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Do a search for MTHFR there was a recent discussion with some really good links and great info :-)
Posts: 845 | From Northeast | Registered: May 2011
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My son is dealing with the C mutation, the A mutation and with a COMT polymorphism. We are awaitng the results of further genetic testing.
Since these are issues that some autistic children deal with, we decided to see a nutritionist who deals with a lot of autistic children along with those with chronic disease. She uses the Amy Yasko protocol for those with methylation issues.
Since my son has been on her diet and supplement protocol, he has improved dramatically. His seizure activity has lessened and he is dealing with much less anxiety.
For the last two months we have not been treating for Lyme and Co's and he is continuing to do well.
Once the methylation issues are under control we will treat for parasites, yeast and heavy metals and then see what remains of Lyme and the Co's.
At least that is the plan and we all know what happens to plans.
Once we get the results of the full genetic testing, we will hopefully have a better idea of what is going on.
If you are interested in the name of the nutritionist who is in NJ, please PM me and I will be happy to share.
Take Care, Karen
I think that this is just the beginning of what we need to deal with
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Pinelady
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IMO it is the prion like proteins of Borrelia and other organisms that are carrying them that are cause for them seeing it as a gene mutation...
They have found 3 prion like proteins in Bb so far. The other bacteria and parasites are exhibiting stealth but it has not been defined yet in the proteins. Yet they know they are swapping genes with many...
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Thanks RC1 .....I have looked at previous posts about MTHFR but will check again.
Dan's Mom thanks so much for your info, will send you a pm.
Pinelady, I apologize for my ignorance......I don't fully understand the technical info on the link you posted......are you saying that it may not be a gene mutation at all but some protein related to the lyme bacteria......please explain, this is very interesting.....thanks for posting this.
Posts: 574 | From New Jersey | Registered: Feb 2004
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Pinelady
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Yes JJ29. You are not ignorant---this is life changing new information.
http://www.ncbi.nlm.nih.gov/pubmed/21943430 2011 Sep 21 THANK YOU SO MUCH CHINA! Fibril Formation of the Rabbit/Human/Bovine Prion Proteins.---Together, these results suggest that the strong inhibition of fibrillization of the rabbit PrP
by the crowded physiological environment and the absence of such a protease-resistant fragment for the rabbit protein could be two of the reasons why rabbits are resistant to prion diseases.
THANK YOU CHINA... Furthermore, Western blots identified that the levels of the endogenous TPPP in the brains of scrapie-infected experimental hamsters were significantly reduced. http://www.ncbi.nlm.nih.gov/pubmed/21857997
I suspect they will find the same in birds...Heat factors reduce many known infectious pathogens and could subsequently reduce its resistance in a lower body temp. host by haveing less infections in the first place to fold in the proteins..
But this proves that HSP's are merely an illusion and should not be used in vaccine.
We review the origins of the quasispecies concept and its relevance for RNA virus evolution, viral pathogenesis and antiviral treatment strategies. We emphasize a critical point of quasispecies that refers to genome collectivities as the unit of selection, and establish parallels between RNA viruses and some cellular systems such as bacteria and tumor cells. We refer also to tantalizing new observations that suggest quasispecies behavior in prions, perhaps as a result of the same quantum-mechanical indeterminations that underlie protein conformation and error-prone replication in genetic systems.
If substantiated, these observations with prions could lead to new research on the structure-function relationship of non-nucleic acid biological molecules.
http://www.ncbi.nlm.nih.gov/pubmed/21947943 Thank You U. of Alberta.....In this study, we utilized RT-PCR arrays to compare RNA expression levels of 84 markers for pro and anti- apoptotic signalling pathways following exposure of HFNs to either Aβ(1-42) (20 μM) or human amylin (2 μM). ----------Imagine that 84 Markers....LOL
http://www.ncbi.nlm.nih.gov/pubmed/21952878 2011 Sep 28. [Epub ahead of print] Prion Protein Coding Gene (PRNP) Variability in Sheep from Turkey and Iran.-------Turkey working for the People!!
