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Post by lilsissy on Jan 6, 2010 23:14:51 GMT -5
This just in,http://www.thenmo.org/
Left: A Morgellons fiber: 0.1 mm. Right: Morgellons sufferer Cindy Casey shows the scars left by the disease on her arms. The rest of her body bears similar marks. -Photo by Will Atkins Corinne Carson 15.APR.09
Conference on strange disease held in Oak Hill area
It sounds like science fiction. People report strange unknown fibers emerging from under their skin in hues of blue, red, white, black, even turquoise. Researchers report that the fibers are made of cellulose, which is not normally found in the human body, and some have even found fibers coated in metal. Some fibers have been observed to move. The fibers are accompanied by an intolerable feeling of something crawling, stinging or biting under the skin, a feeling that gets worse at night. This torment is accompanied by a variety of other symptoms, including skin lesions and "brain fog" and the symptoms are sometimes shared by whole families, and even their pets.
The condition, known as Morgellons Disease, is not officially recognized by the mainstream medical community and sufferers are often diagnosed with other skin illnesses or told that they are suffering from a psychological condition known as delusions of parasitosis – in other words, that it is all in their head.
Although the mainstream medical community does not recognize the illness, on one day out of the year, the often self-diagnosed Morgellons patients and sympathetic medical professionals and allies gather for their international conference. This year, that conference was held April 4th in Southwest Austin at the Westoak Woods Baptist Church.
The conference is sponsored by the Charles E. Holman Foundation, a non-profit that states its mission is to support "research, education, diagnosis and treatment of Morgellons Disease" and included lectures from sympathetic medical professionals and researchers. Charles Holman is the late husband of Cindy Casey RN, a Morgellons patient. He founded the "New Morgellons Order" to raise awareness of the disease after accompanying his wife to a number of doctors' appointments and watching as she was told she was crazy. The foundation was renamed in his honor when he died of a heart attack in 2007 and his wife Casey took over as the executive director.
Cindy Casey's story is like many others. She began experience symptoms of chronic fatigue and occasional skin lesions as far back as 1997. By 2003, the lesions had become so prevalent and excruciating, with the characteristic fibers emerging from her skin and the intense itching, pain and cognitive problems or "brain fog" that she decided to seek treatment.
Like many "Morgies" as Morgellons patients sometimes call themselves, Casey was told by several dermatologists that she suffered from delusional parasitosis, a condition in which the patient hallucinates the sensation of bugs crawling under the skin, often accompanied by skin wounds caused from excessive itching or picking at the skin.
In an intermission during the conference, Casey rolled back her sleeve and lifted her pant leg to reveal arms and legs covered with numerous lesions and discolored whiter skin where she said previous lesions had healed. "They start out as little pimple marks and then they become open wounds, so I have them in all different stages," she said.
Other patients came up, lifting their skirts and pant legs to reveal the same lesions dotting their skin. Some had lesions under white cotton gloves or hidden under handkerchiefs tied over their head.
Of the lesions, Casey said, "They are so painful it's hard to describe – the itching is worse. It's just this insatiable itch that you can't even describe. I've had poison ivy and those things itch bad but this is just, it's just so bad it makes you want to come unglued."
Casey, like many others at the conference, credits Ginger Savely, DNP, a nurse practitioner famous for treating the controversial Morgellons and Chronic Lyme diseases, for finally showing her respect and compassion, and for giving her treatment that she says has reduced the number of lesions and the severity of her pain and itching.
Savely, who has a PHD in nursing, is practically worshipped in Morgellons and Lyme circles. She gave two lectures at the conference, one in which she described case studies of various Morgellons patients she has treated, and another discussing treatment options for the disease. While acute Lyme disease has finally become recognized by the medical community, Chronic Lyme, in which the Lyme symptoms persists after the normal course of antibiotics, is still controversial. Many doctors do not believe it exists.
Not only is Chronic Lyme real, Savely maintains, but it has a strong association with Morgellons. She discovered the connection while treating Chronic Lyme patients in her practice in Austin. She found that approximately 10 percent of her chronic Lyme patients had the fibers, lesions and skin-crawling sensations characteristic of Morgellons. As news of the Morgellons phenomenon spread over the Internet, she started hearing from more patients who came to her for Morgellons treatment. She says overall, about 95 percent of Morgellons patients she has treated are co-infected with Lyme disease.
Savely postulates that Lyme may weaken the immune system, making patients more vulnerable to whatever pathogen causes Morgellons, but she admits she does not know what that pathogen is.
