MAF 314 (probiotic gcmaf)

[stef2011]

Dr. Cheney will show the results of 1 month trial of maf 314 on CFS/XMRV infected patients on the 22-25 september Ottawa conference (http://www.iacfsme.org/)

Prof. Ruggiero 27 e 29 sept a Padova http://www.siai2011.azuleon.org/

due to the extraordinary results professor ruggiero and the other scientists involved agreed to explain people on how to do maf314 in our home kitchens

we know that first weeks of maf 314 made a rise of cd4,cd8 and nk cells in aids and healthy subjects...much more potent than chemical gcmaf i am doing now

[stef2011]

there is no prof it has an effect on hbv at all so i suggest not to use this for hbv now
maf314 can be bought in austria (dr Uta Santos-König vienna) and germany kassel (dont have the name of clinic now)

[Jeff912000]

Hi Stef

Where can i prurchase MAF314.  

[April9903]

Thanks for the info. I honestly do not understand many things but anyway I'll follow this post as this is also one of the hopes of cure for us.....

[stef2011]

redlabs.com have also cytokine tests, this way we may have a clue of wht we do with gcmaf to immune system

[stef2011]

i just posted the most interesting parts of this last study because if we use gcmaf or maf 314 we can use cd counts and cytokine tests to see if maf or gcmaf are having an effect

for example in my case cd4/cd8 ratio was 0.4 while they say acute are usually 2:1 ratio.so with my gcmaf therapy i need to increase cd4 at least more than double

[stef2011]

Interferon-g findings

The data on IFN-g production by PHA stimulated peripheral blood mononuclear cells from the studied patients revealed a highly significant (P < 0.001) increase among the acute HBV group as compared to the healthy subjects and chronic cases (Table 6). However, IFN-g production among the chronic cases revealed a highly significant decrease (P  0.05) when compared to the controls (Table 6). The results published by Kakumu et al (1989) [22], Inowa et al (1989) [23], Fuji et al (1987) [24], Ikeda et al (1986) [25] and Abb et al (1985) [26] were in accordance with the present data. The findings of defective IFN production in patients with chronic HBV infection reported in our study and by other investigators had led to the hypothesis that this might be a primary defect which could have been instrumental in the early stages of infection in permitting continued viral infection. These have led to the speculation that a defect in the ability to produce sufficient IFN during acute viral hepatitis may lead to chronic infection. Our data enabled us to suggest that IFN levels were statistically highly correlated (P < 0.001) to IL-2 levels. Both cytokines increased in acute HBV cases and control subjects, and both decreased in the chronic cases (data not presented).

The release of IL-2 by Th1 cells seemed to be the main stimulus for the sequential synthesis of IFN-g . When exogenous IL-2 was added to peripheral blood lymphocytes (PBL) in culture, there was a significant increase in the amount of IFN-g [23]. When both cytokines were correlated to Th subsets they were statistically insignificant. This was explained by the fact that measurement of Th subset in the present study did not specifically identify Th1, the main inducer of IFN-g and IL-2.

So, not only the phenotypic analysis of Th subsets was a must but also their functional differences should be studied to confirm the hypothesis proposed that defective Th1 was the main element underlying viral persistence in chronic HBV infections.