CaliforniaLyme
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posted
Klempners latest- **************************************** 1: Biochem Biophys Res Commun. 2007 May 2;
Borrelia burgdorferi-induced monocyte chemoattractant protein-1 production in vivo and in vitro.
Zhao Z, McCloud B, Fleming R, Klempner MS. Section of Infectious Diseases, Boston University Medical Center, 650 Albany St., Boston, MA 02118, USA.
Matrix metalloproteinase 9 (MMP-9) is selectively upregulated in erythema migrans (EM) lesions with acute Lyme disease. This study explored whether upregulation of MMP-9 was associated with monocyte chemoattractant protein 1 (MCP-1) production, and Borrelia burgdorferi (B. burgdorferi) could induce MCP-1 production in vivo and in vitro.
The results indicated that expression of MCP-1 was significantly increased in U937 cells by B. burgdorferi. The activity of MMP-9 could be elevated by recombinant MCP-1 (rMCP-1) in U937 cells. MMP-9 was not upregulated by B. burgdorferi in fibroblasts.
However, the expression of MCP-1 was significantly increased in the presence of B. burgdorferi in fibroblasts.
The level of MCP-1 in EM lesions and in serum of patients with acute Lyme disease was also significantly elevated compared to that for healthy controls.
The secreted MCP-1 may affect the production of MMP-9 in fibroblasts and/or macrophages.
PMID: 17485071
-------------------- There is no wealth but life. -John Ruskin
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CaliforniaLyme
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Upregualtion of MMP-9 is a marker of Lyme AND of ALS, had that on the old ALS/Lyme page as a marker for the twain- oh- and I know a GBS person who later was diagnosed Lyme- ****************************************** 1: J Neuroimmunol. 2005 Feb;159(1-2):146-54.
The pro and the active form of matrix metalloproteinase-9 is increased in serum of patients with amyotrophic lateral sclerosis.
Demestre M, Parkin-Smith G, Petzold A, Pullen AH. Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, University College London, Queen Square, London WC1N 3BG, UK. [email protected]
Pro and active-matrix metalloproteinase-9 (MMP-9) was measured in sera from patients with amyotrophic lateral sclerosis (ALS), Guillain-Barre syndome (GBS), and healthy subjects.
Both forms of MMP-9 were elevated in sera of ALS and GBS patients, compared with healthy controls. It has been postulated that elevated MMP-9 reflects damage to peripheral nerve and muscle. This possibility was investigated in sera, and tissue extracts of sciatic nerves and muscle from mice 5 and 12 days after axotomy of the sciatic nerve.
Pro-MMP-9 was elevated in sera and extracts of damaged nerve and muscle, suggesting such damage may be followed by elevated pro-MM9-9 in sera. Active MMP-9 was only elevated in the sera.
However, in situ activation of MMP-9 is tightly regulated and localised, and probably difficult to demonstrate by ELISA, resulting in a short half-life active MMP-9, implying any active MMP-9 in the serum may have a more immediate origin than injured muscle or nerve, for example circulating blood cells.
PMID: 15652414
-------------------- There is no wealth but life. -John Ruskin
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CaliforniaLyme
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1: Neurochem Int. 2003 Aug;43(3):191-6.
Increased plasma levels of matrix metalloproteinase-9 in patients with Alzheimer's disease.
Lorenzl S, Albers DS, Relkin N, Ngyuen T, Hilgenberg SL, Chirichigno J, Cudkowicz ME, Beal MF. Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, Room F-610, New York, NY 10021, USA.
Matrix metalloproteinases (MMPs) may play a role in the pathophysiology of Alzheimer's disease (AD).
MMP-9 and tissue inhibitors of metalloproteinases (TIMPs) are elevated in postmortem brain tissue of AD patients. MMPs and TIMPs are found in neurons, microglia, vascular endothelial cells and leukocytes.
The aim of this study was to determine whether circulating levels of MMP-2, MMP-9, TIMP-1 and TIMP-2 are elevated in the plasma of AD patients.
We compared AD patients to age- and gender-matched controls as well as to Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS) patients. There was constitutive expression of gelatinase A (MMP-2), and gelatinase B (MMP-9), in all the samples as shown by zymographic analysis.
Levels of MMP-9 were significantly (P=0.003) elevated in the plasma of AD patients as compared to controls. Plasma levels of MMP-2, TIMP-1 and TIMP-2 were unchanged.
