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March20 podcast Dr Hazen
anti-TMA pill in a year or 2 ? (scroll 12 mins)

Additional info: https://youtu.be/811v7RLXP9M
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MEBO TMAU TESTING DISCONTINUED
(2012-2017)

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want listed ? contact info@meboresearch.org

MEBO - UBIOME study 2018

'PRESS RELEASE'

NCT03582826
ClinicalTrials.gov

MEBO Gut Microbiome Study
"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"
Funded by uBiome Research Grant

"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"

Dynamics of the Gut Microbiota in
Idiopathic Malodor Production
& PATM

Started May 2018 - Ongoing

Current people sent kits : 100/100
3 kits per person

NO LONGER RECRUITING

Participation info : LINK English

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BO Sufferers Podcasts

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TMAU Petition world
TMAU UK end total:262
TMAU UK ends 23/01/20
TMAU Petition USA end total 204
USA : Moveon open
TMAU (Dominican)
Metabolomic Profiling Study
NCT02683876

Start : Aug 2016
Stage 1 : 27 Canadian volunteers to test
Latest click here (26 oct) :
17 samples returned


Note : Stage 1 is Canada only.
Return cut-off date : passed
Analysis can take 6/8 weeks
Analysis start in/before Nov
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rareconnect.org TMAU

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Denver TMAU Test Lab survey click here
click to Read more/less

USA survey for anyone who wants to improve Denver TMAU test

begun : Dec22
end : no ending for now

A trainee genetic counselor is working at the Denver TMAU test lab. Probably as part of her training. As a project she wishes feedback on any aspect of the Denver TMAU test and process. You can fill in the survey and/or email her (email address is in survey). It's meant for USA people, but perhaps others can give their view too (as we have so few opportunities).

quote from her rareconnect post

"Hello all! I wanted to make you aware of a research study being conducted to better understand the experience and needs of individuals with trimethylaminuria with a goal of being able to create improved patient and healthcare provider education materials. Any participation is completely voluntary and all responses remain confidential. Feel free to use the contact information within the link with any questions or share the survey with others with TMAU."

see this post for more details

https://www.meboblog.com/2023/01/denver-tmau-test-survey-tbc-who-it-is.html

Sunday, October 6, 2013

FMO3 gene : E158K and E308G

There are a few ways that people can have 'faults' in their DNA that cause them an inability to develop a fully functioning protein of some sort (eg FMO3 protein). Most errors will only affect function by a certain %, say meaning 90% function etc. It's 'null mutants' and deletions that are probably the worst type of errors, that can cause almost total inability to create the protein (usually people have maybe 20% function even if severe). Currently with TMAU, the severe genetic type is associated with having 2 copies of null mutants.

However the most common type of 'errors' are 'Single Nucleotide Polymoprhisms', 'variants' that are missense changes which mean the wrong amino acid is inserted in the 532 amino acids track that go to make a full FMO3 protein. Usually there are many of these missense changes in a gene pool and often do not have any 'clinical' effect on protein formation. However sometimes a missense copy here and there in your FMO3 DNA can compound to possibly affect function to some degree.

2 common polymorphisms for the FMO3 protein are what are known as E158K and E308G. This means that on the 532 amino acid 'DNA railtrack', at codons ('track') 158 and 308 there are missense amino acids. At both 158 and 308 they should be E (Glutamic acid) but instead it is :
158 : should be glutamic acid : instead is lysine
308 : should be glutamic acid : instead is glycine

Apparently, it is estimated that around 50% of the white population carry a copy of the E158K error, and about 20% carry a copy of the E308G error

What researchers do is in the lab use FMO3 DNA and check to see how the 'faults' may affect total formation of the (FMO3) protein. Currently it is thought that carrying a copy of E158K and E308G on the same allelle (i.e. from the same parent) may affect FMO3 function to some degree (say meaning 70%-90% function)

Whether later it will be thought carrying them on either allelle is enough to cause some deficiency is unknown. However it does seem that these little 'SNPs' (not just at 158 and 308) compounded may in the future be predicted to cause problems in the FMO3 DNA 532-track railtrack. To have a copy of one 'null-mutant' as well as these little SNP faults may be enough to put people in the 'risk zone' at times. We will need to wait and see the full picture

Link: amino acid symbols
Link: letter to editor about compound heterozygosity and FMO3 function



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1 comments:

Anonymous said...

mój problem nieświeży oddech już 7 lat , jedyne po czym jest gorzej to amfetamina, gdy zażyje amfetaminę pogarsza się bardzo

przeczytałem ten artykuł

http://jpet.aspetjournals.org/content/288/3/1251?ijkey=d34d01b2247dfb8cd3a932a5beb09e2ea1b7be3c&keytype2=tf_ipsecsha

i pytam- czy jeśli pogarsza się po amfetaminie to mogę mieć tmau1?

Dec 27, 2016, 11:00:00 AM
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