AUTOIMMUNE DISEASES CAUSED BY AN INFECTION?

SeekinTruth

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Re: RHEUMATOID ARTHRITIS CAUSED BY AN AMOEBA INFECTION?

Keeping fingers crossed, Laura. It makes sense that high dose vitamin C helped a lot. Not only does it support the immune system as needed, is a powerful master antioxident - recycling other antioxidents and relieving the oxidative stress, it also detoxes microorganism toxins, particularly mycotoxins (mold/fungus toxins). Should be even more effective in combination with NAC.

Shijing said:
Reading some of the above reminded me of a couple excerpts in the pleomorphism literature that may be relevant:

Hidden Killers: The Revolutionary Medical Discoveries of Professor Guenther Enderlein

Multiple Sclerosis: Halting the Degenerative Process (107-08) said:
[…] Currently, conventional medicine has no cure for the disabling illness, although drugs such as prednisone and ACTH may suppress the severity of attacks, while other medications are used to inhibit the body’s immune response. Physical therapy is also used to help victims learn to cope with their disabilities.

In contrast, Dr. Enderlein showed that multiple sclerosis is an infection that can often be healed. He confirmed that the blood of MS patients is greatly infested by different forms of microbial growth. Dr. Enderlein also revealed that these microorganisms within the patients’ blood are “programmed” to attack and destroy specific tissues of the nervous system, thereby causing progressive paralysis – a contention that helps explain why relatives of MS victims are highly susceptible to the disease. To combat the disease, Dr. Enderlein developed biological medications that are active against some forms of the microbes, which makes it possible to prevent or halt MS symptoms in certain patients.

In my private practice and through research using live blood analysis, I have discovered that treatment with Penicillum frequentans (QUENTAKEHL) offers strong hope that the progress of multiple sclerosis can be stopped. In addition, I sometimes use the medications Aspergillus niger (NIGERSAN) and RECARCIN to fight MS. By rubbing the drop form of the biological medication into the thigh area and other parts of the body, I have been able to successfully stop the disease from progressing and further damaging my patients’ tissues in some cases (injections can also be effectively used, but are not permitted in Sweden). The biological medications destroy the pathogenic microorganisms that attack the tissues, and halt progress of the disease. However, because MS is degenerative and nerve damage already caused by the infection is irreversible, the patients will never return to 100 percent function. As a result, it is critical for patients to receive treatment as early as possible to stop the damage caused by the microorganisms.

Unfortunately, it is not possible to help every MS patient, probably because Dr. Enderlein did not have the opportunity to develop biological medications against the entire complex of microorganisms that produce the MS syndrome. However, many successes against the disease are possible, and many of the patients I treated have remained stable and are doing well years after they initially came to me.

For what it's worth, my mother was diagnosed by MRI with MS in 1996 when she began to drag her foot and quickly became unable to control her leg. She deteriorated fast from first appearance of symptoms. I read Hulda Clark's book The Cure for All Diseases and gave her the herbal parasite program and built a zapper per her instructions. Within weeks of doing Clark's treatments, the whole thing reversed and disappeared. The reason I wanted to try Clark's claims is that I had read The Rife Report: The Cancer Cure That Worked years earlier - which mentioned pleomorphism as background - and her claims and approach were very similar to Rife's. And it paid off.

I also gave Hulda Clark's info and a zapper and herbal parasite program to my friend, whose sister-in-law had recently been diagnosed with cancer a few years ago. They were in a panic as a family. In a few days, they rechecked and the tests came back "indeterminate". But, alas, the doctors scared her and the family into going to the US and getting chemo therapy.
 

Laura

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Re: RHEUMATOID ARTHRITIS CAUSED BY AN AMOEBA INFECTION?

Gaby said:
The allopurinol is indicated in the protocol only for the first week and as an anti-parasitic, hence its high doses as opposed to other medical indications. It is like an anti-parasitic induction phase, making the first week the most difficult one of the protocol.