And this is what really upsets many in the mainstream medical community. They criticize her for prescribing heavy doses of a variety of medications for extended periods, outside the normal medical guidelines, when she doesn't even know what she is attacking or which of her treatments will work.
"I've been told that I'm just randomly giving these different treatments to the patients without knowing what the pathogen is and that's really irresponsible. But I think what's irresponsible is ignoring suffering people and not treating them at all," Savely said, and the crowd erupted into applause.
And treat she does. She first works to heal any co-infections such as Lyme disease, and then prescribes simultaneous heavy doses of antibiotics, de-wormers, anti-fungals and various topical creams, trying various medications on a patient until she finds the ones that work, sometimes treating patients with these medications for years at a time.
"Every patient is unique. The more I treat this illness the stupider I get," she said, explaining how she will often find a treatment that works well for a time and then just stops working, and that what works well for one patient, won't necessarily work for another.
Savely doesn't know why the de-wormers are effective, since there are no "worms" found in Morgellons patients but suspects that they are in someway toxic to the pathogen. When she prescribes them, she says patients experience an immediate worsening of lesions and of the crawling, biting and stinging sensations, which she attributes to a "mass-exodus" of the fibers out of the skin. "I do warn patients, you're going to get worse before you get better. That's to be expected, and the majority do get worse before they get better."
But she says most patients do get better, although not all become completely symptom free. One of Savely's success stories stood up, a woman who Savely said was at one time totally debilitated by the condition but has now been symptom-free for three years.
Despite the success stories, some in the medical community feel Savely's treatments are dangerous. She was forced to leave the state of Texas when the medical board put pressure on her sponsoring physician and she could find no other Austin physician to work with. She now practices in San Francisco, California where the laws governing medical treatment are more liberal.
She says she carefully monitors her patients' liver function and blood count over the course of treatment and has seen only on very rare occasions, very minor adverse affects such as a small elevation in liver function, which she says she easily reverses by reducing the medication. "It sounds scary to the pharmacist and they will try to scare you, but I just haven't seen the problems, and people tolerate them (medications) very well," she said.
Although Savely is willing to treat the disease now, everyone agrees that finding the cause of the disease is necessary to find the most effective treatment. The Center for Disease Control (CDC) is currently investigating Morgellons but they have not published any findings.
But other researchers are also looking into the cause. One such researcher who spoke at the conference is Dr. Raphael Stricker, MD, a clinician who, like Savely, treats Chronic Lyme and Morgellons patients in California. Morgellons skeptics dismiss Stricker's research because he was fired from the University of California in 1990 for allegedly suppressing data in a 1985 research paper on AIDS that would have contradicted his hypothesis. But Stricker has consistently denied the charges and Lyme and Morgellons message boards abound with patients posting messages in his defense.
Stricker presented research he conducted along with Savely and Vitaly Citovsky, Ph.D of the State University of New York at Stony Brook, in which they tested lesions from seven Morgellons patients as well as biopsied skin samples from a healthy control population. They found agrobacterium in all seven Morgellons patients and none was found in the control group.
Agrobacterium is a bacteria that infects plants, causing Crown Gall disease in trees, and it is the only known organism to engage in lateral gene transfer among kingdoms, transferring genes from the plant kingdom to the animal kingdom. The bacterium produces copious amounts of cellulose fibers, and Stricker and others have found the fibers found in Morgellons patients to also be made of cellulose, a plant material.
Skeptics point out that cotton is also made of cellulose fibers. But Forensic scientist Ron Pogue of the Tulsa Police Crime Lab in Oklahoma told ABC News that he checked a sample of Morgellons against every known fiber in the FBI database and found no match. The lab's director, Mark Boese, told ABC that the fibers are "consistent with something that the body may be producing." He added, "These fibers cannot be manmade and do not come from a plant. This could be a byproduct of a biological organism."
Stricker has a theory, but acknowledges a lot of research needs to be conducted to see if his theory is correct. He speculates that agrobacterium, which is found in the soil and also in a high percentage of ticks, is the cause of Morgellons, and that the reason many are co-infected with Lyme is that they may contract Morgellons from the same tick that gave them the Lyme disease.
Furthermore, he notes a very curious finding. Telomerase is an enzyme that ads more DNA to the end of a chromosome after cell division. "Every cell and species has telomerase," said Stricker. "There have been comparative studies of telomerase in different organisms and it's been shown that the telomerase in Lyme and agrobacterium are exactly the same."
