Please send this exchange that Ohm and I had recen

Please send this exchange that Ohm and I had recently to Jay. It should answer a lot of his questions.

https://investorshangout.com/post/view?id=6432436

It is important to understand that while looking at the heat map, you're looking at differences between those values from before the start of the trial to the values at the end of the trial. You are not looking at actual values. All we know is that the values were either elevated or reduced from where it started.

Since all participants had cT1 > 800 ms, we know they had a disease process taking place which produced fat, steatosis and was remodeling scar tissue, but was greater on the side of forming scar tissue vs. resorbing scar tissue.

But both steatosis and fibrosis were happening simultaneously.

Per my post:
Interferon gamma is produced by Th1 cells. IFN-γ is produced predominantly by natural killer cells (NK) and natural killer T cells (NKT) as part of the innate immune response, and by CD4 Th1 and CD8 cytotoxic T lymphocyte (CTL) effector T cells once antigen-specific immunity develops.

Interferon gamma puts the effected Macrophage in the Classical Activation Pathway which is very inflammatory. At the same time, the effected Macrophage is TAKEN OUT OF the Alternative Pathway of metabolizing scar tissue. In this Classical Pathway, induced by the Th1 by exuding Interferon Gamma, the effected Macrophage is commanded to manage the dying hepatocytes. I put out some posts describing what happens in this Pathway a few days earlier, but they are not organized.

The lipid particles are piling up within the hepatocytes. The mitochondrion are failing. The cells are swelling and its becoming a fatty swollen liver. Some hepatocytes are necrotizing, some are committing suicide. The repair of the liver needs to take place and recruitment of blood supply to feed the new hepatocytes which take the place of the old needs to happen. In this situation, the dying Hepatocytes send out a distress call and request the assistance of the immune cells. The Th1 cell responds and sends out Interferon Gamma. The Macrophages in the area respond by going into the Classic Pathway of Macrophage Activation and begin to decide how to handle the dying hepatocytes. Here Interferon Gamma would be increased.

But in 350mg, we saw Interferon Gamma Decreased. We don't know from what to what, we just know it was decreased across the board in 350 and was sharply decreased. Interferon Gamma was still present, but less than prior to initiation of LRM. Why? What did LRM do?

Read the link. I think LRM led to increase in IL-4 or IL-13.

Because when the majority of Macrophages are activated by Th2 cells, they are in the Alternate Pathway and that Pathway is where the Scar Tissue is Metabolized. Some is taken away while some is added. Since we saw a significant decrease in cT1 in >950 ms cT1, there was more taken away than was added. When a Macrophage is activated by Th2, then it is put into the Alternative Pathway, the metabolism of scar tissue pathway AND IS TAKEN out of the Classical Pathway of managing the dying hepatocytes.

The metabolism of scar tissue pathway is non-inflammatory while the managing of the dying hepatocytes is inflammatory. With the addition of 350mg LRM, these patients tended to show that the balance of power of the Activated Macrophages was more in the camp of the metabolism of scar tissue while the Placebo group and 700 normal group who did poorly with respect to reduction of cT1 and PDFF, their Macrophages remained mainly in the Classical Pathway and tried to manage the dying hepatocytes while the steatosis and scar tissue just built up.

LRM effected a change in the management of these Macrophages. It did not effect a change in inflammation, per say. Reduced inflammation was a side effect.

I made a lot of posts two days ago on the operation of these things, but this platform makes it very difficult to find them I have to say.