Vitamin C also helps heal collagen. So if lots of die-off reactions were causing inflammatory tissue reaction, vitamin C sounds like a great one to take. Taking bone broth regularly will also help the gut and the tissues.

Alright, I'll take the damn things though I know they'll make me feel crappy again ... <<<grumble>>> I don't want to miss any chances to kill critters.
 

Shared Joy

Jedi Council Member
Re: RHEUMATOID ARTHRITIS CAUSED BY AN AMOEBA INFECTION?

Hi,
Thank you Laura for opening this thread and thank you All for your input, as it seems that the amoeba infections are so wide spread and appearing under so many form,s that at the end one might find that a large majority of seemingly unrelated diseases can be traced back to it.

For example:

_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078255/

Invasive amoebiasis complicating iflammatory bowel disease
Amoebiasis, which is caused by the intestinal protozoan Entamoeba histolytica, is a ubiquitous parasitic infection affecting approximately 10% of the world's population and causing more deaths every year (100,000 deaths) than any other parasitic infection, with the exception of malaria and schistosomiasis [1–3]. Most individuals with an E. histolytica infection are asymptomatic, but some develop severe invasive disease, such as amoebic colitis. Other manifestations, such as pulmonary, cardiac or brain involvement, are rare. Intestinal amoebiasis can probably also present as a chronic, non-dysenteric syndrome of diarrhoea, weight loss, and abdominal pain that can last for years and mimic inflammatory bowel disease. Fulminant colitis with bowel necrosis leading to perforation and peritonitis occurs in only about 0.5% of cases, but it is associated with a mortality rate of more than 40%. Patients with invasive amoebiasis living in the United Kingdom and other developed countries generally acquire the infection in another country in which the pathogenic species is endemic. Areas that have high rates of amoebic infection include India, Africa, Mexico and parts of Central and South America. Infection with pathogenic E. histolytica is not a common cause of travelers’ diarrhoea, and gastrointestinal infection is uncommon in travelers who have spent less than one month in endemic areas.

Despite the availability of sophisticated investigative procedures, differentiating invasive colonic amoebiasis from idiopathic inflammatory bowel disease (IBD) may be difficult. This case is presented to remind clinicians of the similarities in the clinical presentation and endoscopic features of these two conditions, and to highlight the difficulty in differentiating them.

.....
Discussion
Amoebic colitis is a disease with diverse clinical manifestations that frequently lead to confusing it with other types of colitis. When misdiagnosed as UC, undesirable outcomes might occur from the use of steroids, including colectomy or even death. Clinicians must keep amoebiasis in mind in the differential diagnosis of patients suspected of having UC or Crohn's disease [3]. A recent study in Turkey showed that amoeba infection in patients with IBD, especially those with UC, is more prevalent than in the normal population [4]. With more frequent air travel, amoebic colitis is an important “not to miss” diagnosis even in the developed world. However, it should be noted that amoebiasis can be contracted by people, especially children, who have never been abroad.

The above article also has a case study included.

Also here is some information material on amoeba (intestinal and amoebic liver abscess), description, treatment, some recommendation for prevention

_http://www.patient.co.uk/health/amoebiasis-leaflet

Amoebiasis
E. histolytica is an amoeba. An amoeba is the name given to any single-celled microscopic animal with a jelly-like consistency and an irregular, constantly changing shape. Amoebae are found in water, soil and other damp environments. They move and feed by means of flowing extensions of their body, called pseudopodia. Amoebae are types of germs (protozoa). Protozoa is a more general name for microscopic, single-celled organisms. Some protozoa, including E. histolytica, are important parasites of humans.
....
Most people who become infected with E. histolytica do not develop any symptoms. However, symptoms may develop if the parasite causes inflammation of the lining of your gut. In some people, E. histolytica can also get into the bloodstream from the gut and spread around the body to the liver, lungs and sometimes other organs. Note: the parasites can still be present in the stools of infected people who have no symptoms.
......