He continued, "This is a peculiar coincidence because telomerases are usually completely different among different species and types of bacteria. This suggests when there is co-infection with Borrelia, which causes Lyme disease, and with agrobacterium, the two bacteria can actually help each other by adding pieces of DNA to each other's chromosomes and this could cause variation in both bacteria, that could then lead to changes in what the bacteria are doing in the human body. It's a very interesting possibility that also needs to be examined in further detail."
He added, "My speculation, and it still is speculation, is that Morgellons Disease may represent the first known human illness caused by a plant bacterium. And in fact, when people say they have these fibers attached to the skin that don't come out, that are very adherent, in a way they are kind of turning into plants."
He also noted that his research has found some fibers to have a metallic coating, which could explain why many people have witnessed these fibers moving. He said the metal could become charged with electricity, causing the fibers to move.
"The movement is real," said Casey. "Most everyone you can talk to has seen these things move. It's almost alien. It's like your worst science fiction movie. A lot of us will get together and you can put them on the end of a tweezers and see them moving around almost, like a cobra dance."
But getting together, even if it is just to commiserate about the movement in the fibers, is something that seems to help these patients. Savely said, that in addition to light exercise, nutrition, and her treatment regimen, she urges her patients to seek out human contact.
Because some are afraid Morgellons could be contagious, (there is no evidence to show it is contagious under casual contact) and other are ashamed of their disfiguring lesions, like modern day lepers, many sufferers isolate themselves.
"I think human touch is so important, said Savely. "You can't go with out it. I've had patients come up to me and I give them a hug and they start to cry and they say, 'That's the first time I've touched a human being in five years.' How can you live like that? You know you can't. You can't isolate yourself. You need to be around your family now more than ever."
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Post by skyship on Jan 7, 2010 1:17:46 GMT -5
Conjugation In order to be virulent, the bacterium must contain a tumour-inducing plasmid (Ti plasmid or pTi), of 180 kb, which contains the T-DNA and all the genes necessary to transfer it to the plant cell. Many strains of A. tumefaciens do not contain a pTi. Since the Ti plasmid is essential to cause disease, pre-penetration events in the rhizosphere occur to promote bacterial conjugation - exchange of plasmids amongst bacteria. In the presence of opines, A. tumefaciens produces a diffusible conjugation signal called 30C8HSL or the Agrobacterium autoinducer. This activates the transcription factor TraR, positively regulating the transcription of genes required for conjugation. en.wikipedia.org/wiki/Agrobacterium_tumefaciens=================== we have to prove that teleomeres can be changed and this is done by mitochondria from like organisms mimicking our mitochondria so to integrate, recognizing mitochondria and the teleomeres. lenthening or shorting the 5' end or the short end 3'. so if the same teleomeres in agro are associated with the teleomere damage in lymes d. we have a beginning. the same or beginning CISgenesis. done in plants, same in humans, with the tool used is tRNA from tumour inducing plasmid. In other words senesence, or old age is increased by the replication of this package over and over on the short end. To make someone immortal, you lengthen it. It is genetic specific, where epigenetics comes in because it is SELECTIVE, give some diseases, others immortal life. This morgellons not taking means we are aging faster, while these idiots are extending their lives, in many these are not integrating, but, we have something they do not have. we have primitive genes, we have something that these scientists will never understand, and that is survival mode, it is ingrained in us. We suffer, but yet we know, we have something that cannot be altered. We refuse to sell our souls! Period! Yet, we are caught between life and half life, the radiation we have may sustain us. Like Dr. Staninger says, it is radiant heat from the sun, that will cure us. Not the simulated sunlight we are getting from aerosol operations and chemical illuminent strategy, will explain that later. I propose that aerosol operations carry this teleomere change, through buckyballs, yet to be understood. But, first we must find the beginning change, the blood change has been looked at since early 1900s. when it was labeled a or b or o or rh. That could have been the first with the cd146, muc 18, mel-cam, but the ligand cannot be found, however, I think the ligand relates to fullerenes. the next or previous one goes back to 1974, at conference held to begin the altering of genes. NIH, USDA, FDA, EPA, all involved, DOE began its genomes 2 life program constructing novel or chimeric microbes to clean up water, water tanks, etc. these created chemical/radiative constructions. but, the NIH and their group allowed this to go on with very little if any regulations. Food became the bioweapon, aerosol operations the metallic simulated particles to provide simulated sunlight, or