I had a talk with my favourite vaccine scientist,
julian barden, I am so glad he talks to me. We discussed his discussions with Dr Nesslhehut last week about the speed of vaccine clearance and the MHC class 1 and 2 pathways and vaccine design options.
The take home point was that mhc class 1 gave a hla independent vaccine response, I will seek to confirm and clarif this point. I wished I made it to CMIT this year, but next year will do. I am excited to be going back to germany.
I made another batch of maf 314 yogurt today.
I have to get money and get back to Germany ASAP.
Do you notice as soon as my ass is challenged by this illness I am back into the science.
Lots of emails and calls today. I still did my b17/dmso/dca/goleic
We will redo markers next wednesay arvo, then I will have 9 days of the heavy infusion of the above combo, might go straight map and mct oil on low level to see if i can force the cea down with heavy diet.
the article below confirms whats I have been told and retold here about infection and cancer, and vaccines. Clinical practice has such along way to go. My higher than usual crp 1.6 I think indicates tumour growth.
7 days post vaccine, so no infections seems prudent now, I will run this past doc N when I get to Duderstadt, its what I will be doing. Do you get it? HERE IS THE SIMPLE VERSION, SPEND YOUR ONLY $10,000 A DC VACCINE, SOME KID SNEEZES ALL OVER YOU AT THE AIRPORT, YOUR VACCINE JUST GOT TURNED OFF. NOONE IS CONTROLLING FOR POST INJECTION INFECTIOUS EVENTS. But I suggest you read and contemplate.
Maybe it will be possible with this focused approach to really get better survival rates for all DC patients, when immunotherapists and patients jointly start addressing all of these very complex interactions.
I have not found what Julian was referingtoo above, I will keep on searching.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077019/
When dendritic cells (DCs) encounter signals associated with infection or inflammation, they become activated and undergo maturation. Mature DCs are very efficient at presenting antigens captured in association with their activating signal but fail to present subsequently encountered antigens, at least in vitro. Such impairment of MHC class II (MHC II) antigen presentation has generally been thought to be a consequence of down-regulation of endocytosis, so it might be expected that antigens synthesized by the DCs themselves (for instance, viral antigens) would still be presented by mature DCs. Here, we show that DCs matured in vivo could still capture and process soluble antigens, but were unable to present peptides derived from these antigens. Furthermore, presentation of viral antigens synthesized by the DCs themselves was also severely impaired. Indeed, i.v. injection of pathogen mimics, which caused systemic DC activation in vivo, impaired the induction of CD4 T cell responses against subsequently encountered protein antigens. This immunosuppressed state could be reversed by adoptive transfer of DCs loaded exogenously with antigens, demonstrating that impairment of CD4 T cell responses was due to lack of antigen presentation rather than to overt suppression of T cell activation. The biochemical mechanism underlying this phenomenon was the down-regulation of MHC II–peptide complex formation that accompanied DC maturation. These observations have important implications for the design of prophylactic and therapeutic DC vaccines and contribute to the understanding of the mechanisms causing immunosuppression during systemic blood infections.
SEXY BITS
This is an important question because the outcome of vaccination strategies based on antigen targeting to DCs (14–17), or on loading of DCs with tumor antigens ex vivo (18), might be affected by the maturational status of the DCs. Furthermore, bacterial infections of the blood (sepsis) or parasite infections (e.g., malaria) can cause systemic DC maturation (19–21) and, concomitantly, immunosuppression (21–23). Defining the role of systemic DC maturation on this immunosuppression, and the mechanisms controlling MHC II antigen presentation by DCs, might provide strategies for restoring immunocompetence.
Our results contribute to the understanding of the mechanisms of immunosuppression associated with blood infections such as sepsis (22) and malaria (23). In most scenarios of infection, down-regulation of antigen presentation in mature DCs should have no deleterious consequences because the number of DCs that respond to a given pathogen is probably small. MY MALARIA CAUSED RECURRENCE 1 and SEPSIS RECURRENCE 2,3 and 4. GAME SET AND MATCH TO THE GENIUS. My friends Ren and Phil had sepsis and infections, no wonder the DC Vaccines failed. The clinical ways to address these infections, well Ren left his infected port in for many months, that low grade infection did not just side track the army, it shut down the command and control function. It matures all DC to go after the infection, then the TUMOUR antigen APC just stops. All the money wasted, the time wasted. The TCELLS just not doing anything. NOT specific targetted immune response. THE CALVARY AINT DEPLOYED ITS THAT SIMPLE.
This info will save your life if you are doing dc vaccines.
KETOGENIC DER STUFF - THIS MIGHT BE EASILY OVER LOOKED - EMAIL TO MY KETOGENIC GURUS
julian barden, I am so glad he talks to me. We discussed his discussions with Dr Nesslhehut last week about the speed of vaccine clearance and the MHC class 1 and 2 pathways and vaccine design options.
The take home point was that mhc class 1 gave a hla independent vaccine response, I will seek to confirm and clarif this point. I wished I made it to CMIT this year, but next year will do. I am excited to be going back to germany.
I made another batch of maf 314 yogurt today.
I have to get money and get back to Germany ASAP.
Do you notice as soon as my ass is challenged by this illness I am back into the science.
Lots of emails and calls today. I still did my b17/dmso/dca/goleic
We will redo markers next wednesay arvo, then I will have 9 days of the heavy infusion of the above combo, might go straight map and mct oil on low level to see if i can force the cea down with heavy diet.
the article below confirms whats I have been told and retold here about infection and cancer, and vaccines. Clinical practice has such along way to go. My higher than usual crp 1.6 I think indicates tumour growth.
