A.B.
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@Janet Dafoe (Rose49) has Ron tried insulin or amino acids to see if they normalize results on the impedance test? The basic idea is to activate mTOR which is activated when there are nutrients.
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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@Janet Dafoe (Rose49) has Ron tried insulin or amino acids to see if they normalize results on the impedance test? The basic idea is to activate mTOR which is activated when there are nutrients.
You are spot-on here! We are doing everything we can think of to get funding with the help of OMF. We are hoping fervently that we get one of the NIH Center grants. Any help and ideas about funding are appreciated! Thank you!
Melbourne Bioanalytics have put together this transcript, including slides, of Neil McGregor's talk, I believe they will be doing the same with Chris Armstrong's presentation as well.
https://www.melbournebioanalytics.o...mecfs-by-neil-mcgregor-written-transcription/
Are "G-protein" and "glycoproteins" the same thing?
N-linked glycosylation[edit]
Main article: N-linked glycosylation
N-linked glycosylation is a very prevalent form of glycosylation and is important for the folding of many eukaryotic glycoproteins and for cell-cell and cell-extracellular matrix attachment. The N-linked glycosylation process occurs in eukaryotes in the lumen of the endoplasmic reticulum and widely in archaea, but very rarely in bacteria. In addition to their function in protein folding and cellular attachment, the N-linked glycans of a protein can modulate a protein's function, in some cases acting as an on-off switch.[9]
Importance of N-linked glycosylation in the production of therapeutic proteins[edit]
Many “blockbuster” therapeutic proteins in the market are antibodies, which are N-linked glycoproteins. For example, Etanercept, Infliximab and Rituximab are N-glycosylated therapeutic proteins.
Quite possibly, a key Element behind our problems has to do with Endoplasmic Reticulum (ER) stress, Misfolded Proteins and the the subsequent Unfolded Protein Response (UPR). Anything that impairs proper folding of Proteins within the ER ultimately leads to UPR and the Majority of our problems. At the end of the post you can find relevant References regarding why Methylation problems, Tetrahydrobiopterin Production Impairement, Celiac Disease, N-Linked Glycosylation impairment (among others), all create Stress within the ER and then signal a UPR.
We have previously shown that GlcNAc limits T cell activation/growth and when provided orally to mice, inhibits experimental autoimmune encephalomyelitis, a mouse model of Multiple Sclerosis (MS), as well as autoimmune diabetes in the Non Obese Diabetic mouse model (Grigorian et al., 2011, 2007). GlcNAc has also been given orally (3–6 g/day) to children with refractory inflammatory bowel disease for ~2 years, with 8 of 12 showing clinical improvement without reported toxicities and/or side effects (Salvatore et al., 2000). We have recently observed that serum levels of endogenous GlcNAc are markedly reduced in patients with the progressive form of MS and correlate with clinical disability and imaging measures of neurodegeneration (Alexander Brandt and Michael Demetriou, unpublished data). A pilot study of low-dose oral GlcNAc in MS (3 g/day) increased serum GlcNAc levels and branching in T cells (Barbara Newton and Michael Demetriou, unpublished data). As GlcNAc is a dietary supplement that is for sale ‘over the counter’ in the US, these data suggest that GlcNAc may serve as a safe and inexpensive therapeutic for MS patients and potentially other autoimmune diseases.
This gene encodes a member of the guanine nucleotide-binding protein (G protein)-coupled receptor kinase subfamily of the Ser/Thr protein kinase family. The protein phosphorylates the activated forms of G protein-coupled receptors thus initiating their deactivation. It has also been shown to play a role in regulating the motility of polymorphonuclear leukocytes (PMNs).[6]
@FMMM1
I forgot to mention that the Analytical Methods i use have selected GRK5 (A G-Protein coupled receptor) as potentially relevant to ME/CFS.
I do not know if this type of receptor was found to be relevant by Neil McGregor. A quick search on Phoenix Rising shows no previous mentions regarding this particular receptor.
I liked the presentation about G-proteins worth a watch on youtube
Think it’s part 6 of the symposium on YouTube
I’m not sure how to do links on the phone
I wondered if it ties up with dr Kerr’s work many years ago
Is this the Dr. Kerr? If so, it does look like there may be some overlap, though one would have to look at which subgroups golf patients heceas looking at.Thanks for this. I don't know of Dr Kerr's work but the list of symptoms listed in Dr McGregor's talk looks familiar.