From a week ago.
So i beat prof vogl to work. To the
uniclinik frankfurt. But he answered my 5am emailing about viral delivery metabolic strategeties.
Its so wonderful to have a conventionally terminal illness, a team of innovative doctors and therapists and the resources to make my miracle.
See the photo of vogls empty waiting room. Normally its bursting at the seems.
I got up 5am fresh, alert, ready for a big day. A new therapy attempt remission thanks to dr arno thaller who is quiet famous amongst my existing team
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076631/
In summary, this study demonstrates that KD inhibits mTOR pathway signaling in the brain and liver of healthy rats, and prevents late hippocampalmTOR activation after KA-induced SE. This mTOR inhibition may underlie some of the physiological effects of KD, including growth impairment, anticonvulsant actions, and potential antiepileptogenic effects. Further studies are necessary to prove a causal relationship between mTOR inhibition and antiepileptogenic actions of the KD.
Abstract
Previously we demonstrated that histidine decarboxylase (HDC), which produces histamine from l-histidine, was detected in monocytes/macrophages located in human atherosclerotic lesions. As monocytic migration is a key event of atherogenesis, we investigated whether histamine induces monocytic expression of monocyte chemoattractant protein (MCP)-1 and its receptors CCR2-A and -B, and also endothelial expression of ICAM-1 and VCAM-1. Furthermore, we studied the effect of interleukin (IL)-4, which inhibits the HDC expression, on the expression of MCP-1 and CCR2. Histamine stimulated monocytes, but not macrophages, to express MCP-1 and CCR2-A and -B. The expression of MCP-1 was inhibited by histamine H2 blocker. In contrast, IL-4 enhanced CCR2 expression but not MCP-1. Histamine stimulated endothelial cells to express ICAM-1 and VCAM-1. These results indicate that histamine and IL-4, which are both synthesized in the arterial intima, chronically participates in the pathogenesis of atherosclerosis via the enhanced expression of monocytic MCP-1, CCR2 and endothelial adhesion molecules. http://www.colonchat.net/forum/viewtopic.php?f=1&t=2512
got XXXXXXX my freezer, amongst other goodies.
getting it injected into sites of new disease via needles as guided imaging.
waiting 5 days for replication, then tacing and doing ipt and systemic immunotherapies aimed at taking out virally infected tumour cells.
lots of opportunities to boost the efficacy of the ndv, we will see.
what triggered the growth i think insulin.
considering strategies to temporailyshutdown immune function for the week while ndv replicates in tumour cells,
also looking a strategies to boost blood flow to tumours post arterial viral injection.
got to have some fun trying to stay alive
any suggestions, heck i might do a shot of chemo to kill my immune sysytem.
Maybe some ultra high cimetidine a pre viral injection option to down regulate macrophages.
Just ideas.