Talk:Duchenne muscular dystrophy

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This article was the subject of a Wiki Education Foundation-supported course assignment, between 27 August 2018 and 7 December 2018. Further details are available on the course page. Student editor(s): Vgedwards82!, Ts6t.mtsu, Jat6z, Mam2ex. Peer reviewers: Vgedwards82!, Rma3t-mtsu.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 19:54, 16 January 2022 (UTC)[reply]

Daughters of men with Duchenne

The statement "Daughters of men with Duchenne also have a 50% chance of being carriers" seems to be completely wrong. Any female MUST get an X from her father, who only has 1 X, and if a man has Duchenne's than his 1 X must be infected. In other words, a daughter of a man with Duchenne, it seems to me, MUST be a carrier. I think that whoever wrote the statement got confused because the diagram shows an unaffected father, hence the chance that his daughter may not be a carrier.

--DreamsReign 22:57, 22 February 2006 (UTC)[reply]

Just noting that this has been fixed. --nkayesmith 01:36, 9 August 2006 (UTC)[reply]

Distal or proximal muscles?

Somebody changed the text Distal muscles to proximal muscles in symptoms section. Wikipedia mentions both on the page that proximal muscles redirects to, and I have it from a reliable source (which I should really put here) that the distal muscles are affected. However, upon reading wikipedia's explanation, I don't think either serve to cover all of the affected areas. Perhaps the somebody who changed this could leave an explanation here. Thanks. nkayesmith 01:58, 18 August 2006 (UTC)[reply]

As someone who suffers from the disease, I can tell you that all muscles are eventually affected. However, I'm not sure if proximal or distal muscles are affected first. As far as I know, they are affected at the same time. More accurately, voluntary muscles that aren't used while inactive or while sleeping deteriorate faster than involuntary muscles, such as cardiac muscles that are used all the time. For instance, I am 19 years old. I can't move my legs and can barely move my arms well enough to use a keyboard and mouse, but an ultrasound would reveal a healthy heart. Perhaps the text should be changed to voluntary muscles? --Sylvas 23:58, 26 February 2007 (UTC)[reply]

Possible references

From User talk:Nkayesmith:

Here are a few sources:
  • Emery, 2000, Muscular Dystrophy – The Facts, Oxford University Press, United States of America

NCurse work 13:59, 1 October 2006 (UTC)[reply]

Are there any specific racial groups or geographic areas in which DMD is more common?

I don't mean to sound racist or anything, but I'm doing a report on this disease and I can't find this info anywhere. Are there any specific racial groups or geographic areas in which DMD is more common? It would be really helpful if anyone knew this. --Floog 00:36, 26 March 2007 (UTC)[reply]

As am I, and I cannot find this information. It would be useful to have. GreaseNinja 14:23, 12 November 2007 (UTC)[reply]

I know your not a racist but put it this way, there aren't any racial categories, its just one species of human. And most research suggests that it occurs everywhere and if there is no research between where you live and the instance of duchenne's then you can't write about it. You will have to just state that there is no correlation at the moment between geographical location and the occurence of duchenne's. It is possible that there are some environmental factors that might trigger a mutation, like living next to radiation. But though there are genetic conditions that are common in some ethnic groups, this particular one seems to affect everyone. ScottishAnarchist 15:12, 26 April 2008 (UTC)[reply]

My opinion about this disease it’s related more to genetic factor that we all keep touch with it from the beginning . I think we should develop our research about human genes and avoid its recurrence Mahmoud ateya (talk) 10:26, 6 July 2020 (UTC)[reply]

muscle restoration in an animal model of Duchenne muscular dystrophy

Enough dystrophin accumulated in the muscles of the MD mice so that we could no longer find defects in the muscles when we examined them," says Sweeney (senior author H. Lee Sweeney, PhD, chair of the Department of Physiology at Penn). "For all intents and purposes the disease was corrected by treatment with PTC124." [1] Brian Pearson 05:03, 23 April 2007 (UTC)[reply]

NEJM - antisense oligonucleotide bridges open reading frame and induces dystrophin production. JFW | T@lk 07:51, 27 December 2007 (UTC)[reply]

Other Charities

http://www.actionduchenne.org/ - is a UK based Duchenne MD site, if non-US sites are wanted (though I know that it might make the list very long, if they were addded for all countries... hence not adding it myself. Emmadw (talk) 13:18, 19 April 2008 (UTC) Emma[reply]

A few comments.

Having just read through the article, I have a few suggestions as to how it can be improved.

