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The Spike Protein, AT1 Receptors and Male Infertility Spike Protein exposure has demonstrably resulted in increased AT1R antibodies in those suffering from Post
2025 Apr 7, 7:23am 43 views 1 comment
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HANrongli
2025 Apr 7, 9:25am
Taking vitamin D + zinc, vitamin C, the virus will be blocked from spreading or even extinguishing
https://open.substack.com/pub/rwmalonemd/p/honey-why-do-viral-outbreaks-happen?selection=41dca94a-96db-41c7-b554-1db2185182d9
服用维生素D +锌，高剂量的维生素C，病毒会被阻止传播甚至扑灭
Did you ever wonder why outbreaks of viral diseases seem to happen in occasional (geographically based) waves of infection? And why do these viral waves tend to periodically circle the world?
How about why an outbreak will start, grow, taper off, and then re-emerge a few years later? Whether or not “public health” intervenes?
A natural process has been going on for as long as viruses have been interacting with humans and other animals with immune systems that can adapt to fight different viruses. When some public health organization (or clueless MSM outlet) claims that an outbreak has been “controlled” by actions they have taken, the informed response is to question how much of this “control” was due to natural processes and how much of the “control” can be attributed to the intervention. Sometimes, the natural processes in play can even “mask” or hide harm from a “public health” intervention or policy. This is particularly true for many examples of common viral infectious diseases of childhood.
Most people who are not obsessed with the viral infectious disease just notice local outbreaks. Perhaps when corporate media decides to launch another fear porn campaign for some reason, they might become aware of a regional outbreak within their country- such as the current “outbreak” of measles infection and disease occurring in Texas. They don’t notice that these outbreaks tend to periodically circle or spread across the world, strangely vanish for a few years, and then return.
Some background:
While the devil is in the details, and there is some seriously complicated mathematical modeling required to understand the nuances of outbreak timing (kinetics) and viral evolution during a spreading outbreak (cladistics) in specific situations, the general answer is mostly settled and can be understood without going too deep. But first, so that I can help bridge the gulf between academia and common knowledge, we need to define a very simple equation commonly used to describe how rapidly a virus will spread within a population - before it is even introduced. That equation defines the baseline infectivity of a virus in a specific population - the baseline coefficient of reproduction (R0).
If you were paying attention during COVID, you may have heard of this “coefficient of reproduction” - conveniently called R0 (R naught). R0 is so named because it describes, in an average way, how efficiently a virus will infect, reproduce and spread if nothing is done to slow it down. In a sense, this is a purely ‘academic” concept, but you have to start somewhere. In most cases, when an outbreak gets started, people at risk change their behavior, and some become infected right away and develop natural immunity (lets call this non-pharmaceutical interventions), and may start taking Vitamin D + Zinc, high dose Vitamin C, getting vaccinated (if available), etc. (lets call those things pharmaceutical interventions). These non-pharmaceutical and pharmaceutical interventions will make it harder for the virus to infect, reproduce and spread, and so will reduce R- let’s then call this a new “realistic” coefficient of reproduction R0’. At the start of an outbreak, R0 describes how many people (on average) will be infected by the first person(s) that have been infected. As soon as it starts infecting a population, people will get infected, recover, and develop natural immunity, and this process of acquiring “natural immunity” will start to slow the ability of the virus to spread- let’s call this moving target for the coefficient of reproduction Rn with n= the number of days (or weeks) after the virus enters the population and starts to spread. If either R0 (baseline) is greater than (>) 1 or Rn is >1, the virus will spread in the population.