Amoebic colitis
The E. histolytica parasite can cause inflammation of the lining of your gut (intestines). This condition is known as amoebic colitis. 'Colitis' is a general term used for inflammation of the lining of the large intestine (the colon). 'Amoebic' refers to the fact that the colitis is caused by the amoeba E. histolytica. The disease is often mild and can just lead to tummy (abdominal) pain and diarrhoea. However, more severe inflammation with ulceration of the intestinal lining can occur in some people and so-called 'amoebic dysentery' can develop. (Dysentery is any infection of the intestines, causing severe diarrhoea with blood and mucus.)
.....
Amoebic liver abscess
The E. histolytica parasite can invade right through your gut wall, get into your bloodstream, and pass in your bloodstream to your liver. Once in your liver, it can cause an amoebic liver abscess to form. An amoebic liver abscess contains pus and liquified, dying liver tissue.

Symptoms include fever and right upper abdominal pain with tenderness in this area when a doctor examines you. You may notice that your skin and the whites of your eyes become yellow (jaundiced) and your liver may also become enlarged..

Spread from an amoebic liver abscess
Rarely, an amoebic liver abscess can burst (rupture) and lead to damage to your diaphragm - the thin muscle that separates your chest cavity from your abdominal cavity. This can allow spread of the abscess into your chest cavity, affecting your lungs and your pleura - the membrane that covers your lungs. Symptoms of such a complication include cough, difficulty breathing and pain in your chest when you breathe in.

Also, very rarely, in someone with an amoebic liver abscess, infection can spread to their brain and central nervous system. This can be very serious and it needs quick treatment. Symptoms include headache, felling sick (nausea), being sick (vomiting) and confusion.

Being such a simple organism it can survive in most adverse conditions and is equipped with a complex mechanism of getting inside the tissues, ex.:

_http://content.lib.utah.edu:81/cgi-bin/showfile.exe?CISOROOT=/EHSL-NOVEL&CISOPTR=1181&filename=784.pdf
CLINICAL NEURO-OPHTHALMOLOGY AMOEBAE (AMOEBIASIS)
...
Pathogenesis
E. histolytica exerts a lytic effect on tissue, a characteristic for which the organism is named (10). The amoeba invades the colonic epithelium directly. Its ability to invade and damage tissues seems to sequentially involve adherence to target cells, secretion of proteolytic enzymes, disturbance of intercellular junctions, release of cytotoxins, creation of ion channels, and phagocytosis (11,16,27,28). Adherence precedes cytolysis and depends on a substance called N-acetyl-D-galactosamine (Gal/GalNAc) inhibitable adherence lectin (9), which has a mass of 260 kD and is composed of 170-and
35-kD subunits (29). The 170-kD subunit is the main component that mediates binding to colonic epithelial cells (30). It shares an epitope with human 2 integrins, a subfamily of cell surface glycoproteins expressed exclusively on polymorphonuclear leukocytes (PMNs) and involved in many adhesive and signaling interactions (31). The immunologic similarity of these proteins may explain the ability of E. histolytica to bind to and invade colonic epithelium (11).
Once E. histolytica adheres to host mucosal cells, it damages these cells and the surrounding tissue by means of numerous self-contained proteolytic and hydrolytic enzymes (16,17,32). At the same time, the amoeba lyses host PMNs, thus releasing toxic nonoxidative substances that contribute to the further destruction of host tissues (33–36).

So, it makes it's way into the host's organism by way of dissolving the protective tissue and then releasing toxins inside the cells.
The article also features description of various forms of amoebiasis: liver, intestinal, genitourinary, intracranial abcesses, pleuropulmonaty, pericardial, etc.

I think, is good to know. FWIW
Joy
 

Kasia

Jedi Master
Re: RHEUMATOID ARTHRITIS CAUSED BY AN AMOEBA INFECTION?


Alright, I'll take the damn things though I know they'll make me feel crappy again ... <<<grumble>>> I don't want to miss any chances to kill critters.

Laura, I'm keeping my fingers crossed for your victory in this battle :v:
 

Laura

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Re: RHEUMATOID ARTHRITIS CAUSED BY AN AMOEBA INFECTION?