uv radiation, is between radiant from sun and ultraviolet produced by aerosol operational materials used. Dimers were formed from this UV radiation, the contrived global warming scheme, and from that the homodimers and heterodimers, and more formed. that is next stage. ====================== But, to stick with biological, first, one sees that the food was changed, beginning with e-coli and yeast, in corn. That seems to be where the mobile genetic element comes in. The first thing I noticed when I caught on to the agenda, was the change in the telomeres. the tRNA was tool used, for all transposon, in human, in mammal, in plant. etc. The gall, is infectious, the use of viral particle in roots, if you destroy the roots, you destroy the plant, but the viral package was not used to destroy the root, just to alter the plant genes. This is different than hybridizing in same species. However, how is the viral package forming the gall, disposed of? it continues to replicate. inside the cells, takes on different form. make sense? So, what was this beginning stage, changing the telomeres? Involved folding and unfolding in our DNA from the tRNA in the food. ================== In order to be virulent, the bacterium must contain a tumour-inducing plasmid (Ti plasmid or pTi), of 180 kb, which contains the T-DNA and all the genes necessary to transfer it to the plant cell. so the ti plasmid of pTi contains the T-DNA, lets dig..................... will start with the Sunflower, next post. skyship
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Post by skyship on Jan 7, 2010 2:21:42 GMT -5
T-DNA of pTi-15955 from Agrobacterium tumefaciens is transcribed into a minimum of seven polyadenylated RNAs in a sunflower crown gall tumor. Abstract Northern blot hybridization analysis of polysomal polyadenylated RNA isolated from sunflower crown gall tumor PSCG-15955 demonstrated that a minimum of seven RNAs were transcribed from T-DNA of pTi-15955 from Agrobacterium tumefaciens. The sizes of the T-DNA transcripts were 1.8, 1.6, 1.5, 1.1, 1.0 kilo bases (kb) and two transcripts of 0.8 kb long. The relative abundance of these polyadenylated RNAs varied greatly, the 1.0 kb RNA being the most abundant and the 1.6 kb RNA being the least abundant. Assignment of map locations of the seven polyadenylated RNAs indicated that the conserved region of T-DNA which may play a central role in tumorigenesis contained four RNAs of 1.8, 1.1, 0.8(a) and a portion of 0.8(b) kb long. www.ncbi.nlm.nih.gov/pmc/articles/PMC320558/============================ In humans called TNF tumor necrosis factor. =================================== we have a number. pTi-15955 from ago tume. what are the 7 polyadenylated RNAs in the gall tumor? pTi-15955 not getting anywhere with the number but this may help: This describes the proteins scroll down till you see the large fiber on left. keyhani.ifas.ufl.edu/Agrobacterium.pdf================================= ================================== insertion found in agro descriptions: ====================== . tumefaciens causes crown-gall disease in plants. The disease is characterised by a tumour-like growth or gall on the infected plant, often at the junction between the root and the shoot. Tumors are incited by the conjugative transfer of a DNA segment (T-DNA) from the bacterial tumour-inducing (Ti) plasmid. The closely related species, A. rhizogenes, induces root tumors, and carries the distinct Ri (root-inducing) plasmid. Although the taxonomy of Agrobacterium is currently under revision it can be generalised that 3 biovars exist within the genus, A. tumefaciens or biovar 1, A. rhizogenes or biovar 2, and A. vitis or biovar 3. Strains within biovars 1 and 2 are known to be able to harbour either a Ti or Ri-plasmid, whilst strains of biovar 3, generally restricted to grapevines, can harbour a Ti-plasmid. Non-Agrobacterium strains have been isolated from environmental samples which harbour a Ri-plasmid whilst laboratory studies have shown that non-Agrobacterium strains can also harbour a Ti-plasmid. Many environmental strains of Agrobacterium do not possess either a Ti or Ri-plasmid. These strains are avirulent. The plasmid T-DNA is integrated semi-randomly into the genome of the host cell (Francis and Spiker, 2005. Plant Journal. 41(3): 464.), and the virulence (vir) genes on the T-DNA are expressed, causing the formation of a gall. The T-DNA carries genes for the biosynthetic enzymes for the production of unusual amino acids, typically octopine or nopaline. It also carries genes for the biosynthesis of the plant hormones, auxin and cytokinins. By altering the hormone balance in the plant cell, the division of those cells cannot be controlled by the plant, and tumors form. The ratio of auxin to cytokinin produced by the tumor genes determines the morphology of the tumor (root-like, disorganized or shoot-like). " Agrobacterium in humans Although generally seen as an infection in plants, Agrobacterium can be responsible for opportunistic infections in humans with weakened immune systems,[1][2] but has not been shown to be a primary pathogen in otherwise healthy individuals. A 2000 study published by the National Academy of Sciences suggested that Agrobacterium attaches to and genetically transforms several types of human cells by integrating its T-DNA into the human cell genome. The study was conducted under laboratory conditions and states that it does not draw any conclusions regarding related biological activity in nature.