  • More detail on the aetiology and pathophysiology of the condition would be helpful.
  • Several sections within the article are lacking in citations, particularly the smaller sections at the beginning of the article.
  • The article could do with a good copyedit, with some misspellings and a few words seeming to be merged together.

Hope this is of some use! :-) Colds7ream (talk) 15:30, 1 December 2008 (UTC)[reply]

Occupational therapy

This section appears to have been copied from a University of British Columbia wiki. The material there was built up over numerous edits. I cannot see a copyright policy on that site. It may well be that the content of that wiki is under a suitable licence for transfer to Wikipedia, or that the original editors of the content are the ones doing the transfer and are happy to re-license it under the appropriate Creative commons license, but I think we need an explicit link to the wiki's copyright policy or a statement by the authors.-gadfium 22:05, 27 April 2011 (UTC)[reply]

Also possible in females

I think some ammends should be made to the article. Though much rare, duchene muscular dystrophy can also occur in females due to skewed x chromosome inactivation, so the intro has to be changed


Here is some text I wrote earlier explaining the phenomenon with reference


Skewing can directly affect the expression of a genetic disease because of the interplay between the number of normal cells and mutant cells. Also, skewing can be a good indicator for a disease in the clinical setting as it can hint at the underlying mechanism that are leading to certain types of cells gaining selective advantage. For example, skewed X inactivation has been shown to be correlated with the condition known as Duchenne muscular dystrophy in rare cases of heterozygous females [52]. Duchenne muscular dystrophy produces severe muscular weakness and myopathy in the affected individual. Affected females show strong dominance of the X chromosome containing the mutant dystrophin gene. While it is not yet determined whether the skewness causes the disease or vice versa, because the two occur together, it is a useful clinical tool. Particularly, there seems to be a familial inheritance that leads to some females become mosaics full of the mutant gene. Thus, presenting patients can be analysed for their patterns of x inactivation as well as their families.

Yoshioka M, Yorifuji T, Mituyoshi I (1998) Skewed X inactivation in manifesting carriers of Duchenne muscular dystrophy. Clin Genet 53:102–7 —Preceding unsigned comment added by 130.102.158.15 (talk) 03:18, 12 May 2011 (UTC)[reply]

Exon skipping rewrite

Many errors have cropped up in the exon skipping sequence and the narrative had been lost through small accumulated edits. I rewrote the section, mostly by rearranging existing text. I am not very familiar with the Prosensa/GSK 2'-O-Me phosphorothioate clinical trials, so I assumed the existing text referring to the clinical outcomes was correct. I clipped out some of the discussion of other disease targets for exon-skipping. This section would benefit from some detail on the range of mutations that give rise to DMD and the need for many approved oligos to treat most of the DMD population.

JonMoulton (talk) 21:55, 22 June 2011 (UTC)[reply]

Abortion and DMD

Just noticed that the text:

"Prenatal tests can tell whether their unborn child has the most common mutations, and they may choose to have an abortion."

was changed to:

"Prenatal tests can tell whether their unborn child has the most common mutations."

There are numerous sources in the medical literature[2][3][4][5][6][7] that describe abortion as a fairly common choice in such situations; thus, I've reverted the edit. Rhode Island Red (talk) 06:19, 4 January 2012 (UTC)[reply]

Ongoing research on prostaglandin d synthase inhibitors

At a conference on research results from the ISS, I just saw presentation on a novel treatment of DMD using prostaglandin d synthase inhibition, see [8] and [9]. The ISS was used a platform for growing large and pure protein crystals for x-ray crystallography, but I'm not at all an expert on medicine or medical research, so I'll leave this one for others to evaluate and include. siafu (talk) 16:40, 26 June 2012 (UTC)[reply]

Matrix metalloproteinase inhibitors potential treatment for DMD?

http://hmg.oxfordjournals.org/content/18/14/2584.full

I see no mention of this in the article. One MMPI is doxycycline, a commonly prescribed antibiotic. This could have immediate therapeutic implications. — Preceding unsigned comment added by 75.111.74.238 (talk) 21:40, 22 August 2012 (UTC)[reply]

It's not mentioned nor should it be. It's a simple mouse study with MMPIs. It has no "immediate therapeutic implications" for DMD. It's also a primary source. See WP:MEDREV for guidance. Rhode Island Red (talk) 22:45, 22 August 2012 (UTC)[reply]

