Topic: Today's pieces of the puzzle for RESEARCHERS
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Long...highlight, cut and paste and drop into word to study later.
``Our observations show that (beta)2-subunits play an important role in the
regulation of sodium channel density
and function in neurons
in vivo and are required for normal action potential generation and
control of excitability.''
Forskolin impacts alpha AND beta receptors.
Bb's OspB protein looks to impact NH2 which impacts the androgen (estrogen AND testosterone) receptors (specifically the estrogen receptors which have alpha and beta components).
We (all, guys included) have estrogen receptors throughout our body...even in our brains!
So...certain infected cells and receptors on specific cells -> less cAMP (have less energy). Will explain why below.
This impacts the Na-K pumps (and more - esp. the Mg-ATP pump too).
"Pseudohyponatremia (false low blood sodium levels) occurs when too much water is drawn into the blood; it is commonly seen in people with hypoglycemia (low blood sugar). "
Our cells NEED glucose. It is our PREFERRED sugar. Bb is using fructose, which looks to prevent us from using the "preferred" sugar...glucose.
While chemically, the sugars (glucose, galactose and fructose) are idential (C6H12O6), structurally they are NOT.
If you see the 2 dimensional structure, it becomes apparent.
Glucose and galactose are structurally identical except for the 2nd carbon on the chain. H and OH bonds are "flipped" or mirror images.
Fructose is similar except for the 4th carbon which contains attached to it...H-C-OH.
Once you figure out what H-C-OH is...you will say...Oh, no...not good!
This pathogen really messes up our neurotransmitters and hormones...bigtime... by virtue of its genetic component C-acetyltransferase (needed to make acetylcholine).
If we throw ONE neurotransmitter off, it impacts all the others and more!
This is intereting:
"When sheep are faced with a barking dog (audiovisual stress) or insulin-induced hypoglycemia (metabolic stress) they produce acute rises in adrenocortical hormone (ACTH), cortisol, epinephrine and norepinephrine which
can only be turned off by high doses of estrogen."
If GLUSOSE levels drop, there goes serotonin. Glucose triggers serotonin release!
The 2 major neurotransmitters in our body are: 1.norepinephrine (also called noradrenaline) -> epinephrine (also called adrenaline) and 2. acetylcholine.
Bb is impacting acetylcholine.
We have many more neurotransmitters in our brain. Many are actually made in our gut from NUTRIENTS we consume. (Tryptophan - amino acid - to serotonin, for example.)
Genetic research says Bb has a PKC inhibitor.
Tamoxifen is a man-made estrogen dependent PKC inhibitor. It is used to destroy cancer cells. These inhibitors look to work by REDUCING cAMP...less energy for those cells and then they die.
If too many cells die too fast, this is really hard on our system to handle the "garbage" that remains. So, we try to keep the cells alive. Up goes PKC to counter Bb's PKC inhibitor. PKA also goes up...leave it at that for now. This gets even more complex!
I suspect Bb first damages the endothelial cells that line our blood vessels (they contain no protection since nutrients have to flow in and out of their cell walls) and then may also "infect" the Langerhans cells.
These are our first line of defense (cruising police officers) which envelop these pathogens and are supposed to begin the destruction of Bb and then "present" the antigens (proteins in Bb's outer cell wall) to the T cells in order to make the "right" antibody.
When Bb cloaks itself in the Salp15 protein - which I think contains Na+Al - (OspC) which it picks up in the ticks' saliva this buys Bbs time to infect.
Aluminium displaces Mg. Na carries choline INTO the cells.
Until Bb truly expresses OspA + OspB (and yes, other proteins), we don't mount the appropriate defense.
By then we are in real trouble.
NORMALLY Mg-ATP triggers cAMP. With Mg leaving the cells...the control is kapoot. Bb also has a Mg transporter...
Mg-ATP INactivates PFK...phosphofructokinase...the "rate limiting" enzyme for glycolysis.
Bb is "PFK dependent". It appears PFK1, not PFK2 (thank goodness).
It appears Bb wants/can use ONLY fructose (maybe).
Insulin ACTIVATES PFK1. Several things besides Mg-ATP can INactivate it.
Bb has ways to protect itself (from the superoxide free radical as well as H2O2 destruction).
The ONLY thing that INactivates PFK2 and (ultimately) PFK1 is glucagon.
Sorry, but those who already have diabetes and get lyme are really in a mess. It will make it much harder to regulate the insulin-sugar levels.
Bb also has zinc fingers...histidine and cysteine bound by zinc. (So does HIV.)
Mg and zinc are "gate keepers" for the NMDA receptors. These are the glutamate receptors. If the "gate-keeper'' levels are low...up goes glutamate = "rapid firing".
Glutamate = accelerator GABA = brakes
GABA tries to go up to counter. GABA levels effect dopamine levels in ways we don't yet completely understand.
Back to the zinc fingers...histidine and cysteine bound by zinc...
If Bb is taking from us histidine AND zinc...there goes our immune defense as zinc is really needed to mount a good immune defense.
