The genetic change of Duchenne/Becker type and its hope through WMDROC session and first and second genetic test results

  These days, everyone's life has become a mess because of COVID-19. 

 Even if I do not point out, even though they deny it, some humans in a certain country scientifically researched these things with an unclear purpose, artificially synthesizing the genes to create the worst coronavirus. And because the important management was negligent and spread all over the world, there was no room for anyone to doubt that such a great incident occurred.  

 

These events have ushered in a gloomy era called Corona Blue.

 If it wasn't for this Corona Blue, I would have posted a few more, if not many, useful research data or information. I have regrets about this.

 I have been studying for a long time to stop the muscle destruction in patients with Duchenne or Becker type and some other types of muscular dystrophy, and to increase the weight while using this stop as an inflection point to regenerate the destroyed muscle again.

Among these research processes and experiences, the most curious point was whether there was a possibility or probability as to whether the genes in the nucleus of myocytes correlated with the muscles would follow directly with the gene changes when the muscles are regenerated or not.

 As a researcher, I was always curious because I had no idea of a strategy that could directly interfere with the gene, and I was not curious about the change in this gene as a factor that influences the success or failure of treatment like others.

Needless to say, as an anonymous writer, any scientist, researcher, or expert at a world-renowned research institute could never establish a direct treatment strategy for a gene with such an abnormality, and establish the therapy. It is the current level of medical and medical research that it cannot be published. 

 However, shackled by the theory of genetic origin, the pathogenesis of this disease established by those who advocate for science, they had to frame a strategy based on the treatment of the broken gene that caused the brain to explode.

Therefore, the only treatment strategy that has been introduced is a gene indirect treatment method called exon skipping that has become like a dragonfly. 

When this exon skipping strategy was first established and research started, it was really buzzing as if a dream treatment would be available to DMD/BMD patients with exon defects.

 However, in terms of the clinically obtained effects after making it, it is not possible to achieve not only regeneration of progressively destroyed muscles, but also their stopping.

 The results obtained through samples from the clinically administered experimental subjects are the prediction and expectation that only 1~2% of dystrophin protein transpiration can be detected and thus the progress of muscle destruction can be slowed down to some extent are all its effects.

 In other words, current scientists and researchers on muscular dystrophy are looking for a solution to this disease in terms of the development of gene therapy, either dying or dying, because the cause of the disease is assigned to genes correlated with various types of muscular dystrophy.

On the other hand, I have been emphasizing through several posts on this blog that I put everything, such as the cause of the disease and treatment strategies, on the energy and function, volume, and mass of all organs.

 

 Let's get to the point and let's talk.

 There are two types of diagnosis results by specialists in medical institutions.

 Confirmation, that is, C/W (Consistent With), which obtains the result of diagnosis clearly and reveals it, and R/O (Rule Out), that is, the confirmation of a presumptive diagnosis because the diagnosis result is unclear.      

 

 For a patient with muscular dystrophy born in 1978 during a session of WMDROC, the ongoing muscle destruction was stopped, and the performance and change of muscle regeneration were made through the session as shown in the comparative picture in Fig. 1.

 In order to solve the question of what kind of change will happen to the broken gene, a second genetic test (Fig 4) to compare or contrast with the primary genetic test (Fig 3) that had already been done before the session started was performed.

 As in the case of other patients, it was not intended to be confirmed by medical examination, but in a patient who had already been confirmed long ago by muscle biopsy and genetic test, the progress of muscle destruction was not only stopped, but rather, the muscle was regenerated as shown in the comparative photo in Fig. This is because, if the body improved, we could not help but have a natural curiosity or doubt about how the patient's genetic condition would have changed.

Fig 1

 After registering the patient, he visited D University Hospital in Busan, a medical institution he had been attending for more than 10 years, after 3 years, and showed the doctor in charge of the comparison photo (Fig. 1) of his body from 3 years ago and now that he has improved a lot. As a result of the consultation, they came to the conclusion that he should do the genetic test again at University B hospital in Yangsan and received an outpatient report for genetic retest order (Fig 2) from the attending physician.

Fig 2

                        

After the onset of this disease, the patient was probably the first in the world to have a genetic test again, wondering how the mutated gene has changed again or whether it is still the same.

