|
Post by lilsissy on Oct 12, 2010 22:36:09 GMT -5
I am finding a real fit here with my pain and family history, this has to do with rare blood types. Seems some positive blood type are positive negative . Rh-Negative People have 2 NEGATIVE Blood Factors. Ex. (--) Rh-Positive People have EITHER 2 POSITIVE Blood Factors OR 1 Negative and 1 Positive. Ex (++) OR (+-). arthritis.about.com/od/gene/a/HLAgenes.htmAbnormal fiber deposits can cause fibrosis , stiff ribs red eyes tendon pain Pain in flares weakness The HLA-DR4 gene, which has been associated with rheumatoid arthritis, has also shown involvement in Lyme disease. Lyme disease is caused by a microorganism which is transmitted to humans via deer ticks. Among the symptoms which can develop from Lyme disease are: Multitude of other symptoms Would possibly explain my daughters blood group changes. Possibly she was not grouped correctly to begin with. She has changed to a negative. If one had this gene it would cause an over immune reaction to fight off invasion of transmutation. Has anyone been tested for this, it is a simple blood test. My mom remembers when my sister had her tonsils out the doctors where mad because she did not tell them about her blood but she doesn't remember what it was about the blood. Mom does not know what her blood type is of know what Dad's was. I am a B+ I think but not sure.
|
|
|
Post by lilsissy on Oct 12, 2010 22:40:05 GMT -5
This was the chat which brought this genetic condition to my attention. As you see this gal posting on GodlikeProductions admits she is not a Doctor but she does seem to know her stuff. For lack of a name here , I will refer to her as LADY X. LADY X. www.godlikeproductions.com/forum1/message373159/pg30Re: B L O O D O F T H E G O D S - Are you an Rh Negative blood type? Quote My mom is O+ but I am A-. For the past 4-5 years her doctors have been trying to diagnose issues she is having. Issues resembled RA, MS and Fibromyalgia... HOWEVER, due to my research and persistance with her doctor, I was able to convince them to yest her for a very rare genetic marker that would help to properly diagnose her with an auto immune disease she actually has. The genetic marker is HLA-B27, it is found in less than 1.4-8% of the population, depending on the area of the world you live in....it is literally a needle in a haystack. My mom thought the Doc was going to think I was a nut but he did not. He agreed with my theory and tested her. She came up POSITIVE! Doctor was shocked! I found the needle in the haystack that they spent almost 5 years looking for! Now I have been asked by her physician to accompany her to all her specialist Dr. appts. I order to convey my research, findings and theory, so they can get her the proper tests required to complete the proper diagnosis and begin an actual course of treatment; not just a trial and error of medications that give no relief and create side effects! The Auto Immune disease we are testing for is Ankylosing Spondylitis or AS, you can read more about it at www.RhNegativeRegistry.com. It resembles RA, Lupus, MS and Fibramyalgia but it is it own auto immune issue. I worked hard to put this information together because I do not want to be in my mothers position of pain in 20 years. If you are a person who is Rh- or you are Rh- and have an Rh+ parent with these issues, you could be a candidate. I have a hypothesis that states my reasoning to show this. However, the basic is below. Rh-Negative People have 2 NEGATIVE Blood Factors. Ex. (--) Rh-Positive People have EITHER 2 POSITIVE Blood Factors OR 1 Negative and 1 Positive. Ex (++) OR (+-). If what they say is true and Rh- people have a higher concentration of copper and Rh+ people have a higher concentration of iron, then people who are Rh+ but have the blood factors (+-) are in "dis-ease". People who are (--) or (++) have a fully matching system, eith all iron or all copper. People who are (+-) like my mom, should really be reclassified into their own unique Rh category. They are like half-breeds of iron and copper and the body gets confused. www.facebook.com/topic.php?uid=294068922321&topic=14331I am not a scientist or a genetisist, just an interested researching Rh- blood carrier who would like to see more information on this subject looked at more seriously. I am sick of the medical profession and genetisist telling people the only thing they need to worry their tiny little brains with is getting the RhoGAM shot. What about the rarity of the types and potential issues if a blood donation or transplant is needed! Shouldn't we know the individual position we may be faced with in trying to find matching donors for our rare and most complex blood system. I am working on updating my site with more information as I find it. I am looking for answers and solutions. For instance, a lot of Rh- woman have issues taking birth control...Try to find a birth control out there made specifically for Rh- people. I will save you the time, it does not exsist. We are just stuck to take our chances with getting the side effects from said medication. Try