Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
The following is hard for me to understand, but I believe it maybe vital information for others much smarter than me.
Molybdate increases intracellular 3',5'-guanosine cyclic monophosphate and ***stabilizes vitamin D receptor association with tubulin-containing filaments.***
Abstract With a recently developed method we detected rapid and sequential reorganization of vitamin D receptors (VDR), including their temporary association with fibers, and we showed that calcitriol induces cGMP accumulation around reorganizing VDRs.
In this report we first identified the VDR-associated fibers as microtubules: they show immunoreactivity with tubulin antisera and were sensitive to tubulin-disruptive agents.
Tubulin-disruptive agents also prevented calcitriol-induced alignment and intranuclear accumulation of VDR and cGMP, but did not prevent the initial cGMP accumulation in the cytoplasm.
Then we studied the effect of molybdate on VDR reorganization and on cGMP accumulation.
Sodium molybdate inhibits steroid receptor transformation into a DNA binding form through interaction with the steroid binding region of the receptor.
The mechanism of molybdate effect on steroid receptors is not well understood and the interaction of molybdate with guanylate cyclase has not been investigated.
We found in cells pretreated with molybdate that the addition of calcitriol resulted in a prolonged and accentuated association of VDR and cGMP with the microtubules.
Furthermore, both immunocytology and radioimmunoassay demonstrated that molybdate is a highly potent inducer of guanylate cyclase. Neither calcitriol nor molybdate effect on guanylate cyclase were prevented by methylene blue pretreatment, suggesting that they activate particulate guanylate cyclase.
Pretreatment of cells with dibutyryl-cGMP mimicked molybdate effect on VDR reorganization.
The effect of molybdate on cGMP may participate in molybdate stabilization of steroid receptors.
We suggest that rapid cGMP accumulation after steroid exposure plays a role in facilitation of intracellular transport of the steroid receptor through interaction with microtubules.
Name Molybdate transport system Definition K02020+K02018+K02017+K05776 Class Information Processing; Transport system; Mineral and organic iontransport system Pathway bbz02010 ABC transporters
Orthology K02020 modA; molybdate transport system substrate-binding protein K02018 modB; molybdate transport system permease protein K02017 modC; molybdate transport system ATP-binding protein [EC:3.6.3.29] K05776 modF; molybdate transport system ATP-binding protein
Lymeorsomething
Frequent Contributor (1K+ posts)
Member # 16359
posted
I don't know what this means but it does seem clear that Bb screws with receptors to some degree. Even when my serum hormone levels have been perfectly normal I have experienced deficiency-like symptoms at times.
So Dr. B is probably correct in suggesting that there is some level of receptor disruption and/or blockade.
-------------------- "Whatever can go wrong will go wrong." Posts: 2062 | From CT | Registered: Jul 2008
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Pinelady
Frequent Contributor (5K+ posts)
Member # 18524
posted
Could it be that in Alzheimers the borrelia is not able to cross the BB Barrier and the calcification is a direct result of injury to the Hypothalmic/Thalamic regions?
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
From what I understand the BBB is damaged via the inflammatory cytokines.
Only H1 blockers cross the BBB. These normally make us sleepy, but NOT if given with B6 in a coated capsule (Bendectin).
H2 blocker (ranitidine) was part of "tritec" which destroyed all forms of Bb in the GI track.
LOW B6 and inflammatory cytokines = sleepy.
I think while Bb can be a cause of AD, the primary mischief maker is likely yeast which can trigger histamine when they are knocked off.
From what I've read, Bb itself is NOT TOXIC to our brain cells, it is OUR RESPONSE that triggers the problems.
Posts: 9481 | From Sunshine State | Registered: Mar 2001
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Pinelady
Frequent Contributor (5K+ posts)
Member # 18524
posted
So is it possible those that exhibit a greater response have a higher likelyhood of getting
alzheimers than say those like me who have to
challenge to get a response--for whatever reason/s, will develop a more acute form???
This disease is so craZY.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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