“The people have no voice because they have no information.” — Gore Vidal
A failure of energy metabolism limits the ability of cells to return from an excited active state to a stable resting state. Unresolved excitation causes cells to emit signals indicating the need for repair, inflammatory signals. Pre-existing inflammation is associated with high altitude sickness and the ability to get sick from a corona virus, as well as chronic diseases. This implies that treatment for a so-called “coronavirus infection” should be to reduce cellular excitation and inflammation and normalize energy production. It also implies that these treatments will have favorable effects on cell aging.
The conditions that produce inflammation activate the adaptive exosome system, a retrotransposon system involving a massive block of our DNA, which overlaps with the virus production mechanism. Current approaches to preventing viral disease dangerously ignore this fundamental physiological-genetic system. An important implication of this system’s involvement in health and disease is that we are not defined “somas” produced once by our DNA, but rather adaptive, epigenetic, ongoing creative beings.* 能量代谢的失败限制了细胞从兴奋的活跃状态恢复到稳定的静止状态的能力。未解决的兴奋导致细胞发出信号，表明需要修复，炎症信号。预先存在的炎症与高原病、冠状病毒以及慢性病相关。这意味着所谓的“冠状病毒感染”的治疗应该是减少细胞兴奋和炎症，并使能量产生正常化。这也意味着这些治疗将对细胞衰老产生有利影响。 产生炎症的条件激活了适应性外体系统，这是一个涉及大量DNA片段的逆转录转座子系统，与病毒产生机制重叠。目前预防病毒性疾病的方法危险地忽视了这一基本的生理遗传系统。该系统参与健康和疾病的一个重要含义是，我们不是由DNA产生的“躯体”，而是适应性的、表观遗传的、持续不断的创造性生物。 —- U.S. history has repeatedly hinged on words that didn’t correspond to facts, for example the bombing of Vietnam based on the fictional Tonkin Gulf incident, or the invasion of Iraq based on the yellowcake uranium and other fictional weapons of mass destruction. To explain the present destruction of the normal US economy it would be reasonable to look for some clear image to indicate that China’s new variant corona virus was more dangerous than preceding strains of the virus, but there has been no public information about how to distinguish infections with this new virus from other acute lung problems. According to official medical views, no specific treatment or test was known when the WHO declared the pandemic, so the FDA has bypassed its normal regulations for both tests and drugs. A test, to be useful in diagnosis, determining the exact cause of symptoms, would have to show whether any of the common respiratory disease organisms was present, and naturally, any test has to be tested itself. The CDC has observed that half of the positives on an antibody test, in a population with low prevalence, could be false. A muddle of tests has created confusion even among experts; on May 21, the CDC acknowledged that it was mixing together their counts of antibody tests and PCR virus tests. 美国的历史一再依赖于与事实不符的词语，例如根据虚构的东京湾事件轰炸越南，或根据黄饼铀和其他虚构的大规模杀伤性武器入侵伊拉克。为了解释目前美国正常经济所遭受的破坏，我们有理由寻找一些清晰的图像来表明D614G突变变种冠状病毒比之前的病毒株更危险，但目前还没有关于如何区分这种新病毒感染与其他急性肺部问题的公开信息。根据官方医学观点，世卫组织宣布大流行时，还不知道具体的治疗或检测方法，因此FDA绕过了检测和药物的常规规定。为了有助于诊断，确定症状的确切原因，测试必须显示是否存在任何常见的呼吸道疾病生物体，当然，任何测试都必须进行自身测试。CDC观察到，在低发病率人群中，抗体检测的一半阳性结果可能是假的。混乱的测试甚至在专家中也造成了混乱；5月21日，疾病预防控制中心承认，他们将抗体检测和PCR病毒检测的计数混合在一起。 In March and April, several Stanford professors were arguing that the lethality of the new virus was very similar to that of the familiar influenzas, about 0.25% of those infected. The latest figures from the CDC, published inconspicuously on May 22, were similar, assuming that 35% of infected people could be symptom free; if a higher percentage of infections are symptom free, then the infection-death rate is even lower. 