to find an Rh- OBGYN Specialist....nope, none there either. We are left out in the cold, uneducated on purpose and no taken seriously. If Rh- type O- blood has been Patented and used as a treatment given to Rh+ HIV patients, in order to slow the progression of the disease by 2-5 years; imaging the implication for things like cancer! Our blood does not mutate and cannot be cloned, that is why there is no artificail plasma option for Rh-. So if the problem with cancer is it matastisizes ( I know I spelled that WAY wrong), but it spreads, multiplies, etc. What effect could the introduction of Rh- blood have on a cancer patient have on an Rh+ Person with Cancer. If you are interested in chatting more about it, please email me at info@RhNegativeRegistry.com. IF you have information you think may be important, please share! A symptom for my mom that would have been an early detection hint, if they new it, was the loss of her HAIR COLOR at age 16. Premature greying at a very early age, denotes a stop of melanin production and the decreased production of Vit. B12 and D. Always consult your doctor directly where your health is concerned, but who says you can't lead them by the nose and help them get it right. After all the only oath they take is to "practice medicine", that practice is done on you.
|
|
|
Post by lilsissy on Oct 12, 2010 23:07:31 GMT -5
|
|
|
Post by lilsissy on Oct 12, 2010 23:13:30 GMT -5
Looks like Skytrool was on to this one, lymebusters.proboards.com/index.cgi?board=rash&action=display&thread=6130&page=6cut, In one embodiment of the methods of the invention, the selectable marker is a positive selectable marker gene, a negative selectable marker gene or both. Positive selection marker genes that can be used with the methods and vectors of the subject invention include green fluorescent protein (gfb), â-galactosidase (â-gal), blasticidin deaminase (bsd), dihydrofolate reductase (dhfr) and neomycin (neo). Negative selection marker genes that can be used with the methods and vectors of the subject invention include diptheria toxin-A (DT-A) and thymidine kinase (TK). Other suitable positive and negative selection marker genes are known in the art and can be used according to the present invention. " "Claim 1 of 12 Claims 1. An in vitro method of altering the histocompatibility phenotype of a human stem cell, comprising:
a) deleting adjacent HLA-B and HLA-C MHC genes from a first chromosome;
b) replacing HLA-B and HLA-C MHC genes on a second chromosome with a site specific cassette, said cassette comprised within a vector that includes a site specific recombination sequence selected from LoxP and FRT;
c) inserting a transgene harboring a heterologous HLA allele and a homologous sequence matching the site specific recombination sequence of step b); and d) catalyzing said site specific recombination wherein said transgene becomes incorporated into said second chromosome by site specific recombination to provide a stem cell with altered histocompatibility phenotype. " LINK: tinyurl.com/3au4tqRead more: lymebusters.proboards.com/index.cgi?board=rash&action=display&thread=6130&page=6#ixzz12D1AN7GE
|
|
|
Post by lilsissy on Oct 12, 2010 23:23:30 GMT -5
So if LADY X from Godlike is right
Our blood does not mutate and cannot be cloned, that is why there is no artificail plasma option for Rh-.
and suppose we are postive negative or negative negative
We would be rejecting these cassests for the insertions of transgenes. No artificial would be appropriate for us.
|
|
|
Post by lilsissy on Oct 12, 2010 23:44:02 GMT -5
How to get tested, www.facebook.com/pages/The-Rh-Negative-Registry/294068922321Ask your doctor to test you for the HLA-B27 genetic marker. It will help them diagnose your condition. If they say no, tell them your mom was positive. A genetic predisposition is associated, so if you "tell" them that mom was HLA...-B27+ they have to test you. I suggest a Rheumologist and a Naturopathic doctor be requested if you are positive. Feel free to email me if you have questions. If you share symptoms, I may be able to point you in a direction to help your diagnosis. JessicaSee More October 8 at 4:32am ·
|
|
|
Post by skyship on Oct 13, 2010 20:44:17 GMT -5
I think we are the B factor, and evidently, it has been said that the B if changed to Z form, and that is in invertis and other jnk autorecessives. I am B+ as well....... That z form has a bacteria that is replacing blood to make it O. All universal blood types, which then takes it away from us, our native blood. History: www.madehow.com/Volume-5/Artificial-Blood.htmlabove is artificial: but is HLA-B27 ligands artificial? something called the merlin gene, and the Magicin on chromosome 22? more on that later. nf1 and nf2 genes, all involved in cytoskeleton reorganization. Stole our bloodline, under the guise of cytoskeleton reorganization. What a trick, note the merlin gene and the magicin. new thread for that one. Skyship
|
|
|
Post by skyship on Oct 13, 2010 21:56:21 GMT -5
......"a stem cell with altered histocompatibility phenotype. "
THE PROTOTYPE.
