1/ A 🧵 on the latest (preprint) paper by @CGATist et. al. The paper mentions that "Significant female and male traits were indicative of chronic inflammation, insulin resistance and liver disease" : Tagging @JennieJacques1 medrxiv.org/content/10.110…
2/ Differentially expressed proteins were used as inputs to the software framework I have been using in order to identify promising research targets. Note that "Liver disease" has been identified as early as 2017 as a potential target using certain analytical methods.
3/ Moreover, on a document I circulated among #MECFS researchers in 2017, issues with Glucose metabolism and Inflammatory processes have been also identified ("Liver disease" also mentioned) :
4/ We begin with differentially expressed proteins appearing on Figure 5. A ranking is generated according to the relevance of each medical topic. Below are the results. Note the relevance of "protein stability" and transferases among others :
5/ Next, the same ranking is generated for proteins appearing on figure 6c. Here are the rankings for males and females :
6/ ..and from the same figure (6c) below is the relevance ranking of proteins that were found to be differentially expressed in both males and females. Note the high ranking of the liver and transferases.
7/ Transferases is one of the concepts that consistently received very high rankings. And there was evidence about this as early as 2017. From the same document mentioned in (3) :
8/ According to #ChatGPT, the following are factors that affect transferases functioning. Tagging @scott_scientist for environmental toxins. Note the mention on "Protein folding" which is directly related to ER Stress (found in #MECFS patients by Hwang ) et.al
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1/ After reading posts related to #MECFS24 working group meeting, I saw that some speakers shared slides attempting to look at a bigger picture. First, a tweet by @JanetDafoe shows the following slide by Chris Armstrong.
2/ I do not know if Chris wants to hypothesize with this slide that Gulf War Illness , #MECFS , Post-treatment Lyme disease syndrome and #LongCOVID are actually the same syndrome. If true, could other syndromes belong to this bigger picture?
3/ Below is a snapshot from @MEAssociation . Could #MECFS be triggered also by medications, in this case Accutane (Isotretinoin)? Interestingly, a "Post-Accutane Syndrome" exists. Source : meassociation.org.uk/2013/01/parlia…
1/ This is a major -and hopefully exciting- update on the use of #AI and #networkanalysis methods to research #MECFS. As new research was becoming available, it was sent to the #AI framework in order to identify most promising research targets. Here are the results :
2/ The #AI framework suggests that we look into sulfation, disulfide bonds, cysteine metabolism and cysteine residues. Some of these concepts have been identified but given the latest research, the confidence for their relevance has increased even more.
3/ In a presentation by Dr Shuzhao Li (@jacksonlab - cc @Derya_ ) we see certain metabolites from #MECFS patients being different from HCs. Observe how many metabolites are related to sulfation (red arrows) and cysteine (green rectangle). Note DHEA-S :
1/ This is a thread on the latest study by @microbeminded2 @resiapretorius . The study (see attached) identified issues of complement activation, endothelium function and downregulation of the coagulation system : et.al
2/ In the study we find a table that lists a number of proteins that were found to be significantly different from healthy controls. Among them we find a Vitamin K-related protein named "Protein S" ,Lactotransferrin (Lactoferrin) and Thrombospondin-1
3/ Also, previous research has identified impaired LXR/RXR and RHOGDI signalling (@DrMaureenHanson ) , ABCA1 (@fereshtehjahan1) and Thrombospondin-1. Looking from a greater perspective we have one more study that could be pointing us to efferocytosis.
1/ Thread related to the latest paper (preprint) by Li et. al and the use of LOLA for amelioration of #MECFS and #LongCOVID symptoms. This work may have identified a greater issue (hypothesis) which will be discussed here and have also been communicated to authors of the study.
2/ Among others, the paper identified low levels of asparagine. From the wikipedia entry of asparagine we read that it is essential for proper N-Linked glycosylation (shown below)
3/ From the same wikipedia entry, we find mentions of N-AcetylGlucosamine (NAG). Interestingly, the potential use of NAG was discussed on a document that I circulated in 2017 where N-Linked Glycosylation was also mentioned.
1/ After seeing a tweet by @Naomi_D_Harvey, about N-Acetylglucosamine (NAG) ,I would like to post a thread : The role of N-Linked glycosylation (which I mentioned briefly to @BhupeshPrusty in Berlin recently) , ER Stress and NAG. All links will be given at the end of this thread
2/ I begin with what has been written about the subject : Below we see a tweet I posted (2017) where N-Linked Glycosylation is mentioned. If we follow the link we read about the importance of N-Linked glycosylation and endoplasmic reticulum stress (right)
3/ In the same post we read about the use of NAG for inhibiting experimental autoimmune encephalitis. However, supplementing with NAG has a danger (Note this is a hypothesis)... If viruses use products of N-Linked Glycosylation to thrive (see right) then it is possible that...
1/ We now look at the 4th hypothesis named "Could vascular damage caused by massive
inflammatory events underlie a relapse/recovery
phenotype of ME/CFS and Long COVID?" from @JeffLubell_C19 which can be found in the @patientled patient-generated hypotheses.
2/ The hypothesis suggests that a relapse/recovery pattern takes place among #MECFS and #LongCOVID patients and also discusses associations of hypermobile #EhlersDanlos, chiari malformation,tethered cord syndrome and mast cell activation with these syndromes.
3/ According to the hypothesis, during a relapse , substantial vascular damage occurs which can be attributed to inflammatory processes. These inflammatory processes can be triggered by mast cell activation, acute infection and ischemia/reperfusion injury