Pronunciation of Duchenne

Webster's New World Dictionary uses 'doo chen' [with diacretical marks] to instruct pronunciation of the word 'Duchenne'. How is (pronounced [dyʃɛn] / /duʊˈʃɛn/ an improvement on that simple elegant instruction? It's not only not an improvement, it's incomprehensible. It should not be here, in an encyclopedia, which is not the place for pet projects such as 'IPA', whatever that is. Jack B108 (talk) 21:15, 6 May 2013 (UTC)[reply]

You are welcome to add a WP:RESPELL version of the pronunciation to supplement the IPA.-gadfium 23:01, 6 May 2013 (UTC)[reply]
Please don't try to edit war style changes into articles. Can you tell me what percentage of our readers understand IPA? --Anthonyhcole (talk · contribs · email) 22:50, 7 May 2013 (UTC)[reply]
You should debate whether Wikipedia should use IPA somewhere more central, such as the village pump. An individual article talk page is not appropriate. Also, I did not add the IPA, I am merely defending it against removal. The onus is on you to get a consensus to remove it.-gadfium 22:57, 7 May 2013 (UTC)[reply]
I had not realised that this had been added so recently, so I'll leave it off the article for the time being to see if other editors would like to comment on its relevance. The IPA added was:
pronounced [dyʃɛn] / /duʊˈʃɛn/
I'm not fluent in IPA myself, but this is still helpful in telling me how to pronounce the name.-gadfium 23:14, 7 May 2013 (UTC)[reply]

Cardiac issues

doi:10.1161/CIRCULATIONAHA.114.015151 JFW | T@lk 22:16, 6 May 2015 (UTC)[reply]

Muscle stem cells

New (primary) source:

  • "Dystrophin expression in muscle stem cells regulates their polarity and asymmetric division". Nature Medicine. 16 November 2015. doi:10.1038/nm.3990. {{cite journal}}: Cite uses deprecated parameter |authors= (help)

LeadSongDog come howl! 21:47, 16 November 2015 (UTC)[reply]

  • "EGFR-Aurka Signaling Rescues Polarity and Regeneration Defects in Dystrophin-Deficient Muscle Stem Cells by Increasing Asymmetric Divisions". Cell Stem Cell. 31 January 2019. doi:10.1016/j.stem.2019.01.002. {{cite journal}}: Cite uses deprecated parameter |authors= (help)

"Rare"?

The opening sentence states "Duchenne muscular dystrophy (DMD) is a rare X-linked recessive form of muscular dystrophy, affecting around 1 in 3,600 boys". Is 1 in 3,600 boys truly rare? The reference does not include that implication. Axl ¤ [Talk] 19:56, 28 March 2016 (UTC)[reply]

See rare disease. This appears to qualify by the definitions given there for the US, Japan and Europe. If this is not sufficient, I suggest you ask at Wikipedia talk:WikiProject Medicine as this potentially affects many medical articles.-gadfium 05:58, 29 March 2016 (UTC)[reply]
While the incidence of DMD fits (some of) the numerical definitions given in that article, there does not seem to be a reliable source that specifically calls out DMD as rare. In the absence of such a source, that interpretation is synthesis and does not belong in Wikipedia's DMD article. I am removing "rare" from the article. Axl ¤ [Talk] 10:29, 29 March 2016 (UTC)[reply]
Although it's relatively rare, it is one of the most common X-linked genetic disorders. That kind of wording could satisfy both perspectives on rarity.MartinezMD (talk) 10:58, 29 March 2016 (UTC)[reply]

External links modified

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unaffected/carrier women

if it is x-chromosome linked shouldn't that mean women should have twice the chance of getting DMD? how come it isn't? — Preceding unsigned comment added by 2A02:1810:3622:5C00:E925:CF72:F6BA:A76F (talk) 00:24, 3 July 2016 (UTC)[reply]

See X-linked recessive inheritance.-gadfium 04:05, 3 July 2016 (UTC)[reply]

BIG lancet neurology review

doi:10.1016/S1474-4422(18)30024-3 JFW | T@lk 15:27, 14 February 2018 (UTC)[reply]

What is the approved DMD treatment to elevate dystrophin levels

What is the approved DMD treatment to elevate dystrophin levels ? New Scientist (8 Sept 2018 p14) says there is one (that produces dystrophin at 0.4% of normal levels) but this WP article does not seem to mention it. - Rod57 (talk) 20:26, 8 September 2018 (UTC)[reply]

Rod57, that is eteplirsen from Sarepta Therapeutics. It is only useful for some mutations. JonMoulton (talk) 18:55, 8 July 2019 (UTC)[reply]