Laura said:
Gaby said:
The allopurinol is indicated in the protocol only for the first week and as an anti-parasitic, hence its high doses as opposed to other medical indications. It is like an anti-parasitic induction phase, making the first week the most difficult one of the protocol.

Vitamin C also helps heal collagen. So if lots of die-off reactions were causing inflammatory tissue reaction, vitamin C sounds like a great one to take. Taking bone broth regularly will also help the gut and the tissues.

Alright, I'll take the damn things though I know they'll make me feel crappy again ... <<<grumble>>> I don't want to miss any chances to kill critters.

Replying to myself sorta.

This exchange triggered something in my mind - something the Cs said a long time ago that I had never figured out what it might mean, but this discussion sheds an all new light on it. It was back when I was doing the "bloodline" research.

9 August 1997 said:
Q: Next question: is there any relationship between the fact
that Roger de Mortimer, the carrier of the last of the
line of the Welsh kings, was the lover of Isabella of
France, who was the daughter of Philip the Fair, the
destroyer of the Templars, and the murder of Edward II,
the first of the English Prince of Wales?

A: Templars are a setup, insofar as persecution is concerned.
Remember your "historical records" can be distorted, in
order to throw off future inquiries, such as your own.

Q: I know that. I have already figured that one out! But,
it seems that no one else has made this connection. I
mean, the bloodlines that converge in the Percys and the
Mortimers are incredible!

A: You should know that these bloodlines become parasitically
infected
, harrassed and tinkered with whenever a quantum
leap of awareness is imminent.


Q: Whenever a quantum leap...

A: Such as "now."

I started to ask a couple follow up questions but it seems that this topic diverted the Cs off onto one of the most interesting of their revelations. So do read the entire session.

Then, about a year later, I tried to get some follow-up clues on 13 June 1998. Read that one also.
 

Laura

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Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

Gaby said:

Thanks.

And doesn't the info in those session just make you go "Huh?" If it is true (and seems to be so), how many people are affected? Is this one of the purposes of alien abduction? To infect people of potential with parasites? Yeah, I know, I could be making a lot of assumptions, but this just puts a whole new spin on a lot of things.

And indeed, that allopurinol makes me feel crappy so it must be doing something. By the way, I did a whole anti-fungal thing a few years ago, I mean serious anti-fungals. It did make me sick, but not as sick as this business has done.
 

Gaby

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Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

I was reviewing the August session from the Wave a couple of days ago. It is eye-opening! Ponerology and other material can be very complementary, but this reality can truly be stranger than fiction!

I remember that from all medical lessons I received on little critters, parasitology was just the creepiest of them all. It didn't helped that my teacher was fascinated by them. He made us look at them in the microscope and draw them so we wouldn't forget them. Ah!! It still gives me the chills!
 

Laura

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Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

So far today, taking the allopurinol and one cortisone, I've done okay. I was somewhat nauseated for a time, and a little brain fog for a time, and crankiness because I felt tired, but nothing over the top. All in all, not too bad.
 

genero81

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Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

Laura said:
Laura said:
Gaby said:
The allopurinol is indicated in the protocol only for the first week and as an anti-parasitic, hence its high doses as opposed to other medical indications. It is like an anti-parasitic induction phase, making the first week the most difficult one of the protocol.

Vitamin C also helps heal collagen. So if lots of die-off reactions were causing inflammatory tissue reaction, vitamin C sounds like a great one to take. Taking bone broth regularly will also help the gut and the tissues.

Alright, I'll take the damn things though I know they'll make me feel crappy again ... <<<grumble>>> I don't want to miss any chances to kill critters.

Replying to myself sorta.

This exchange triggered something in my mind - something the Cs said a long time ago that I had never figured out what it might mean, but this discussion sheds an all new light on it. It was back when I was doing the "bloodline" research.

