1,608 research outputs found
Fossilised Neanderthal Matrilineal Societies, Neo-Neanderthal Hybrids, Endosymbiotic Actinidic Archaea and Civilisational Diseases
Neanderthal genes have been related to human disease. The human genome has been found to have up to 10 percent Neanderthal genes. The pyruvate dehydrogenase gene as well as those coding for MHC alleles are of Neanderthal origin. Neanderthal genes have been related to autism and autoimmune disease. There is high incidence of autism and Neanderthal anthropometry in the matrilineal and Dravidian language speaking nair community of Kerala. The autistic brain is comparable to the large-sized Neanderthal brain. Metabolic patterns were compared among the following groups: matrilineal nairs, non nairs, autism, schizophrenia and systemic diseases to find out a pattern of Neanderthal metabolism. The aim of the study aimed to detect fossilized Neanderthal matrilineal societies and new Neanderthal hybrids in relation to civilisational diseases. Four groups, 25 numbers in each group were chosen for the study—the autistic population diagnosed according to DSM criteria, the normal nair population, the normal non-nair population and civilisational disease group including metabolic syndrome x, alzheimer’s disease, cancer, schizophrenia and multiple sclerosis. Archaeal cholesterol catabolism as well as PDH activity, glycolytic pathway, the GABA shunt, porphyrins, homocysteine and ammonia metabolism were studied to find out a pattern of Neanderthal metabolism. Autistic metabolonomic patterns include low pyruvate dehydrogenase activity, mitochondrial dysfunction, GABA shunt, Warburg glycolytic phenotype, hyperammonemia, hyperhomocysteinemia, porphyria, low cholesterol/bile acid levels and a similar pattern is seen in the normal nair population of Kerala. Neanderthal metabolonomic patterns include a low efficiency PDH activity. Autistic and matrilineal societies like nair can be considered as remnants of the Neanderthals. The autistic and nair population have increased cytochrome F420 activity suggestive of endosymbiotic archaeal growth resulting in PDH and mitochondrial suppression. The increased archaeal digoxin synthesis later on shuts down the metabolic machinery the neuronal and other tissue cells and the human cells and tissues including the brain are taken over by an atavistic actinidic colony network. This leads onto a Neanderthal hybrid zombie syndrome. The increased archaeal growth in ice age conditions contributed to the neanderthal evolution and similar endosymbiotic archaeal growth related to global warming leads to neanderthalisation of homo sapiens. The autistic and neanderthalic metabolonomic patterns are also seen in civilisational diseases like syndrome X, schizophrenia, cancer, multiple sclerosis and alzheimer’s disease. The results suggest neanderthalisation of the humans due to global warming and archaeal growth. The Neanderthalisation of the human species is the basis of the global autistic, schizophrenic and civilisational disease epidemic—epidemic Neanderthal hybrid zombie syndrome. The matrilineal societies are fossilized Neanderthal remnants and neoneanderthal hybrids contribute to civilisational diseases
The Homo Neanderthalis and the Dravidians: A Common Origin and Relation to Harappan Civilisation and Vedas
INTRODUCTION: The postulated Lemurian part of the Indian sub-continent in South India is inhabited by the dominant Nair community. The dominant Nair community also has a high incidence of autism. Neanderthal anthropometric features have been described in autism. Neanderthal metabolonomics have also been described in autism. It is possible that homo neanderthalis would have originated in the super continent which occupied the southern ocean. The island of Sumatra is home to another human species homo floresiensis which lived along with homo neanderthalis. This suggests an oceanic origin of homo neanderthalis in the supercontinent in the southern ocean. Recurrent Tsunamis would have forced the migration of homo neanderthalis to the Eurasian land mass especially to Harappa, Sumeria, Etruscia, Egypt and Basque country. There is a high incidence of Neanderthal genes in the Basque population. The language spoken in Harappa, Sumeria, Etruscia, Egypt and Basque country had a Dravidian sub-stratum. The population in these areas are matrilineal and female dominant.MATERIALS AND METHODS: Neanderthal anthropometric features were evaluated in the Nair community and in autism. The parameters checked include dolichocephalic skull, prominent supraorbital ridge and mid face large flat nose and ring finger index finger ratios.RESULTS: The Nair community had a high prevalence of Neanderthal anthropometric features. Neanderthal anthropometric features were also dominant in autism.CONCLUSION: This suggests an out of oceania hypothesis for the origin of homo neanderthalis