There were no significant changes of MMP-2, MMP-9, TIMP-1 and TIMP-2 levels in PD and ALS samples. TIMP-1 and TIMP-2 were significantly correlated with MMP-9 in the AD patients. ApoE genotyping of plasma samples showed that levels of MMP-2, TIMP-1 and TIMP-2 and MMP-9 were not significantly different between the ApoE subgroups.
These findings indicate that circulating levels of MMP-9 are increased in AD and may contribute to disease pathology.
PMID: 12689599
-------------------- There is no wealth but life. -John Ruskin
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CaliforniaLyme
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: J Neurol Sci. 2003 Mar 15;207(1-2):71-6. Links Tissue inhibitors of matrix metalloproteinases are elevated in cerebrospinal fluid of neurodegenerative diseases.Lorenzl S, Albers DS, LeWitt PA, Chirichigno JW, Hilgenberg SL, Cudkowicz ME, Beal MF. Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street Room A-501, New York, NY 10021, USA.
Matrix metalloproteinases (MMPs) are implicated in the pathogenesis of diseases such as Alzheimer's Disease (AD) and amyotrophic lateral sclerosis (ALS). Increased expression of MMP-9 and TIMPs has been reported in postmortem AD and ALS brain tissue, as well as in ALS cerebrospinal fluid (CSF) and plasma.
Although individual studies of MMP and TIMP expression in CSF have included AD and ALS samples, there are no studies comparing the expression of these proteins between neurodegenerative diseases.
We measured the levels of matrix metalloproteinases (MMPs)-2 and -9 and the tissue inhibitor of MMPs (e.g. TIMP-1 and TIMP-2) in CSF samples from patients with Parkinson's Disease (PD), Huntington's Disease (HD), AD and ALS as compared to age-matched control patients.
There was constitutive expression of the proform of gelatinase A (proMMP-2) on zymography gels in all CSF samples. Unexpectedly, there was an additional gelatinolytic band at 130 kDa of unknown etiology in the CSF samples of patients with PD (61% of patients studied), AD (61%), HD (25%) and ALS (39%). Levels of TIMP-1 were significantly elevated in CSF samples from all disease groups. TIMP-2 was significantly increased in CSF of AD and HD patients. MMP-2 levels did not differ significantly between groups.
These findings show that TIMPs are elevated in the CSF of patients with neurodegenerative diseases suggesting a potential role of these endogenous inhibitors of matrix metalloproteinases in neurodegenerative diseases.
PMID: 12614934
-------------------- There is no wealth but life. -John Ruskin
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Marnie
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Definitions:
MCP1: Monocyte chemotactic protein-1, a member of the small inducible gene (SIG) family, plays a role in
the recruitment of monocytes to sites of injury and infection.
The gene for MCP1 is on chromosome 17 in region 17q11.2-q12.
MPC1 has been found in the joints of people with rheumatoid arthritis where may serve to recruit macrophages and perpetuate the inflammation in the joints. MPC1 has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
MCP1 has also been called small inducible cytokine A2 (SCYA2) and monocyte chemotactic and activating factor (MCAF).
" Metalloproteases, on the other hand, seem to be a common feature in most bacterial pathogens."
(Metalloprotease,by definition, means attracted to metals - usually in the mitochondria.)
It is an enzyme.
A pathogen is a disease causing bacteria.
The mitochondria are the "powerhouses" of the cells where energy - ATP is made.
Top genes for aluminum oxide...MMP2, MMP9, etc.
THAT comes as no surprise!
Figure out what the SALP 15 protein contains!
MMP9 collagenase among others.
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oxygenbabe
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The one product I've found tremendously helpful with this is comitras--from Atrium Biotech. A medical doctor with lyme told me about it a few years ago and said it really helped but it was so expensive I ignored him. Recently I felt such an intuitive urge to try it, I ordered it. It arrives frozen and is purified peptides of shark cartilage known to downregulate the MMP's. I feel significantly better when I take it--it seems to eliminate that fractured, buzzing, feeling and increase my well being and energy. Its very expensive!
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CaliforniaLyme
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How expensive?!! It sounds interesting!!! I believe MMP-9 is as you would say Marnie- "a piece of the puzzle"*)!!)!*!!!! Do you have a link for it>?