skyship
|
|
|
Post by skyship on Oct 14, 2010 13:31:20 GMT -5
Notice the last paragraph. Lil sissy ..." most common in the U.S. are HLA B27*05 and HLA B27*02." The Test 1. How is it used? 2. When is it ordered? 3. What does the test result mean? 4. Is there anything else I should know? How is it used? The HLA-B27 test is primarily ordered to help strengthen or confirm a suspected diagnosis of ankylosing spondylitis (AS), Reiter’s syndrome (reactive arthritis), or sometimes anterior uveitis. The HLA-B27 test is not a definitive test that can be used to diagnose or rule out a disorder. It is used as one piece of evidence in a constellation of signs, symptoms, and lab tests to support or rule out the diagnosis of certain autoimmune disorders, such as AS and Reiter's syndrome. Both AS and Reiter’s syndrome are chronic progressive conditions that occur more frequently in men than women, and the first symptoms usually occur when a patient is in his early 30's. Ankylosing spondylitis is characterized by pain, inflammation, and a gradual stiffening of the spine, neck and chest. Reiter’s syndrome is a group of symptoms that includes inflammation of the joints, urethra, eyes, and skin lesions. Often, the initial symptoms of these autoimmune disorders are subtle and may take several years before characteristic degenerative changes to bones and joints are visible on X-rays. Anterior uveitis is associated with recurring inflammation of the structures of one or both eyes. The HLA-B27 test may be ordered as part of a group of tests used to diagnose and evaluate conditions causing arthritis-like chronic joint pain, stiffness, and inflammation. This group of tests may include an RF (rheumatoid factor) with either an ESR (erythrocyte sedimentation rate) or a CRP (C-Reactive protein). HLA-B27 is sometimes ordered to help evaluate someone with recurrent uveitis that is not caused by a recognizable disease process. ^ Back to top When is it ordered? An HLA-B27 test may be ordered when a patient has acute or chronic pain and inflammation in his spine, neck, chest, eyes, and/or joints, and the doctor suspects an autoimmune disorder that is associated with the presence of HLA-B27. Doctors frequently must rely on their clinical findings and the HLA-B27 test result when diagnosing ankylosing spondylitis, and other HLA-B27 related disorders, because the characteristic changes to the bones may not be detectible for several years. Under these circumstances, HLA-B27 is not diagnostic but adds additional information, increasing or decreasing the likelihood that the patient has ankylosing spondylitis. An HLA-B27 may also be ordered when a patient has recurrent uveitis. ^ Back to top What does the test result mean? HLA-B27 will be present or absent. If it is present, then the HLA-B27 antigen exists on the surface of the body’s white blood cells and other nucleated (containing a nucleus) cells. If a patient has HLA-B27 and has symptoms such as chronic pain, inflammation, and/ or degenerative changes to his bones (as seen on X-ray), then it supports a diagnosis of AS, Reiter’s syndrome, or another autoimmune disorder that is associated with the presence of HLA-B27. This is especially true if the patient is young, male, and if he experienced his first symptoms before the age of 40. If HLA-B27 is not present, then the association is not there. This does not, however, mean that the person does not have the suspected condition, as a certain percentage of patients with each disorder will be HLA-B27 negative. A positive HLA-B27 in a person who does not have symptoms or a family history of HLA-B27 associated disease is not clinically significant. It does not help predict the likelihood of developing an autoimmune disease. If a patient does have an associated disorder, the presence of HLA-B27 cannot be used to tell which disease is present, how quickly it will progress, its severity, prognosis, or the degree of organ involvement. ^ Back to top Is there anything else I should know? Whether or not HLA antigens will be present is