Not to mention...our WBCs MUST HAVE GLUCOSE.
Calprotectin, in our neutrophils - most abundant WBCs - binds to zinc. That's how those WBC are defending. Unfortunately they are only made about every 3 weeks. (Cells are made, destroyed, made...all at different times.)
Bb cannot stand a lot of oxygen. Notice I said a LOT. A lot of free radicals are formed as a protective measure and combine with nitrogen to make NO...nitric oxide to dilate blood vessels.
Bb can defend itself from those free radicals (superoxide, H2O2) to a degree, but these free radicals sure as heck mess with our DNA! They break the hydrogen bonds holding our DNA together it appears.
This is why hyperbaric chambers HELP. This is where ozone saunas HELP.
I believe the latter (saunas) actually "fry" Bb because it seems (reported here) the persons who do those saunas do NOT have a herx afterwards as opposed to those who do hyperbaric chambers using O2,
NOT trivalent, O3.
DO NOT BREATHE OZONE!!!
Delta....as in d-galactose.
The galactose-H(+) membrane-transport protein, GalP...contains cysteine.
If L-cysteine is too low (remember Bb's use of it to make its zinc fingers)...no transport of Omega 3s into the cells.
"Here we show that forskolin is a remarkably specific
inhibitor of energized D-galactose transport
by the GalP sugar-H+ symport protein..."
That makes me wonder if Bb is not only using fructose, but galactose as well?
"In addition, forskolin inhibited the influx of other carbohydrates including galactose, ribose, and fructose."
No mention of glucose!!!
Which IS the ideal, preferred sugar for our cells.
Glucose levels up -> insulin release (beta cells) to stimulate uptake of glucose -> glucagon released (alpha cells) -> halt (inactivate) PFK1 and PFK2.
Apart from insulin, beta cells release C-peptide, a byproduct of insulin production, into the bloodstream in equimolar quantities. Measuring the levels of C-peptide can give a practitioner an idea of the viable beta cell mass.
β-cells also produce amylin, also known as IAPP, islet amyloid polypeptide, a protein with unknown function.
C-peptide is a peptide which is made when proinsulin is split into insulin and C-peptide.
C-peptide functions in repair of the muscular layer of the arteries.
C-peptide may also exerts beneficial therapeutic effects on diabetic neuropathy
Amylin, or Islet Amyloid Polypeptide (IAPP), is a 37-residue peptide hormone secreted by pancreatic β-cells at the same time as insulin (in a roughly 100:1 ratio).
Although amylin's normal role may not yet be fully known, it aids in limiting glycemic excursions by slowing gastric emptying, promoting satiety, and
inhibiting inappropriate secretion of glucagon,
a catabolic hormone that opposes the effects of insulin and amylin.
Glugagon not released = up goes insulin, amylin, C-peptide via pancreatic beta cells.
IAPP was identified independently by two groups as the major component of diabetes-associated islet amyloid deposits in 1987.[1
Glucagon is not being released? Why would the body be allowing this to happen...or?
GLU-R (glucagon receptor) signals through both adenylate cyclase- and also
mediates an ***increase in intracellular calcium***,
consistent with earlier descriptions of dual glucagon signaling pathways in hepatocytes (liver cells).
Glucagon receptors are also expressed on islet b cells, where they are coupled to stimulation of insulin secretion.
Calcium, our most abundant mineral can help to regulate our pH in a lactic acidosis situation...as Bb ferments sugar to lactic acid...as well as WE produce additional via TNF alpha and NO upregulating this acid.
The path our body takes looks to upregulate SPECIFIC alpha receptors and downregulate SPECIFIC beta receptors.
Glucagon stimulates an exocytotic response from a cells in a PKA-dependent manner. These actions were
blocked by a glucagon antagonist des-His1-[glu9]-glucagon-amide.
Histidine containing amide blocking glucagon?
Histidine availability alters glucagon gene expression in murine αTC6 cells.
Glucagon release is being blocked due to low levels of histidine which Bb is using for its zinc fingers?
Impacting cyclase activity:
Under conditions where both glucagon and hormonal stimulation of adenylyl cyclase activity increase with increasing concentrations of glucagon...
Forskolin, a direct activator of adenylate cyclase, stimulates cAMP production in islet cells. The effects of forskolin on the release of somatostatin, glucagon, and insulin were studied using the isolated, perfused dog pancreas.
It was found that concentrations ranging from 0.075 microM-1 microM stimulated the secretion of somatostatin, glucagon, and insulin in a dose-related manner.
This gets confusing because...
(Most other research indicates forskolin halts glucagon. Quote follows.)
Forskolin, which are known to raise intracellular cAMP levels, all caused a reduction in glucagon receptor mRNA expression -
In LIVER cells. It reduces the RECEPTOR functioning. It is released, but the liver cells don't take it up.
In pancreatic cells, forskolin appears to trigger the release of glucagon and insulin (and somatostatin), but in LIVER cells forskolin reduces the receptor to ``accept'' glucagon?