-------------------- There is no wealth but life. -John Ruskin
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treepatrol
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Matrix metalloproteinase (MMP; MMP-9) are enzymes that open tunnels through the tissues of the body in order to deliver inflammatory cytokines and other biochemicals.
MMPs are essential for substances to be able to move around the body,but excessive levels of MMPs develop when inflammation is too high. MMP-9 is frequently discussed in relation to people with TBI. High levels of MMP-9 means high levels of cytokines are being delivered to body tissues, causing lots of trouble everywhere else.
This elevated inflammation = elevated cytokines = increased inflammation and elevated risk of other inflammatory diseases.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
posted
Not surprisingly, MMP-9 are also known to be elevated in MS, too.
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Marnie
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This is long, but please, please, please read!
Not technical (I tried hard), but a on-line discussion!
Like you, I naturally thought the things upregulated (including TNF alpha) need to be downregulated, to control the infection.
Let's look at this another way. Let's upregulate the things that are being downregulated instead of visa versa.
I believe the body is NOT making mistakes. I believe the things that go up and the things that go down do so (or have done so - past tense) for very good reasons.
I think the body is trying to find a way to keep us alive while trying hard to fight a really mean pathogen.
But it needs help.
We know, for example, that at the OUTSET of this disease, Mg levels dropped DRAMATICALLY. Over time (because it is stored in fat)we know vitamin E levels drop too (anti-oxidant).
Think of these as DEFENSIVE moves.
Okay, this pathogen (#1) needs glucose. It uses ours and deprives our cells of this nutrient.
Think of the infected cell as a house. There's a party going on in that house and everyone is eating and drinking, getting along very smoothly.
Along comes an uninvited guest who eats all the food and drinks all the beverages leaving none for the others. Besides, this creep leaves a mess behind too.
ALL OUR CELLS NEED GLUCOSE. ESPECIALLY our brain cells. Our WBCs, our defense cells (including antibodies) absolutely MUST HAVE glucose.
So...when the INTRACELLULAR energy supply is kapoot because Bb is breaking down glucose, the body triggers the liver to MAKE glucose.
This is called gluconeogenesis.
If you think depriving yourself of carbs (source of glucose) is a good idea...think again.
The body WILL find a source...which is EXACTLY what Bb wants it to do!
Gluconeogenesis happens in the liver. It is the generation of glucose (6 carbon chain, with O and H's at different spots, in different configurations)from things OTHER THAN carbon.
Gluconeogenesis is the generation of glucose from NON-sugar carbon substrates like pyruvate, lactate, glycerol, and...pay attention...***glucogenic amino acids*** (PRIMARILY, but not exclusively) alanine and glutamine.
The amino acids are building blocks of protein. They contain NITROGEN. These and other amino acids go DOWN as maybe utilized to MAKE glucose.
So...our body, when a pathogen takes from us glucose for its own energy, MAKES MORE GLUCOSE.
Another thing is happening...to get that glucose INTO the cell...we need insulin to be released.
Glucagon does this...up it goes. Interesting, but I just learned that glucagon ALSO functions to INactivate a liver enzyme called HMG CoA reductase, effectively shutting off VLDL...very low density lipoprotein release (containing choline)from the liver.
Bb, in order to make its cell wall..needs lipoproteins.
NORMALLY Mg INactivates this enzyme, but MUSCLE levels of Mg have dropped "significantly" (understatement).
Mg and glucose are both needed to make healthy antibodies. Both are in short supply.
We're in trouble...fast. Mg is an anti-inflammatory and anti-histamine and we react to this pathogen - to its outer cell wall proteins (antigens) very much like we react to "allergens".
In a manner of speaking, our reaction is an allergic reaction.
So...what to do?
Gi Gi is right! We must get glucose levels UP. But the RIGHT kind of glucose is absolutely critical.
If we watch carefully how our body is responding and figure out how to support this response, we just might "win" the battle.
We must get glucose levels up which would halt gluconeogenesis?
But...which form of glucose (believe me, that is critical!)? I'll talk about that in a minute.
Glucose is "alkaline" (positive charge).
This bugger is making the system far too acidic.
Yes, acids (negative charges) do indeed knock out infections...but too many harm healthy cells.
Think of it this way...when we exercise a LOT, our body produces a LOT of lactic acid and our NK cell levels NORMALLY drop. They aren't "needed"...the entire system is already acidic to destroy precancerous cells.