Peer Review

I have read your contribution to the article of DMD. Great job overall. If you look carefully at the first sentence, it was overrepresented in the previous sections of the article. I think if you start without defining what DMD is, it would still be a great addition that you have made. Also, in the second sentence, you mentioned that the life expectancy varies but maybe forgot addressing the factors that affect the life expectancy of the patients. 2nd paragraph, 3rd sentence, you forgot to use a comma before "such". Same paragraph, 5th sentence, you wrote "forties" and "fifties". It is not a problem. It is just not consistent with how you wrote 30s in the first paragraph. Other than that, it was all great. I hope this helps. Rma3t-mtsu (talk) 07:20, 18 November 2018 (UTC)[reply]

Ref

Which ref supports this

"Duchenne muscular dystrophy results when a change in the base sequence of the human dystrophin mRNA results in encoding a protein which would be missing a functional C-terminal (downstream) end. This can be due to a deletion or insertion mutation changing the reading frame of the RNA or to the introduction of a premature stop codon (a nonsense mutation) into the DMD gene (which encodes dystropin). Exon skipping can be used to treat some mutations causing DMD. If a deletion has altered the reading frame of the mRNA, the codons downstream (in the 3' direction) of the mutation are altered and no longer encode the correct amino acids. Translated into protein, such an mRNA would encode a protein with amino acids at its C-terminal end that are different from the amino acids of healthy dystrophin; this altered dystrophin would not carry out the biological functions it does in healthy cells. Sometimes an exon adjacent to the deletion has a number of bases that can restore the reading frame of the downstream codons if that adjacent exon is "skipped", that is, if the spliceosome can be induced to splice out the adjacent exon so it is no longer in the mature mRNA. Steric-blocking antisense oligos can cause such skipping either by blocking snRNP binding sites near the splice junctions or by blocking splice regulatory elements (such as exonic splicing enhancers, intronic splicing suppressors, etc.). The approved DMD drug eteplirsen (ExonDys51) blocks an exonic splicing enhancer to trigger skipping of exon 51, frameshifting downstream sequence. When used in a person with one of the appropriate DMD-causing mutations (referred to as a mutation amenable to exon 51 skipping) eteplirsen can restore a healthy reading frame in the downstream dystrophin RNA sequence and restore production of a functional C-terminal amino acid sequence of the dystrophin protein. Use of exon-skipping oligos to treat another sort of mutation, genetic duplications, is in an earlier stage but is progressing. Exon skipping oligos can potentially be used to treat nonsense mutations by skipping the exon containing the mutation (though if skipping that exon induces a frameshift, additional exon(s) would have to be skipped to restore the reading frame)."

And why is it all in the research section? Eteplirsen is discussed already. Doc James (talk · contribs · email) 04:34, 27 December 2018 (UTC)[reply]

"healthy reading frame", "exon skipping can be used to treat", "functional C-terminal amino acid sequence of the dystrophin protein"... jeez! Not that it is inherently incorrect, but thanks for moving this double Dutch out of the mainspace. — kashmīrī TALK 09:53, 27 December 2018 (UTC)[reply]

Link

Perhaps this link can be added to the page ?: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6205228/ Genetics4good (talk) 08:51, 14 February 2019 (UTC)[reply]

Contradictory

Introduction section gives a statistic of 1/5000, Epidemiology gives 1/3500, both with citation. Should it be listed as contested?— Preceding unsigned comment added by Данјул Финеган (talk • contribs)

I see the 5000. I don't see the 3500. Could you point it out please? Generally if both are reliable and give different numbers, I would put it as a range (e.g. rates range from 1 in 5000 to 1 in 3500) and reference each. MartinezMD (talk) 13:28, 10 May 2019 (UTC)[reply]

"https://en.wikipedia.org/w/index.php?title=Duchenne_muscular_dystrophy&diff=896425217&oldid=896418964"Данјул Финеган (talk) 11:39, 13 May 2019 (UTC)[reply]

The text is confusing as there are prevalance can be a. prevalence in a fetus in the whole fetus population, b. prevalence at birth out of e.g. all men born and c. say prevalance at a certain age - e.g. say age 5.
However as people pretty much die before 30 then a whole population prevalence is also going to be wrong (and more dependent on the age profile of a community).
Given the widespread testing and then aborting of possible fetuses then the population level will drop in countries that carry out this testing and abortion election where this is a preferred cultural choice. CLARITY can make this clear and show the prevalence - what is done for other cases? DO we give a figure based on actual live births?? Does this take abortion into account? 91.154.169.156 (talk) 18:27, 16 November 2023 (UTC)[reply]

Why list eteplirsen under research?