If R0 or Rn with is or becomes less than (<) 1, viral spread will be slow and will quickly die out. In that case, each infected person will infect less than one other person, and the outbreak will be extinguished. Make sense? Simple stuff 您是否曾经想过为什么在偶尔（基于地理）感染的波浪中似乎发生病毒疾病的爆发？ 为什么这些病毒波倾向于定期绕世界圈？
为什么爆发会开始，成长，逐渐减少，然后几年后重新出现呢？ “公共卫生”是否干预？
只要病毒一直与人类和其他具有免疫系统的动物相互作用，可以适应不同的病毒。 当某些公共卫生组织（或无知的MSM出口）声称，他们采取的行动“控制”了爆发时，有明智的回应是质疑这种“控制”是多少是由于自然过程造成的，而“控制”的数量可以归因于干预措施。 有时，游戏中的自然过程甚至可以“掩盖”或从“公共卫生”干预或政策中隐藏伤害。 对于许多常见的儿童期病毒感染疾病的例子尤其如此。
大多数不着迷于病毒传染病的人只是注意到当地爆发。 也许当公司媒体出于某种原因决定发起另一场恐惧色情运动时，他们可能会意识到其国家内发生的区域爆发，例如目前在德克萨斯州发生麻疹感染和疾病的“爆发”。 他们没有注意到这些爆发往往会定期绕过或散布在世界各地，奇怪地消失了几年，然后返回。
一些背景：
虽然魔鬼在细节中，并且在特定情况下，在传播爆发（分子式）期间，需要一些严重复杂的数学建模，以了解爆发时间（动力学）和病毒演变的细微差别，但总体答案大多是解决的，并且可以理解，而无需太深。 但是首先，这样我就可以帮助弥合学术界和常识之间的海湾，我们需要定义一个非常简单的方程式，通常用于描述病毒在人群中的速度传播的速度 - 甚至在引入之前。 该方程定义了特定人群中病毒的基线感染性 - 基线繁殖系数（R0）。
如果您在Covid期间关注，您可能已经听说过这种“繁殖系数” - 方便地称为R0（R Nothing）。 R0之所以如此命名，是因为它平均描述了病毒将如何有效地感染，繁殖和扩散，如果什么都没有采取任何措施来减慢它。 从某种意义上说，这是一个纯粹的“学术”概念，但是您必须从某个地方开始。在大多数情况下，当爆发开始时，处于风险的人会改变其行为，有些人会立即感染并产生自然免疫力（让我们称这种非药物干预措施），并可能开始服用维生素D +锌，高剂量的维生素C，如果可以接触到这些东西（如果可以接种）（如果可以接种）等。 非药物和药物干预将使病毒更难感染，繁殖和传播，因此将其称为新的“现实”繁殖系数R0，在爆发开始时，R0平均将被恢复到首次感染的人。 发展自然的免疫力，并且获得“自然免疫力”的这种过程将开始减慢病毒传播的能力 - 让我们将这个移动的目标称为繁殖rn系数，而n =病毒进入人群后的天数（或几周），并开始扩散。 如果任何R0（基线）大于（>）1或RN> 1，则该病毒将在人群中扩散。
如果使用IS或rn变为或少于（<）1，则病毒传播会很慢，并且很快就会消失。 在这种情况下，每个受感染者的感染都比另一个人少，疫情将被扑灭。 有意义吗？ 简单的东西
https://open.substack.com/pub/rwmalonemd/p/honey-why-do-viral-outbreaks-happen?selection=41dca94a-96db-41c7-b554-1db2185182d9
服用维生素D +锌，高剂量的维生素C，病毒会被阻止传播甚至扑灭
Did you ever wonder why outbreaks of viral diseases seem to happen in occasional (geographically based) waves of infection? And why do these viral waves tend to periodically circle the world?
How about why an outbreak will start, grow, taper off, and then re-emerge a few years later? Whether or not “public health” intervenes?
A natural process has been going on for as long as viruses have been interacting with humans and other animals with immune systems that can adapt to fight different viruses. When some public health organization (or clueless MSM outlet) claims that an outbreak has been “controlled” by actions they have taken, the informed response is to question how much of this “control” was due to natural processes and how much of the “control” can be attributed to the intervention. Sometimes, the natural processes in play can even “mask” or hide harm from a “public health” intervention or policy. This is particularly true for many examples of common viral infectious diseases of childhood.
Most people who are not obsessed with the viral infectious disease just notice local outbreaks. Perhaps when corporate media decides to launch another fear porn campaign for some reason, they might become aware of a regional outbreak within their country- such as the current “outbreak” of measles infection and disease occurring in Texas. They don’t notice that these outbreaks tend to periodically circle or spread across the world, strangely vanish for a few years, and then return.
