Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
First, simplified...Bb locks onto plasminogen which converts to plasmin which Bb "coats" itself in. Plasmin is a serine protease (they break up proteins) and this allows Bb to disseminate (spread).
The following is a discussion of how to halt the serine proteases which allow Bb to "travel around"...pave the way. Hopefully, we will find a SAFE way to do that!
I have been very scared/cautious re: the use of colloidal silver.
I still am not SURE it is completely safe, but... I need to admit I found the following reasons WHY colloidal silver might help:
We know Bb locks onto plasminogen. This triggers: the conversion of plasminogen to plasmin and is believed to trigger Bb's invasion.
"Host-derived plasmin plays a critical role in mammalian infection by Borrelia burgdorferi. The Lyme disease spirochete expresses several plasminogen-binding proteins.
Bound plasminogen is converted to the *serine protease plasmin* and thereby may facilitate the bacterium's dissemination throughout the host by degrading extracellular matrix.
Bb apparently "cloaks" itself in plasmin which is a serine protease.
Serine proteases or serine endopeptidases (newer name) are proteases (***enzymes that cut peptide bonds in proteins***) in which one of the amino acids at the active site is serine.
Plasminogen (Bb binds to it) to plasmin:
"The extracellular serine protease tissue plasminogen activator (tPA) that converts plasminogen into plasmin is abundantly expressed throughout the central nervous system.
Surface receptors for plasminogen are expressed by many gram-positive and gram-negative bacteria and may play a role in the dissemination of organisms by binding plasminogen, which upon conversion to plasmin.
"125I labeled plasminogen binding to both the 70-kDa protein and Osp A was inhibited by ;90%
with a 1,000-fold ***excess of unlabeled plasminogen***."
The above is not the first time this has been found to work. When the SARS virus scare was happening, researchers figured out what it locks onto (an enzyme) and GAVE MORE of that enzyme and the virus locked onto the excess and did not infect the person.
In the case of lyme, it looks like giving excess plasminogen (asap) may help...a lot. Let Bb bind to the excess.
That makes excess plasminogen our 1st line of defense.
Here is something else:
"125I-labeled plasminogen binding by B. burgdorferi was also inhibited by the lysine analog - aminocaproic acid."
(Lysine analog? What about lysine itself?)
Available as a drug: AMICAR (aminocaproic acid) is 6-aminohexanoic acid, which acts as an *inhibitor of fibrinolysis*.
Fibrinolysis is a normal body process that keeps naturally-occurring blood clots from growing and causing problems.
If we INHIBIT that...
Primary fibrinolysis refers to the normal breakdown of clots.
So...the above drug, by inhibiting fibrinolysis, might then increase the risk of blood clots which can't be/are not broken down?
"Thrombin activatable fibrinolysis inhibitor (TAFI) is a regulator of endogenous fibrinolysis.
Conclusions: Our results suggest that low-molecular-weight heparins influence TAFI and other hemostatic parameters in hemodialyzed patients to a lesser degree than unfractionated heparin.
Increased TAFI is possibly due to thrombin appearance during hemodialysis with *unfractionated heparin*."
Not for kids:
"Recent evidence suggests that the clinical outcomes of unfractionated heparin therapy in children are poor, as determined by target-range achievement and adverse-event rates. These reports of poor outcomes may be related to an age-dependent mechanism of action of unfractionated heparin."
There can be a boomerang effect (clots form) after heparin treatment.
Next, another way?
"Oxidative inactivation of plasmin and other serine proteases by
copper and ascorbate.
Oxidation of the zymogens Glu-plasminogen and single-chain urokinase-type plasminogen activator by Cu(II) and ascorbate resulted in the failure of these molecules to generate active enzymes when treated with plasminogen activators or plasmin, respectively.
The active site His residue may be the target of oxidative inactivation, as evidenced by the ***partial protection afforded plasmin by the addition of Zn(II), histidine,*** or the platinum derivative, platinum(II) (2,2':6',2"- terpyridine) chloride.
Because platelets contain micromolar concentrations of Cu and leukocytes are rich in ascorbate, Cu-dependent site-specific oxidation might play a role in modulating proteolytic events and the life span of thrombi formed at sites of tissue injury."
Copper and vitamin C?
Bb has "zinc fingers which look to be made of Cysteine and Histidine bound to/by Zinc.
Another question:
Is Bb's OspC (outer surface protein C)like OUR protein C?
Protein C is a major physiological *anticoagulant*.
It is a vitamin K-dependent serine protease enzyme (EC 3.4.21.69) that is
activated by thrombin
into activated protein C (APC). The activated form (with protein S and phospholipid as a cofactor) degrades Factor Va and Factor VIIIa.
It should not be confused with C peptide or c-reactive protein or protein kinase C.
The protein C pathway's key enzyme, activated protein C, provides physiologic antithrombotic activity and exhibits both anti-inflammatory and anti-apoptotic (me: anti-cell death) activities.
Its actions are related to development of thrombosis and ischemic stroke.
The protein C pathway of the coagulation of the blood involves the influences of lipids and lipoproteins and the study of the strong epidemiologic association between hyperlipidemia and hypercoagulability.
Mutations in protein C, when leading to insufficient protein levels or activity, predispose to thrombosis.
Repeating: protein C is an anticoagulant protein that is a vitamin K dependent *serine protease* which is activated by the presence of thrombin.
