治疗的唯一方法。 我将继续为全面了解这种病毒及其蛋白质的途径。 我们可以留下没有石头。 祝大家新年快乐！ 我希望你的假期愉快，充满和平，快乐，希望和爱。 我们有很多东西可以发现，很多人都可以帮助治愈。