Some background:
While the devil is in the details, and there is some seriously complicated mathematical modeling required to understand the nuances of outbreak timing (kinetics) and viral evolution during a spreading outbreak (cladistics) in specific situations, the general answer is mostly settled and can be understood without going too deep. But first, so that I can help bridge the gulf between academia and common knowledge, we need to define a very simple equation commonly used to describe how rapidly a virus will spread within a population - before it is even introduced. That equation defines the baseline infectivity of a virus in a specific population - the baseline coefficient of reproduction (R0).
If you were paying attention during COVID, you may have heard of this “coefficient of reproduction” - conveniently called R0 (R naught). R0 is so named because it describes, in an average way, how efficiently a virus will infect, reproduce and spread if nothing is done to slow it down. In a sense, this is a purely ‘academic” concept, but you have to start somewhere. In most cases, when an outbreak gets started, people at risk change their behavior, and some become infected right away and develop natural immunity (lets call this non-pharmaceutical interventions), and may start taking Vitamin D + Zinc, high dose Vitamin C, getting vaccinated (if available), etc. (lets call those things pharmaceutical interventions). These non-pharmaceutical and pharmaceutical interventions will make it harder for the virus to infect, reproduce and spread, and so will reduce R- let’s then call this a new “realistic” coefficient of reproduction R0’. At the start of an outbreak, R0 describes how many people (on average) will be infected by the first person(s) that have been infected. As soon as it starts infecting a population, people will get infected, recover, and develop natural immunity, and this process of acquiring “natural immunity” will start to slow the ability of the virus to spread- let’s call this moving target for the coefficient of reproduction Rn with n= the number of days (or weeks) after the virus enters the population and starts to spread. If either R0 (baseline) is greater than (>) 1 or Rn is >1, the virus will spread in the population.
If R0 or Rn with is or becomes less than (<) 1, viral spread will be slow and will quickly die out. In that case, each infected person will infect less than one other person, and the outbreak will be extinguished. Make sense? Simple stuff 您是否曾经想过为什么在偶尔（基于地理）感染的波浪中似乎发生病毒疾病的爆发？ 为什么这些病毒波倾向于定期绕世界圈？
为什么爆发会开始，成长，逐渐减少，然后几年后重新出现呢？ “公共卫生”是否干预？
只要病毒一直与人类和其他具有免疫系统的动物相互作用，可以适应不同的病毒。 当某些公共卫生组织（或无知的MSM出口）声称，他们采取的行动“控制”了爆发时，有明智的回应是质疑这种“控制”是多少是由于自然过程造成的，而“控制”的数量可以归因于干预措施。 有时，游戏中的自然过程甚至可以“掩盖”或从“公共卫生”干预或政策中隐藏伤害。 对于许多常见的儿童期病毒感染疾病的例子尤其如此。
大多数不着迷于病毒传染病的人只是注意到当地爆发。 也许当公司媒体出于某种原因决定发起另一场恐惧色情运动时，他们可能会意识到其国家内发生的区域爆发，例如目前在德克萨斯州发生麻疹感染和疾病的“爆发”。 他们没有注意到这些爆发往往会定期绕过或散布在世界各地，奇怪地消失了几年，然后返回。
一些背景：
虽然魔鬼在细节中，并且在特定情况下，在传播爆发（分子式）期间，需要一些严重复杂的数学建模，以了解爆发时间（动力学）和病毒演变的细微差别，但总体答案大多是解决的，并且可以理解，而无需太深。 但是首先，这样我就可以帮助弥合学术界和常识之间的海湾，我们需要定义一个非常简单的方程式，通常用于描述病毒在人群中的速度传播的速度 - 甚至在引入之前。 该方程定义了特定人群中病毒的基线感染性 - 基线繁殖系数（R0）。
如果您在Covid期间关注，您可能已经听说过这种“繁殖系数” - 方便地称为R0（R Nothing）。 R0之所以如此命名，是因为它平均描述了病毒将如何有效地感染，繁殖和扩散，如果什么都没有采取任何措施来减慢它。 从某种意义上说，这是一个纯粹的“学术”概念，但是您必须从某个地方开始。在大多数情况下，当爆发开始时，处于风险的人会改变其行为，有些人会立即感染并产生自然免疫力（让我们称这种非药物干预措施），并可能开始服用维生素D +锌，高剂量的维生素C，如果可以接触到这些东西（如果可以接种）（如果可以接种）等。 非药物和药物干预将使病毒更难感染，繁殖和传播，因此将其称为新的“现实”繁殖系数R0，在爆发开始时，R0平均将被恢复到首次感染的人。 发展自然的免疫力，并且获得“自然免疫力”的这种过程将开始减慢病毒传播的能力 - 让我们将这个移动的目标称为繁殖rn系数，而n =病毒进入人群后的天数（或几周），并开始扩散。 如果任何R0（基线）大于（>）1或RN> 1，则该病毒将在人群中扩散。
