古菌共生和地高辛状态调节智人和尼安德特人的进化——地高辛是尼安德特人的一种激素

R. Kurup, P. A. Kurup
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引用次数: 0

摘要

导语:气候变化和全球变暖/冰河时代导致人体系统内共生的锕系古菌生长和胆固醇分解代谢导致内源性地高辛合成。在自闭症和母系社区中检测到的内共生古细菌生长增加,自闭症和尼安德特人的发病率增加,这导致地高辛作为尼安德特人激素的结论。与气候变化和全球变暖有关的内共生古细菌生长增加以及由此产生的内源性地高辛合成导致智人尼安德特化,人类疾病导致智人灭绝。地高辛可以抑制逆转录酶活性和RNA编辑,从而抑制内源性逆转录病毒的生长。这产生了抑制HERV表达和跳跃基因现象产生在人类基因组的动态。HERV相关跳跃基因在突触多样性、HLA表达、免疫调节和代谢多样性中起着至关重要的作用。地高辛使钠-氢交换发生改变,产生酸性pH值,并像生长因子一样使成体细胞发生干细胞转化。干细胞有一个独特的代谢,增加糖酵解和抑制PDH和线粒体功能。这会导致癌症和代谢综合征。地高辛干扰RNA编辑可导致RNA病毒突变和广泛传播的RNA病毒流行。地高辛干扰HERV表达和RNA编辑,从而抑制基因组、代谢、神经和免疫多样性,从而产生自身免疫性疾病、癌症、代谢综合征、变性、精神分裂症和自闭症,这些疾病在人群中以流行病的速度增加。材料和方法:在母系社区、SLE、多发性硬化症、帕金森病、阿尔茨海默病、中枢神经胶质瘤、多发性骨髓瘤、伴有CAD和CVA的代谢综合征x、精神分裂症和自闭症中,评估内源性地高辛水平和血清细胞色素F420水平作为古菌生长的标志物。每组15个数字,每个患者有一个年龄和性别匹配的对照。Elisa法测定内源性地高辛,分光光度法测定细胞色素F420。统计分析采用方差分析。结果:内源性地高辛水平和细胞色素F420水平在母系尼安德特人社区、SLE、多发性硬化症、帕金森病、阿尔茨海默病、中枢神经胶质瘤、多发性骨髓瘤、伴有CAD和CVA的代谢综合征x、精神分裂症和自闭症中升高。内源性地高辛和细胞色素F420水平在非母系智人群体中较低。结论:智人具有较低水平的内共生放线菌和较低的地高辛合成。智人的自身免疫性疾病、癌症、精神分裂症、自闭症和代谢综合征的发病率较低。内共生的放线菌古菌生长和地高辛合成导致智人的尼安德特化,导致人类病理和灭绝。尼安德特人有更高的锕系古菌共生率和地高辛合成率,自身免疫性疾病、癌症、精神分裂症、自闭症和代谢综合征的发病率更高。放线菌分泌地高辛作为尼安德特人激素的功能。
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Archaeal Symbiosis and Digoxin Status Modulates Evolution of Homo Sapiens and Homo Neanderthalis - Digoxin Is a Neanderthal Hormone
Introduction: The climate change and global warming/ice age results in endosymbiotic actinidic archaeal growth in the human system and cholesterol catabolism resulting in endogenous digoxin synthesis. The increased endosymbiotic archaeal growth detected in autism and matrilineal communities with increased incidence of autism and neanderthalic origin leads to the conclusion that digoxin acts as neanderthalic hormone. The increased endosymbiotic archaeal growth and resultant endogenous digoxin synthesis in relation to climate change and global warming results in neanderthalisation of homo sapiens and human disease resulting in homo sapien extinction. Digoxin can inhibit reverse transcriptase activity and RNA editing resulting in suppression of endogenous retroviral growth. This produces inhibition of HERV expression and jumping gene phenomena producing in adynamicity of the human genome. HERV related jumping genes are crucial in synaptic diversity, HLA expression and immunomodulation as well as metabolic diversity. Digoxin produces alteration in sodium-hydrogen exchange producing an acidic pH and acts like a growth factor producing stem cell transformation of adult cells. Stem cells have a distinct metabolism with increased glycolysis and suppression of PDH and mitochondrial function. This can result in cancer and metabolic syndrome. The digoxin interference with RNA editing can lead to mutated RNA viruses and wide spread RNA viral epidemics. The digoxin interference with HERV expression and RNA editing and resultant inhibition of genomic, metabolic, neural and immune diversity produces autoimmune disease, cancer, metabolic syndrome, degenerations, schizophrenia and autism which are increasing at epidemic rates in human population. Materials and Methods: Endogenous digoxin levels and serum cytochrome F420 levels as a marker of archaeal growth were estimated in matrilineal communities, SLE, multiple sclerosis, parkinson’s disease, alzheimer’s disease, CNS glioma, multiple myeloma, metabolic syndrome x with CAD and CVA, schizophrenia and autism. 15 numbers were included in each group and each patient had an age and sex matched control. Endogenous digoxin was estimated by Elisa and cytochrome F420 estimated by spectrophotometry. The statistical analysis was done by ANOVA. Results: Endogenous digoxin levels and cytochrome F420 levels were elevated in matrilineal neanderthalic communities, SLE, multiple sclerosis, parkinson’s disease, alzheimer’s disease, CNS glioma, multiple myeloma, metabolic syndrome x with CAD and CVA, schizophrenia and autism. Endogenous digoxin and cytochrome F420 levels were low in non-matrilineal homo sapien population. Conclusion: Homo sapiens tend to have low levels of endosymbiotic actinidic archaea and low digoxin synthesis. Homo sapiens have low incidence of autoimmune disease, cancer, schizophrenia, autism and metabolic syndrome. The neanderthalisation of homo sapiens consequent to endosymbiotic actinidic archaeal growth and digoxin synthesis produces human pathology and extinction. Homo neanderthalis have higher rates of actinidic archaeal symbiosis and digoxin synthesis with higher incidence of autoimmune disease, cancer, schizophrenia, autism and metabolic syndrome. Actinidic archaeal secreted digoxin functions as a Neanderthal hormone.
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