Whatever the case, any hopeful expectation of the outcome was not at all hoped for.

He was a prosecutor who did not have any mental burden because it was just to relieve doubts and relieve curiosity.

 This is because, through the session of WMDROC, what this patient had already wanted to achieve as a stop and regeneration of the ongoing muscle destruction was sufficiently obtained.

 Also, one of the biggest reasons for not being able to have great expectations for the genetic change was that the regeneration rate of the muscles on the knee of the patient, which had an unusually poor healing speed, affected gait, was insignificant, so it was still not completely regenerated.

 It is because it is a progress of a session where it is not possible to predict how many more regenerative muscles will need to be made and attached to the area in the future with how many more sessions, and the amount of muscle needed and the amount of treatment needed.

 The primary genetic test was performed as shown in the photo below (Fig 4) when muscular dystrophy was suspected at the age of 26 when the onset of the disease began.

   [Gathering]

   2004-07-28 11:34:04

   [Inspection Date]

  was done on 2004-08-02

   [Results and Interpretation]

   As a result of DMD genetic test, deletion of exson 45,46,47,48 site was confirmed,

   [Confirmation (C/T)]

  DMD/BMD due to exon deletions in the DMD gene

    

   [sample]

peripheral venous blood

         

  Fig 3. Report on the results of the first genetic test conducted on Aug. 2, 2004

Through the WMDROC session, the progress of muscle destruction due to muscular dystrophy has been stopped and the regeneration of the muscle is changing, so even the change in the gene is suspected or curious, so I did it again as an outpatient treatment at B University Hospital in Yangsan , The contents of the secondary genetic test performed in that way are as shown in Fig. 4 below,

[Gathering]

2021-04-08

[Inspection Date]

2021-05-07 15:38,

[result]

As a result of the MLPA test for all exons of the subject's Dystrophin gene, deletion patterns were found in Exon 45,46,47,48.

[Clinical information]

R/O, Becker muscular dystrophy

Fig 4 Second genetic test result report conducted on May 7, 2021   

 

   

Here, we need to compare the first test result report in 2004, which is the initial onset period, and the result report in 2021, the second test period, as a chart (Fig 6) to make a comparative comparison.

                      Fig 5  Comparison of 1st and 2nd genetic test results report

Inspection Round	1st	2nd
Sample collection	2004-07-28 11:34:04	2021-04-08
Inspection Date	2004-08-02	2021-05-07 15:38,
Test results	As a result of the DMD genetic test, the deletion of exon 45,46,47,48 was confirmed.	As a result of the MLPA test for all exons of the subject's Dystrophin gene, deletion patterns were found in Exon 45, 46, 47, and 48.
Medical diagnosis	C/T DMD/BMD due to exon deletions in the DMD gene	R/O, Becker muscular dystrophy

  

  There is a subtle but clear difference between the test results and the medical diagnosis of one or two periods with a time difference of 17 years.

Confirmation of deletion of Exon 45,46,47,48 -> Exon 45,46,47,48 showed a deletion pattern, indicating the result is insignificant and there is a difference in expression, so it may be overlooked maybe

 However, when a nurse collects a sample, there is a separate expert who mixes the sample and analyzes and judges it professionally.

 2004.08.02 In the first test conducted at K University Hospital in Busan, the interpreter in the Screening Test Report under the title of Result & Interpretation "DMD genetic test showed that the deletion of exons 45, 46, 47, 48 was found. confirmed".

 Naturally, neurologists confirm and report these readings as confirming C/T (Consistent with ; consistent with) DMD/BMD due to exon deletions in the DMD gene (DMD/BMD due to exon deletions in the DMD gene) The final diagnosis of Iran was made, not the doctor's discretion.

Looking at the second test result report 17 years later, on May 7, 2021, at University B Hospital in Yangsan,

As a Lab Physician Report, the result was "The MLPA test for all exons of the Dystrophin gene of this test subject showed deletion patterns in Exon 45, 46, 47, and 48."