如果使用IS或rn变为或少于（<）1，则病毒传播会很慢，并且很快就会消失。 在这种情况下，每个受感染者的感染都比另一个人少，疫情将被扑灭。 有意义吗？ 简单的东西
Spike Protein exposure has demonstrably resulted in increased AT1R antibodies in those suffering from Post-COVID Vaccination Syndrome.
WALTER M CHESNUT
APR 7
穗蛋白，AT1受体和雄性不孕症尖刺蛋白暴露在患有后伴侣后疫苗接种综合征的那些中产生了AT1R抗体。 沃尔特M Chesnut
https://open.substack.com/pub/wmcresearch/p/the-spike-protein-at1-receptors-and
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The changes of AT1 concentrations in the testes of normal C57BL/6 mice (A), RAB mice (B), and ± AT1KO mice (C) during the second (○) and fourth weeks (□). Error bar indicates the mean ± SD and significances are indicated as ∗ p < 0.01
One of the most challenging aspects of researching SARS-CoV-2 and its Spike Protein is that so many findings contain conflicting results. In today’s discussion, we look at the sera of post-COVID vaccination controls and those who suffer from post-COVID vaccination syndrome. In the cohort of those suffering from post-COVID vaccination syndrome, we find an increased presence of AT1R antibodies, yet those vaccinated without developing the syndrome have decreased levels.
A subset of eight of the analyzed receptor antibodies differed significantly (p < 0.0001) between post-vaccination sera (6 months after the last vaccination) in the control cohort and post-vaccination sera (>5 months after the last vaccination) of PACVS-afflicted persons. Six of these antibodies (AT1R, ETAR, M2R, M3R, β2-adr-R, MASR) were significantly (p < 0.0001) higher in PACVS subjects than in post-vaccination controls. Coincidentally, these six receptor antibodies exhibited vaccination-associated decreases in controls,
Chronic Fatigue and Dysautonomia following COVID-19 Vaccination Is Distinguished from Normal Vaccination Response by Altered Blood Markers
https://www.mdpi.com/2076-393X/11/11/1642
What the article does not discuss about these antibodies is what we will now discuss. The angiotensin II type 1 receptor mentioned above (AT1R) is a very important receptor. It is a key player in cardiovascular signaling pathways.
The importance of the renin angiotensin aldosterone system in cardiovascular physiology and pathophysiology has been well described whereas the detailed molecular mechanisms remain elusive. The angiotensin II type 1 receptor (AT1 receptor) is one of the key players in the renin angiotensin aldosterone system. The AT1 receptor promotes various intracellular signaling pathways resulting in hypertension, endothelial dysfunction, vascular remodeling and end organ damage. Accumulating evidence shows the complex picture of AT1 receptor-mediated signaling; AT1 receptor-mediated heterotrimeric G protein-dependent signaling, transactivation of growth factor receptors, NADPH oxidase and ROS signaling, G protein-independent signaling, including the β-arrestin signals and interaction with several AT1 receptor interacting proteins. In addition, there is functional cross-talk between the AT1 receptor signaling pathway and other signaling pathways. In this review, we will summarize an up to date overview of essential AT1 receptor signaling events and their functional significances in the cardiovascular system.