在3月和4月，几位斯坦福大学教授争论说，新病毒的杀伤力与熟悉的流感病毒非常相似，约占感染者的0.25%。CDC在5月22日不显眼地公布的最新数据也很相似，假设35%的感染者没有症状；如果没有症状的感染比例更高，那么感染死亡率甚至更低。 With no public explanation of the pathophysiology of the “new disease,” the vacuum was filled by rumors that it was a virus escaped from germ warfare labs, alternately said to be from Wuhan or Fort Detrick, and several broadly circulated articles denied that such a virus was even possible to engineer, conflicting with articles in major journals in recent years describing exactly that engineering (de Haan, et al., 2008; Graham and Baric, 2010). In the absence of empirical information about the nature of the disease, but with the rumors creating fear of a uniquely horrible disease, hospitals have been instructing doctors to treat patients with breathing problems in very aggressive and invasive, and standardized, ways. 在没有公开解释“新疾病”病理生理学的情况下，真空被一种病毒从细菌战实验室逃逸的传闻所填补，或者说是从武汉或德特里克堡逃逸的，并且一些广为传播的文章否认这种病毒甚至可以制造，与近年来主要期刊上描述该工程的文章相冲突（de Haan等人，2008；格雷厄姆和巴里克，2010年）。在缺乏关于疾病性质的经验信息的情况下，但随着谣言制造了对一种独特可怕疾病的恐惧，医院一直在指示医生以非常激进、侵入性和标准化的方式治疗呼吸问题患者。 A couple of doctors in the US said publicly that those treatments aren’t appropriate for the real disease. Cameron Kyle-Sidell has made two videos observing that his patients’ symptoms resemble those of people with high altitude pulmonary edema, a feature of which is very low carbon dioxide as well as low oxygen. Another doctor in New York, Isaac Solaimanzadeh, suggested using calcium channel blockers and acetazolamide to treat the new disease, because of their therapeutic effect in high altitude pulmonary edema. He didn’t mention it, but both of these drugs can correct the tissue deficiency of carbon dioxide. 美国的几位医生公开表示，这些治疗方法不适合真正的疾病。卡梅隆·凯尔·赛德尔（Cameron Kyle Sidell）制作了两个视频，观察到他的患者的症状类似于高原肺水肿患者的症状，其特征是二氧化碳和氧气都非常低。纽约的另一位医生Isaac Solaimanzadeh建议使用钙通道阻滞剂和乙酰唑胺治疗这种新疾病，因为它们对高原肺水肿有治疗作用。他没有提到，但这两种药物都可以纠正组织中二氧化碳的缺乏。 In Germany, Luciano Gattinoni (Gattinoni, et al., 2020) pointed out that the standard ventilation protocol wasn’t conforming to the best knowledge of respiratory physiology. He observed that in one conventional hospital the mortality of respiratory patients was 60%, while in a nearby hospital following his more rational method, the mortality of respiratory patients was zero. 在德国，Luciano Gattinoni（Gattinoni等人，2020年）指出标准通气方案不符合呼吸生理学的最佳知识。他观察到，在一家传统医院，呼吸系统疾病患者的死亡率为60%，而在附近的一家医院，按照他更合理的方法，呼吸系统疾病患者的死亡率为零。 High altitude physiology is obviously confusing to the many doctors who have scoffed at the comparison of the new disease to high altitude pulmonary edema. This is because of the way physiology is taught. At low altitude, when a tissue’s oxygen consumption increases beyond the blood’s ability to deliver oxygen, as in an intensely working muscle, the tissue activates the glycolytic process, converting glucose to lactic acid as a source of additional energy. Carbon dioxide is seen as nothing but a waste disposal problem. This view has led to the concept of the “high altitude lactate paradox,” referring to the fact that maximal exertion at high altitude doesn’t increase lactic acid production in the normal way. Neglecting the role of carbon dioxide in suppressing the formation of lactic acid, they also neglect all of its other essential metabolic effects, including its role as the factor whose absence results in the syndromes of altitude sickness, and ventilatorinduced lung damage (Sinclair, et al., 2002; Cummins, et al., 2010; Contreras, et al., 2012). 