 As with the test result report at K University-affiliated hospital in the first period, if the MLPA test for all exons of the subject reported that deletion was confirmed in Exon 45, 46, 47, 48, accordingly, the attending physician had to make a Contest with ;

 A report showing the appearance of a deletion cannot be a report confirming the deletion, which means a meaning close to the nature of the absence.

 

Make a diagnosis of Becker-type muscular dystrophy of medical condition (R/O) by referring to the contents of the laboratory doctor's report, the medical history through consultation with the patient, and the opinion of the specialist at University D who entrusted the outpatient treatment it has become

 Compared to Confirm a deletion, the word seems to be a deletion pattern is an expression that cannot be given an equivalent meaning.

 Perhaps these subtle genetic changes made it possible to stop the ongoing muscle destruction, regenerate the muscle, and secure the patient's life.

 The fact that medical institutions and specialists with public credibility make a final medical diagnosis for a patient who has already been confirmed and has progressed with the disease is a sign of a revolutionary genetic change.

  Because, figuratively, it was as if it had changed from the original to the fake.

 If the inspection in the 1st period made a conclusion of the invasion of the enemy by confirming and reporting the enemy troops in front of the guards who were looking at the four main guards at the forefront, the inspection in the 2nd period was a report that it looked like an enemy army, and the commander said that there was It's like coming to a conclusion that it seems like it.

 Destruction proceeded rapidly and the patient's muscle, whose weight had dropped to 51.3 kg, entered regenerative treatment from rest to close to 70.0 kg. It took a lot of time and effort to arrive at the treatment (Fig. 7, 8) of the attempt to prepare the space so that it was filled, and it was accompanied by trial and error several times to modify the treatment direction during the session.

Fig 6 2021.05.20 Weight

그림 7 자전거 운동

  

In order to draw these results and write this article, the patient had to undergo a second examination and waited for the results to come out for more than six months after the former post.

 In addition, there were concerns that the deleted gene would change and could not be observed.

 If the deleted gene is not observed, rather than being recognized for the achievement of direct treatment of the gene, the world, researchers, scientists, medical practitioners, patients, and their caregivers, and most or most of the members of myopathy groups and their members are the authors I will drive this patient to be a scammer on the go-stop gambling board.

 Also, they thought that the first test was wrong, the second test was wrong, and they would be the target of distrust and excuses that focused on the first and second genetic tests performed by these patients themselves.

 I am well aware that this deletion pattern of exon will not disappear easily in the electrophoresis of the genetic test unless 100% complete treatment can be achieved for this patient.

Fig 8. MLPA analysis chart of Duchenne type patient with #45,46,47,38,49,50 exon deletion

 

The meaning of exon deletion, deletion, or deletion of the DMD gene as we know it is accepted as the absence of an exon, and it is recognized and believed by the author.

 However, as the MLPA analysis in Fig. 9 above shows, if the fluorescence intensity of each exon is <0.75 on the vertical axis, it is an exon deletion, 0.75 < normal <1.3, and >1.3 if duplicate or duplicate ( Duplication).

Compare it with anyone type of tree or plant. If it grows to a general average height, it is normal, if it grows too far and grows steadily, it becomes duplicated or duplicated. Even though germination occurred, it did not grow properly, so it could not reach the normal height and if it was defective, it would be deleted. In terms of the human physique, a dwarf who is much shorter than the normal height will be deleted, and if the height exceeds the level of a normal person, it will be classified as a duplicate.

One exon in the DMD gene is only one of the 79 steps to make the dystrophin protein.

  However, from among the four nucleic acids adenine, guanine, cytosine, and thymine, three of them are selected dozens of times and these are mixed dozens of times like this and that.

  After this dozen of nucleic acid mixing work is finished, it takes a brief break (intron), and then the next step should be continued by mixing dozens of times to the next step.

  Because this mixing operation and the resting process are performed 79 steps, there are 79 exons.

  No one can deny that the genuine dystrophin protein that nourishes the muscle cell membrane will be produced only when these 79 processes are successfully completed.     

If we look at the fluorescence ratio in the diagram in Fig. 8 above, anyone can immediately know that the ratio of fluorescence will be low due to insufficient energy to be supplied to carry out the process of a defective exon.

 Conversely, in the case of duplication or duplication of exons, the supplied energy is excessive, so that anyone can know that the ratio of fluorescence is increased.

