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Wednesday, February 21, 2018 4:50 AM | Venöse Multiple Sklerose, CVI & SVI, CCSVI Volg link
Isolated synthetic “Vitamin” D has really everything a proper Cancer does need to develop. You just have to take it long enough & in high dosages.

“Calcitriol Directly Sensitizes Renal Tubular Cells to ATP-Depletion- and Iron-Mediated Attack”, Fred Hutchinson Cancer Research Center 1999

Vitamin Ds have been reported to have diverse effects
on cell homeostasis, leading to suggestions that they
have therapeutic applications extending beyond their
traditional actions on the Ca21/parathyroid/bone
axis. As some of these potential indications carry an
inherent risk of acute renal failure (ARF; eg , cancer
chemotherapy and organ transplantation), the goal
of this study was to assess whether vitamin Ds di-
rectly affect renal tubule injury responses. Cultured
human proximal tubular (HK-2) cells were exposed to
physiological or pharmacological doses of either cal-
citriol (D3) or a synthetic vitamin D2 analogue (19-
nor) for 3 to 48 hours. Their impact on cell integrity
(percent lactate dehydrogenase (LDH) release and tet-
razolium dye MTT uptake) under basal conditions and
during superimposed injuries (ATP depletion/Ca21
ionophore or iron-mediated oxidant stress) were de-
termined. As vitamin Ds can be anti-proliferative, cell
outgrowth ([3H]thymidine uptake and crystal violet
staining) was also tested. Finally, the action of D3 on
in vivoARF (glycerol-induced myoglobinuria) and iso-
lated proximal tubule injury responses were assessed.
D3 induced a rapid, dose-dependent increase in HK-2
susceptibility to both ATP-depletion/Ca21-ionophore-
and Fe-mediated attack without independently affect-
ing cell integrity or proliferative responses. In con-
trast, D2 negatively affected only Fe toxicity and only
after relatively prolonged exposure (48 hours). D3
dramatically potentiatedin vivo ARF (two- to three-
fold increase in azotemia), suggesting potential in
vivo relevance of the above HK-2 cell results. Proxi-
mal tubules, isolated from these glycerol-exposed
mice, suggested that D3 can worsen tubule injury de-
spite a parodoxic suppression of H2O2production. In
contrast, D3 had a mild negative impact on cellular
energetics (depressed ATP/ADP ratios), and it accen-
tuated plasma membrane phospholipid breakdown.
The latter was observed in both glycerol-treated and
control tubules, suggesting a primary role in the in-
jury-potentiation effect of D3. Vitamins D(s) may di-
rectly, and differentially, increase proximal tubule
cell susceptibility to superimposed attack. This prop-
erty should be considered as new uses for these
agents are defined.
(Am J Pathol 1999, 154:1899 –1909)

full paper:
Venöse Multiple Sklerose, CVI & SVI, CCSVI