[3] There is a conjectured connection with Morgellons syndrome. Dr. Stricker, along with Dr. Citovsky, MRF board member from the State University of New York at Stony Brook and an expert on plant pathogens, reported in January, 2007, that Morgellons skin fibers appear to contain cellulose. Five skin samples of Morgellons patients contained evidence of DNA from Agrobacterium.[4]" www.answers.com/topic/agrobacterium-1=========================== Agrobacterium radiobacter: a recently recognized opportunistic pathogen. Edmond MB, Riddler SA, Baxter CM, Wicklund BM, Pasculle AW. Division of Infectious Diseases, University of Pittsburgh School of Medicine, Presbyterian University Hospital, Pennsylvania. Over the past decade, an increasing number of infections due to Agrobacterium radiobacter have been reported. Observation of three cases of bacteremia due to this organism prompted a review of the English-language literature. Nineteen cases of significant disease have previously been reported. In more than one-half of the cases, bacteremia was the primary manifestation, often associated with the presence of an intravascular catheter. Other clinical syndromes (peritonitis, urinary tract infection, and endocarditis) have been described. Infection is strongly related to the presence of plastic foreign material, and effective treatment often requires removal of the device. Because antimicrobial sensitivity is variable, treatment must be based on sensitivity data for the individual isolate. tinyurl.com/ycncvgrwww.ncbi.nlm.nih.gov/pubmed/8452950?ordinalpos=1&itool=EntrezSystem2.PEntrez. Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl. Pubmed_Discovery_RA&linkpos=2&log$=relatedreviews&logdbfrom=pubmed ============================ Since the Ti plasmid is essential to cause disease, pre-penetration events in the rhizosphere occur to promote bacterial conjugation - exchange of plasmids amongst bacteria. In the presence of opines, A. tumefaciens produces a diffusible conjugation signal called 30C8HSL or the Agrobacterium autoinducer. This activates the transcription factor TraR, positively regulating the transcription of genes required for conjugation. opines Chemical structure Chemically, opines fall into two major structural classes: 1. The vast majority are secondary amine derivatives formed by condensation of an amino acid, either with a keto acid or a sugar. The first subcategory includes the nopaline and octopine families. The nopaline family (nopaline, nopalinic acid, leucinopine, glutaminopine, succinamopine) is formed when alpha-ketoglutarate serves as the keto substrate in the condensation reaction. The octopine family (octopine, octopinic acid, lysopine, histopine) is formed when pyruvate is involved in the condensation reaction. The second subcategory includes the mannityl family (mannopine, mannopinic acid, agropine, agropinic acid) formed by the condensation of an amino-acid with mannose. 2. Agrocinopines form a small, separate class of opines. Chemically they are sugar-phosphodiesters. For example, agrocinopine A is a phosphodiester of sucrose and L-arabinose. [edit] Nomenclature The name opine comes from octopine, the first opine discovered in 1927, not in crown galls, but in octopus muscle. According to Oxford English Dictionary, the word opine was first used in print in 1977. Usually, the name of newly discovered opines has the ending "-opine". Exceptions are nopaline and strombine. On the other hand, not all molecule names ending in "-opine" are opines. For example, atropine, stylopine, europine, and lycopine belong to different classes of molecules. en.wikipedia.org/wiki/Opinescontinue...........next post......... skyship
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Post by skyship on Jan 7, 2010 3:17:57 GMT -5
It is hard to follow the science, because it is misleading, but here is how telomerase works. notice the short end and the replication on long end. faculty.plattsburgh.edu/donald.slish/Telomerase.htmlbut, I will keep at it, somewhere we will find the info that created this change in us. I believe the acetosyringone is involved as are the chvA, chvB, and pscA, Ti and Ri plasmids. acetosyringone: this seems to have been made up, so aconym covering for what it really is. will look at the chvA: ================ "Brucella, Agrobacterium, and Rhizobium belong, according to 16S rRNA sequences, to the -2 subgroup of the Proteobacteria (28). Complete-genome sequencing reveals similarities in transport, metabolic capabilities, and genome structure with these soil- and plant-associated bacteria. Extensive gene synteny between chromosome 1 and the genome of the plant symbiont Mesorhizobium loti emphasizes the similarity between this animal pathogen with plant pathogens and symbionts. A limited repertoire of genes homologous to known bacterial virulence factors were identified (13, 31, 44). Several studies revealed common themes between animal and plant pathogens and endosymbionts. For example the Brucella two-component regulatory system BvrS-BvrR (39) is highly similar to the twocomponent regulatory systems ChvG-ChvI of Agrobacterium tumefaciens (9) and ExoS-ChvI of Sinorhizobium meliloti (10). These two-component regulatory systems are equivalent to the Salmonella PhoP-PhoQ (40) and the Bordetella bronchiseptica BvgA-BvgS systems (42). iai.asm.org/cgi/reprint/72/4/2263.pdfbordetella, brucella related to Lymes? skyship this tells me that the virus stays in the plant>?