As they move for the truth it should be found as suspected that the proteins/genetics are only dependent on the infections that are hiding. With the introduction of cys technology our genes no longer became our own... They became God Like in the stealth proteins that can swap genes and still hide them all in our DNA...Whatever that is...They really don't know... While Kaiser just spent millions on decoding 100,000 of their employee and patients genetic codes I suspect they can tell us nothing of whats real...For that they are going to have to go back to pre vaccine yrs. because the stealth is already being spread in our vectors of disease...so even those who have never been jabbed are also likely to be infected...
2 yrs. ago I had someone tell me--We are all sick...I did not have the mindset to take that in, but upon further investigations into old research I had followed involving vaccines--namely Wakefields claims of seeing Measles DNA in the bowels of Autistic patients and the outbreak of MadCow and Lyme---all within 4 yrs. of each other....I understood what they were trying to tell me... And they were right...
This should have and could have been stopped 30yrs. ago but we were thrown under the bus to protect profits.. Because they knew and did nothing including selling the tech. to other countries and letting them infect their people as well..
We have other countries using the TBEV not knowing what it is or what it does...Like all the others---never challenged in stealth.. So we all could in theory be infected with everything including plant diseases...
Because they listened to the CDC jerks who said Morgellons was Delusional Parasitosis for the last 10 yrs. Knowing that Pam3cys and what they now describe for Pam2cys as well cause viral/fungal synergy..
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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UPCOMING FDA WORKSHOP ON CONTAMINANTS IN THE BLOOD SUPPLY. HERE IS OUR CHANCE TO TALK ABOUT BORRELIAL SPHEROPLASTS AND IDSA'S REFERENCES ACKNOWLEDGING THE EXISTENCE OF THIS FORM: Public Workshop - Data and Data Needs to Advance Risk Assessment for Emerging Infectious Diseases Re www.fda.gov
Abstract Synthetic lipoidal peptides based on viral protein sequences have been prepared. These peptides contain an N-palmitoyl group at the N-terminal residue, which is a modified cysteine, containing a S-[2,3-bis(acyloxy)-(2-R,S)-propyl] moiety. When this residue (Pam3Cys) is at the N-terminus of a synthetic peptide, it acts as potent immunoadjuvant to enhance both IgM and IgG antibody responses to the attached peptide. Conventional analytical procedures (e.g., Edman degradation and amino acid analysis) are either not applicable due to the N-terminal modification, or do not provide confirmation of the intact structure. Chromatographic analysis is also hindered by the tendency of these lipoidal Pam3Cys peptides to form large aggregates, and in some cases to be permanently adsorbed on reversed phase columns. We have applied several mass spectrometric techniques, including fast atom bombardment (FAB), electrospray ionization (ESI) and matrix assisted laser desorption ionization (MALDI) to characterize the intact structures of a number of different Pam3Cys synthetic peptides. The MALDI-MS has been found to be the most sensitive for the analysis of the structure of Pam3Cys peptides.
So you see they were using jello on the wall and did not even know what it did or what it even was once it was altered....
But no one cared then and still today they do nothing to stop the 1 in 38 kids being infected in the name of profit so they can keep their syndrome of Autism or whichever one they want to bless you with. AIDS/LYME/MADCOW/MS/ALS/Parkinsons/Autism/CFS/ME/Lupus/Lymphoma/Alzheimers/GWS/Kawasaki's/etc. etc. etc. is all the same thing.... http://www.sovereignindependent.com/?p=27585 http://www.sovereignindependent.com/?p=27585
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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University of KY. has identified 3 of Borrelia's proteins to be prion like in their stealth ability. http://nar.oxfordjournals.org/content/38/16/5443.full EbfC preferentially binds the palindromic sequence GTnAC, where �n� can be any base, with all erp Operator 2 regions containing two adjacent EbfC-binding sites "What this says is exactly what it means". The n may be any peice of any organism folded within the protein to cause disease.
http://www.ncbi.nlm.nih.gov/pubmed/21946761 2011 Oct;33(7):712-5. Cutaneous Manifestations of B-Cell Chronic Lymphocytic Leukemia Associated With Borrelia burgdorferi Infection Showing a Marginal Zone B-Cell Lymphoma-Like Infiltrate.