The Porphyrins, Origin of Life in Biological Universe and Evolution/Regulation of the Human System
Objectives: Actinidic archaea have been related to thepathogenesis of schizophrenia, malignancy, metabolicsyndrome x, autoimmune disease and neuronaldegeneration. An actinide dependent shadow biosphere ofarchaea and viroids in the above mentioned disease statesis described. Actinidic archaea have a mevalonate pathwayand are cholesterol catabolizing. They can use cholesterolas a carbon and energy source. Archaeal cholesterolcatabolism can generate porphyrins via the cholesterolring oxidase generated pyruvate and GABA shuntpathway. Archaea can produce a secondary porphyria byinducing the enzyme heme oxygenase resulting in hemedepletion and activation of the enzyme ALA synthase.Porphyrins have been related to schizophrenia, metabolicsyndrome x, malignancy, systemic lupus erythematosis,multiple sclerosis and Alzheimer’s diseases. The roleof archaeal porphyrins in regulation of cell functionsand neuroimmunoendocrine integration is discussed.Porphyrins are prebiotic molecules which are involved inabiogenesis and origin of life.Methodology: Plasma from fasting heparinisedblood was used and the experimental protocol was asfollows (I) Plasma+phosphate buffered saline, (II) sameas I+cholesterol substrate, (III) same as II+rutile 0.1 mg/ml, (IV) same as II+ciprofloxacine and doxycycline eachin a concentration of 1 mg/ml. The following estimationswere carried out: Cytochrome F420, free RNA, free DNA,polycyclic aromatic hydrocarbon, hydrogen peroxide,pyruvate, ammonia, glutamate, succinate, glycine, deltaaminolevulinic acid and digoxin. The study also involvedestimating the following parameters in the patientpopulation- Hexokinase, porphyrins, pyruvate, glutamate,ammonia, succinic acid, serine, glycine, HMG CoAreductase, cytochrome C, blood ATP and heme oxygenase.Results: Plasma of control subjects showed increasedlevels of the above mentioned parameters with afterincubation for 1 hour and addition of cholesterolsubstrate resulted in still further significant increase inthese parameters. The plasma of patients showed similarresults but the extent of increase was more. The additionof antibiotics to the control plasma caused a decreasein all the parameters while addition of rutile increasedtheir levels. The addition of antibiotics and rutile to thepatient’s plasma produced the same changes but theextent of change was more in patient’s sera as comparedto controls. There was upregulated archaeal porphyrinsynthesis in the patient population which was archaeal inorigin as indicated by actinide catalysis of the reactions.The cholesterol oxidase pathway generated pyruvatewhich entered the GABA shunt pathway. This resulted insynthesis of succinate and glycine which are substratesfor ALA synthase. The study showed the patient’s bloodhad increased heme oxygenase activity, increased serine,glycine, succinic acid and porphyrins. The hexokinaseactivity was high. The pyruvate, glutamate, ammonia,GABA and succinic acid levels were elevated indicatingblockade of PDH activity, and operation of the GABAshunt pathway. The cytoC levels were increased in theserum indicating mitochondrial dysfunction suggestedby low blood ATP levels. This was indicative of theWarburg’s phenotype. The HMG CoA reductase activitywas high indicating cholesterol synthesis.The RHCDpopulation had values similar to the patient population.The LHCD population had opposite values.Conclusion: An actinide dependent shadow biosphereof archaea and viroids in the above mentioned diseasestates is described. The archaeal porphyrins can contributeto the pathgenesis of metabolic syndrome x, malignancy,psychiatric disorders, autoimmune disease, AIDS, prion disease, neuronal degeneration and epileptogenesis.Archaeal porphyrin synthesis is crucial in the pathogenesisof these disorders. Porphyrins may serve as regulatorymolecules modulating immune, neural, endocrine,metabolic and genetic systems. The porphyrins photooxidationgenerated free radicals can produce immuneactivation, produce cell death, activate cell proliferation,produce insulin resistance and modulate conscious/quantal perception. Porphyrins can regulate hemisphericdominance. The archaeal porphyrins functions as keyregulatory molecules with mitochondrial benzodiazepinereceptors playing an important role. The role of porphyrinsin abiogenesis and origin of life as well as biologicaluniverse is discussed.Key words: Actinide; Archaea; Porphyrins; GABAshunt; Peripheral Benzodiazepine receptor; Deltaaminolevulinic aci