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Post by skyship on Jan 7, 2010 5:03:04 GMT -5
CITOVSKY KNOWS ALL ABOUT AGROBACTERIUM, HE HELPED WRITE THIS ARTICLE, FOLKS. Odyssey of Agrobacterium T-DNA."Most recently, transfer of DNA from Agrobacterium to human cells has been documented (Kunik et al., 2001), indicating that although the T-DNA odyssey always starts from and ends at the same point (the Agrobacterium cell) it may reach on its way different targets (bacterial, yeast, plant or human cells). Vol. 48 Agrobacterium T-DNA 631" www.actabp.pl/pdf/3_2001/623-635.pdfskyship
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Post by lilsissy on Jan 7, 2010 6:39:09 GMT -5
we have to prove that teleomeres can be changed and this is done by mitochondria from like organisms mimicking our mitochondria so to integrate, recognizing mitochondria and the teleomeres.
Thank you for that Sky,
the mitochondria always jumped out at me , I always felt that was played with but could not connect it . Also feel that Neuron type cells have been reconstructed and expressed throughout the myofasuclar. Wonder also if sperm cells were mutated for locomotion or actin , myosin motors.
Do you believe thy changed our telemers with AGRO or Brucella type?
The first I heard of telemers was about 1990 when they said they could use them for eternal life but we would develop cancer as it allows cancerous cells to continue too.. So when they answered the cancer problem they could then extend life.
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Post by lilsissy on Jan 7, 2010 6:51:25 GMT -5
AGRO,,from your link
Infection is strongly related to the presence of plastic foreign material,
PEDOT?
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Post by skyship on Jan 7, 2010 10:29:05 GMT -5
I got the whole of it. Lets see Pedot, first. PEDOT: "In one study [3] PEDOT nanofibers are produced from vanadium pentoxide nanofibers by a nanofiber seeding method. In this procedure EDOT is dissolved in an aqueous solution of camphorsulfonic acid (CSA) and a vanadium pentoxide nanofiber sol-gel and radical cationic polymerization is initiated by addition of ammonium persulfate. The resulting polymer precipitates from solution and has a general composition (PEDOT)(CSA)0.11-(HSO4)0.12(Cl)0.11(H2O)0.19. Washing with dilute hydrochloric acid removes the vanadium compound. The presence of the vanadium pentoxide seeds make the difference between the formation of PEDOT nanofibers (100 to 180 nanometer diameter and one to several micrometres long) and the formation of a more conventional granular morphology. When applied to a solid substrate such as PET, PEDOT non-woven films have slightly less optically transparency and about half the conductance of commercial PEDOT:PSS / PET films." en.wikipedia.org/wiki/Poly(3,4-ethylenedioxythiophene) Nanofiber seeding Nanofiber Seeding is the process to control the bulk morphology of chemically synthesized electronic organic polymers. Description A new synthetic approach, called nanofiber seeding,[1] was developed to control the bulk morphology of chemically synthesized electronic organic polymers. Bulk quantities of nanofibers of conducting polymers such as polyaniline, can be synthesized in one step without the need for any template. Conventional synthesis yields polyaniline having granular morphology. However, if the conventional reaction is seeded by 2-4 mg (seed quantities) of added nanofibers, the bulk morphology changes dramatically from granular to nano-fibrillar. When the reaction is seeded by vanadium pentoxide nanofibers, this method can be extended to all major classes of conducting polymers, including polypyrrole, PEDOT and polythiophene etc.[2][3] en.wikipedia.org/wiki/Nanofiber_seedingvanadium pentoxide nanofibers. HERE is the vanadium........ cyclic polymers: www.scribd.com/doc/13251806/Cyclic-Polymers-Semlyen-JA-Kluwer-2002================================== The Human Cell as an Environment for Horizontal Gene Transfer ir.canterbury.ac.nz/bitstream/10092/1374/1/thesis_fulltext.pdfvery long, wading through. skyship
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Post by aqt on Jan 7, 2010 17:41:10 GMT -5