 That is, in any stage of the exon, if the energy supplied for this purpose is insufficient or excessive, the process of the exon is ruined.

 If it is insufficient, it will be ruined by a defect, if it is excessive, it will be ruined by duplication or duplication.

 My opinion and judgment is that although the fluorescence of the missing exons 45,46,47,48 of the above patient did not exceed 0.75> and did not change to a normal exon, it was It is impossible to deny the possibility that a change in the fluorescence ratio at the time of genetic testing has risen to close to 0.75, which is the boundary ratio between defect and normal.

Therefore, in the second genetic test, as a laboratory doctor's report (Lab. Physician Report), the result was "The MLPA test for all exons of the Dystrophin gene of this test subject showed a deletion pattern in Exon 45, 46, 47, and 48. "It seems that he is using the art of expression.

 On the one hand, even if any change did not come, at least during the session, would this ratio of fluorescence soar to normal, or would it work to produce dystrophin while crossing the fluorescence value of 0.75, which is the borderline between defect and normal? I also have my doubts that

 The reason is that only then, all exons of the DMD gene will operate normally and dystrophin protein will be produced again in the muscle cells that are undergoing destruction, and only when new dystrophin made normally is produced and provided, the progress of muscle destruction is stopped. be able to do it

 In addition, this is because only when a sufficient supply of these proteins is continuously maintained, muscle regeneration and retrograde treatment toward the restoration of normal weight, as shown in the comparative photo in Fig. 1 above, are possible.

Here, if the term “deletion” refers to a condition of 100% fluorescence ratio of 0.0000,,,,,,,, it is the direct gene therapy

 With such a fluorescence ratio of 0.000,,,,,,,, gene direct treatment becomes an impossible creation area that even God cannot do, indeed, there is no prospect.

 However, regardless of the degree of fluorescence, exons treated as deletions because their fluorescence is weaker than that of normal exons can be treated directly if the fluorescence ratio can be raised to the normal level. The development of these technologies is the problem.

 Gene direct treatment means that we have to do research to think about what is needed and how to raise or lower this ratio.

 While the entire cell survives, the amount of power that is sufficient to do its job or the energy that the exon can carry out smoothly must be produced and provided by the mitochondria, and must also be delivered to the nucleus of the cell.

 Mitochondria are energy factories that burn fat to produce and supply energy sources for cells.

 In order for mitochondria to sufficiently perform their job of generating energy sources for cells by burning fat, the mitochondria themselves must be healthy and must have sufficient strength to carry out the energy source production of these cells by themselves.

 Otherwise, fats that need to be burned to make an energy source cannot be burned in a timely and proper manner, and fat accumulates.

 In this way, fat accumulates and clumps, which we call pseudohypertrophy in medical terms.

 This pseudohypertrophy invades and occupies important muscle areas of the body where muscle tissue should be, and destroys those muscles.

         

I have been conducting a session in which the energy that can reinforce the energy source for driving the mitochondria, where these mitochondria themselves can work healthy, is viewed as the energy of the universe and is drawn into the patient's body.

 Adopting in the session the way mitochondria are empowered to become healthy and capable of their full capacity is a non-existent choice in the possibility of treating myopathy, which requires stopping the destruction of ongoing muscles and regenerating new ones. Because it will be the only way.

  This approach is not just a tailored approach for deleted or duplicated genes, or a targeted session.

 If the body condition and muscle of the patients with myopathy improve, the muscle cells also get better, and when the muscle cells get better, the cell nucleus gets better, and when the cell nucleus gets better, these faulty genes in the cell nucleus are also proportional to it. It is using the mechanism of the link that hopes to get better and the ripple power of the chain reaction.   

                 

When the Buddha passed away in Kushinagar, India, as his will, he spoke of the impermanence of conduct.

 All actions are not always done, and they are subject to change or evolution under the influence of the surrounding environment and conditions. If you reject these changes, you will be put out of business. This is a law of nature.

 When muscle destruction is stopped and muscle is regenerated, the condition of the body changes, and the body has a change.

 Depending on the condition of the gene, the state of the body may be dominated, but it is natural as a natural phenomenon that the gene should also have proportional changes according to these conditions of the body and the new state of change.