More to the this ``brew'':
``Forskolin induction of glucagon-CAT activity in STC-1 cells''
Okay...what the heck are those?
STC cells are glycoproteins. The ``CAT'' looks to stand for catecholamines.
Forskolin induces glucagon and catecholamine (norepinephrine and epinephrine) in very specific cells.
Ahhh...the 2 main neurotransmitters in our bodies are: acetylcholine and norepinephrine. We will thus ``downregulate'' acetylcholine in those cells by upregulating norepinephrine?
(STC-1 cells, a cholecystokinin-secreting cell line)
Cholecystokinin is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin, previously called pancreozymin, is secreted by the duodenum, the first segment of the small intestine, and causes the release of digestive enzymes and bile from the pancreas and gallbladder.
If the STC-1 cells aren't working properly...
These results indicate that in STC-1 cells a potassium current is increased by agents that stimulate CCK secretion, presumably by increasing the level of cytosolic calcium.
The observed STC1 suppression of progesterone,
but not estradiol,
production further suggests the potential role of this paracrine hormone as a luteinization inhibitor.
Intestinal cholecystokinin (CCK)-secreting NE (neuroendrocrine) cell line STC-1.
Thus, GABA is involved in the fine tuning of CCK secretion from the gut NE cell line STC-1.
Gastrointestinal neuroendocrine (NE) cells synthesize, store and secrete gamma-aminobutyric acid (GABA).
From these data it can be concluded that glucagon stimulated acid production in the stomach from immature rats, and this effect does
NOT seem to involve the same adenylate cyclase
activated by histamine.
HCL is dependent on glucagon. If HCL drops...no digestion. Eventually no nutrients broken down to be absorbed = goodbye neurotransmitters.
Induction of ketogenesis and fatty acid oxidation by glucagon and cyclic AMP in cultured hepatocytes (liver cells) from rabbit fetuses.
Glucagon and cAMP ->breaking down fats (ketogenesis) to make acetyl CoA. Both sugars and fats are needed to make acetyl CoA. This appears to be what Bb is doing.
Looks like the body is trying to stop the breakdown of fats (ketogenesis which would be triggered by glucagon but the liver cell receptors won't allow uptake it) to supply the amino acids Bb needs.
All of this confusion is due to Bb using 2 pathways simultaneously...Bb's use of sugar as well as the use of fats to make acetyl CoA.
Should you exercise...certainly not for 90 minutes! ;-)
Our results support the concept that different forms of stress may
similarly reduce
counterregulatory responses to
subsequent hypoglycemia.
The blunting in counterregulatory responses induced by prior exercise (epinephrine down 37%, norepinephrine down 40%, glucagon down 58%, growth hormone down 62%, pancreatic polypeptide down 44%, MSNA down 90%, EGP down 70%) was similar in magnitude to that previously reported after antecedent
hypoglycemia.''
Simplified:
In summary, two bouts of exercise (90 min at 50% V˙ O2 max) significantly reduced glucagon, catecholamines, growth hormone, pancreatic polypeptide, and EGP responses to subsequent hypoglycemia.
We conclude that, in normal humans, antecedent prolonged moderate exercise blunts neuroendocrine and metabolic counterregulatory responses to subsequent hypoglycemia.
Acetyl CoA (from sugar and fats) + C-acetyltransferase + choline-> acetylcholine (simplified)
Bb is using OUR supply of sugars and fats. It is BREAKING THEM DOWN.
Bb has a gene for C-acetyltransferase.
Bb can NOT breakdown acetylcholine.
Once more getting back to forskolin:
Forskolin has been used to stimulate adenylyl cyclase. However, we found that forskolin inhibited voltage-sensitive Ca2+ channels (VSCCs) in a cyclic AMP (cAMP)-independent manner
in PC12 cells.
What the heck are those?
Neuronally differentiated PC12 cells have been used as a model for habituation. These cells secrete norepinephrine
in response to extracellular ATP, as well as other stimulants, and the response is diminished with repetitive stimulation.
This loss of neurosecretory responsiveness displays characteristics commonly associated with habituative learning.
Inactivation of the ATP-gated channel may be proportionately faster in response to lower ligand concentrations, allowing habituation to be more rapid in response to stimuli of weaker intensity.
PC12 cells secrete the enzyme acetylcholinesterase (AChE) *while at rest*, and increase the overall rate of this secretion 2-fold upon depolarization.
Acetylcholinesterase is used to BREAKDOWN acetylcholine.
By inhibiting Ca channels in PC12 cells, do we keep acetylcholine levels UP for longer...thus facilitating learning?
Bottom line... today forskolin looks like it MIGHT be very beneficial from MANY, not just one,respect.
Because the body is so darned complex...we do NOT know ALL the implications. But this is certainly in ``test mode'' to treat MANY diseases.
Too many of us are Mg deficient to begin with.
We NEED Mg attached to our energy carrier, ATP as Mg-ATP to control cAMP levels, to INactivate PFK, to INactivate HMG CoA reductase, to make healthy, not fab damaged antibodies specifically designed to fight Bb, to act as an anti-inflammatory and anti-histamine...the list goes on.