genetically determined. Their production is controlled by genes that are passed from parents to children. If one of your family members has a HLA-B27 related disease that affects the joints of the spine (AS or other related condition) and you have the HLA-B27 antigen, then you have a higher risk of developing a similar disease. With new genetic testing methods, it is now possible to separate HLA-B27 into subtypes. So far, about fifteen different subtypes have been identified. The most common in the U.S. are HLA B27*05 and HLA B27*02. How the presence of these specific subtypes affects the likelihood of developing an autoimmune disease is not yet known. www.labtestsonline.org/understanding/analytes/hla_b27/test.htmlskyship
|
|
|
Post by skyship on Oct 14, 2010 13:35:23 GMT -5
A viral peptide?Different HLA-B27 Subtypes Present the Same Immunodominant Epstein-Barr Virus Peptide ... Interest in the B27 family stems from its very strong linkage with ankylosing spondylitis and related spondyloarthropathies This represents by far the clearest example of an HLA-linked disease in humans, and, indeed, there are strong grounds for believing that HLA- B27 molecules are directly involved in the disease process (15), probably as targets of an immunopathological response. Of several mechanisms proposed in this regard (16), one of the most interesting postulates a role for CTL responses directed against an "arthritogenic" peptide, of cellular or microbial origin, which is selectively presented by HLA-B27 In this context, at least five of the above B27 subtypes are known to be disease linked. These are the widespread B27.05 sub- type, the B27.01 and B27.02 subtypes found in Caucasian populations, and the B27.04 and B27.06 subtypes found in South East Asian populations (16, 18). The implication is, therefore, that all five B27 subtype molecules must be capable of binding and presenting the same arthritogenic peptide de- spite differences in the structure of their peptide binding grooves. www.ncbi.nlm.nih.gov/pmc/articles/PMC2191177/pdf/je1783879.pdf======================= What is this B-27 molecule? is a EBV peptide for sure ==================== Molecular mimickry between HLA B27 and Yersinia, Salmonella, Shigella and Klebsiella within the same region of HLA alpha 1-helix.Two new examples of amino acid homology between HLA B27 and microbes triggering HLA B27-associated diseases are described. An outer membrane protein YadA (Yersinia adhesin, previously called Yop1) of Yersinia enterocolitica and Y. pseudotuberculosis shares a linear tetrapeptide with HLA B27.
.... "A cationic outer membrane protein OmpH of Salmonella typhimurium shares homology with five amino acids of HLA B27 in a non-linear fashion. The four amino acids of YadA are also notably included in the hexapeptide identical between Klebsiella pneumoniae nitrogenase and HLA B27, and three of them occur in the pentapeptide shared by a Shigella flexneri protein and HLA B27. Antibodies against synthetic peptides including HLA B27 homologues sequences of YadA and OmpH were observed in one-third of the patients with HLA B27 associated diseases. ",,,,,,'www.ncbi.nlm.nih.gov/pmc/articles/PMC1554211/...."arthritis-triggering microbes and HLA B27" How in the hell can arthritis tirgger microbes? takes us right back to the Llambda bacteriophage, the injection is from the yersinia YOP Llambda, a bunch of sheep, is that all we are! a holes...... Maybe we are too GENTILE? I do know that EPV and CMV are are the viral components. geno cide killing the genes that tell our stories. Follow the father, everything concentrated on Mother and mitochondrial genes, trace the father lineage back. Bringing down the patriarch, was always the aim, cannot accept the fact who Eve really was, can they? It was she who brought the animal genes in?, the father not Adam. If there were 7 eves, who were all the fathers? ================ Mother earth, father time....... =================== HLA alpha 1-helix ...................... skyship
|
|
|
Post by skyship on Oct 14, 2010 14:30:04 GMT -5