You see the NK cells ONLY work when out pH is just right...slightly alkaline. Then, and only then, to they "squirt" the precancerous cells with a...get this...free radical...to destroy them. Every day, about 4 precancerous cells are destroyed this way.
So...in order to fight, in order for our own immune cells to be able to work, the system needs to be slightly alkaline, which is why the blood sugar levels are varying so much.
It makes no sense to acidify the entire body. We must TARGET only the pathogen and only the cells it is in...slowly and very carefully. Our OWN immune system knows very well how to do this.
When cells die off, they are broken down and release nutrients - proteins -> amino acids we either breakdown and re-use (if the level is low) or get rid of (if there is an excess). This is an overwhelming job and it can lead to death. Too many proteins released and broken down too fast will shut down the kidneys. Too acidic. The kidney cells respond to acids and can be damaged by them as their job is to maintain the acid-base(alkaline) balance...otherwise known as the pH balance.
Bb has a PKC inhibitor. These inhibitors specifically cause cell death...prematurely. Cell is still viable, just sick. So we try to keep the cell ALIVE while, at the same time, destroy the pathogen that is damaging it.
Depending on the pathogen...this can be an overwhelming job. Every day all our lives we are fighting off germs that we are exposed to.
Normally...the system works very well.
Tamoxifen is a man-made PKC inhibitor. It specifically destroys cancer cells that are estrogen dependent.
Now...the body does not want sick cells to die prematurely, but tries to figure out ways to stop the UNDERLYING INFECTION that is disrupting those cells and damaging the DNA within those cells (DNA = hydrogen bond between protein chains).
It does this in quite an amazing way. It upregulates glucose to supply energy to the immune system fighters. And it either heats up the body or lowers the temperature according to the need. Cold...REDUCES inflammation. Makes sense, right? (Why your body temp. is low.)
Many cells become glucose deficient. Whatever pathogen is in them (bacterial/viral) is using glucose -> lactic acid and damaging the mitochondria (powerhouses) - the #s drop.
Oxygen is in those cells, just in the wrong form...lone free oxygen radicals because they do indeed destroy most pathogens...esp. the H2O2 we make and destroy every split second. (Works in something like 1/400,00th of a second! Make, gone, make, gone.)
NORMALLY acids (including H2O2..a weak acid) DO destroy pathogens.
Problem is...Bb has devised a way to protect itself from the powerful superoxide (O) free radical, NO (nitric oxide) as well as H2O2.
Normally NO dilates the vessels. If it is inhibited, the body responds appropriately. It develops collateral circulation which "feed the cancer cells" or...
What if...(as some believe) the reason WHY this is happening is to deliver the body defense nutrients, the proteins, the antibodies, etc. that are needed to destroy the underlying infection?
Hence...we develop ways to "starve" those cells of nutients. We do radiation therapy...a really strong negative charge to hit those cells (and the pathogen)and which also damages the collateral circulation vessels.
If that isn't "enough", we make all the "similar" cells toxic via chemotherapy.
Getting back to cells dying...due to PKC inhibitors (there are MANY specific ones!)
WHICH Inhibitor Bb is employing matters...a LOT.
It looks like Bb is stopping the activity of PKC DELTA.
Now..this is weird! The Greek symbol for delta is a triangle. Tri...trivalent...ozone...O3. AND it is the 4th letter in the Greek alphabet.
Co-incidence? Inhibit P D E 4? (Forskolin?)
Just trivia...maybe.
Delta.
If Bb is INhibiting PKC delta, our response looks to be UPregulating PKA alpha and TNF alpha...while some "gamma" too. In addition, it appears Bb also is "downregulating" to an extent, beta in addition to delta.
Alpha looks to be a "inflammatory" approach. Gamma "anti-oxidant".
That would be logical.
But what if...what if...we "counter" Bb's PKC delta inhibitor by instead UPregulating PKC delta?
By...
What if we give a "delta" form of sugar...would we thus "downregulate"...gluconeogenesis? In other words, trigger glycolysis by supplying MORE of a d-sugar and thus drive gluconeogenesis down?
And prevent the loss of the nitrogen in the amino acids involved?
Would that sugar restore the energy to our own immune system cells to attack?
Would Bb be unable to make its cell wall?
Or...by supplying a d-sugar, will glucagon levels DROP and then HMG CoA reductase will release VLDL to supply our body with the choline it needs to MAKE acetylcholine...and downregulate epinephrine (cortisol from)?