7 days post vaccine, so no infections seems prudent now, I will run this past doc N when I get to Duderstadt, its what I will be doing. Do you get it? HERE IS THE SIMPLE VERSION, SPEND YOUR ONLY $10,000 A DC VACCINE, SOME KID SNEEZES ALL OVER YOU AT THE AIRPORT, YOUR VACCINE JUST GOT TURNED OFF. NOONE IS CONTROLLING FOR POST INJECTION INFECTIOUS EVENTS. But I suggest you read and contemplate.
Maybe it will be possible with this focused approach to really get better survival rates for all DC patients, when immunotherapists and patients jointly start addressing all of these very complex interactions.
I have not found what Julian was referingtoo above, I will keep on searching.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077019/
When dendritic cells (DCs) encounter signals associated with infection or inflammation, they become activated and undergo maturation. Mature DCs are very efficient at presenting antigens captured in association with their activating signal but fail to present subsequently encountered antigens, at least in vitro. Such impairment of MHC class II (MHC II) antigen presentation has generally been thought to be a consequence of down-regulation of endocytosis, so it might be expected that antigens synthesized by the DCs themselves (for instance, viral antigens) would still be presented by mature DCs. Here, we show that DCs matured in vivo could still capture and process soluble antigens, but were unable to present peptides derived from these antigens. Furthermore, presentation of viral antigens synthesized by the DCs themselves was also severely impaired. Indeed, i.v. injection of pathogen mimics, which caused systemic DC activation in vivo, impaired the induction of CD4 T cell responses against subsequently encountered protein antigens. This immunosuppressed state could be reversed by adoptive transfer of DCs loaded exogenously with antigens, demonstrating that impairment of CD4 T cell responses was due to lack of antigen presentation rather than to overt suppression of T cell activation. The biochemical mechanism underlying this phenomenon was the down-regulation of MHC II–peptide complex formation that accompanied DC maturation. These observations have important implications for the design of prophylactic and therapeutic DC vaccines and contribute to the understanding of the mechanisms causing immunosuppression during systemic blood infections.
SEXY BITS
This is an important question because the outcome of vaccination strategies based on antigen targeting to DCs (14–17), or on loading of DCs with tumor antigens ex vivo (18), might be affected by the maturational status of the DCs. Furthermore, bacterial infections of the blood (sepsis) or parasite infections (e.g., malaria) can cause systemic DC maturation (19–21) and, concomitantly, immunosuppression (21–23). Defining the role of systemic DC maturation on this immunosuppression, and the mechanisms controlling MHC II antigen presentation by DCs, might provide strategies for restoring immunocompetence.
Our results contribute to the understanding of the mechanisms of immunosuppression associated with blood infections such as sepsis (22) and malaria (23). In most scenarios of infection, down-regulation of antigen presentation in mature DCs should have no deleterious consequences because the number of DCs that respond to a given pathogen is probably small. MY MALARIA CAUSED RECURRENCE 1 and SEPSIS RECURRENCE 2,3 and 4. GAME SET AND MATCH TO THE GENIUS. My friends Ren and Phil had sepsis and infections, no wonder the DC Vaccines failed. The clinical ways to address these infections, well Ren left his infected port in for many months, that low grade infection did not just side track the army, it shut down the command and control function. It matures all DC to go after the infection, then the TUMOUR antigen APC just stops. All the money wasted, the time wasted. The TCELLS just not doing anything. NOT specific targetted immune response. THE CALVARY AINT DEPLOYED ITS THAT SIMPLE.
This info will save your life if you are doing dc vaccines.
KETOGENIC DER STUFF - THIS MIGHT BE EASILY OVER LOOKED - EMAIL TO MY KETOGENIC GURUS
have been home on holidays away from treatments in Germany for 4 weeks, my tumour marker cea just jumped to 42 from 9 in 5 weeks while i have been in heavy ketosis ie always ketones > 3 topped at 6.6 which I thought excellent. My glucose has been as low as 2.7 after good exercise but more like between 3.5 and 5 most days. I thought this was pretty good. My weights stable and I feel excellent. Just did a 5 day yoga retreat.
My friend raised the issue of DER, any comments. I just eat sensibly and easily stay in good ketosis now. I dont count the grams, been too lazy, trying to relax.
Do I need to for ensuring low calories. I thought as long as glucose < keytones I was pretty safe.
The CEA spike however indicates I may need something better.
That said I never expected the K diet on its own to do the work of reducing the tumour burden, I always reserved that for my immunotherapies, but the diet certainly stresses the tumour cells.
THE EMAIL FROM A FRIEND
In one of the experiment mentioned by Dr Seyfried in his book (pg 293), he reported “The results show that DER (Dietary Energy Restricted) significantly reduces tumor growth whether the mice are fed a standard high carbohydrate diet (SD) or a high fat, low carbohydrate KD (Ketogenic Diet)” and on the same page, “Our results show that brain tumor growth is influenced more by diet energy content than by diet nutrient composition”.
If this is correct and applicable to human or other human cancer, then maybe ketosis, heavy or otherwise, is not the key but rather the total energy (or calories) intake?
IN THE CONTEXT OF THE EFFORT OF THE DIET, ITS REASONABLE TO GET THE BEST BENEFIT FROM THE DIET, I WILL ATTEMPTED TO PUSH CALORIES DOWN. I HAVE JUST BEEN RANDOMLY SWIGGING MCT OIL. I WILL GO TO SPECIFIC QUANTITIES LIKE I USED TO. MY STABLE WEIGHT, SMALL INCREASE AND GOOD KETOSIS MADE ME VERY CONTENT WITH MY KETOGENIC DIET.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355893/ vit d and cancer, EXCELLENT!