高原生理学显然让许多医生感到困惑，他们嘲笑将这种新疾病与高原肺水肿进行比较。这是因为生理学的教学方式。在低海拔地区，当组织的耗氧量增加超过血液输送氧气的能力时，如在剧烈工作的肌肉中，组织会激活糖酵解过程，将葡萄糖转化为乳酸作为额外能量的来源。二氧化碳被视为废物处理问题。这一观点引出了“高原乳酸悖论”的概念，即在高原上最大限度的运动不会以正常方式增加乳酸的产生。他们忽略了二氧化碳在抑制乳酸形成中的作用，也忽略了其所有其他基本代谢效应，包括其作为导致高原反应综合征和通气性肺损伤的因素的作用（Sinclair，et al.，2002；康明斯等人，2010年；孔特雷拉斯等人，2012年）。 This CO2-negligent approach to physiology has affected medicine for 100 years. When Otto Warburg discovered that aerobic glycolysis is the defining feature of cancer, the presence of a little extra lactate in the blood, displacing CO2, didn’t appear to most doctors and biologists to be medically important, though a little extra carbon dioxide could arouse concern. Ignoring that 30 years of slightly elevated lactate might lead to cancer or other degenerative disease, those who taught physiological chemistry also had little interest in the idea of chronic metabolic hyperventilation—losing a little too much CO2 even at sea level. Cumulative injury of all sorts contribute to a background of inappropriate excitation and inflammation. 这种忽视二氧化碳的生理学方法已经影响了医学100年。当奥托·沃伯格发现有氧糖酵解是癌症的决定性特征时，血液中存在一点多余的乳酸，取代了二氧化碳，在大多数医生和生物学家看来，这在医学上并不重要，尽管一点多余的二氧化碳可能会引起关注。忽略了30年的乳酸略微升高可能会导致癌症或其他退化性疾病，那些教授生理化学的人也对慢性代谢性过度换气的想法兴趣不大，即使在海平面上也会损失过多的二氧化碳。各种累积性损伤都会导致不适当的兴奋和炎症。 In studies related to asthma, it has become well known that abnormally low CO2, hypocapnia, constricts the airways, and elevated CO2, hypercapnia, relaxes them (El Mays, et al., 2011; Choudhury, et al., 2012); various mechanisms, affecting intracellular calcium, are known to be involved. The causes of relative hyperventilation continue to be disputed. 在与哮喘相关的研究中，众所周知，异常低二氧化碳（低二氧化碳）会使气道收缩，而高二氧化碳（高二氧化碳）会使气道松弛（El Mays，et al.，2011；Choudhury等人，2012年）；已知涉及影响细胞内钙的各种机制。相对换气过度的原因仍有争议。 The basic principles of respiration, the Bohr and Haldane effects, describe the physical equilibria of oxygen and CO2 in people who have adapted to living at different altitudes. The Haldane effect describes the fact that increased oxygen pressure decreases the amount of carbon dioxide retained by hemoglobin, and decreased oxygen pressure increases the amount of CO2 retained. A steady increase of retained CO2 with increasing altitude occurs in those who adapt. People who fail to adapt experience a loss of CO2, with an increase of lactate. 呼吸的基本原理，波尔效应和霍尔丹效应，描述了适应不同海拔高度生活的人的氧和二氧化碳的物理平衡。霍尔丹效应描述了这样一个事实：增加氧气压力会减少血红蛋白保留的二氧化碳量，降低氧气压力会增加保留的二氧化碳量。随着海拔的升高，那些适应环境的人体内残留的二氧化碳会稳步增加。 不能适应的人会经历二氧化碳的减少，乳酸的增加。 It has become increasingly common to treat altitude sickness with carbon dioxide. A few people have argued for a long time that mechanical ventilation would be less harmful if a mixture of CO2 and O2 were used (Laffey and Kavanagh, 1999; Kregenow and Swenson, 2002), analogously to the therapeutic effect of CO2 in high altitude sickness (Harvey, et al., 1988). 用二氧化碳治疗高原反应已变得越来越普遍。一些人长期以来一直认为，如果使用二氧化碳和氧气的混合物，机械通风的危害会更小（Laffey和Kavanagh，1999；Kregenow和Swenson，2002），类似于二氧化碳对高原病的治疗作用（Harvey等人，1988年）。 In a state of chronic stress, oxidative energy production is low, and mediators of inflammation are likely to be chronically increased; there is typically a chronically increased production of lactate, and/or decreased oxidation of it. In this state, the increased ventilation caused by high altitude will cause an increased loss of carbon dioxide, increasing the pH of the blood, which increases the formation of lactic acid. The lactate increases the leakiness of capillaries and loss of fluid, and decreases the ability of oxygen to diffuse from the alveolus to the erythrocyte. Since carbon dioxide diffuses many times more rapidly than oxygen, this diffusion barrier results in low blood CO2 at the same time as hypoxia. Even at sea level, an increase of lactate immediately increases the lungs’ diffusion barrier. 