We have heavy chain, I have the dimers to prove it, as well lil sissy, The dimers form from prions............... so the sup 35 forming prions that fold and unfold in the viral components EPV and CMV change the B form. Link to chlamydia? ================= HLA B27 in health and disease: a double‐edged sword? Secondly, a strong cytotoxic T‐cell response to an HLA B27‐restricted peptide epitope from Chlamydia trachomatis was found in a patient with ReA. This peptide, derived from a bacterium known to trigger ReA, is thus a candidate ‘arthritogenic’ peptide. We have also found evidence that HLA B27 has an unusual cell biology compared with other HLA molecules. HLA B27 demonstrates an unusual ability to form heavy chain homodimers in vitro. Dimerization is dependent upon disulphide bonding through an unpaired cysteine at position 67. Remarkably these dimers lack β2 microglobulin, previously thought to be an essential component of all mature MHC class 1 molecules. HLA B27 homodimer formation has also been demonstrated in certain cell lines in vivo, and preliminary data suggest that significant numbers of T cells from patients with spondyloarthropathy express a ligand for HLA B27 homodimers. These findings have extended our understanding of the beneficial immunologic function of HLA B27, and have also led us to propose the testable new hypothesis that HLA B27 heavy chain dimerization may be involved in the pathogenesis of spondyloarthritis. rheumatology.oxfordjournals.org/content/41/8/857.fullmessed with our B blood!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! ..."HLA B27‐restricted peptide epitope from Chlamydia trachomatis was found in a patient with ReA. : skyship
|
|
|
Post by skyship on Oct 14, 2010 16:04:56 GMT -5
Change of histone 3 and 4 and b type blood cell During the inflammatory response to an implanted biomaterial, monocytes undergo a striking phenotypic progression of differentiation into macrophages, which may subsequently fuse to form foreign body giant cells (FBGCs). macrophages, monocytes, adhesive, adhesive structure development, cytoskeletal reorganization, podosomes, phenotypic, restriction, specializations, Cytokine-induced FBGCs, extreme periphery, FBGCs, F-actin, FBGC, paxillin, ventral plasma membrane, 1 micron, ventral cell membrane, fuse, foreign, differentiation, striking phenotypic, monocytes undergo, cytokine-induced FBGC formation, optical slicing capabilities, podosome adhesive structures, inflammatory, punctate filamentous f-actin structures, cytoplasmic staining, ring staining, www.cytok.com/showabstract.php?pmid=9857213skyship
|
|
|
Post by aqt on Oct 14, 2010 16:45:29 GMT -5
HLA -B27
HeLA
remember her?
infinite/immortal cells.
**lightbulb!!**
aqt
|
|
|
Post by skyship on Oct 15, 2010 2:37:53 GMT -5
These are not Hela though. These are and people with the antigen on their B blood cells, rh or not......... Blood type A not targeted with this antigen, but B is........
=============== In autoimmunity. HLA types are inherited, and some of them are connected with autoimmune disorders and other diseases. People with certain HLA antigens are more likely to develop certain autoimmune diseases, such as Type I Diabetes, Ankylosing spondylitis, Celiac Disease, SLE (Systemic Lupus Erythematosus), Myasthenia Gravis, inclusion body myositis and Sjögren's syndrome. HLA typing has led to some improvement and acceleration in the diagnosis of Celiac Disease and Type 1 diabetes; however for DQ2 typing to be useful it requires either high resolution B1*typing (resolving *0201 from *0202), DQA1*typing, or DR serotyping. Current serotyping can resolve, in one step, DQ8. HLA typing in autoimmunity is being increasingly used as a tool in diagnosis. In Celiac disease it is the only effective means of discriminating between 1st degree relatives who are at risk from those who are not at risk, prior to the appearance of sometimes irreversible symptoms such as allergies and secondary autoimmune disease. en.wikipedia.org/wiki/Human_leukocyte_antigen================== So