Solve ME/CFS Webinar--Deyra Unutmaz-- July 19, 2018

Gemini

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"Crossroad of the Immune Response and the Microbiome" is the topic Derya Unutmaz, ME/CFS Collaborative Research Center Director at Jackson Labs will cover on a July 19, 2018 webinar from 1 to 2PM EDT.

The Webinar is sponsored by the Solve ME/CFS Initiative and Registration is required here:

https://solvecfs.org/solve-mecfs-initiative-webinars/
 
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mariovitali

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Yes i did.

Unfortunately there was not very specific information about ME/CFS but he did mention Artificial Intelligence and Machine Lerning numerous times which brought a smile on my face ;-)
 

Learner1

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Did anybody watch the presentation ? Any online video ? Or can somebody list the salient points ?
They said it was being recorded snd woulf be available from Solve ME/CFS via YouTube.

Very interesting presentation. The basic idea was they will investigate micribiome composition, metabolites made by the microbiome, and how it relates to the biochemistry of ME/CFS patients. He spoke of personalized medicine, customizing treatments for the individual.
 

Moof

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It was really interesting, and it struck me (not for the first time) that only a few years ago it wouldn't have been possible to process the truly staggering amount of data that these researchers need to produce to investigate the microbiome and its relationship to the immune system. It sounded as if they plan to put it on YouTube fairly soon, so look out for it at the Solve channel?

https://www.youtube.com/user/SolveCFS
 

Gemini

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Here's a brief overview of the Webinar talk; same talk was given at the CFSAC last month, transcript here:
https://www.hhs.gov/ash/advisory-committees/cfsac/meetings/2018-06-20/transcripts-day-2.html

* Begins with a quick tutorial on immune system functioning & types of diseases that can occur, i.e., autoimmunity, chronic inflammation, etc.

*Major point: A person's "immune profile" is based on their history of exposures & is unique to each person; likewise the microbiome is also "personalized" to each person. This is very good as you said @Learner1 @mariovitali

* Research approach will be top-down: Genomics> Transcriptomics> Proteomics> Metabolomics

*Goal is to identify "metabolites" that could be used as treatments to "re-program" the immune response

*Will require computational & systems biology, AI and machine learning. Also brought a smile to my face @Moof CFSAC transcript has even more detail on study sizes, data, etc.

*Patient samples will come from the Bateman Clinic & local patients. Note in the CFSAC talk he also mentions requesting samples from the CureME Biobank in the UK

*He said he has "immune profile" data & will be writing a paper on that

*He concluded by introducing his team members & their specialties:
https://JAXmecfs.com/team/
 
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ljimbo423

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*Major point: A person's "immune profile" is based on their history of exposures & is unique to each person; likewise the microbiome is also "personalized" to each person.
That comment also jumped out at me.

A persons unique "immune profile" and unique microbiome as Derya Unutzman called them, most likely have a huge impact on the cytokine profiles seen in ME/CFS and why they can't find a common cytokine profile or signature.
 

Gemini

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A persons unique "immune profile" and unique microbiome as Derya Unutzman called them, most likely have a huge impact on the cytokine profiles seen in ME/CFS and why they can't find a common cytokine profile or signature.
Good point @ljimbo423! Many researchers have looked for one that's for sure!

Just read the CFSAC transcript where he describes his "different" approach & fields probing questions from the Committee [starts halfway down the page on day 2].

He strongly believes ME/CFS is an "immunological disease" in the "ugly" category on his "Good-Bad-Ugly" chart.

The "immune system falls off a cliff" and doesn't recover is how he puts it then asks, "Why doesn't the immune system "reset" to a steady state like it normally does?"

Examining three things that "regulate" immune functioning: the immune system itself(immune profile), the microbiome, and the metabolome in each patient, generating huge amounts of data, then using a systems biology approach:

"we're trying to link using machine learning, artificial intelligence approaches the types of symptoms the patient has, the type of metabolome, the type of immune profile, the type of microbiome, bring this together. It's literally putting the patient back together...and can we associate these with... disease duration or the severity and so on."

"we have to consider the patient as a whole..."

"one person's set point might be another person's abnormality..."

He hopes this method will "molecularly" define subgroups and common and personalized features within them.

When patient advocate Donna Pearson asked if he considered outbreaks, i.e., when a group of people are stricken at the same time, he said he wasn't looking at initial triggers.

Her excellent question helped me distinguish his work from immunologist Mark Davis'.
 

ljimbo423

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"we're trying to link using machine learning, artificial intelligence approaches the types of symptoms the patient has, the type of metabolome, the type of immune profile, the type of microbiome, bring this together. It's literally putting the patient back together...and can we associate these with... disease duration or the severity and so on."
Fascinating stuff!

When patient advocate Donna Pearson asked if he considered outbreaks, i.e., when a group of people are stricken at the same time, he said he wasn't looking at initial triggers.

Her excellent question helped me distinguish his work from immunologist Mark Davis'.
Good point. Nice to know researchers are tackling this from different angles and perspectives.
 

Wally

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@Gemini - I was confused by you comment about Donna Pearson’s question at the CFSAC meeting asking if Unutmaz research would consider outbreaks of this illness. You said said that the answer that he would not be looking at initial triggers of outbreaks helped you distinguish his work from Mark Davis.

I did not realize that Mark Davis was or is looking for the initial trigger of cluster outbreaks (like those that are well documented in the mid 1980’s at Incline Village, Nevada or Lyndonville, N.Y.). Can you point me to where there is information about the research being conducted by Mark Davis that he is looking for the initial trigger for those or other cluster outbreaks?
 

Gemini

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@Gemini - I was confused by you comment about Donna Pearson’s question at the CFSAC meeting asking if Unutmaz research would consider outbreaks of this illness. You said said that the answer that he would not be looking at initial triggers of outbreaks helped you distinguish his work from Mark Davis.
@Wally, sorry for the confusion.

Last year there was a great deal of interest and excitement when Mark Davis presented his T-cell clonal expansion research at the OMF Community Symposium indicating he was pursuing its cause, pathogen or autoimmune.

His presentation is on YouTube here:

Tracing back to the cause of T-cell clonal expansion could indicate what is perpetuating ME/CFS and lead to treatments which address this core aspect of the disease.

While a T-cell expert himself Unutmaz's research is taking a different approach.

As @ljimbo423 points out its nice that researchers are tackling this from different angles and perspectives. That's what I meant by distinguish. Hopefully that helps.