The downward spiral ...Mg loss...is disasterous.
[ 22. April 2007, 01:07 PM: Message edited by: Marnie ]
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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I read a post of a person on another board who is taking this with great results - off his thyroid meds (T3 - I think) in 6 weeks. Enzymatic therapy is the brand he used. He is only dosing every other day now because it is working so well
Here is the definition
Coleus Forskohlii Herb Extract This "power" herb has an active ingredient in it called forskolin. It has been used in ayruvedic medicine for many years. Forskolin's basic mechanism of action is that it increases the amount of cyclic AMP (adenosine monophosphate) in cells by activating an enzyme called adenylate cyclase. Cyclic AMP (cAMP) is one of the most important secondary messengers in the cell. It is considered to be one of the most important cell regulating compounds.
Under normal circumstances, cAMP forms by adenylate cyclase activation due to hormonal stimulation at the cell receptor site. However, forskolin seems to bypass this reaction and allows for an increase in intracellular cAMP to occur. Why is it important to increase cAMP levels? Well, there are several benefits of this to athletes including relaxation of the arteries and smooth muscles, lowering blood pressure, enhanced insulin secretion (which can help drive carbohydrates and protein into muscle cells for energy and recovery), increased thyroid hormone function (which can help enhance metabolic rate), and significantly increase lipolysis (fat burning). Forskolin also seems to benefit other cellular enzymes as well.
The breakdown of fat for fuel (lipolysis) is actually regulated by cAMP. Forskolin has been shown to not only enhance lipolysis but it may also inhibit fat storage from occurring. This is very good news for individuals trying to lose bodyfat and get lean. Another way that forskolin may allow for fat loss to occur is by stimulating thyroid hormone production and release. Thyroid hormone controls metabolism and can enhance metabolic rate, which may translate into more fat loss.
One of the overlooked benefits of forskolin includes its stimulation of digestive enzymes, which can allow individuals to digest and assimilate their food better. It has been shown to increase nutrient absorption in the small intestine.
Forskolin has been shown to be safe and effective and has a great amount of potential as a sports supplement. As with most dietary supplements, more human research is needed but the future looks bright for this compound.
Forskolin is a labdane diterpene that is produced by the plant Plectranthus barbatus. Forskolin is commonly used to raise levels of cyclic AMP (cAMP) in the study and research of cell physiology. Forskolin resensitizes cell receptors by activating the enzyme adenylyl cyclase and increasing the intracellular levels of cyclic Adenosine Monophosphate (cyclic AMP or cAMP). Cyclic AMP is an important signal carrier that is necessary for the proper biological response of cells to hormones and other extracellular signals. It is required for cell communication in the hypothalamus/pituitary gland axis and for the feedback control of hormones.
Benefits
-Inhibition of platelet activation and degranulation. - Inhibition of mast cell degranulation and release of histamine and other allergic compounds. - Increased force of contraction of the heart muscle. - Relaxation of the arteries and other smooth muscles, vasodilation. - Increased insulin secretion. - Increased thyroid function (and therefore metabolic rate). - Reduced adipose assimilation and increased lipolysis of fats.
-------------------- Nori Posts: 109 | From Virginia | Registered: Mar 2006
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Foggy
Frequent Contributor (1K+ posts)
Member # 1584
posted
Marnie, have U shared any of your research w/LLMDs or Columbia?
Posts: 2451 | From Lyme Central | Registered: Aug 2001
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I take Forslean by Sabinsa, which is a extract of the Coleus Forskohlii plant, standardized for Forskolin (mines 10% forskolin).
I try to take between 300mg-1g a day. It may have been the reason my intra ocular pressure is now normal (was high before). My optometrist was really happy and interested that I managed to normalize my eye pressure.
Sabinsa is working on making Forskolin eye drops for glaucoma.
You can buy cheap bulk forslean at http://www.beyondacenturyonline.com/ . If you decide to encapsulate it yourself, wear a mask and preferably do it near an air filter, because its very fine and can be a hazard to inhale.
I think it also helps some with fatigue too. It seems to absorb best on a fairly empty stomach when taken with something fatty, as it's fat soluble (I just take a swig of olive oil).
My 2 cents anyway.
-------------------- "You know, the worst, meanest, nastiest, ticks in the world are politicks," - Steve Nostrum Posts: 242 | From South NJ | Registered: Dec 2006
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Foggy...I've tried. Some of your LLMDs have "listened" and "Willy" himself did send me a reply years ago! I saved it.
His letter to me started, "This is to acknowledge receipt of your October 16th letter, in regard to use of metals on the physiology of borrelia burgdorferi and other spirochetes."
If you didn't catch the word "metals"...you missed the point!
Minerals - metals. The NIH is concerned about metals. Why?
""Metalloproteases, on the other hand, seem to be a common feature in most bacterial pathogens."