The Extinction of Homo Sapiens and Symbiotic Neanderthalisation: Relation to Archaeal Mediated RNA Viroidsand Amyloidosis
Introduction: Prion proteins have been implicated in systemic disorders like neurodegenerations, cancer and metabolic syndrome. The beta amyloid in Alzheimer’s disease, alpha synuclein in parkinson’s disease, the TAR protein in frontotemporal dementia and copper zinc dismutase in motor neuron disease behaves like prion proteins. Prion proteins like behavior is also seen in the tumour suppressor P53 protein in cancer and the islet cell associated amyloid in diabetes mellitus. Prion diseases are conformational diseases. The abnormal prion protein seeded into the system converts the normal proteins with prion like domains to abnormal configuration. This abnormal protein resists digestion by lysosomal enzymes after its half-life is over and results in deposition of amyloid plaques. This produces organ dysfunction. Prion phenomena were initially described for Creutzfeldt Jakob’s disease, but now it is found to be wide spread in chronic disease pathogenesis. Ribonucleoproteins are well known to behave like prion proteins and form amyloid. We have demonstrated actinidic archaea which secretes RNA viroids in metabolic syndrome, neurodegenerations, cancer, autoimmune disease, schizophrenia, autism and CJD. The RNA viroids can bind with normal proteins with prion like domains eg., superoxide dismutase and produce a ribonucleoprotein resulting in prion phenomena and amyloidogenesis.Materials and Methods: The following groups were included in the study:- alzheimer’s disease, multiple sclerosis, non-hodgkin’s lymphoma, metabolic syndrome x with cerebrovascular thrombosis and coronary artery disease, schizophrenia, autism, seizure disorder, creutzfeldt jakob disease and acquired immunodeficiency syndrome. There were 10 patients in each group and each patient had an age and sex matched healthy control selected randomly from the general population. The blood samples were drawn in the fasting state before treatment was initiated. Plasma from fasting heparinised blood was used and the experimental protocol was as follows (I) Plasma+phosphate buffered saline, (II) same as I+cholesterol substrate, (III) same as II+cerium 0.1 mg/ml, (IV) same as II+ciprofloxacine and doxycycline each in a concentration of 1 mg/ml. Cholesterol substrate was prepared as described by Richmond. Aliquots were withdrawn at zero time immediately after mixing and after incubation at 37oC for 1 hour. The following estimations were carried out:- Cytochrome F420, free RNA, Cytochrome F420 was estimated flourimetrically (excitation wavelength 420 nm and emission wavelength 520 nm). Results: Plasma of control subjects showed increased levels of the above mentioned parameters with after incubation for 1 hour and addition of cholesterol substrate resulted in still further significant increase in these parameters. The plasma of patients showed similar results but the extent of increase was more. The addition of antibiotics to the control plasma caused a decrease in all the parameters while addition of cerium increased their levels. The addition of antibiotics to the patient’s plasma caused a decrease in all the parameters while addition of cerium increased their levels but the extent of change was more in patient’s sera as compared to controls. Discussion: The actinidic archaeal growth results in increased digoxin synthesis and phenotypic conversion of homo sapiens to homo Neanderthals as reported earlier. The increased actinidic archaeal growth is due to global warming and these results in neanderthalisation.Homo neanderthalis tend to have more of civilisational diseases like metabolic syndrome, neurodegenerations, cancer, autoimmune disease, schizophrenia, autism and CJD. Actinidic archaeal secreted RNA viroids may play a crucial role in amyloid formation and pathogenesis of these disorders. The evolution and origin of homo sapiens and homo neanderthalis is on the basis of actinidic archaeal symbiosis and digoxin synthesis. Extreme climate change related increased actinidic archaeal symbiosis and digoxin synthesis results in homo neanderthalis. The homo sapien species results from inhibition of actinidic archaeal symbiosis and endogenous digoxin synthesis by normal global climate. Thus there are evolutionary swings between the two human species depending on extremes of climate and archaeal symbiosis. Endogenous