9 August 1997 said:
Q: Next question: is there any relationship between the fact
that Roger de Mortimer, the carrier of the last of the
line of the Welsh kings, was the lover of Isabella of
France, who was the daughter of Philip the Fair, the
destroyer of the Templars, and the murder of Edward II,
the first of the English Prince of Wales?

A: Templars are a setup, insofar as persecution is concerned.
Remember your "historical records" can be distorted, in
order to throw off future inquiries, such as your own.

Q: I know that. I have already figured that one out! But,
it seems that no one else has made this connection. I
mean, the bloodlines that converge in the Percys and the
Mortimers are incredible!

A: You should know that these bloodlines become parasitically
infected
, harassed and tinkered with whenever a quantum
leap of awareness is imminent.


Q: Whenever a quantum leap...

A: Such as "now."

I started to ask a couple follow up questions but it seems that this topic diverted the Cs off onto one of the most interesting of their revelations. So do read the entire session.

Then, about a year later, I tried to get some follow-up clues on 13 June 1998. Read that one also.

That bit about bloodlines being parasitically infected was on my mind all day yesterday. Glad you brought it up. Actually harassed is an excellent description for how my psoriasis has effected me. Not life threatening, but a pain in the you know what. Although people have died from it. I have a friend who used to nurse who remembers a patient who suffered terribly and then died, back before they had the treatment options they do now.
 

Shared Joy

Jedi Council Member
Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

Hi,

I woke up this morning thinking about the lectin - virus -amoeba sequence.
It is sort of matter (lectin) - information (virus) - microorganism (amoeba).

As the next study show, they are interconnected when acting in the organism (please bear with me, I'm not a microbiologist...)

_http://www.ncbi.nlm.nih.gov/books/NBK1907/

quote:
This chapter describes examples of proteins on the surface of microorganisms (adhesins or hemagglutinins), secreted proteins (heat-labile toxins), thei rglycan partners on mammalian cell surfaces (receptors), and insights into the molecular interactions that take place.
Viruses, bacteria, and protozoa express an enormous number of glycan-binding proteins or lectins. Many of these microbial lectins were originally detected based on their ability to aggregate red blood cells (i.e., to inducehemagglutination). The first microbial hemagglutinin identified was in the influenza virus, and it was shown by Alfred Gottschalk in the early 1950s to bind to erythrocytes and other cells though sialic acid residues of cell-surface glycoconjugates.
Many adhesins contain carbohydrate-recognition domains (CRDs) that bind to the same carbohydrates as endogenous mammalian lectins (see Chapter 26). Like animal cell lectins, some microbial adhesins bind to terminal sugar residues, whereas others bind to internal sequences found in linear or branched oligosaccharide chains. Detailed studies of the specificity of microbial lectins have led to the identification and synthesis of powerful inhibitors of adhesion that may form the basis for therapeutic agents for treating infection (see Chapter 51).
….
VIRAL GLYCAN-BINDING PROTEINS
By far, the best-studied example of a viral glycan-binding protein is the influenza virus hemagglutinin, which binds to sialic acid–containing glycans. The affinity of this interaction is relatively low, like that of other glycan-binding proteinswith their glycan ligands, but the avidity for cell membranes increases because of oligomerization of the hemagglutinin into trimers and the high density of glycan receptors present on the host cell (see Chapter 27). Binding is a prerequisite for fusion of the viral envelope with the plasma membrane and for uptake of the virus into cells. The specificity of the interaction of the hemagglutinin with host glycans varies considerably for different subtypes of the virus.

BACTERIAL ADHESION TO GLYCANS
Bacterial lectins occur commonly in the form of elongated, submicroscopic, multisubunit protein appendages, known asfimbriae (hairs) or pili (threads), which interact with glycoprotein and glycolipid receptors on host cells.

Other binding specificities have been described as well (Table 34.2). The specificity of binding can explain the tissue tropism of the organism. The columnar epithelium that lines the large intestine expresses Galα1–4Gal-Cer, whereas the cells lining the small intestine do not. Thus, Bacterioides, Clostridium, E. coli, and Lactobacillus only colonize the large intestine under normal conditions.