It takes a LOT of Mg to displace zinc which is binding Bb's histidine-cysteine zinc fingers.
We know zinc also binds to vitamin C because this is what zinc lozenges contain. We are the only animals that do not MAKE vitamin C.
But first we have to deal with that Salp15 protein Bb picks up! This protein may/may not contain Na and Al. It took me a long time to try to find that ( I think this protein is bound to those 2 "metals". But it is logical. Al displaces Mg and Na carries choline into the cells.
Many universities and research hospitals will NOT read documented research from other (competing) universities/research hospitals.
Which is really, really sad and stupid.
We need to SHARE what we know from every aspect...
It should be a JOINT EFFORT...involving:
Microbiologists, endocrinologists, neuroscientists, nutritionists, etc.
Brainstorming...pulling all the pieces together because this is INCREDIBLY complex.
I believe we already DO have the answer. It is just buried in the mounds of information. Lots of people have puzzle pieces but are not sharing them and no one is putting the puzzle TOGETHER.
For whatever reason(s) it appears to take 2 years to completely clear this infection via certain route(s) after Bb gains a foothold.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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I am taking a lot of Mg. Still going downhill. Tested low on zinc, so I am supplementing that. Still going downhill.
It seems awfully complicated to me, not just your explanations which I hardly ever understand because of all the biochemistry.
Does any of this have to do with T cell function? Cave just posted an article on infection damage to functioning T cells. So, is there anything that improves T cell function? And how does that fit if part of the damage from infection is caused by the proinflammatory cytokines? If you boost immune function, will that just make it worse? These may sound like simple minded questions, but I don't see any of the big guns having answers to this yet.
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
There IS a lot of "truth" to Edgar Cayce's use of castor oil packs to treat arthritis...
IF you understand the very complicated "whys". What is castor oil? Where does it come from? What does it contain? How does it work?
History has a funny way of repeating itself until we catch on!
Bb is breaking down sugars and fats.
We NEED sugar (glucose!) and fats (amino acids) in order to MAKE all our proteins..including our OWN myelin sheath that surrounds our nerves.
Mg levels spiral down for many reasons and we begin to lack the ability to hang onto it.
(Mg levels DIVE at the outset. I'm talking GRAMS, not milligrams.)Destruction happens fast, rebuilding takes TIME.
Calcium is more "reactive"...the body will use its largest store of THIS mineral to keep the pH in balance. This FURTHER depletes Mg levels...for starters.
Mg works with B6. All the B vitamins work together.
TIMING IS CRITICAL.
The kidneys will dump "excess" within a 2 hour time frame.
There are MANY nutrients Bb is taking FROM us. There are MANY we use to fight.
Restoring the balance so we CAN fight is NOT EASY!
Lou if you "Google" the words: depletes magnesium...you will find about 2,500+ websites.
One should stand out...
The one that says "chronic stress".
Stress can come from fighting infections as well as our "interpretation" of our boss' yelling i.e., physical and environmental triggers.
Trivia fun fact:
The scientific name for the castor plant, Ricinus communis, has a much more logical derivation.
Communis means common in Latin, and castor plants were already commonly naturalized in many parts of the world when the eighteenth century Swedish naturalist Carolus Linnaeus (Karl von Linn�) was giving scientific first and last names to plants and animals over 200 years ago.
Ricinus is the Latin word for tick
and is the specific epithet for the Mediterranean sheep tick (Ixodes ricinus).
Apparently Linnaeus thought the seeds looked like ticks, particularly large ticks engorged with blood."
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
More for the experts reading (I hope):
We finally resolved this issue with the observation that the sulfate ion greatly altered the response of STC-1 cells to monomeric dodecanoic acid (lauric acid in coconut oil).
In the presence of sulfate, STC-1 cells will only respond to dodecanoic acid aggregates
whereas when sulfate is replaced with chloride
the cells clearly respond to dodecanoic acid (lauric acid in coconut oil) monomers which are completely in solution.
In summary, we propose that dodecanoic acid can stimulate STC-1 cells via two separate pathways
one involving fatty acid monomers in solution
and one involving fatty acid aggregates.
Which pathway dominates depends on the presence of sulfate in the extracellular medium.
Curious: ***!!! "forskolin-stimulated chloride secretion across T84 epithelial cell monolayers with a Ki of 8 �M."
And:
"There is a possibility that prolonged use of QUESTRAN, since it is a
chloride form of anion
exchange resin, may produce hyperchloremic acidosis."
And...
"In lactic acidosis, the movement of lactate intracellularly in exchange for chloride occurs via an antiport.
It has been found that when lactic acidosis occurs in association with grand mal seizures then as many as 30% of this group of patients may present with a ***hyperchloraemic*** component to their acidosis.
This is an interesting situation because the lactic acidosis is due solely to muscular over-production, occurs rapidly & can be severe BUT it also resolves rapidly.
This should therefore be a `pure' lactic acidosis initially without any respiratory compensation or evidence of other acid-base problem.
So if we find a hyperchloraemic component this clearly suggests that the lactate is being taken up by some cells in exchange for chloride.
