7 /21
-If they trigger the Metabolic Trap which will shut down the enzymatic activity of IDO1, then it can't make kynurenine, and then it can't make NAD. If it can't make NAD, it can't grow.
8 /21
-Technically one problem is they don't want the yeast to consume tryptophan by any other pathway.
-Have looked into yeast, all genes have been sequenced and they understand their function, have found several genes that consume tryptophan for other purposes.
#12
-If you wash out the high level of tryptophan + put in low level of tryptophan, it starts growing again.
-OR if you leave high level of tryptophan but give yeast kynurenine it starts growing again, even in presence of high tryptophan + absence of enzyme activity.
14 /21
-Another reason to do this. Now have system where they can shut down enzyme in Metabolic Trap + only way the cell can grow is to get rid of tryptophan.
-Human cells not quite the same, it's not growth, it's kynurenine which is critical factor.
15 /21
-If this was true in human cells the only way to make kynurenine would be to get rid of the tryptophan. Only way to get rid of tryptophan is to convert it to kynurenine.
-That's why it's called a trap, you get into it, you can't get out.
16 /21
-However if they find compound that will 'block the block'--the inhibition that tryptophan has over the enzyme, then will reactivate IDO1, then IDO1 will consume the tryptophan and the cells will produce kynurenine.
"We have now done proteomics (the large-scale study of proteins) and metabolomics (an analysis of the metabolism) in cerebrospinal fluid (CSF) and blood plasma from about 40 Intensive Care Unit COVID-19 patients. "
"Our next step will be the large-scale metabolomic study of plasma from a larger cross-section of less severe COVID-19 patients (where we have no possibility to collect CSF) not admitted into the ICU."
"In parallel, we are performing CSF proteomics and blood plasma metabolomics in around 50 Herpes Simplex Encephalitis patients (a rare infection with a related neurological disorder). The data from this cohort will provide a valuable baseline for neuroinflammation..."