by removing this B antigen, it makes it O universal blood, I think>========== They are converted by enzymes...........lil sis..............Universal red blood cells—enzymatic conversion of blood group A and B antigens the idea of converting blood group A and B antigens to H using specific exo-glycosidases capable of removing the immunodominant sugar residues was pioneered by Goldstein and colleagues at the New York Blood Center in the early 1980s. Conversion of group B RBCs to O was initially carried out with α-galactosidase extracted from coffee beans. These enzyme-converted O (ECO) RBCs appeared to survive normally in all recipients independent of blood group. The clinical trials moved from small infusions to single RBC units and finally multiple and repeated transfusions. A successful phase II trial utilizing recombinant enzyme was reported by Kruskall and colleagues in 2000. Enzymatic conversion of group A RBCs has lagged behind due to lack of appropriate glycosidases and the more complex nature of A antigens. Identification of novel bacterial glycosidases with improved kinetic properties and specificities for the A and B antigens has greatly advanced the field. Conversion of group A RBCs can be achieved with improved glycosidases and the conversion conditions for both A and B antigens optimized to use more cost-efficient quantities of enzymes and gentler conditions including neutral pH and short incubation times at room temperature. Of the different strategies envisioned to create a universal blood supply, the ECO concept is the only one, for which human clinical trials have been performed. This paper discusses some biochemical and clinical aspects of this developing technology. tinyurl.com/2aueemd================ now again, we find what bacteria is replacing that antigen......... ECO concept: novel bacterial glycosidases with improved kinetic properties and specificities for the A and B antigens=================== Use for coverting b blood: GH110 in B. fragilis and thetaiotaomicron strains. Members of one subfamily have exclusive specificity for the branched blood group B structures, whereas members of a newly identified subfamily represent linkage specific α1,3-galactosidases that act equally well on both branched blood group B and linear α1,3Gal structures. We determined by one-dimensional 1H NMR spectroscopy that GH110 enzymes function with an inverting mechanism, which is in striking contrast to all other known α-galactosidases that use a retaining mechanism. The novel GH110 subfamily offers enzymes with highly improved performance in enzymatic removal of the immunodominant α3Gal xenotransplantation epitope. BfGal110A and BfGal110B, two α-galactosidase variants from B. fragilis; BtGal110A and BtGal110B, two α-galactosidase variants from B. thetaiotaomicron; SaGal110A, α-galactosidase from S. avermitilis; SgGal110A, α-galactosidase from S. griseoplanus 2357; www.jbc.org/content/283/13/8545.abstract================ skyship
|
|
|
Post by skyship on Oct 15, 2010 2:57:14 GMT -5
List of 110's: some of these are fungus? and bacteria, prob archaea as well. www.jbc.org/content/early/2008/01/28/jbc.M709020200.full.pdfEDM26187 Lentisphaera araneosa EAV34087 Shewanella woodyi AM259273 Streptomyces griseoplanus (SgGal110A) CAJ33349 Streptomyces avermitilis (SaGal110A) CAJ33352 Bacteroides thetaiotaomicron (BtGal110A) CAH09922 Bacteroides fragilis (BfGal110A) EDM21756 Bacteroides caccae CAJ33353 Bacteroides thetaiotaomicron (BtGal110B) EDM21147 Bacteroides caccae CAJ33351 Bacteroides fragilis (BfGal110B) ABR37834 Bacteroides vulgatus ABR44546 Parabacteroides distasonis EDN88509 Parabacteroides merdae EDN46502 Opitutaceae bacterium EDN46254 Opitutaceae bacterium will check these out................ this should be found in our blood, then, that HLA-B27 test should show these antigens? Skyship
|
|
|
Post by skyship on Oct 15, 2010 2:58:23 GMT -5
something to attack those bacterias cold stop the exchange?
MIght stop the bacteria from forming the biofilms.?
And or altering the blood cells?