This movement of the acid anion intracellularly is one mechanism responsible for a hyperchloraemic component in some types of high anion gap acidosis. "
"Deficiency of chloride is rare. However, when it does occur, it results in a life threatening condition known as alkalosis."
"Chloride deficiency leads to a situation where the kidney reabsorbs more
bicarbonate anion
than usual because there is not sufficient chloride anion present.
Reabsorption of an anion is necessary to maintain electroneutrality as Na+ & K+ are reabsorbed so the deficiency of chloride leads to a re-setting upwards of the maintained plasma bicarbonate level.
Chloride and bicarbonate are the only anions present in appreciable quantities in extracellular fluid so a deficiency of one must lead to an increase in the other because of the strict requirement for macroscopic electroneutrality."
"This medicine contains the active ingredient acetylcholine chloride, which is a compound produced naturally by the body's nervous system."
My guess...Bb wouldn't be too happy with that bicarbonate! (OH)
"Thus, SOD1 acquires peroxidase activity at physiological pH only in the presence of HCO3 2 or structurally similar anions. Alterations in pH that shift the HCO3 2/CO2 equilibrium as occur in disease processes such as ischemia, sepsis, or shock would modulate the peroxidase function of SOD1."
Questran...more chloride overall Forskolin...remove chloride from specific cells
Depends on your point of view.
P.S. Melatonin, if I remember correctly, stimulates bicarbonate release. It looks like the body wants us to do just that.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
whoops
-------------------- 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.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
quote:Originally posted by Marnie: P.S. Melatonin, if I remember correctly, stimulates bicarbonate release. It looks like the body wants us to do just that.
Thats the reason I had a herxiemer Like reaction the first few days when I took it {melatonin} for sleep...
Now whats peppermint do Marnie???
-------------------- 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.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
Antiviral effect of aqueous extracts from species of the Lamiaceae family against Herpes simplex virus type 1 and type 2 in vitro.Nolkemper S, Reichling J, Stintzing FC, Carle R, Schnitzler P. Institute of Pharmacy and Molecular Biotechnology, Department of Biology, University of Heidelberg, Heidelberg, Germany.
Aqueous extracts from species of the Lamiaceae family were examined for their antiviral activity against Herpes simplex virus (HSV). Extracts from lemon balm (Melissa officinalis), peppermint (Mentha x piperita), prunella (Prunella vulgaris), rosemary (Rosmarinus officinalis), sage (Salvia officinalis) and thyme (Thymus vulgaris) were screened. Their inhibitory activity against Herpes simplex virus type 1 (HSV-1), type 2 (HSV-2) and an acyclovir-resistant strain of HSV-1 (ACV (res)) was tested in vitro on RC-37 cells in a plaque reduction assay. The 50% inhibitory concentrations (IC (50)) of the extracts for HSV plaque formation were determined in dose-response studies. All test compounds showed a high antiviral activity against HSV-1, HSV-2 and ACV (res). In order to identify the mode of antiviral action, the extracts were added to the cells or viruses at different stages of infection. Both types of Herpes virus including ACV (res) were considerably neutralized after treatment with the extracts prior to infection. At maximum non-cytotoxic concentrations of the extracts, plaque formation was significantly reduced by > 90% for HSV-1 and HSV-2 and > 85% for ACV (res). In time-response studies over a period of 2 hours, a clearly time-dependent activity was demonstrated. These results indicate that the extracts affect HSV before adsorption, but have no effect on the intracellular virus replication. Therefore, the extracts exert their antiviral effect on free HSV and offer a chance to use them for topical therapeutic application against recurrent HERPES infections.
PMID: 17091431 [PubMed - indexed for MEDLINE]
-------------------- 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.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
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Giardia lamblia: the effects of extracts and fractions from Mentha x piperita Lin. (Lamiaceae) on trophozoites.Vidal F, Vidal JC, Gadelha AP, Lopes CS, Coelho MG, Monteiro-Leal LH. Department of Histology and Embryology, Laboratory of Microscopy and Image Processing, State University of Rio de Janeiro, Av. Prof. Manoel de Abreu, 444, 3 degrees andar, Maracana, Rio de Janeiro, RJ 20550-170, Brazil.
Giardia lamblia is a parasite that causes giardiasis in humans and other mammals. The common treatment includes different classes of drugs, which were described to produce unpleasant side effects. Mentha x piperita, popularly known as peppermint, is a plant that is frequently used in the popular medicine to treat gastrointestinal symptoms. We examined the effects of crude extracts and fractions from peppermint against G. lamblia (ATCC 30888) on the basis of trophozoite growth, morphology and adherence studies. The methanolic, dichloromethane and hexanic extracts presented IC(50) values of 0.8, 2.5 and 9.0microg/ml after 48h of incubation, respectively. The aqueous extract showed no effect against the trophozoites with an IC(50)>100microg/ml. The aqueous fraction presented a moderate activity with an IC(50) of 45.5microg/ml. The dichloromethane fraction showed the best antigiardial activity, with an IC(50) of 0.75microg/ml after 48h of incubation. The morphological and adhesion assays showed that this fraction caused several alterations on plasma membrane surface of the parasite and inhibited the adhesion of G. lamblia trophozoites. Cytotoxic assays showed that Mentha x piperita presented no toxic effects on the intestinal cell line IEC-6. Our results demonstrated antigiardial activity of Mentha x piperita, indicating its potential value as therapeutic agent against G. lamblia infections.