These and many more reasons are why we need millions going to help the people. But this is everything about Lyme because it could have and should have been stopped 30 yrs. ago but they lied and said it was easy to cure and easy to treat....Now they feign ignorance once again. By leaving out important findings so they don't miss profits. http://www.ncbi.nlm.nih.gov/pubmed/21947773 Interleukin-10 Alters Effector Functions of Multiple Genes Induced by Borrelia burgdorferi in Macrophages to Regulate Lyme Disease Inflammation.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017414 We found that Nod2 mediates induction of pro-IL-1β, TNF-α, IL-6, IFN-α and CXCL10 in response to B. burgdorferi in BMDM in vitro. However, our results with an in vivo model of B. burgdorferi infection revealed two important findings. First, Nod2 does not appear to play an important role in the control of B. burgdorferi infection in mice and in fact, may hinder control.
How long does it take stupid at the CDC/IDSA to ignore for profit to the point of total pop. infection a strain highly suspect to be viral like? 2 yrs.? 10 yrs.? 30 yrs.? What difference does it make they are highly incompetent but still stick their hands out as experts asking for mo money to find something else to kill us with a little quicker.... http://www.ncbi.nlm.nih.gov/pubmed/21175079 2010 Nov Abstract During spring and fall 2009, 60 wild turkeys (Meleagris gallopavo) harvested by Tennessee hunters were surveyed for Borrelia spp. by
sampling their blood, tissue, ...and attached ticks. In both seasons, 70% of turkeys were infested with juvenile Amblyomma americanum;
one spring turkey hosted an adult female Ixodes brunneus.
Polymerase chain reaction assays followed by DNA sequencing indicated that 58% of the turkeys were positive for the spirochete Borrelia miyamotoi,
with tissue testing positive more frequently than blood (P = 0.015).
Sequencing of the 16S-23S rRNA intergenic spacer indicated > or = 99% similarity to previously published sequences of the North American strain of this spirochete.
Positive turkeys were present in both seasons and from all seven middle Tennessee counties sampled.
No ticks from the turkeys tested positive for any Borrelia spp.
This is the first report of B. miyamotoi in birds; the transmission pathways and epidemiological significance of this high-prevalence spirochetal infection remain uncertain.
Stupid Must Not go here anymore....They claim they found it yrs. ago....They knew and did nothing.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady, thank you for these links and your related comments...... it's all very interesting ...... I must admit that my lyme brain is overwhelmed by it all.
I totally agree that knowledge and research related to this disease has probably been available for a long time and has been ignored and /or suppressed largely due to the profit motives of a variety of interest groups.
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Pinelady
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Profit motives---such as that recently exhibited by Kaiser Permenente? Surely not...
They can decode 100,000 of their patients and employee's genetic codes, while the people that needed their help from the CDC's contract to find the cause and origin of Morgellons money was just wasted?
Now we get to suffer even longer by not knowing what it is while they figure out where to invest their knowledge to get the most bang for our bucks...LOL
http://www.ncbi.nlm.nih.gov/pubmed/21946761 2011 Oct; Cutaneous Manifestations of B-Cell Chronic Lymphocytic Leukemia Associated With Borrelia burgdorferi Infection Showing a Marginal Zone B-Cell Lymphoma-Like Infiltrate.
http://jem.rupress.org/content/158/6/2127.full.pdf Published December 1, 1983 STRUCTURAL ANALYSIS OF THE VARIABLE MAJOR PROTEINS OF BORRELIA HERMSII BY ALAN G. BARBOUR,* OSMAR BARRERA, AND RALPH C. JUDD* From the Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of AUergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840
Borrelia hermsii, a spirochete and an agent of relapsing fever, undergoes spontaneous antigenic variation both in vivo (1, 2) and in vitro (2). The rate of serotypic change is estimated to be 10-3-10 -4 per cell per generation (2).