在慢性应激状态下，氧化能产生量较低，炎症介质可能长期增加；通常，乳酸的产量会长期增加，和/或乳酸的氧化减少。在这种状态下，高海拔引起的通风增加将导致二氧化碳损失增加，增加血液的pH值，从而增加乳酸的形成。 乳酸会增加毛细血管的渗漏和液体的流失，并降低氧气从肺泡扩散到红细胞的能力。由于二氧化碳的扩散速度比氧气快很多倍，这种扩散屏障导致血液中二氧化碳含量低，同时缺氧。即使在海平面上，乳酸的增加也会立即增加肺部的扩散屏障。 Thinking of the infection as the disease, and therefore considering the “receptor,” “entry,” and replication of the virus to be sufficient to explain the damage to infected cells, tissues, and organs, and defining the disease as an inflammation of the respiratory tree and lung, the hospital system went into action. Failing to think of the intestine (which is infected as easily as the nose and lungs), the meaning of events throughout the organism, including the lungs, is misunderstood. The infection can serve as one of the factors increasing inflammation and stress, suppressing energy function, but the relevant disease to be treated is that unstable state of counter-productive, energy-depleting excitatory and inflammatory signals. 将感染视为疾病，因此认为病毒的“受体”、“进入”和复制足以解释对受感染细胞、组织和器官的损害，并将疾病定义为呼吸树和肺部的炎症，医院系统开始行动。如果不考虑肠道（肠道和鼻子和肺一样容易感染），那么整个有机体（包括肺）中事件的含义就会被误解。感染可作为增加炎症和压力、抑制能量功能的因素之一，但需要治疗的相关疾病是产生反作用、消耗能量的兴奋性和炎症信号的不稳定状态。 Healthy individuals aren’t harmed by the presence of the virus, so the nature of the defect that makes some people susceptible should be the focus of attention. Some important factors have already been identified: living at high altitude provides 3- or 4-fold protection (Arias-Reyes, et al., 2020), and being a young woman is even more protective. In Italy, 70% of the deaths are men, but deaths increase sharply among post-menopausal women. 健康的个体不会受到病毒的危害，因此使一些人易受感染的缺陷的性质应该是关注的焦点。已经确定了一些重要因素：生活在高海拔地区可以提供3到4倍的保护（Arias Reyes，et al.，2020），而年轻女性的保护作用更大。在意大利，70%的死亡是男性，但绝经后女性的死亡人数急剧增加。 The lungs are especially sensitive to activation of the so-called “calcium channels,” i.e., calcium uptake by cells, by hypoxia, causing constriction of blood vessels, but increased carbon dioxide, which increases during adaptation to altitude, reverses the hypertension caused by hypoxia (Baudouin and Evans, 1993; Chuang, et al., 2011). Calcium channel blockers, paralleling that effect of CO2, are effective treatments for high altitude pulmonary hypertension. Like acetazolamide, the other recognized treatment for altitude sickness, calcium channel blockers inhibit carbonic anhydrase, facilitating the body’s retention of CO2. To the medical scoffers who deny that CO2 has a constructive physiological role, the exaggerated pulmonary constriction at high altitude is the cause of the lung failure, while in the respiratory distress caused by Covid-19 that contriction is a consequence of the disease (Luks and Swenson, 2020), and neither is a result of a CO2 deficiency. 肺对所谓的“钙通道”的激活特别敏感，即细胞通过缺氧吸收钙，导致血管收缩，但在适应高原期间增加的二氧化碳增加，逆转了缺氧引起的高血压（Baudouin和Evans，1993；庄等人，2011年）。钙通道阻滞剂是治疗高原肺动脉高压的有效药物，与二氧化碳的作用类似。 与乙酰唑胺一样，钙通道阻滞剂也可以抑制碳酸酐酶，促进身体吸收二氧化碳。对于否认二氧化碳具有建设性生理作用的医学嘲笑者来说，高原上过度的肺收缩是肺衰竭的原因，而在新冠病毒-19引起的呼吸窘迫中，这种贡献是疾病的结果（Luks和Swenson，2020），两者都不是二氧化碳缺乏的结果。 