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treepatrol
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Inhibition by the essential oils of peppermint and spearmint of the growth of pathogenic bacteria.Imai H, Osawa K, Yasuda H, Hamashima H, Arai T, Sasatsu M. Functional Foods Section, Central Laboratory, Lotte Company Ltd, Urawa, Saitama, Japan.
The effects of the, essential oils of peppermint (Mentha piperita L.), spearmint Mentha spicata L.) and Japanese mint (Mentha, arvensis L.), of four major constituents of the esssential oil of peppermint, and of three major constituents of the essential oil of spearmint, on the proliferation of Helicobacter pylori, Salmonella enteritidis, Escherichia coli O157:H7, methicillin-resistant Staphylococcus aureus (MRSA) and methicillin sensitive Staphylococccus aureus (MSSA) were examined. The essential oils and the various constituents inhibited the proliferation of each strain in liquid culture in a dose-dependent manner. In addition, they exhibited bactericidal activity in phosphate-buffered saline. The antibacterial activities varied among the bacterial species tested but were almost the same against antibiotic-resistant and antibiotic-sensitive strains of Helicobacter pylori and S. aureus. Thus, the essential oils and their constituents may be useful as potential antibacterial agents for inhibition of the growth of pathogens.
Effects of essential oil from mint (Mentha piperita) on Salmonella enteritidis and Listeria monocytogenes in model food systems at 4 degrees and 10 degrees C.Tassou CC, Drosinos EH, Nychas GJ. National Agricultural Research Foundation, Institute of Technology of Agricultural Products, Lycovrysi, Greece.
The effect of mint (Mentha piperita) essential oil (0.5, 1.0, 1.5 and 2.0%, v/w) on Salmonella enteritidis and Listeria monocytogenes in a culture medium and three model foods; tzatziki (pH 4.5), taramosalata (pH 5.0) and pate (pH 6.8), inoculated at 10(7) cfu g-1, at 4 degrees and 10 degrees C for ca 1 week was studied. In the culture medium supplemented with the essential oil, no growth was observed over 2 d at 30 degrees C determined by a conductance method with a Malthus 2000 growth analyser. Salmonella enteritidis died in tzatziki in all treatments and declined in the other foods except for pate at 10 degrees C as judged with viable counts. Listeria monocytogenes populations showed a declining trend towards the end of the storage period but was increased in pate. Mint essential oil antibacterial action depended mainly on its concentration, food pH, composition, storage temperature and the nature of the micro-organism.
PMID: 7615414 [PubMed - indexed for MEDLINE]
1: Probl Tuberk Bolezn Legk. 2006;(9):43-5. Links [Use of essential oil of peppermint (Mentha piperita) in the complex treatment of patients with infiltrative pulmonary tuberculosis][Article in Russian] Shkurupii VA, Odintsova OA, Kazarinova NV, Tkrachenko KG. The paper describes the effects of peppermint (Mentha piperita) essential oil inhaled by patients with infiltrative pulmonary tuberculosis in the penitentiary system. This procedure is shown to be most effective in infiltrative pulmonary tuberculosis in the phase of resorption of infiltrates and/or closure of decay cavities. The efficiency is determined by the rapid positive changes in a tuberculous process, which appear as a rapider regression of tuberculous inflammation, causing small residual changes. This procedure may be used to prevent recurrences and exacerbations of pulmonary tuberculosis.
PMID: 17128800 [PubMed - indexed for MEDLINE]
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treepatrol
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up for marnie
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I read it Marnie what do you make of what they said?
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treepatrol
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They said: 1st part CONCLUSIONS: Peppermint oil in the intestinal lumen inhibits enterocyte glucose uptake via a direct action at the brush border membrane. So stops or slows down glucose sugar from being used?
2nd part Inhibition of secretion by serosal peppermint oil is consistent with a reduced availability of calcium.
2nd part I aint grasping brainfa*t
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Limonene is a hydrocarbon, classed as a terpene. It is a colourless liquid at room temperatures with an extremely strong smell of oranges. It takes its name from the lemon, as the rind of the lemon, like other citrus fruits, contains considerable amounts of this chemical compound, which is responsible for much of their smell. Limonene is a chiral molecule, and as is common with such forms, biological sources produce one specific enantiomer: the principal industrial source, citrus fruit, contains D-limonene ((+)-limonene), which is the (R)-enantiomer (CAS number 5989-27-5, EINECS number 227-813-5). Racemic limonene is known as dipentene.[1]
As the main odour constituent of citrus (plant family Rutaceae), d-limonene is used in food manufacturing and some medicines, e.g., bitter alkaloids, as a flavoring, and added to cleaning products such as hand cleansers to give a lemon-orange fragrance. See: orange oil.