TOXINS THAT BIND GLYCANS
A number of secreted bacterial toxins also bind to glycans (Table 34.3). The best-studied example is the toxin fromVibrio cholera (cholera toxin), which consists of A and B sub-units in the ratio AB5. Its crystal structure shows that the B subunits bind to the Galβ1–3GalNAc moiety of GM1 ganglioside receptors through CRDs located on the base of the subunits (Figure 34.6). The A subunit is loosely held above the plane of the B subunits, with a single α-helix penetrating through a central core created by the pentameric B subunits. Upon binding to membrane glycolipids through the B subunits, the A subunit is delivered to the interior of the cell by an unknown mechanism. In cholera toxin, the affinity of the B subunit for its glycan ligand (GM1) is unusually high compared to the binding of related AB5 toxins from Shigella dysenteria, Bordetella pertussis, and E. coli to their glycan receptors (Kd in the nanomolar range for cholera toxin B subunit vs. millimolar range for Shiga toxin B subunit binding to Pk determinants). In both examples, the formation of the pentameric complex greatly increases the avidity of the interaction. This phenomenon is being exploited to make oligovalent glycan ligands as protective agents against the toxin.
………
PARASITE LECTINS
In addition to viruses and bacteria, a number of parasites also utilize glycans as receptors for adhesion (Table 34.4).Entamoeba histolytica expresses a 260-kD heterodimeric lectin that binds to terminal galactose/N-acetylgalactosamine residues on glycoproteins and glycolipids. Binding may have a role in attachment, invasion, and cytolysis of intestinal epithelium, and it may function in binding the amoeba to bacteria as a food source. The lectin is heterodimeric, with a transmembrane subunit of 170 kD and a glycosylphosphatidylinositol (GPI)-anchored subunit of 35 kD. The glycan-binding site is located in a cysteine-rich domain. The importance of this receptor in virulence has been established by antisense silencing of the adhesin and by expression of a dominant-negative form of the light subunit. Thus, the adhesin is a potential target to manage E. histolytica infection (see Chapter 40).

end guote

Well, as we can see, these critters use one another and the environment to proliferate in the body.

But more important is to understand the mechanism of diseases in order to:
- prevent weakening of the immune system
- reduce toxic load of whatever origin, be it received from exterior or generated internally by those microorganisms
- use the microorganisms' own metabolism characteristics to prevent their proliferation.

I think that the most important steps are
- paleo/keto diet, as all this critters prime necessity is to adhere to the host cells, and preferred are tissues with high carbohydrate content
- I would also suggest that weekly whole body baths with salt, sodium bicarbonate, borax, magnesium sulfate would help strengthen the immune system, detoxify, reduce overall body acidity/inflammation, also kill germs. Nora Gedgaudas said that transdermal administration is 80% more efficient than assimilation via guts.
- She also, emphasize the role of L-glucosamine in enhancing the secretory IgA response of our endothelium, and tissue repair, which is the body's first line defense. Other similar substances are featured in the above article.


The last sequence quoted contain a rather puzzling remark (at least for me, but I might be mistaken).

quoted again:
PARASITE LECTINS
In addition to viruses and bacteria, a number of parasites also utilize glycans as receptors for adhesion (Table 34.4).Entamoeba histolytica expresses a 260-kD heterodimeric lectin that binds to terminal galactose/N-acetylgalactosamine residues on glycoproteins and glycolipids. Binding may have a role in attachment, invasion, and cytolysis of intestinal epithelium, and it may function in binding the amoeba to bacteria as a food source. The lectin is heterodimeric, with a transmembrane subunit of 170 kD and a glycosylphosphatidylinositol (GPI)-anchored subunit of 35 kD. The glycan-binding site is located in a cysteine-rich domain. The importance of this receptor in virulence has been established by antisense silencing of the adhesin and by expression of a dominant-negative form of the light subunit. Thus, the adhesin is a potential target to manage E. histolytica infection (see Chapter 40).