Eteplirsen was approved several years ago in the USA. Why is it listed under the research section? It is a medication. There are oligos for other exons, such as golodirsen (to skip exon 53) and casimersen (to skip exon 45), that are still in clinical trials.JonMoulton (talk) 19:16, 8 July 2019 (UTC)[reply]

Likely because those of us following this page aren't involved with DMD treatment closely enough to have seen the approval. Of note in the approval announcement, and may be worth including in the article (unless there's been further data to say otherwise), is the FDA's statement that "A clinical benefit of Exondys 51, including improved motor function, has not been established". So approved, but not yet established to be helpful apparently. MartinezMD (talk) 21:29, 8 July 2019 (UTC)[reply]
FDA approval has been extremely controversial, and the agency's own committee recommended against it. Read more here: [10]. Eteplirsen has been refused marketing authorisation in Europe, too.[11] In my view it is only correct to describe eteplirsen as a compound with no confirmed efficacy. — kashmīrī TALK 08:17, 9 July 2019 (UTC)[reply]

Challenge to the statement "This represents about 1.5% of cases."

The sentence in question is in the Exon-skipping section.

Two sentences from Scoto et al. 2018 support a different number (found under 1.1 DMD: Antisense oligonucleotides(AONs)):

"The most common mutations affecting DMD boys are out-of-frame deletions removing one or more exons, found in approximately 65% of DMD boys."

"As an example,skipping exon 51 restores the reading frame of ~ 15% of all the boys with deletions."

15% of deletions treatable by exon 51 and 65% of DMD cases being deletions gives 9.7% of all DMD cases treatable by skipping exon 51. This is considerably greater than the 1.5% that is cited in this Wikipedia article in the Exon-skipping section. The sentence with the 1.5% claim cited Scoto et al. 2018 for support. However, I cannot find the 1.5% figure in that cited paper. I believe the 1.5% figure is false. Can anyone offer evidence for it? JonMoulton (talk) 18:32, 10 July 2019 (UTC)[reply]

1.5% is just basic math - it's 10% of all DMD cases, 15% of whom may benefit, equals 1.5% of all cases of DMD. I think the source is saying it could be as high as 70% of these cases, which then equals 7% of all cases of DMD. We have to be careful with the math and not mixing things up for the reader. MartinezMD (talk) 19:59, 10 July 2019 (UTC)[reply]
You write: "it's 10% of all DMD cases". What is 10% of all DMD cases? I agree that 15% of 10% is 1.5%, but your premise is not clear. I do not find that defined in the paper you cited. What does the 10% figure describe? JonMoulton (talk) 16:46, 11 July 2019 (UTC)[reply]
I didn't write this section of the article or cite a paper; I'm just looking at the article. I'm referring to "Antisense oligonucleotides (oligos), structural analogs of DNA, are the basis of a potential treatment for 10% of people with DMD.[43]" and then " "As an example, skipping exon 51 restores the reading frame of ~ 15% of all the boys with deletions. It has been suggested that by having 10 AONs to skip 10 different exons it would be possible to deal with more than 70% of all DMD boys with deletions."[43]" Where citation 43 is referring to the journal article Genetic therapies for inherited neuromuscular disorders. MartinezMD (talk) 17:07, 11 July 2019 (UTC)[reply]

Golodirsen information posted and removed. I am reposting now.

On 17 March 2020, I posted the following in the treatment section: In December 2019 the antisense oligo golodirsen (Vyondys 53) received US FDA approval[1] for the treatment of cases that can benefit from skipping exon 53 of the dystrophin transcript.

The above is true and documented with the embedded links.

Later on 17 March 2020, Doc James removed that information.

I am now reinstating the post and, if Doc James chooses to again remove information about the second approved antisense drug for Duchenne Muscular Dystrophy from the Duchenne Muscular Dystrophy page, I request that a reason for that action be documented here.