The antigenic repertoire of B. hermsii (2) may be as extensive as that of another vector-transmitted and blood-borne pathogen,
Trypanosoma brucei, a eucaryote
(3, 4). Examination of four variants or serotypes found among the progeny of a single B. hermsii organism revealed that each serotype had an abundant protein of unique apparent molecular weight (5). Immunofluorescence and radioiodinelabeling studies indicated that these variable proteins, the pI proteins, were located on the surface. Serotype-specific monoclonal antibodies bound to homologous but not heterologous pI proteins (5). The pII protein was the other major protein found in whole cell lysate of each serotype (5). In contrast to pI proteins, the pII proteins had the same apparent molecular weight in each serotype, were less accessible than the pI proteins for iodine labeling, and were recognized in western blots by heterologous as well as homologous polyclonal antiserotype sera (5). As it appears likely that antigenic variation is based on the spontaneous appearance in a borrellia population of an organism possessing an antigenically "novel" pI protein, we are studying the structure of the pI proteins. Of particular importance for models of the genetic mechanism of antigenic variation is the amount of structural relatedness among the different pI proteins. We analyzed the pI and pII proteins of serotypes C, 7, and 21 with one- and two-dimensional (l-D, 2-D) I peptide-mapping procedures.
The results indicated that whereas all pII proteins are identical,
What if all this time they knew that we were also being infected with Trypanosomes that were eveloped in fungus to remain hidden from the tryst ? http://www.hindawi.com/journals/jna/2010/840768/ Volume 2010 (2010) Overview of DNA Repair in Trypanosoma cruzi, Trypanosoma brucei, and Leishmania major ---------Can't splain it away....LOL
Are the prion proteins and immune suppression the root cause of Morgellons? And if so what implications do the GMO have on the existance of man as we know him in the 1 in 38 now being diagnosed with Autism, the 1 every min. being diagnosed with Alzheimers, the one every 10 mins. being diagnosed with MS....
Stupid cannot live here anymore if man is to survive....
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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Appl Environ Microbiol. 2011 Sep 30. [Epub ahead of print] Cotransmission of divergent relapsing fever spirochetes by artificially infected Ornithodoros hermsi. Policastro PF, Raffel SJ, Schwan TG. Source
Medical Entomology Section, Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840 USA. Abstract
The soft tick Ornithodoros hermsi, which ranges in specific arboreal zones of western North America, acts as vector for the relapsing fever spirochete Borrelia hermsii.
Two genomic groups (GGI and GGII) of B. hermsii are differentiated by multilocus sequence typing,
yet are codistributed in much of the vector's range.
To test whether the tick vector can be infected via immersion, non-infected, colony-derived O. hermsi larvae were exposed to reduced humidity conditions before immersing in culture suspensions of several GGI and GGII isolates.
We tested for spirochetes in ticks by immunofluorescence microscopy, and in mouse blood by quantitative polymerase chain reaction of the vtp locus to differentiate spirochete genotypes.
The immersed larval ticks were capable of spirochete transmission to mice at the first nymphal feeding.
Tick infection with mixed cultures of DAH (vtp6; GGI) and MTW-2 (vtp5; GGII) isolates resulted in ticks that caused spirochetemias in mice consisting of MTW-2 or both DAH and MTW-2.
These findings show that this soft tick species can acquire B. hermsii by immersion in spirochete suspensions,
that GGI and GGII genotypes can coinfect the tick vector by this method,
and that these spirochetes can be cotransmitted to a rodent host.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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I believe it will be found the only difference will be the time allowed that is needed for the infectious proteins to fold and then remain hidden in the DNA..Such as the TN tick/turkey study.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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I was on the trail of prions when one of my listmembers sent me a link to this site. I cannot express how totally impressed I am with the quality and depth of information and connections that are being made here. It has been my experience that those with morgellons, lyme, and other harsh and debilitating diseases are the most intelligent people on the planet.
thank you for all of these resources.
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Catgirl
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Glad you found us Patrick. Welcome!
Most (if not all) of the people here have minds open enough that they don't just swallow whatever conventional medicine dishes out. This is where we meet. share and grow. There is so much more. Also, Pinelady rocks!
Fyi, we don't use our real names here. You can go to profile to edit.
-------------------- --Keep an open mind about everything. Also, remember to visit ACTIVISM (we can change things together). Posts: 5418 | From earth | Registered: Mar 2011
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