The presence of lactate corresponds to some degree of reductive excess in cells, and the degree of reduction regulates the “calcium channels,” controlling the excitatory effects of intracellular calcium (Wang, et al., 1997; Iesaki and Wolin, 2000; Schach, et al., 2007). Reduction by stress and/or lactate “activates the channels,” tightening vascular smooth muscle, and activating a wide range of other cell activities, including inflammation, exosome secretion, and viral replication (Savina, et al., 2003; Chen, et al., 2019). Exosome production during stress is part of the body’s normal restorative function (Zhang, et al., 2017); it’s only when protective factors such as progesterone and carbon dioxide are lacking that their production becomes counter-productive. 乳酸的存在对应于细胞中某种程度的还原过量，还原程度调节“钙通道”，控制细胞内钙的兴奋效应（Wang等人，1997；Iesaki和Wolin，2000年；Schach等人，2007年）。应激和/或乳酸的减少“激活通道”，收紧血管平滑肌，并激活广泛的其他细胞活动，包括炎症、外泌体分泌和病毒复制（Savina等人，2003；陈等人，2019年）。应激期间产生的外小体是身体正常恢复功能的一部分（Zhang等人，2017年）；只有当孕酮和二氧化碳等保护性因素缺乏时，它们的产生才会适得其反。 Progesterone and its neuroactive metabolites including tetrahydroprogesterone or allopregnanolone, are very effective “calcium channel blockers” (Todorovic, et al., 2004; Pathirathna, et al., 2005; Hu, et al., 2007). A major function of progesterone is the inactivation of the estrogen receptor; estrogen and its “receptor” are powerful activators of cellular calcium uptake (Sarkar, et al., 2008). 孕酮及其神经活性代谢物，包括四氢孕酮或别孕烯酮，是非常有效的“钙通道阻滞剂”（Todorovic等人，2004年；Pathirathna等人，2005年；Hu等人，2007年）。孕酮的主要功能是使雌激素受体失活；雌激素及其“受体”是细胞钙摄取的强大激活剂（Sarkar等人，2008）。 Studies of progesterone’s effects on recovery of nerve function after traumatic brain damage have found that vitamin D increases its effectiveness. By improving calcium homeostasis, opposing the effects of the parathyroid hormone which activates calcium channels, vitamin D (25-hydroxycholecalciferol) is coming to be considered a neurosteroid (Groves, et al., 2014; Gezen-Ak and Dursun, 2019), as well as an essential factor in immunity (Pfeffer and Hawrylowicz, 2012). 关于孕酮对创伤性脑损伤后神经功能恢复的影响的研究发现，维生素D可提高其功效。通过改善钙稳态，对抗激活钙通道的甲状旁腺激素的作用，维生素D（25-羟基胆钙化醇）逐渐被视为神经甾体（Groves，et al.，2014；Gezen Ak和Dursun，2019），以及免疫的一个基本因素（Pfeffer和Hawrylowicz，2012）。 Intracellular calcium is essential for all aspects of the viral cycle—entry, gene replication, maturation, and release—while also disturbing the cell’s own functions. “Evidence has emerged that pharmacologically targeting the calcium channel or calcium release from the endoplasmic reticulum … can obstruct virus lifecycles” (Chen, et al., 2019). 细胞内钙对病毒周期进入、基因复制、成熟和释放的各个方面都至关重要，同时也干扰细胞自身的功能。“有证据表明，药理学上针对钙通道或内质网释放的钙……可以阻碍病毒的生命周期”（Chen等人，2019年）。 A few doctors recognize that progesterone supplementation might seem reasonable for preventing or treating the corona virus problem, though they don’t seem to know about its already established antiviral effects (Pfahler, et al., 1987; Muñoz, et al., 2007; Hall, et al., 2016), or the mechanisms involved. Other doctors (Sharon Nachman), following their cliché thinking instilled by estrogen industry advertising, and believing that estrogen is “the female hormone” that explains women’s health advantages, have begun a study, treating the corona infection in men with estrogen patches. Old men’s estrogen levels, especially if their health is poor, can be higher than that of women of the same age, while their progesterone is always lower. 一些医生认识到，补充孕酮对于预防或治疗冠状病毒问题似乎是合理的，尽管他们似乎不知道其已经确定的抗病毒作用（Pfahler等人，1987年；Muñoz等人，2007年；Hall等人，2016年）或相关机制。其他医生（Sharon Nachman）遵循雌激素行业广告灌输的陈词滥调，相信雌激素是解释女性健康优势的“女性激素”，已经开始了一项研究，用雌激素贴片治疗男性的冠状动脉感染。老年男性的雌激素水平，尤其是当他们的健康状况不佳时，可能会高于同龄女性，而他们的孕酮水平总是较低。 