Abstract Background: Telomerase is a ribonucleoprotein that copies a short RNA template into telomeric DNA, maintaining eukaryotic chromosome ends and preventing replicative senescence. Telomeres differentiate chromosome ends from DNA double-stranded breaks. Nevertheless, the DNA damage-responsive ATM kinases Tel1p and Mec1p are required for normal telomere maintenance in Saccharomyces cerevisiae. We tested whether the ATM kinases are required for telomerase enzyme activity or whether it is their action on the telomere that allows telomeric DNA synthesis.Results: Cells lacking Tel1p and Mec1p had wild-type levels of telomerase activity in vitro. Furthermore, altering telomere structure in three different ways showed that telomerase can function in ATM kinase-deleted cells: tel1 mec1 cells senesced more slowly than tel1 mec1 cells that also lacked TLC1, which encodes telomerase RNA, suggesting that tel1 mec1 cells have residual telomerase function; deleting the telomere-associated proteins Rif1p and Rif2p in tel1 mec1 cells prevented senescence; we isolated a point mutation in the telomerase RNA template domain (tlc1-476A) that altered telomeric DNA sequences, causing uncontrolled telomeric DNA elongation and increasing single strandedness. In tel1 mec1 cells, tlc1-476A telomerase was also capable of uncontrolled synthesis, but only after telomeres had shortened for >30 generations.Conclusion: Our results show that, without Tel1p and Mec1p, telomerase is still active and can act in vivo when the telomere structure is disrupted by various means. Hence, a primary function of the ATM-family kinases in telomere maintenance is to act on the substrate of telomerase, the telomere, rather than to activate the enzymatic activity of telomerase. www.cell.com/current-biology/abstract/S0960-9822(01)00391-8
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Post by aqt on Jan 7, 2010 17:44:09 GMT -5
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Post by aqt on Jan 7, 2010 17:48:56 GMT -5
The role of DNA damage response proteins at telomeres—an “integrative” model tiny.cc/637wOAbstract Telomeres are specialized structures at chromosome ends which play the key role in chromosomal end protection. There is increasing evidence that many DNA damage response proteins are involved in telomere maintenance. For example, cells defective in DNA double strand break repair proteins including Ku, DNA-PKcs, RAD51D and the MRN (MRE11/RAD51/NBS1) complex show loss of telomere capping function. Similarly, mouse and human cells defective in ataxia telangiectasia mutated (ATM) have defective telomeres. A total of 14 mammalian DNA damage response proteins have, so far, been implicated in telomere maintenance. Recent studies indicate that three more proteins, namely BRCA1, hRad9 and PARP1 are involved in telomere maintenance. The involvement of a wide range of DNA damage response proteins at telomeres raises an important question: do telomere maintenance mechanisms constitute an integral part of DNA damage response machinery? A model termed the “integrative” model is proposed here to argue in favour of telomere maintenance being an integral part of DNA damage response. The “integrative” model is supported by the observation that a telomeric protein, TRF2, is not confined to its local telomeric environment but it migrates to the sites of DNA breakage following exposure of cells to ionizing radiation. Furthermore, even if telomeres are maintained in a non-canonical way, as in the case of Drosophila, DNA damage response proteins are still involved in telomere maintenance suggesting integration of telomere maintenance mechanisms into the DNA damage response network. drosophelia....diptera....the fly
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Post by aqt on Jan 7, 2010 17:50:35 GMT -5
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Post by aqt on Jan 7, 2010 17:57:14 GMT -5
A protein called Ku is essential for NHEJ. Ku is a heterodimer of the subunits Ku70 and Ku80. In the 9 August 2001 issue of Nature, Walker, J. R., et al, report the three-dimensional structure of Ku attached to DNA. Their structure shows beautifully how the protein aligns the broken ends of DNA for rejoining. users.rcn.com/jkimball.ma.ultranet/BiologyPages/D/DNArepair.html
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Post by skyship on Jan 7, 2010 23:08:49 GMT -5
Oh my gosh, aqt,
this is from one of the models: arabidopsis thaliana This means that a gene from this plant is is used at ends of teleomeres to repair the double strand breaks, but is homologous to to the unit KU70 and Ku80, but the KU is a heterodimer, a subunit of the units.
