So I posted a rant here the other day about how I am out here in Colorado and didnt get any sleep near the city,
I blamed it on the mattress. I still think thats 80% true.
However I did post that I slept GREAT up in Indian Hills which is far away from the City and actually more in the mountains.
I just thought of something. Perhaps it was because there were less EMFs up there.
After all I didnt get cell service and my room was in the basement surrounded by concrete.
I slept GREAT!!!!!!!!!!!!!!!!!!!!!!
Posted by lymeHerx001 (Member # 6215) on :
Im waiting for NM Taliz to chime in.....
Posted by Marnie (Member # 773) on :
Radiofrequencies are part of the electromagnetic spectrum.
There maybe a link:
However,the role of PKCdelta in radiosensitivity and cell cycle regulation remains unclear.
Overexpression of PKCdelta increased Ca2+-independent PKC activity without altering other PKC isoforms (PKCalpha, -beta1, -epsilon, and -zeta), and extracellular regulated protein kinase (ERK [?]) 1/2 activity was also increased in PKCdelta-specific manner.
***A clonogenic survival assay showed that PKCdelta-overexpressed cells had more radiosensitivity and pronounced induction of apoptosis than control cells.***
Flow cytometric analysis revealed that PKCdelta made the cells escape from radiation-induced G(2)-M arrest.
Moreover, p53 and p21(Waf) induction by radiation were higher in PKCdelta-overexpressed cells than control cells, and PKCdelta-mediated apoptosis was reduced, when radiation-induced ERK1/2 activity was inhibited by PD98059.
Furthermore, PKCdelta antisense and rottlerin, PKC inhibitor-abrogated PKCdelta-mediated radiosensitivity and reduced ERK1/2 activity to the control vector level.
These results demonstrated that PKCdelta overexpression enhanced radiation-induced apoptosis and radiosensitivity via ERK1/2 activation, thereby abolishing the radiation-induced G(2)-M arrest and finally apoptosis.
Cell Growth Differ. (2002) PMID: 12065247
Bb has a PKC inhibitor which looks to be PKCD.
A PKCD inhibitor. Rottlerin is a man-made PKCD inhibitor.
It appears we try to activate PKCD (one form of estrogen, E2, does this)...and so do other things.
Prostate cancer cells LACK PKCD.
It is believed if the cells contained PKCD they would die...a good thing if the cell is cancerous.
Now...we have to be careful because too many cells dying too fast is not good.
What triggers cell death?
Cytochrome C.
What keeps the cells alive?
If cytochrome C is bound to something else OR if it is oxidized.
Will the cell then live on forever?
I don't think so. Every cell has a specific length of time it survives before it is destroyed and replaced. Our stomach cells (because the stomach is so acidic) are replaced very often.
Posted by lymeHerx001 (Member # 6215) on :
Im bumping this again. It was wonderfull the sleep I got.