Nitric oxide is a powerful oxidant that can destroy viruses, and it happens to dilate blood vessels. Doctors have almost unanimously recommended it to treat the corona virus infection; however, it is associated with inflammation (Weidinger, et al., 2015), and promotes fibrosis, and fibrosis is a sequela of coronavirus disease. An increased amount of nitric oxide in the exhaled breath is a clear predisposing factor for high altitude sickness (Ren, et al., 2015). Progesterone is a respiratory stimulant that increases the hypoxic ventilatory response, and a low hypoxic ventilatory response is another predisposing factor to high altitude sickness. Progesterone inhibits the formation of nitric oxide (Wolfson, et al., 2015), while estrogen increases it (Lima, et al., 2014). 一氧化氮是一种强大的氧化剂，可以破坏病毒，它会扩张血管。医生们几乎一致建议用它来治疗冠状病毒感染；然而，它与炎症有关（Weidinger等，2015），并促进纤维化，纤维化是冠状病毒病的后遗症。呼出气体中一氧化氮含量的增加是高原病的明显易感因素（Ren，et al.，2015）。孕酮是一种呼吸兴奋剂，可增加低氧通气反应，低低氧通气反应是高原病的另一个易感因素。孕酮抑制一氧化氮的形成（Wolfson等，2015），而雌激素增加一氧化氮的形成（Lima等，2014）。 For years, corona viruses have been known to bind to the angiotensin converting enzyme 2 (ACE2), and that enzyme has been known to have protective effects, destroying angiotensin, and losartan, an angiotensin receptor blocker, has been known to be protective against corona viruses. Angiotensin increases intracellular calcium, and losartan lowers intracellular calcium. In reaction to the new corona virus, a few groups responded quickly, treating successfully with antiinflammatory things—losartan, cinanserin (a serotonin antagonist), aspirin, and azithromycin or erythromycin, which lower intracellular calcium. Aspirin’s effects overlap those of losartan, and it downregulates the angiotensin receptor, ATR1 (Mitra, et al., 2012). 多年来，已知冠状病毒与血管紧张素转换酶2（ACE2）结合，并且已知该酶具有保护作用，破坏血管紧张素，并且已知血管紧张素受体阻滞剂氯沙坦对冠状病毒具有保护作用。血管紧张素增加细胞内钙，氯沙坦降低细胞内钙。在对新冠病毒的反应中，一些小组反应迅速，成功地用消炎药物氯沙坦、辛那西林（一种血清素拮抗剂）、阿司匹林和阿奇霉素或红霉素治疗，这些药物可以降低细胞内钙。阿司匹林的作用与氯沙坦的作用重叠，并下调血管紧张素受体ATR1（Mitra等人，2012年）。 Meanwhile, medical media, such as Lancet, immediately warned against the use of anti-angiotensin drugs, as if the authors and editors hadn’t been reading respiratory physiology in recent years. This is because of the stupefying effects of the receptor dogma. Having identified ACE2 as the “coronavirus receptor,” nothing physiological matters. Graded, holistic effects, involving simultaneous changes in many “receptors,” in which rising inflammation can lead to viral replication, suggesting many safe therapeutic interventions, simply don’t fit into the paradigm of product “development” and marketing. 与此同时，医学媒体，如《柳叶刀》（Lancet），立即警告不要使用抗血管紧张素药物，就好像作者和编辑近年来没有阅读呼吸生理学一样。这是因为受体教条的麻木效应。在确认ACE2为“冠状病毒受体”后，没有任何生理问题。分级的整体效应，包括许多“受体”的同时变化，其中炎症加剧可导致病毒复制，表明许多安全的治疗干预措施，根本不符合产品“开发”和营销的范式。 The closed, authoritarian nature of the medical profession makes it a perfect tool for political manipulation. Obstructing the use of rational treatments, the profession has been mobilized to promote the militarization of the national response to the latest respiratory virus, the history of which shows the massive involvement of the US military. Ralph Baric’s publications on the corona virus, as well as dissenting opinions among virologists and in government (Nature, Nov. 12, 2012; The Scientist Magazine, Nov. 16, 2012), make it clear that military-motivated gain of function virus research has been able to override a presidential moratorium, and the actions of Eric Schmidt and his National Defense Commission on Artificial Intelligence (proposing responses to growing Chinese power), and his recent appointment by Governor Cuomo to help reorganize New York’s schools, health system, and economy, offer new perspectives on the government’s surprising actions. The fact that Italy and Iran last year signed an agreement to participate in China’s expansive trade plan might be relevant to evaluating the meaning of this novel flu season. 