Now instead of LOWERING cholesterol, our body can MAKE what it needs (our cell walls are made up of cholesterol as is the myelin sheath that surrounds the nerves).
Bb has a C-acetyltransferase enzyme. Is it using that enzyme so we don't have enough? This enzyme is needed to make acetylcholine.
Bb can NOT breakdown acetylcholine.
What if we kept acetylcholine levels up by blocking the receptors? They are called nicotinic receptors! What if we used a nicotine patch? Nitroglycerine patches do dilate vessels. (Nitrogen + a sugar?)
By blocking those receptors (they aren't actually blocked, it is a "timing" issue), we keep the level of that neurotransmitter higher for longer. Much like how Prozac works on serotonin receptors. It blocks the receptors, thus keeping serotonin present longer before it is "taken apart".
We make the neurotransmitters and take them apart as needed at astounding speed.
What if we restore the HPA axis via Phosphatidyl Serine? It may take "higher" doses than normal to do this. Supposedly this corrects the cortisol level...if high, makes it lower, if low, makes it higher. Will this drive the pituitary to release growth hormone?
What is the risk regarding cancerous cells?
If we make the system more "alkaline" via a d-sugar, will our NK cells take over?
Will PSA levels RISE? Protein "markers"..."Here...hit THIS cell. This is the one infected."
What about the heart? Well...it sure as heck needs a lot of glucose...for energy.
What about yeast? How will they react to a d-sugar?
Is a delta sugar the ONE sugar Bb cannot use? Is Bb's PKC inhibitor PKC DELTA?
Bb can use many sugars in their various forms.
Now...d-ribose is a sugar that is used to make RNA.
RNA is odd. It is identical to DNA except that it contains one extra OXYGEN molecule.
Now, Gi Gi has posted that d-galactose is the sugar to use. Unfortunately, it is not readily available OTC, but d-ribose IS.
Would it work?
Stay with me...PLEASE.
I found this:
"***"Of the compounds tested,
only D-ribose was capable of stimulating ß-galactosidase synthesis ."***
I think that is alpha, gamma.
"Lactase
An enzyme found in mammals, honeybee larvae, and some plants.
It is a ß-galactosidase which hydrolyzes lactose to galactose and glucose.
Hydrolyzes = break a bond in a molecule by adding WATER!
(Trivia: some cosmetics "hydrolyze" the area under our eyes to correct dark circles. The blood vessels are WEAK and LEAKING. It helps to keep those vessels healthy!)
In mammals, lactase appears in the intestinal secretion from the intestinal villi, and exerts its effect on lactose in chyme. "
(Is lactase low because Mg is needed to make it and Bb transports Mg out of the cells?)
Lactose (milk sugar) is converted by a ß-galactosidase (stimulated by d-ribose)to D-glucose and
D-galactose, (yo, Gi Gi!)
which are then taken up by the cell.
D-Glucose is channeled into glycolysis
while D-galactose can be converted by two different pathways.
Beside the common Leloir pathway, we identified a novel pathway for D-galactose utilization in fungi.
Genetic engineering of the pathways is used to alter the flux rates through the different pathways catabolizing lactose/D-galactose."
The change in metabolite accumulation in the different pathways directly influences the induction of cellulases."
Cellulases.
Now...here's another tidbit:
"The B-glucuronidase Klotho hydrolyses and activates the TRPV5 channels. These look to be calcium channels.
Once again, I think Bb is somewhat triggering a "beta" response (Il1 beta), but to a lesser degree than an "alpha" response (TNF alpha) via inhibiting delta. It appears we also use gamma as a defense.
Instead of blocking TNF alpha and IL1 Beta, what if we instead "promote" delta?
Years ago, several lyme patients went to Italy to try DNP (an acid in a class with cyanide) to "speed up glycolysis". The idea was to heat the cells and kill all forms of Bb. Unfortunately for one it was deadly because this depleted the MINERALS..K would go first. The body got hot, the oxygen demands soared.
What if we instead trigger glycolysis by giving the cells a SUGAR that it has to process via glycolysis?
Can we kill Bb with "sweetness"?
Or..will it trigger hypo (LOW) glycemia by stimulating insulin secretion?
What is the impact of ribose on collagen (which looks to be being broken down)?