"MECHANISM OF THROMBIN BINDING BY FIBRIN"
But going back to the beginning...to *prevent* lyme, it looks like INHIBITING the breakdown of fibrin (fibrinolysis)is suggested.
If fibrin then is "free to" bind to thrombin, does this then inhibit Bb's (and OUR!)Protein C which is activated by thrombin?
In other words...let's "encourage"/allow fibrin to bind to thrombin to keep thrombin away from Bb so it can't make/activate its OspC...if it is like our protein C.
Another drug:
Suramin - IV, hospital only, very dangerous, but...look at the things it is used for ("Google" suramin)! Sleeping sickness, cancer...
Curious: "Suramin and derivatives thereof as topical microbicide and contraceptive " (brand new patent -2009)
This post has talked about ways we might PREVENT Bb from disseminating.
Once Bb has a "foothold", I still believe there are other ways to deal with the infection...
I believe Rife and Far infrared (phototherapy) can indeed help, but I also believe it is critical to restore Mg levels after these "electromagnetic" treatments. And MgCl looks to be the "right" form. We CAN use our skin to absorb MgCl (which ideally would be given in IV doses), but MgCl IS available over the internet and can be diluted (I used distilled water) and applied to the skin.
Ancora Imparo!
Posts: 9481 | From Sunshine State | Registered: Mar 2001
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lymie tony z
Frequent Contributor (1K+ posts)
Member # 5130
posted
Really interesting stuff!
I'll have to relay this to my llmd in training and see what he has to say.
Would you mind emailing this to me Marnie?
I guess I could email it to myself huh! duhh!
Thanks,
zman
-------------------- I am not a doctor...opinions expressed are from personal experiences only and should never be viewed as coming from a healthcare provider. zman Posts: 2527 | From safety harbor florida(origin Cleve., Ohio | Registered: Jan 2004
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Bb BINDING to our plasminogen is supposed to be inhibited via Amicar.
But it looks as though Bb (via it's "zinc fingers" can, to a degree, "compete").
IF, I repeat, IF one of Bb's outer surface proteins is (Osp C) is like OUR Protein C...that protein is an anti-coagulant.
One would THINK, Bb is "depriving us" of the nutrients needed to make our own protein C -> hypercoagulation/"thick blood"...which is USUALLY the case.
Good luck. God Bless. This is one very very incredibly complex pathogen that is disrupting so much.
Posts: 9481 | From Sunshine State | Registered: Mar 2001
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TerryK
Frequent Contributor (5K+ posts)
Member # 8552
posted
Thanks for posting this Marnie. I really think you should be sharing your research with LLMD's and other lyme researchers. Have you considered talking to ILADS about some of your research?
Terry
Posts: 6286 | From Oregon | Registered: Jan 2006
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Pinelady
Frequent Contributor (5K+ posts)
Member # 18524
posted
Yes, when I read silver binds to them somehow
and they used a silver sol. to stain them,
turns them brown,
It might work or help.
Now if I could get rid of this burning hot neck.
Could it be they are trapped there?
Too heavy to move anywhere else?
I hope? Why do lymies complain of this hot burning neck?
-------------------- 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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METALLlC BLUE
Frequent Contributor (1K+ posts)
Member # 6628
posted
Reading this post made me realize just how low my IQ really is.
-------------------- I am not a physician, so do your own research to confirm any ideas given and then speak with a health care provider you trust.
seekhelp
Frequent Contributor (5K+ posts)
Member # 15067
posted
Same with me Metallic Blue. I just look at her postings and say things that make you go hmmmmm... Posts: 7545 | From The 5th Dimension - The Twilight Zone | Registered: Mar 2008
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posted
marnie does it make sense to remove fibrin from the blood with wobenzyme..making it harder for the spirochetes to survive..i realy herx bad on wobenzyme alone..i also have hypercoagulation..
Posts: 593 | From long island ny | Registered: Apr 2006
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TerryK
Frequent Contributor (5K+ posts)
Member # 8552
posted
Blue, Taking the time to learn the vocabulary makes a huge difference.
Very time consuming and not always doable but if you want to understand it, that is a start.
I often save the post and figure I'll go back to it and sometimes I do and a lot of times I don't.
Terry
Posts: 6286 | From Oregon | Registered: Jan 2006
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
Dear Marnie, As usual, I appreciate all your work very much, but most of it goes right over my head.
FWIW, I can tell you I have a friend, whose husband is also sick, and they've both been taking C.S. for several years now.
They are not any worse, but they are not any better either.
klutzo
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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posted
Marnie, this is jumping around a bit for me. You propose controlling the dissemination of Bb by controlling the binding of plasminogen to surface proteins (there appear to be several that bind Pgn), and then indicate a drug that binds plasminogen (aminocaproic acid).
It seems the rest of the post focuses on inhibiting fibrinolysis, but I do not see how that is the point. The important thing is controlling the binding of plasminogen by Bb, but controlling it by binding pgn rather than binding the surface proteins on Bb is a loosing battle.
We need the plasminogen - I think that thrombosis is a larger risk than Lyme in this case. Finding a pgn analogue that binds the surface proteins of Bb would be a great thing, but I would think that the action of a drug like that would not be locallized to Bb, but I would be happy to be shown wrong.
Posts: 263 | From Capital Region, NY, USA | Registered: Jun 2008
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