医学界封闭、专制的本质使其成为政治操纵的完美工具。由于阻碍了合理治疗的使用，该行业被动员起来，推动国家对最新呼吸道病毒的反应军事化，其历史表明美国军方的大规模参与。拉尔夫·巴里克关于冠状病毒的出版物，以及病毒学家和政府的不同意见（自然杂志，2012年11月12日；《科学家》杂志，2012年11月16日）明确指出，出于军事动机的功能增益病毒研究已经能够推翻总统的禁令，以及埃里克·施密特及其国防委员会在人工智能方面的行动（提出应对不断增长的中国实力的建议），而他最近被库莫州长任命帮助重组纽约的学校、卫生系统和经济，为政府令人惊讶的行动提供了新的视角。意大利和伊朗去年签署了参与中国扩大贸易计划的协议，这一事实可能与评估这一新奇流感季节的意义有关。 Since the recognition that only 1% or 2% of our DNA consists of “our genes,” and that around 48% shows features specifying retroviruses, many geneticists are suggesting that retroviruses, transferring their RNA information into our DNA, are our ancestors. The reason for this crazy thought is probably to avoid as far as possible the radical abandonment of the Central Dogma of genetics, that information flows only from nucleic acids to proteins. Now that the protective and adaptive functions of exosomes and retrotransposons have been clarified, the more obvious inference might be that we are the ancestor of retroviruses, though the real implication is that we are essentially adaptive, epigenetic, creative beings. The “germ line” is everywhere, not insulated in the gonads. 由于认识到只有1%或2%的DNA由“我们的基因”组成，并且大约48%的DNA显示出特定于逆转录病毒的特征，许多遗传学家认为逆转录病毒是我们的祖先，将其RNA信息转移到我们的DNA中。这种疯狂想法的原因可能是为了尽可能避免彻底抛弃遗传学的中心教条，即信息只从核酸流向蛋白质。现在，外显体和逆转录转座子的保护和适应功能已经阐明，更明显的推论可能是我们是逆转录病毒的祖先，尽管真正的含义是我们本质上是适应性、表观遗传和创造性的生物。“生殖系”无处不在，在性腺中没有绝缘。 Vaccine adjuvants are designed to produce systemic inflammation, and that involves some degree of activation of our innate immunity with its epigenetic adaptive potential. Recognizing that a barely recognizable background of inflammation predisposes to develop serious sickness from a corona virus, it’s important to consider the role of the recent great expansion of the influenza vaccination campaigns in Italy and the US, especially directed at older people, in the current increased incidence of corona infections. Several studies, designed to judge the effectiveness of the influenza vaccine, reported that the vaccine might be about 45% effective in reducing influenza infections, but that the vaccinated people were much more likely to have other respiratory infections, including corona virus infections. 疫苗佐剂被设计用于产生全身炎症，这涉及到我们的先天免疫及其表观遗传适应潜力的某种程度的激活。在科罗娜啤酒中，认识到难以识别的炎症背景易导致严重疾病，因此考虑当前在意大利和美国的流感疫苗接种活动的重大扩展，尤其是针对老年人，在当前科罗娜啤酒感染率增加的情况下，重要的是。几项旨在判断流感疫苗有效性的研究报告称，该疫苗在减少流感感染方面可能有45%左右的有效性，但接种疫苗的人更可能患有其他呼吸道感染，包括冠状病毒感染。 Focus on the induction of antibodies by vaccines to define immunity has led to a dangerous disregard for the basic facts of health. The present testing of a vaccine containing the RNA that specifies the most destructive spike protein of the corona virus, the part that inactivates our protective ACE2 enzyme, is being done in a culture that avoids consideration of the meaning of our massive endogenous system of RNA-responsive reverse transcriptases and retroelements. The consequences of incorporating the spike protein of the virus into our genetic repertoire are hard to imagine. The mindless activation of our huge epigenetic system of retroelements, with no knowable benefits, should be stopped. 专注于通过疫苗诱导抗体来定义免疫力导致了对健康基本事实的危险忽视。目前对一种含有RNA的疫苗的测试，该RNA指定了冠状病毒最具破坏性的棘突蛋白，该蛋白是使我们的保护性ACE2酶失活的部分，该疫苗的测试是在一种文化中进行的，这种文化避免了考虑我们大量的内源性RNA应答逆转录酶和逆转录酶元件系统的意义。