PMID: 9494092
"A method for preparing cross-linked collagen, and cross-linked collagen products. The method includes incubating collagen in a solution including water, at least one polar solvent and at least one sugar, to form cross-linked collagen. The accompanying figure shows the effect of treatment with reducing sugar (D-ribose) and alcohol on particulate collagen degradation by bacterial collagenase ."
if you're suggesting using a d-ribose supplement, I think there are people here who have taken it. If I remember correctly, some have reported an increase in energy.
I was tested for MMP-9 and TNF-A last fall. TNF-A was a little elevated, but MMP-9 was not remarkably high, although the lab's range is huge. Mine was toward the bottom end.
I was taking doxycycline, only stopped a couple of days before the test. I would be willing to bet it was keeping the MMP-9 low, it's been shown to do that in joints.
Also, MMP-9 can go up very quickly, at least according to Dr. Shoemaker.
Perhaps you could get some input about "d-ribose".
Thank you for keeping the grey matter stimulated.
I had few markers of inflammation, but I my symptoms just scream it. Ipuprofen doesn't help, so it's not primarily prostaglandins. Antihistamines don't work well for me, but it doesn't seem to be histamine either.
There is something else, some chemical or chemical that is part of this disease. . . I keep hoping for the answer, and the magic pill.
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Marnie
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posted
Go to the last link...!!! Look at the figure (picture).
It is not JUST d-ribose.
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
More...
Cancer cells are undermethylated .
Methionine is almost the first amino acid used.
It is used by several bacteria, including E.Coli.
"Its level of methylation is influenced by D-ribose, D-galactose, and certain structural analogues of them."
"T-cell receptor beta chain gene rearrangement in acute myeloid leukemia always occurs at the allele that contains the
undermethylated J beta 1 region ."
Undermethylated BETA region.
So...it may well be that d-ribose and d-galactose levels are severely low in lyme -> undermethylation and this impacts beta...
Here is the molecular formula for methionine:
C5H11NO2S.
Guess what.
Here is the formula for penicillamine!
C5H11NO2S.
Look alike, don't they?!
More expensive than say...SAMe...
"A less expensive readily available starting material is d-ribose, which has the right # of carbon atoms, but requires the oxidation at C1 and...
Inversion of sterochemistry at C-4.
You wouldn't believe the number of google links to C-4!
Leaves from tobacco (nicotine - acetylcholine receptors are nicotinic receptors) show that when malate (malic acid) with a 14C label
on the C4 position
is supplied to the xylem stream, 14C is fixed in cells ."
Looks like this is common to many pathogens.
(Amino sugars such as D-glucosamine and D-galacosamine have an amino goup instead of a hydroxyl group at the C-2 position. Many of you know this helps, but doesn't cure.)
If glucose influx into the liver is low (e.g. hypoglycemia) then very little F-6-P will be around, so there will be very little F-2, 6-BP.
Which translates to: gluconeogenesis is kicking in...the liver is not taking up glucose, but is instead MAKING it from non-carbon sources. In this situation, AMP levels are low too. Acetyl CoA is up, glucagon is up, citrates are up.
Now...the liver, is "deprived" of glucose for its own energy...perhaps.
"PFK 2 is active when insulin (beta cells) is present; inhibited when cAMP levels are high from glucagon (alpha cells) stimulation."
Glucagon is trying to raise cAMP, but this inhibits PFK2 and thus inhibits insulin release?
Epinephrine (adrenaline) also raises cAMP.
The body is doing everything it can to increase cAMP.
Sit tight...the best is yet to come.
Remember when I said one of the amino acids used in gluconeogenesis was alanine? Well...it is a marker for protein catabolism - protein breakdown!
If you need bypass surgery...it is important that you know this recent information:
PHOENIX, AZ, FEB 20, 2007-People with coronary artery disease (CAD) may require coronary artery bypass surgery.
Today, some patients are candidates for an alternative surgery using an "off-pump" cardiopulmonary bypass (OPCAB) technique, which eliminates the use of a heart-lung machine.
Still, the surgery carries many risks due, in part, to a depletion of adenosine triphosphate (ATP), which cells use as their primary source of energy.
A study led by David Perkowski, MD, Susan Wagner, RN, Alan Marcus, MD, and John St. Cyr, MD, PhD showed that patients undergoing off pump bypass surgery who took an oral D-ribose supplement before surgery demonstrated significant improvements in their cardiac indices, a measure of heart pump function.