skyship
|
|
|
Post by skyship on Oct 16, 2010 15:54:06 GMT -5
Virology Erythroviruses belong to the Parvoviridae family of small DNA viruses.[7] It is a non-enveloped, icosahedral virus that contains a single-stranded linear DNA genome. Approximately equal proportions of DNA of positive and negative sense are found in separate particles. At each end of the DNA molecule there are palindromic sequences which form "hairpin" loops. The hairpin at the 3' end serves as a primer for the DNA polymerase.[8] It is classified as erythrovirus because of its capability to invade red blood cell precursors in the bone marrow.en.wikipedia.org/wiki/Parvovirus_B19======================== This has to be what was used to change blood. I see the "hairpin" loops are important, have seen these in my specimens. Have seen the fake dna strand and it does show 2 strands as well. Invade red blood cell precursors.......... or progenitors, that could be what Carnicom saw on the cells? any other viruses that have that capacity? Erythroviruses: ================ Novel Human Erythrovirus Associated with Transient Aplastic Anemia The B19 PCR assay yielded a product that hybridized only very weakly to the B19-specific probe and whose sequence diverged more from those of 24 B19 viruses (11 to 14%) than the divergence found within the B19 group (<= 6.65%). Restriction enzyme analysis of the V9 genome revealed that this genetic divergence extended beyond the amplified region. Interestingly, serological tests failed to demonstrate a response characteristic of acute B19 infection. V9 could be a new erythrovirus, and new diagnostic tests are needed for its detection. jcm.asm.org/cgi/content/abstract/37/8/2483------------------------- so what is this V9? new thread::::::::::::: OM....... Nasa's echinocytes? skyship
|
|
|
Post by skyship on Nov 15, 2010 1:53:19 GMT -5
The three-dimensional structure of the Class I Human Histocompatibility Protein, HLA-B27 has been determined at 2.1 angstroms resolution. If your Web Browser has been suitably configured, download this crystal structure of Human MHC Class I, [1HSA] (563Kb) - this is a dimer [Bbk|BNL|Hal] www.cryst.bbk.ac.uk/pps97/assignments/projects/coadwell/004.htm===================== Orthorhombic space group? Crystals are of the orthorhombic space group P2(1)2(1)2(1 Has to do with geometry shapes....etc..... crystals more on that later...... =================== MHC I and MHC II In fact, major histocompatibility complex (MHC), the most gene-rich section of the human genome, is one of the major reasons for the wide diversity of the immune system. Interestingly, MHC allele frequencies vary by racial group. Major Histocompatibility Complex (MHC): a hidden clue to human social behavior? MHC is a major contributor to the human immune system, and one of the most polymorphic regions of the genome. This hints at a population-gene interaction, where large numbers of unique alleles at the same locus (equation 1) distributed throughout a population increases the probability of species survival. Interestingly, polymorphism is also high with genes that contribute to human behavior. A case for group selection The diversity of the immune system, where unique alleles are spread across a population, rather than being overloaded on to the same individual genome, is one of the more interesting events in evolution. It is perhaps an excellent case for the hotly contested theory of group selection, that is, selection of genes at the level of the population, as opposed to the phenotype. Communicable disease may best be defended by a distribution of unique alleles across a population. That is, a larger set of distinct alleles spread across a population may provide greater survival rates to epidemics than overloading an individual's genome with the same set of unique alleles. MHC loci exhibit unusually high levels of heterozygosity (Lewin, 1989). Extreme polymorphism at MHC loci has been proposed to be maintained by natural selection at the level of the population. One such mechanism involves the hypothesis that certain pathogens acquire MHC antigens from their primary host, subsequently carrying them to the next host, which will benefit by genetic variation in the MHC, which will treat the pathogens with the hitchhiking MHC antigens like intruders (Andersson, 1987). Had the next victim had identical MHC alleles as the first, the pathogens would be harder to detect and eliminate. see images of two. MHCs neuropolitics.org/defaultmar10.aspskyship
|
|
|
Post by lilsissy on Nov 15, 2010 2:40:29 GMT -5
I don't know if this helps but I have carried EBV extremely high about 8 times to high for years also Herpes type 1 ( mouth type).
|
|
|
Post by HARPREET SINGH on May 27, 2015 2:18:09 GMT -5
HLA B27 POSTIVW WHAT I DO I AM SUFFERING 5 YEAR AGO PLEASE HELP ME
|
|
|
Post by preet on May 27, 2015 4:29:19 GMT -5
hello my selp preet ,i am 21 year ,but mu hla b27 is postive ,i feel not good ,i alwayes feel stifness ,tierd and lazy feeling,
|
|
|
Post by skyship on Jun 13, 2015 0:08:09 GMT -5
I know the feeling and pain. Keep using protocols recommended in treatments, remmedies posts.