digoxin can be considered as a Neanderthal hormone. The results show that there was increase in cytochrome F420 in CJD and other disease groups indicating increased archaeal growth. There was also an increase in free RNA indicating self-replicating RNA viroids in CJD and other disease groups. The RNA viroid generation was catalysed by actinides. The RNA viroids can bind with proteins having prion like domains forming ribonucleoproteins. These ribonucleoproteins can give an abnormal conformation to the protein resulting in generation of abnormal prions. The abnormal prions can act as a template to convert normal proteins with normal configuration to abnormal conformation. This can result in amyloidogenesis. The abnormal configured proteins will resist lysosomal digestion and accumulate as amyloid producing disease states and extinction
THE EFFECTS OF FIELD EMITTED ELECTRONS ON RF SURFACE
The ever-growing demand for higher RF gradients has
considerably increased the risk of breakdown in
accelerating structures. Field emission is the most
common form of RF breakdown that generates free
electrons capable of inflicting irreversible damages on the
RF surface. This paper presents a systematic experimental
and simulation programme to understand possible sources
and their influence on RF cavity operatio
Endosymbiotic Actinidic Archaea and Viroids -- A Model for Abiogenesis and Viral, Prokaryote, Eukaryotic, Primate and Human Evolution
Aim: A hypothesis regarding endosymbiotic actinidic archaea as having evolved from isoprenoid organisms by abiogenesis is presented in this paper. An actinidc archaea/ viroid mediated model of prokaryote, viral, eukaryotic, primate and human evolution is discussed. Endomyocardial fibrosis along with the root wilt disease of coconut is endemic to Kerala with its radioactive actinide beach sands. Actinides like rutile and organisms like phytoplasmas and viroids have been implicated in the etiology of these diseases. Actinidic archaea has been related to the pathogenesis of schizophrenia, malignancy, metabolic syndrome x, autoimmune disease and neuronal degeneration. Actinidic archaea have a mevalonate pathway and cholesterol catabolism. A hypothesis of cholesterol as the primal prebiotic molecule synthesised on actinide surfaces with all other biomolecules arising from it and a self replicating cholesterol lipid organism as the initial life form is presented. A cholesterol based theory of abiogenesis and its role in the evolution of actinidic archaea is discussed. The origin of viruses, prokaryotes, eukaryotes, primates and humans from the initial isoprenoid organism derived actinidic archaea is postulated. Methods: Plasma from fasting heparinised blood was used and the experimental protocol was as follows (I) Plasma+phosphate buffered saline, (II) same as I+cholesterol substrate, (III) same as II+rutile 0.1 mg/ml, (IV) same as II+ciprofloxacine and doxycycline each in a concentration of 1 mg/ml. The following estimations were carried out:- Cytochrome F420, free RNA, free DNA, polycyclic aromatic hydrocarbon, hydrogen peroxide, dopamine, serotonin, pyruvate, ammonia, glutamate, cytochrome C, hexokinase, ATP synthase, HMG CoA reductase, digoxin and bile acids. Results: Plasma of control subjects showed increased levels of the above mentioned parameters with after incubation for 1 hour and addition of cholesterol substrate resulted in still further significant increase in these parameters. The plasma of patients showed similar results but the extent of increase was more. The addition of antibiotics to the control plasma caused a decrease in all the parameters while addition of rutile increased their levels. The addition of antibiotics and rutile to the patient’s plasma produced the same changes but the extent of change was more in patient’s sera as compared to controls. Conclusion: An actinide dependent shadow biosphere of archaea and viroids in the above mentioned disease states is described. Metal actinides in beach sands have been postulated to play a role in abiogenesis. Cholesterol is the primal prebiotic molecule synthesised on actinide surfaces with all other biomolecules arising from it. A self replicating cholesterol lipid organism could be the initial life form. A cholesterol based abiogenesis is a more likely evolutionary option and the actinidic archaea and viroids would have evolved from it. The origin of viruses, prokaryotes, eukaryotes, primates and humans from the initial isoprenoid organism derived actinidic archaea is discussed.Key words: Actinide; Archaea; Viroid; Eukaryote; Prokaryote; Virus; Primate; Human; Evolutio
- …