"PF inhibits activation-mediated loss of superantigen-reactive CD4 as well as CD8 T cells in vivo without significantly affecting their activation, and inhibits activation-induced death and caspase induction in stimulated CD4 as well as CD8 T cells in vitro without preventing the induction of activation markers.
Consistent with this ability to prevent activation-induced death in not only CD4 but also CD8 T cells, PF also enhances the persistence of CD8 T cell responses in vivo."
Bb is a CO2 fixation bacteria. Which blood vessels do you think it hangs out in?
Arteries or veins?
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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AliG
Frequent Contributor (1K+ posts)
Member # 9734
posted
perfusion defects & hypoperfusion?
low CD-57?
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
It is a PDE1-5 inhibitor. Is that what you need to know?
Yes, I "NO"...misspelling intentional.
But healing the CD4 cells looks to be paramount.
Beta-1,3-glucuronyltransferase 1 (glucuronosyltransferase P), also known as B3GAT1 or CD57, is a human
gene.
Read my PKCD sentences...how gene transcriptions get messed up. Phosphate transfer kapoot?
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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