|
|
HLA B27 antigen sufferer
Guest
|
Post by HLA B27 antigen sufferer on Jan 29, 2016 12:48:17 GMT -5
I am finding a real fit here with my pain and family history, this has to do with rare blood types. Seems some positive blood type are positive negative . Rh-Negative People have 2 NEGATIVE Blood Factors. Ex. (--) Rh-Positive People have EITHER 2 POSITIVE Blood Factors OR 1 Negative and 1 Positive. Ex (++) OR (+-). arthritis.about.com/od/gene/a/HLAgenes.htmAbnormal fiber deposits can cause fibrosis , stiff ribs red eyes tendon pain Pain in flares weakness The HLA-DR4 gene, which has been associated with rheumatoid arthritis, has also shown involvement in Lyme disease. Lyme disease is caused by a microorganism which is transmitted to humans via deer ticks. Among the symptoms which can develop from Lyme disease are: Multitude of other symptoms Would possibly explain my daughters blood group changes. Possibly she was not grouped correctly to begin with. She has changed to a negative. If one had this gene it would cause an over immune reaction to fight off invasion of transmutation. Has anyone been tested for this, it is a simple blood test. My mom remembers when my sister had her tonsils out the doctors where mad because she did not tell them about her blood but she doesn't remember what it was about the blood. Mom does not know what her blood type is of know what Dad's was. I am a B+ I think but not sure.
|
|
HLA B27 antigen sufferer
Guest
|
Post by HLA B27 antigen sufferer on Jan 29, 2016 12:49:14 GMT -5
I am finding a real fit here with my pain and family history, this has to do with rare blood types. Seems some positive blood type are positive negative . Rh-Negative People have 2 NEGATIVE Blood Factors. Ex. (--) Rh-Positive People have EITHER 2 POSITIVE Blood Factors OR 1 Negative and 1 Positive. Ex (++) OR (+-). arthritis.about.com/od/gene/a/HLAgenes.htmAbnormal fiber deposits can cause fibrosis , stiff ribs red eyes tendon pain Pain in flares weakness The HLA-DR4 gene, which has been associated with rheumatoid arthritis, has also shown involvement in Lyme disease. Lyme disease is caused by a microorganism which is transmitted to humans via deer ticks. Among the symptoms which can develop from Lyme disease are: Multitude of other symptoms Would possibly explain my daughters blood group changes. Possibly she was not grouped correctly to begin with. She has changed to a negative. If one had this gene it would cause an over immune reaction to fight off invasion of transmutation. Has anyone been tested for this, it is a simple blood test. My mom remembers when my sister had her tonsils out the doctors where mad because she did not tell them about her blood but she doesn't remember what it was about the blood. Mom does not know what her blood type is of know what Dad's was. I am a B+ I think but not sure.
|
|
|
Post by HLA antigen on Jan 29, 2016 13:13:33 GMT -5
Have you used Accutane or it s newer version Isoretinon/ These can cause calcium deposits. The newer form of Accutane hits patients, ladies quicker than the original Accutane. It is hormonal driven and the antigen suppresses the antibody which fights acne. When a woman uses Accutane back in the 80s, they did not know they had this until they hit menopause because then the hormones change. you will probably have trouble with your menstrual cycle and may not be able to conceive or if you can conceive, your male children will not be able to have children as is my case
|
|
|
Post by ErikaGaf on Mar 10, 2019 8:39:40 GMT -5
|
|
|
Post by LesDush on Sept 11, 2019 3:48:30 GMT -5
Cialis Online Cheap buy cialis Kamagra Gelatina Orale 25 Mg Amoxicillin Eyes First Aid Amoxicillin Sunlight Exposure
|
|
|
Post by JoeUrime on Jan 5, 2020 21:41:07 GMT -5
I am the head web developer for the Email Extractor and Internet Search Engine Scraper by Creative Bear Tech. Essentially, this search engine scraper can scrape many of the search engines, including Google, Bing, AOL, Yandex alongside social network sites networks including Facebook, Instagram, Twitter, LinkedIn, Yellow Pages, Google Maps and so much more. I feel it will be a lot easier if you read through the comprehensive tutorial at blockchainlifemag.com/2019/05/21/guide-email-extractor-and-search-engine-scraper-by-creative-bear-tech. The application is not official yet, but as soon as it is, it will be available on creativebeartech.com We are at the present time beta testing the software and searching for beta tester and software reviewers. You will receive the complete licence key for the computer software and can even scrape B2B contact details for your own industry. If interested, please give me a shout on Facebook www.facebook.com/Creative-Bear-Tech-2284249764963533/or just reply to this thread.
|
|
|
Post by Katieurbat on Aug 8, 2020 23:23:44 GMT -5
|
|
|
Post by Katieurbat on Aug 11, 2020 16:03:08 GMT -5
|
|