Limonene is increasingly being used as as a solvent for cleaning purposes, such as the removal of oil from machine parts, as it is produced from a renewable source (citrus oil, as a byproduct of orange juice manufacture.) Limonene works as paint stripper when applied to painted wood. The (R)-enantiomer is also used as botanical insecticide.
The (S)-enantiomer, also known as l-limonene (CAS number 5989-54-8, EINECS number 227-815-6), is used as a fragrance in some cleaning products. In contrast to the citrus (orange-lemon) scent (see above) of d-limonene, the enantiomer l-limonene has a piney, turpentine-like odor.
Limonene is very common in cosmetic products.
Chemistry Limonene is a relatively stable terpene, which can be distilled without decomposition, though it forms isoprene when passed over a hot metal filament. It is easily oxidised in moist air to carveol and carvone[4] . Oxidation using sulfur leads to p-cymene and a sulfide.
Limonene occurs naturally as the (R)-enantiomer, but it can be racemised to dipentene simply by heating at 300 �C. When warmed with mineral acid, limonene forms the conjugated diene terpinene, which can itself easily be oxidised to p-cymene, an aromatic hydrocarbon. Evidence for this includes the formation of Diels-Alder α-terpinene adducts when limonene is heated with maleic anhydride.
It is possible to effect reaction at one of the double bonds selectively. Anhydrous hydrogen chloride reacts preferentially at the disubstituted alkene, whereas epoxidation with MCPBA occurs at the trisubstituted alkene. In both cases the second C=C double bond can be made to react if desired. Limonene is also very common in cosmetic products.
In another synthetic method Markovnikov addition of trifluoroacetic acid followed by hydrolysis of the acetate gives terpineo
[edit] Biosynthesis Limonene is formed from geranyl pyrophosphate, via cyclisation of a neryl carbocation or its equivalent as shown.(5) The final step involves loss of a proton from the cation to form the alkene
Safety information General Limonene and its oxidation products are skin irritants, and limonene-1,2-oxide (formed by aerial oxidation) is a known skin sensitizer. Most reported cases of irritation have involved long-term industrial exposure to the pure compound, e.g. during degreasing or the preparation of paints. However a study of patients presenting dermatitis showed that 3% were sensitized to limonene.(6)
Limonene causes renal cancer in male rats, but not in female rats or in mice of either sex, due to binding of the metabolite limonene-1,2-oxide to α2u-globulin, a protein produced only by male rats. There is no evidence for carcinogenicity or genotoxicity in humans. The IARC classifies d-limonene under Class 3: not classifiable as to its carcinogenicity to humans.
Europe Limonene is listed in annex 1 of the directive 67/548/EEC under index number 601-029-00-7 [2]. The pure substance is classified as irritant (Xi) and dangerous for the environment (N). The following risk and safety statements are obligatory:
R10: Flammable. R38: Irritating to skin. R43: May cause sensitization by skin contact. R50/53: Very toxic to aquatic organisms, may cause long-term adverse effects in the aquatic environment. S2: Keep out of the reach of children. S24: Avoid contact with skin. S37: Wear suitable non-latex gloves. S60: This material and its container must be disposed of as hazardous waste. S61: Avoid release to the environment. Refer to special instructions/Safety data sheets. Limonene is not specifically mentioned in directive 1999/45/EC, and so the labelling of preparations containing this compound is at the discretion of the manufacturer.
Canada Limonene is classified [3] under the categories
B3: Combustible liquid D2B: Toxic material causing other toxic effects The presence of limonene in a preparation at a concentration greater than 1.0% must be disclosed.
Australia Limonene is listed in Class 3, flammable liquids, Packing Group III, under the Australian Dangerous Goods Code.
Notes and references J. L. Simonsen, The Terpenes Volume I (2nd edition), Cambridge University Press, 1947. E. E. Turner, M. M. Harris, Organic Chemistry, Longmans, Green & Co., London, 1952. Wallach, Annalen der Chemie, 246, 221 (1888). Blumann & Zeitschel, Berichte, 47, 2623 (1914). J. Mann, R. S. Davidson, J. B. Hobbs, D. V. Banthorpe, J. B. Harborne, Natural Products, pp308-309, Addison Wesley Longman Ltd., Harlow, UK, 1994. ISBN 0-582-06009-5. IARC Monographs on the evaluation of carcinogenic risks to humans 1999, 73, 307-27. Source: European Chemicals Bureau. Source: CSST Workplace Hazardous Materials Information System. The CAS and EINECS numbers in the table are for the racemic mixture: the relevant numbers for the two enantiomers are given in the text. M. Matura et al., J. Am. Acad. Dermatol. 2002, 33, 126-27. External links Detailed description of d-limonene from Biochem Corp. Links to external chemical sources
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treepatrol
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upy
-------------------- 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.
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