Mitochondriopathy - Renal, Lung, Liver, GIT, Bone and Joint Diseases
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- Indbinding:
- Paperback
- Sideantal:
- 444
- Udgivet:
- 12. juli 2023
- Størrelse:
- 150x28x220 mm.
- Vægt:
- 679 g.
- 2-15 hverdage.
- 12. december 2024
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Beskrivelse af Mitochondriopathy - Renal, Lung, Liver, GIT, Bone and Joint Diseases
Actinidic archaea has been related to global warming and renal, lung, liver, GIT, bone and joint diseases. The growth of endosymbiotic actinidic archaea in relation to climate change and global warming leads to neanderthalisation of the humans. Neanderthal metabolonomics include the Warburg phenotype and cholesterol catabolism resulting in hyperdigoxinemia. Digoxin produced by archaeal cholesterol catabolism produces neanderthalisation. The human mitochondria has the cytochrome P450 enzymes required for steroidal synthesis. The mitochondria can synthesize the aglycone part of the digoxin. The archaeal RNA viroids hybridizing with mitochondrial RNA can get converted to mitochondrial DNA by reverse transcriptase and can form part of the mitochondrial DNA. This transfers the information for the synthesis of the sugar moiety from the archaea to the mitochondria. They can form supermitochondria and superbugs synthesizing digoxin. The mitochondrial digoxin can regulate the sodium-calcium exchange into the cell membrane and modulate mitochondrial function. A mitochondriopathy is the basis of renal, lung, liver, GIT, bone and joint diseases.
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