AT1 receptor signaling pathways in the cardiovascular system
https://pmc.ncbi.nlm.nih.gov/articles/PMC5607088/
I studied this receptor in the context of knockout. Knockout is when you eliminate the expression of a gene, and I found something very interesting yet disturbing. AT1R has other vital functions, particularly in the reproductive system. When you knockout AT1R in male mice testes, they become infertile. Antibodies binding to a receptor impair its functionality. It can be as if they were “knockedout” since they cannot carry out their normal tasks.
Knocking out AT1R had a dramatic effect on the ability of male mice to reproduce. No females that spent time with the KO males became pregnant, and the sperm was malformed.
The pregnancy rate of female mice was determined in one week of cage closure with male mice in Control and ± AT1KO groups. None of the female mice mated with ± AT1KO male mice became pregnant. Moreover, the pregnancy rate in 2-week normal mice was 50%, and the pregnancy rate in 4-week normal mice was 55% (Table 5). The plasma testosterone levels were detected in these mice but no significant difference was found (data not shown).
The total deformity rate was 59% in ± AT1KO mice, significantly (P < 0.01) higher than those in normal mice (19%) and in ARB mice (25%). Enlarged (fat) head appeared to be the mostly increased deformity in spermatozoa from ± AT1KO mice (201/642, compared to 26/990 in control group and 23/708 in ARB group). Spermatozoa with no hook and folded tails were also significantly increased.
Decreased angiotensin receptor 1 expression in ± AT1 Knockout mice testis results in male infertility and GnRH reduction
https://rbej.biomedcentral.com/articles/10.1186/s12958-021-00805-1
Why is this important? Because we know the Spike Protein mRNA is found in the testes.
Biodistribution of lipid-nanoparticle in rat, Pfizer study November 2020. From TGA FOI reply 2389-6 [5] (p. 45).
‘Spikeopathy’ Part 1: COVID-19 Spike Protein Is Pathogenic, from Both Virus and Vaccine mRNA
https://www.researchgate.net/publication/373210100_'Spikeopathy'_Part_1_COVID-19_Spike_Protein_Is_Pathogenic_from_Both_Virus_and_Vaccine_mRNA
And now we have evidence for something which the NIH has, so far, vehemently denied.
Based on the studies published so far, there is no scientific proof of any association between COVID-19 vaccines and fertility impairment in men or women.
The impact of COVID-19 vaccines on fertility-A systematic review and meta-analysis
https://pmc.ncbi.nlm.nih.gov/articles/PMC9464596/
We now have a mechanism by which Spike Protein mRNA vaccines may indeed cause male infertility. Males suffering from post-COVID Vaccination Syndrome should have fertility tests. We need to determine if this is occurring in humans.
Still, the questions remain. Why does this only happen in some? And, if we are repeatedly exposed to the Spike Protein, will it eventually happen in all?
Thank you, as always, for your dialogue, readership and support.