很难想象将病毒的棘突蛋白纳入我们的基因库的后果。我们应该停止盲目地激活我们庞大的表观遗传逆转录酶元件系统，因为它没有任何已知的好处。 —- ===== 参考文献 ===== Respir Physiol Neurobiol. 2020 Apr 22 : 103443. Does the pathogenesis of SAR-CoV-2 virus decrease at high-altitude? Arias-Reyes C, Zubieta-DeUrioste N, PomaMachicao L, Aliaga-Raudan F, Carvajal-Rodriguez F, Dutschmann M, Schneider-Gasser EM, Zubieta-Calleja G, and Soliza J. Crit Care Med. 1993 May;21(5):740-6. Action of Carbon Dioxide on Hypoxic Pulmonary Vasoconstriction in the Rat Lung: Evidence Against Specific Endothelium-Derived Relaxing Factor-Mediated Vasodilation. Baudouin SV, Evans TW. Cells. 2019 Dec 30;9(1):94. Host Calcium Channels and Pumps in Viral Infections. Chen X, Cao R, Zhong W. American Journal of Respiratory and Critical Care Medicine 2012;185:A2848. Investigations Of Mechanisms Of Carbon Dioxide-Induced Bronchial Smooth Muscle Relaxation. Choudhury P, El Mays TY, Snibson K, Wilson R, Leigh R, Dennis J, Nelson DE, Green F. Kaohsiung J Med Sci. 2011 Aug;27(8):336-43. Effect of Carbon Dioxide Inhalation on Pulmonary Hypertension Induced by Increased Blood Flow and Hypoxia. Chuang IC, Yang RC, Chou SH, Huang LR, Tsai TN, Dong HP, Huang MS. Crit Care Med 40:2622–2630. Hypercapnic acidosis attenuates ventilation-induced lung injury by a nuclear factor-kappaB-dependent mechanism. Contreras M, Ansari B, Curley G, Higgins BD, Hassett P, O'Toole D, Laffey JG. J Immunol. 2010 Oct 1;185(7):4439-45. NF-κB links CO2 sensing to innate immunity and inflammation in mammalian cells. Cummins EP, Oliver KM, Lenihan CR, Fitzpatrick SF, Bruning U, Scholz CC, Slattery C, Leonard MO, McLoughlin P, Taylor CT. Hormones (Athens). 2019 Mar;18(1):17-21. Molecular Basis of Vitamin D Action in Neurodegeneration: The Story of a Team Perspective. Duygu Gezen-Ak, Erdinç Dursun. J Virol. 2010 Apr;84(7):3134-46. Recombination, Reservoirs, and the Modular Spike: Mechanisms of Coronavirus Cross-Species Transmission. Graham RL, Baric RS. Annu Rev Nutr. 2014;34:117-41. Vitamin D as a Neurosteroid Affecting the Developing and Adult Brain. Groves NI, McGrath JJ, Burne THJ. Methods Mol Biol. 2008;454:229-36. Manipulation of the Coronavirus Genome Using Targeted RNA Recombination With Interspecies Chimeric Coronaviruses. de Haan CAM, Haijema BJ, Masters PS, Rottier PJM. PLOS Pathog. 2016;12:e1005840. Progesterone-Based Therapy Protects Against Influenza by Promoting Lung Repair and Recovery in Females. Hall OJ, Limjunyawong N, Vermillion MS, Robinson DP, Wohlgemuth N, Pekosz A, Mitzner W , Klein SL. (Implanted, rather than physiologically dosed, progesterone was used.) Lancet. 1988 Sep 17;2(8612):639-41. Effect of Carbon Dioxide in Acute Mountain Sickness: A Rediscovery. Harvey TC, Raichle ME, Winterborn MH, Jensen J, Lassen NA, Richardson NV, Bradwell AR. Neuropsychopharmacology volume 32, pages1477–1489(2007). Inhibition of Evoked Glutamate Release by Neurosteroid Allopregnanolone Via Inhibition of L-Type Calcium Channels in Rat Medial Prefrontal Cortex. Hu AQ, Wang ZM, Lan DM, Fu YM, Zhu YH, Dong Y & Zheng P. Arterioscler Thromb Vasc Biol. 2000 Nov;20(11):235965. Thiol Oxidation Activates a Novel Redox-Regulated Coronary Vasodilator Mechanism Involving Inhibition of Ca2+ Influx. Iesaki T, Wolin MS. Eksp Klin Farmakol. 2012;75(12):19-21. [Role of Estradiol in Hypoxia-Induced Pulmonary Hypertension in Female Rats]**. [Article in Russian] Kovaleva IuO, Artem'eva MM,Ilatovskaia ME, Medvedev OS, Medvedeva NA.