JonMoulton (talk) 18:47, 18 March 2020 (UTC)[reply]

Once again Doc James has removed the note about regulatory approval of golodirsen as a therapeutic for Duchenne Muscular Dystrophy. No reason was given. I am reposting the information on the drug approval. JonMoulton (talk) 19:19, 18 March 2020 (UTC)[reply]

On 19 March 2020 Doc James again removed the information about regulatory approval of golodirsen as a drug for Duchenne Muscular Dystrophy. I am reposting the information. JonMoulton (talk) 16:23, 19 March 2020 (UTC)[reply]

it is already in the article, the same section, next paragraph "The antisense oligo golodirsen was approved for medical use in the United States in 2019 for the treatment of cases that can benefit from skipping exon 53 of the dystrophin transcript.[28]", so I removed it again. MartinezMD (talk) 16:32, 19 March 2020 (UTC)[reply]

Thanks. I had missed that the approval note for golodirsen had been combined with ataluren in one paragraph. While it seems odd to group the compounds that way (the mechanisms of eteplirsen and golodirsen, both exon skippers, are far more similar than either is to ataluren, a stop-codon-readthough compound) I am satisfied that the note on approval is somewhere in the text. JonMoulton (talk) 19:18, 19 March 2020 (UTC)[reply]

References

  1. ^ U.S. Food and Drug Administration, Silver Springs, Maryland. News Release: FDA grants accelerated approval to first targeted treatment for rare Duchenne muscular dystrophy mutation, December 12, 2019. Archived December 13, 2019, at the Wayback Machine

Possible separate page for "dystrophinopathy"

I ran across this issue while editing calpainopathy. When referring to dystrophinopathies, there is no good place to link to. Would a small stub page be appropriate, in which Duchenne and Becker are linked? I'm not experienced enough to go ahead and act.. — Preceding unsigned comment added by Lukelahood (talk • contribs) 16:11, 7 May 2020 (UTC)[reply]

Additionally, Template:Muscular_dystrophy uses dystrophin, a protein, as the category containing duchenne and becker. Lukelahood (talk) 16:44, 7 May 2020 (UTC)[reply]

I went ahead and created the dystrophinopathy page.Lukelahood (talk) 21:49, 8 May 2020 (UTC)[reply]

Orphaned references in Duchenne muscular dystrophy

I check pages listed in Category:Pages with incorrect ref formatting to try to fix reference errors. One of the things I do is look for content for orphaned references in wikilinked articles. I have found content for some of Duchenne muscular dystrophy's orphans, the problem is that I found more than one version. I can't determine which (if any) is correct for this article, so I am asking for a sentient editor to look it over and copy the correct ref content into this article.

Reference named "FDA PR":

I apologize if any of the above are effectively identical; I am just a simple computer program, so I can't determine whether minor differences are significant or not. AnomieBOT⚡ 16:25, 13 August 2020 (UTC)[reply]

Notable Cases: Jack Johnson (Owen Farrell)

Anything that speaks against adding this paragraph unter Notable Cases?

Jack Johnson came to be known to the rugby community because Owen Farrell celebrates all his pionts by interlocking his fingers to symbolize "Joining Jack" since 2014 to raise public awareness and sponsorship of finding a cure.[12][1][2]

Cheers, Eltirion (talk) 09:05, 17 July 2021 (UTC)[reply]

We do list people with the particular disease, but only those who themselves are notable. Being publicly known only because of being talked about by a notable person is insufficient – on Wikipedia, notability is not inherited. Also, Express is not really an acceptable source. — kashmīrī TALK 15:43, 17 July 2021 (UTC)[reply]

References

  1. ^ Millar, Joey (2017-03-18). "Owen Farrell celebration: Here's why England rugby star does THIS symbol after scoring". Express.co.uk. Retrieved 2019-03-14.
  2. ^ Hughes, David (2019-02-01). "Owen Farrell celebration: what the sign made by the England rugby star means". inews.co.uk. Retrieved 2019-03-14.

GW501516

I heard on a 2017 podcast that a reformulated GW501516 that hopefully would not cause cancer was entering Phase 1 trials for DMD. What was the outcome of that? Even a negative result would be interesting either on that article or this one. -- Beland (talk) 07:09, 22 August 2021 (UTC)[reply]

Ah, found some more info: the corporate sponsor is Mitobridge, founded by Ron Evans, according to [13]. I think that might be the MTB-1 or MA-0211 announced on August 8, 2017 at [14]? -- Beland (talk) 07:22, 22 August 2021 (UTC)[reply]

Genetics

Duchenne's muscular dystrophy in boys 41.113.75.197 (talk) 18:37, 10 April 2022 (UTC)[reply]

The entire article is about the genetics of DMD in boys with the mention of the exceptionally rare cases in girls. What exactly are you proposing? MartinezMD (talk) 20:42, 10 April 2022 (UTC)[reply]
Retrieved from "https://mdwiki.org/wiki/Talk:Duchenne_muscular_dystrophy"