It just remembered me something about light-interference to modify DNA, from session of 26 November 1994

A: Light wave alteration.

Q: (L) And light waves, actual light waves, affect DNA?

A: Yes.

Q: (T) What was the origin of the light waves?

A: Our center.

Q: (L) What is your center?

A: Our realm. STO.

Q: (L) So, how did the Lizzies use the light from the Service to Others realm...

A: They used sophisticated technology to interrupt light frequency waves.
..................
A: Are you ready? DNA core is as yet undiscovered enzyme relating to carbon. Light waves were used to cancel the first ten factors of DNA by burning them off. At that point, a number of physical changes took place including knot at top of spine. Each equally reflected in the ethereal.

Maybe, just maybe, this could be also the way we get sick, in order to contact "needed diseases" which will help learn and evolve? Too many people can't learn from it, just stay ill.
It's such a complex situation.
I could use some help to connect the dots here, if any.

FWIW
Joy
 

SeekinTruth

The Living Force
FOTCM Member
Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

Shared Joy, there's a lot to consider in that post. Right now I just wanted to add that there's some evidence that the information or signal goes both ways. For example, grains, and their lectins and anti-nutrients, have virus-like qualities, eating lots of carbs can attract infections (or even bring latent/dormant ones into active phase), starting in the ancient world, there are accounts of survivors of plagues being meat eaters, etc. So there's a lot there, plus how much truth or lies we "assimilate" could also be part of attracting not only the devastating space rocks, but the ones that bring the "alien" microbes. FWIW.
 

nicklebleu

The Living Force
FOTCM Member
Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

Shared Joy said:
The lectin is heterodimeric, with a transmembrane subunit of 170 kD and a glycosylphosphatidylinositol (GPI)-anchored subunit of 35 kD. The glycan-binding site is located in a cysteine-rich domain. The importance of this receptor in virulence has been established by antisense silencing of the adhesin and by expression of a dominant-negative form of the light subunit. Thus, the adhesin is a potential target to manage E. histolytica infection (see Chapter 40).

Shared Joy,

There might be a misunderstanding from your side.

"Light" in this context refers to "with minor weight" and not to "photon emission", as it refers to the smaller subunit (of "weight" 35 kD - Dalton (D) is a measure of atomic mass and kD is kilo-Dalton) versus the bigger subunit of 170 kD. That's what is referred to as "heterodimeric" - hetero (different), dimeric (composed of two things), so the lectin is composed of two subunits of different mass.

Hope that helps!
 

Shared Joy

Jedi Council Member
Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?

nicklebleu said:
Shared Joy said:
The lectin is heterodimeric, with a transmembrane subunit of 170 kD and a glycosylphosphatidylinositol (GPI)-anchored subunit of 35 kD. The glycan-binding site is located in a cysteine-rich domain. The importance of this receptor in virulence has been established by antisense silencing of the adhesin and by expression of a dominant-negative form of the light subunit. Thus, the adhesin is a potential target to manage E. histolytica infection (see Chapter 40).

Shared Joy,

There might be a misunderstanding from your side.

"Light" in this context refers to "with minor weight" and not to "photon emission", as it refers to the smaller subunit (of "weight" 35 kD - Dalton (D) is a measure of atomic mass and kD is kilo-Dalton) versus the bigger subunit of 170 kD. That's what is referred to as "heterodimeric" - hetero (different), dimeric (composed of two things), so the lectin is composed of two subunits of different mass.

Hope that helps!

Thank you Nicklebleu, you are right, this is what happens when I get into something I don't understand and interpret it ad literam. I should be more careful.
Joy
 

Laura

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Re: AUTOIMMUNE DISEASES CAUSED BY AN AMOEBA INFECTION?


Reporting in: today was a good day. I took all my doses of allopurinol, took NO cortisone, and felt fine all day. I did have a bit of tiredness and took two short naps, but other than that, I had no pain, no nausea, no symptoms like that at all. In fact, there is a strange feeling of "lightness" to my limbs that I can't quite describe.
 
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