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Mitochondrion: Natural Transplant

Aaron S Wallman*

Clinical Fellow in Neonatal-Perinatal Medicine, Columbia University Medical Center, United States

*Corresponding Author:
Aaron S Wallman
Clinical Fellow in Neonatal-Perinatal
Medicine, Columbia University Medical
Center, United States.
Tel: 310-502-5889
Email: aaron.wallman@yahoo.com

Received date: October 25, 2016; Accepted date: November 22, 2016; Published date: November 24, 2016

Citation: Aaron S Wallman. Mitochondrion: Natural Transplant. Health Syst Policy Res.2016, 3:4 doi: 10.21767/2254-9137.100054

 
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Opinion Article

According to Dr. Helen A. Tuppen, the mitochondria are independent of the nuclear genome, and its replication does not coincide with the cell’s cycle. In addition, Dr. Tuppen believes it has a higher number of mutations than the nucleus. In the case of the mitochondrial mutations from their oxidation are the following disorders: bipolar, diabetes, dementia, epilepsy, strokes, heart disease, and aging. According to Tuppen, their repair system is not enough to counteract the oxidation damage, and they lack protective histones along with reduced cellular ATP.

If the mitochondria became a part of eukaryote cells when oxygen entered the atmosphere in substantial amounts, then I would consider them as more a transplant as an ancestor than as an integral part of the cell [1]. According to an article in Scientific American, our descendants of mitochondria are a type of bacteria which leads to a disorder like heart disease or neurodegeneration. Such puzzles as disorders are from the absence of introns and not from following the patterns of codons according to Professor Williams [2]. As the ancestors of mitochondria, I believe that the bacteria lead to this absence of introns and lack of normal codon patterns.

On this basis I propose that the introns emerge with a normal pattern of codons in the mitochondria from the correct doses of reversine. In a study about thyroid cancer cells, reversine, a chemical compound which is already known to turn a muscle cell into a progenitor cell and then turn into either a bone or a fat cell, has the potential to arrest or cause apoptosis to the thyroid cancer cells which are from a given mitochondria [3,4]. In another study, Dr. Ruxix discovered that with reversine we can cause the change of a rat’s neurons. Based on these two studies, I believe that the ideal amount of reversine on mitochondria are ideally measured by a robot and becomes the ancestor of mitochondria which are bacteria, as the Scientific American article previously mentioned [5,6]. As reversine does this suggested act, I believe the apoptosis of this bacteria’s inherent infection occurs as it is renewed into a new and normal mitochondria. Therefore, the mitochondria operate without genes jumping into the nucleus as Dr. Hume observes in her article. She also believes that keeping these genes locally in the mitochondria gives the cells a way to control themselves. In my opinion, the presence of intron and codon patterns will occur from such control with reversine and other elements [7].

For example, Dr. Hinckle in his article on oxidation phosphorylation suggests that reversine with another element known as phosphorous and its oxygen has a possible and positive affect on the mitochondria. Based on his study, I believe that stressing the oxygen of reversine and an element like phosphorous, an important source of metabolism, lead to new and normal mitochondria. All in all, a correct dosage of reversine used with other elements or a variation of it is what I propose for others to consider as a means to end a given disorder from a certain mitochondria of cells.

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