穗蛋白，AT1受体和雄性不孕症尖刺蛋白暴露在患有后伴侣后疫苗接种综合征的那些中产生了AT1R抗体。 沃尔特M Chesnut APR 7在APP中阅读AT1浓度在第二个（○）和第四周期间的正常C57BL / 6小鼠（A），RAB小鼠（B），RAB小鼠（B）和±AT1KO小鼠（C）的验证中的变化 误差栏表示平均值±SD和意义，表示为* P <0.01研究SARS-COV-2最具挑战性的方面之一，其尖峰蛋白质是许多发现含有相互冲突的结果。 在今天的讨论中，我们看看后Covid疫苗接种控制的血清和患有Covid疫苗接种综合征的人。 在患有后Covid疫苗接种综合征的人的队列中，我们发现AT1R抗体的存在增加，然而在不发育综合征的情况下接种疫苗的那些疫苗的水平降低。 分析的受体抗体中的八个子集（P <0.0001）在对照队列和疫苗接种后的疫苗接种赛（最后一次疫苗接种后6个月）之间有显着（P <0.0001），PAC的疫苗接种后血清（> 5个月） 这些抗体中的六种（AT1R，ETAR，M2R，M3R，β2-ADR-R，MASR）显着（P <0.0001）在PACVS受试者中高于接种后对照。 巧合，这六种受体抗体在Covid -19疫苗接种后的对照，慢性疲劳和脱血神经组阴量表现出接种相关的降低，从而通过改变血迹HTTPS://www.md来区分正常疫苗接种响应 上述血管紧张素II型受体（AT1R）是一个非常重要的受体。 它是心血管信号传导途径的关键球员。 肾素血管紧张素醛固酮系统在心血管生理学和病理生理学中的重要性得到了很好的描述，而详细的分子机制仍然难以捉摸。 血管紧张素II型1受体（AT1受体）是肾素血管紧张素醛固酮体系中的关键球员之一。 AT1受体促进各种细胞内信号传导途径，导致高血压，内皮功能障碍，血管重塑和终端器官损伤。 累积证据显示AT1受体介导的信号传导的复杂图片; AT1受体介导的异映型G蛋白依赖性信号传导，生长因子受体的转移剂，NADPH氧化酶和ROS信号传导，G蛋白无关的信号传导，包括β-incketIn信号和与几个AT1受体的相互作用相互作用。 另外，AT1受体信号传导路径和其他信令途径之间存在功能串扰。 在本文中，我们将总结最新概述基本AT1受体信号传导事件及其心血管系统中的功能意义。 AT1受体信号传导途径在心血管系统中HTTPS://pmc.ncbi.nlm.nih.gov/artlicle/pmc5607088/我在淘汰赛的背景下研究了这个受体。 敲除是消除基因表达的时候，我发现了一些非常有趣但令人不安的东西。 AT1R具有其他重要功能，特别是在生殖系统中。 当你在雄性小鼠睾丸中敲门时，它们变得不孕。 与受体结合的抗体损害其功能。 它可以就像他们“淘汰赛”一样，因为他们无法进行正常的任务。 敲门率对雄性小鼠繁殖的能力具有显着影响。 没有女性与KO男性共度时期怀孕，精子畸形。 雌性小鼠的妊娠率在一周的笼闭合中测定，用雄性小鼠和±AT1KO组。 没有雌性小鼠与±AT1KO雄性小鼠怀孕。 此外，2周正常小鼠的妊娠率为50％，4周正常小鼠的妊娠率为55％（表5）。 在这些小鼠中检测到血浆睾酮水平，但没有发现显着差异（未显示数据）。 总畸形率为59％±AT1KO小鼠，显着（P <0.01）高于正常小鼠（19％）和Arb鼠标（25％）。 扩大（脂肪）头似乎是从±AT1KO小鼠（201/642）的精子畸形的畸形，而ARB组中的对照组26/790和Abb组中的23/708）。 没有钩子和折叠尾巴的精子也显着增加。 减少血管紧张素受体1表达±AT1敲除小鼠睾丸导致男性不孕症和GNRH减少HTTPS://RBEJ.BIOMedCentral.com/articles/10.1186/S12958-021-00 因为我们知道在睾丸中发现尖刺蛋白mRNA。 在大鼠脂质纳米粒子的生物分布，辉瑞研究11月20日期。从TGA FOI回复2389-6 [5]（第45页）。 'spikeopathy'第1部分：covid-19穗蛋白是致病性的，来自病毒和疫苗mRNA https://www.researchgate.net/publication/373210100'spikeopathy'_part 基于迄今为止发布的研究，在男性或女性的Covid-19疫苗和生育障碍之间没有科学证明。 Covid-19疫苗对生育率的影响 - 系统审查和荟萃分析https://pmc.ncbi.nlm.nih.gov/articles/pmc9464596/我们现在拥有sp的机制 患有Covid疫苗接种综合征的患者应具有生育率测试。 我们需要确定是否发生在人类中。 仍然存在问题。 为什么这只发生在某些情况下？ 而且，如果我们反复接触到尖刺蛋白，它最终会发生在所有情况下？ 衷心感谢您的对话，读者和支持。