 My direct gene therapy strategy is to aim for gene therapy according to these laws of nature or its laws.

 Regardless of the Duchenne/Becker type, the gene therapy for any type of muscular dystrophy should be a high-end cure that can only be seen at the final stage of changing the body condition to be healthy so that it is close to normal. to do, and to be

 In the treatment of the Duchenne/Becker type, the priority is to save the patient's life, increase the digestion, and improve the body's ability to use the body.

 After fixing all this and that, in the end, it is this gene therapy that ultimately can be fixed or not, fixed or not, must be fixed or not.

 It is not a disease that has to be all-inclusive from the beginning or from the beginning to the end of the gene therapy that is completely blind.

 If the broken genes of these patients are corrected, muscles are automatically created, so that all myopathic patients can have normal muscles and return to normal people like everyone else.

 I warn you that the hopes and desires of trial-and-error gene therapy can eventually lead to the loss of a patient's life.   

Everyone likes chicken that is delivered to order.

 Look at the leftover chicken leg bones.

 A chicken leg bone cannot have as much flesh as a pig's foot.

   In gene therapy for these myopathy, new muscles made by regenerating degenerated skeletal muscle as gene therapy must be attached to the patient's skeleton and built up one after another.

However, if the first treatment to fix the large, thick, hard, and strong bones and joints of the stunted or thin patient cannot be performed, the treatment of this disease cannot be expected at all.

 That's why, look at these chicken legs and pig's feet, and also think about it.

 At least not as many people who know me as I am who see or believe that gene therapy, whether indirectly or directly, can be the alpha and omega for myopathy.

 In the past, Zhuangzi 莊子 compared people's foolishness and said:

 What a fish needs is a gourd of water right now, not an arrogant river that flows ten miles away,,,,,,,,,

 Although it is not perfect, bringing about this level of change is of great significance and reward to the above patient and the author, and motivates the role that can spur the treatment of this disease. It seems that it will be a reason or opportunity to give a little attention to other patients and their families who have believed that they will not be cured.

Why are humans and chimpanzees considered the same apes?

 Because the genetic information is 98% identical and the difference is only about 2%, it is classified as a zoologically similar species.

 But some scientists are also saying.

 The possibility of evolution in which these genes will change by 2% in millions of years is a huge tornado that blows away this garbage in a huge garbage dump full of all sorts of rubbish, and this and that mixes together in a jumbled way. What is less than the probability of a jet being created by chance is a change in genes.

 Even if there is a difference in wind speed, if it is possible to directly leave traces of such wind on the gene to appear in the results of genetic testing, it will be a significant cornerstone contributing to the development of direct gene therapy.

 This is because, no matter how well this patient manages his/her health, it is absolutely irreversible for these defective genes of DMD / BMD to be improved or changed.

 Even if such a reversible change is brought about, the change cannot be expected in this patient's lifetime.

 Even if gene transfer is passed down from generation to generation, it is impossible for anyone to promise or specify how many hundreds or thousands of years it will take.

What they need is the fact that we are going to disclose the above data to reveal it, but rather than denying my opinion, the dystrophin protein is increased according to the change in the gene even though gene therapy was not done anyway, so the progress of muscle destruction is stopped, and the muscle is rather damaged. Addressing the question of whether the muscle can be regenerated and reattached with the mechanism of this disease would be the first priority.

 Because of these negative people, the established facts of the test results or the changes in the muscles of the patient's body are not accepted as facts and cannot be overlooked as they are simply buried as unconfirmed information or treated as deceptive false information.

 While reluctant to acknowledge any signs of such changes in the patient's body, how can we vaguely expect gene therapy to return the broken genes of myopathic patients to normal?

  Such a wish would be like expecting a tornado to blow through the garbage heap, causing all kinds of garbage to flutter and then come back together to form a jumbo jet.

  It is a change in a patient with myalgia that must be pointed out as a writer, so I am leaving this post with the patient's consent.

  I hope that patients, their families, researchers, and medical personnel who are interested in gene therapy due to this disease will have their own meaning or interpretation by comparing the above two-gene test results to understand this disease. I hope to publish this.