D-Ribose has already been shown to increase functional capacity for patients with congestive heart failure (CHF) by improving diastolic heart function, ventilation, exercise capacity, and
oxygen uptake efficiency.
Corvalen, which was used in the study, is a proprietary D-ribose product of Bioenergy Life Science, Inc.
http://www.bioenergy.com, a privately held, Minneapolis-based life sciences company whose core technology lies in the development and commercialization of products based on the physiological benefits of D-ribose in health and wellness."
C-4 decarboxylase involved in cholesterol (is a steroid protein) biosynthesis...as in Bb's cell wall formation?
While cruising for more C-4 information:
"These reslute indicated that flavones or flavonols that contain C5, C7 and C4' hydroxyl groups are
potent inhibitors of P-450 enzyme activities
induced by Aroclor 1254 (P-450IA1 and P-450IA2), and may potentially be useful as chemopreventive agents against heterocyclic amine-induced mutagenesis or carcinogenesis."
P450...as in alcohol DEHYDROGENASE? This bugger can breakdown alcohol?
Flagyl INactivates that liver enzyme.
So...if "Delta" is being downregulated, is this surprising (not):
Gamma delta T cells accumulate at epithelial barriers and at sites of inflammation in various infectious and autoimmune diseases, yet little is understood about the function of tissue-infiltrating gamma delta T cells.
We observe that gamma delta T cells of the V delta 1 subset accumulate in synovial fluid of human Lyme arthritis and are intensely cytolytic toward a wide array of target cells.
Particularly striking is that the cytolytic activity is highly prolonged, lasting for at least 3 wk after stimulation of the gamma delta T cells with Borrelia burgdorferi.
Cytolysis is largely Fas ligand, which is transcriptionally regulated. This also manifests in a substantial level of
self-induced apoptosis of the gamma delta T cells.
In this capacity, certain gamma delta T cell subsets may serve as cytolytic
sentinels
at sites of inflammation, and perhaps at epithelial barriers.
� Published in J Immunol. 2003 Mar 1;170(5):2702-10. J Immunol. 2003 Mar 1;170(5):2702-10.
Are the T cells dying because Bb is downregulating PKC delta in them? Do they lack enough D-ribose for energy to sustain the fight?
Several enzymes are responsible but the two most important enzymes for alcohol metabolism are known as ADH (alcohol dehydrogenase) and cytochrome P450.
ADH converts alcohol into acetaldehyde, which is one of the principal culprits in producing the hangover effect.
The level of activity of these two enzymes can vary greatly from person to person.
This may explain why some people are able to drink large amounts of alcohol and never appear to suffer from a hangover.
They may simply be metabolising more alcohol through the cytochrome P450 system, which does not result in unpleasant hangover symptoms.
Breaking alcohol down via alcohol dehydrogenase.
P450 upregulated = drugs less effective.
Women have less alcohol dehydrogenase than do men. We can't breakdown alcohol as easily as most men.
How does this make women more vulnerable to lyme? Statistically, it sure appears to hit more women than men, but does hit both. Remember the cat discussion? They rarely get lyme (compared to dogs), but can. Humm...gotta find an old file...
Meanwhile...
This fact was used to determine the stereospecificity at C4 of NAD(P) for the NADP-dependent alcohol dehydrogenase from...
Only Flagyl...?
Of course not...
Acetylcarnitine inhibits alcohol dehydrogenase This finding is unique in that this is the first report of this function of acetylcarnitine and it is a novel interaction between two important nutrients, niacin and carnitine . PMID: 7945297
Carnitine is not an amino acid is the strictest sense. It is actually a substance related to the B vitamins. It's main function is to transport long chain fatty acids, which are burned within the cells, mainly in the mitochondria. This is a major source of energy for the muscles. It inhibits alcohol induced fatty liver. (Want more? I am copying from my nutrition book)
L-carnitine comes from L-tyrosine and L-Methionine.
D-ribose and/or D-galactose AND acetylcarnitine )ALC).
If this causes a herx response...PERSONALLY, I'd have on hand the 3rd OTC supplement in the "Universal Remedy" to bind the "toxins". Careful..it also binds nearly EVERY drug!
I do NOT know if this is totally "safe", what doses or timing!!!
I remember now...
"Plasma total carnitine concentration in the females was significantly lower than that of males."
That's why this is primarily a "chick" thing...and why we get so little attention, perhaps.
[ 11. May 2007, 08:06 PM: Message edited by: Marnie ]
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