====================== Identification of Ku70 and Ku80 homologues in Arabidopsis thaliana; evidence for a role in the repair of DNA double-strand breaksn higher organisms such as mammals and plants, DNA double-strand breaks (DSBs) are repaired preferentially by non-homologous end joining (NHEJ) rather than by homologous recombination. The NHEJ pathway is mediated by Ku, a heterodimer of ≈70 and 80kDa subunits, which contributes to various aspects of the metabolism of DNA ends in eukaryotic cells. On the basis of their preicted sequence similarity to human Ku70 and Ku80, cDNAs encoding the first plant homologues of these proteins (AtKu70 andAtKu80, respectively) have now been isolated from Arabidopsis thaliana. AtKu70 and AtKu80 share 28.6 and 22.5% amino acid sequence identity with human Ku70 and Ku80, respectively. Yeast two-hybrid analysis demonstrated that AtKu70 and AtKu80 form a heterodimer, and electrophoretic mobility-shift assays revealed that this heterodimer binds to double-stranded telomeric and non-telomeric DNA sequences, but not to single-stranded DNA. The AtKu heterodimer also possesses single-stranded DNA-dependentATPase and ATP-dependent DNA helicase activities. Reverse transcription and the polymerase chain reaction revealed that AtKu70 and AtKu80 genes are expressed widely but at low levels in plant tissues. The expression of these two genes in cultured cells was markedly increased in response to the generation of DSBs by bleomycin or methylmethane sulfonate. These results suggest that the evolutionarily conserved Ku70-Ku80 heterodimer functions in DSB repair by the NHEJ pathway in A. thaliana. d.wanfangdata.com.cn/NSTLQK_NSTL_QK5652440.aspx========================== Arabidopsis thaliana (A-ra-bi-dóp-sis tha-li-á-na; thale cress, mouse-ear cress or Arabidopsis), is a small flowering plant native to Europe, Asia, and northwestern Africa.[1] A spring annual with a relatively short life cycle, Arabidopsis is popular as a model organism in plant biology and genetics. Its genome is one of the smallest plant genomes[2] and was t he first plant genome to be sequenced. Arabidopsis is a popular tool for understanding the molecular biology of many plant traits, including flower development and light sensing......" Leaves are covered with small unicellular hairs (called trichomes). The flowers are 3 mm in diameter, arranged in a corymb; their structure is that of the typical Brassicaceae. The fruit is a siliqua 5–20 mm long, containing 20–30 seeds.[3][4][5][6] Roots are simple in structure, with a single primary root that grows vertically downwards, later producing smaller lateral roots. These roots form interactions with rhizosphere bacteria such as Bacillus megaterium.[7]Arabidopsis can complete its entire life cycle in six weeks. The central stem that produces flowers grows after about three weeks, and the flowers naturally self-pollinate. In the lab Arabidopsis may be grown in petri plates or pots, under fluorescent lights or in a greenhouse.[8]" en.wikipedia.org/wiki/Arabidopsis_thaliana============ mmmm might be interesting to grow some and compare to our fibers? =============== What is this Ku protein? Eukaryotic Ku is a heterodimer of two polypeptides, Ku70 (XRCC6) and Ku80 (XRCC5), so named because the molecular weight of the human Ku proteins is around 70 kDa and 80 kDa. The two Ku subunits form a basket-shaped structure that threads onto the DNA end.[1] Once bound, Ku can slide down the DNA strand, allowing more Ku molecules to thread onto the end. In higher eukaryotes, Ku forms a complex with the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to form the full DNA-dependent protein kinase, DNA-PK.[3] Ku is thought to function as a molecular scaffold to which other proteins involved in NHEJ can bind. Both subunits of Ku have been experimentally knocked out in mice. These mice exhibit chromosomal instability, indicating that NHEJ is important for genome maintenance.[4][5] In many organisms, Ku has additional functions at telomeres in addition to its role in DNA repair." note image: looks like DNA is cornered! en.wikipedia.org/wiki/Ku_(protein)Now, how is this done, if it doesn't adhere to plants? I know the a. thaliana has been used as a tool in gmo crop modification, but, how else does it do this for us? Making us part of earths dna, symbiosis, all around! There must be another mechanism. to deliver it to us who need the ends of our telomeres fixed. mmmmmmmmm............ Why do we have double strand helix breaks? something is causing that! mmmmmmmmmm well, the picture is unfolding, somewhat. skyship
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Post by skyship on Jan 8, 2010 0:11:00 GMT -5
Answered my own question, what is causing the teleomere breaks. .....from your #10 post, aqt............ ionizing radiation. mmmmmmm ...."A model termed the “integrative” model is proposed here to argue in favour of telomere maintenance being an integral part of DNA damage response. The “integrative” model is supported by the observation that a telomeric protein, TRF2, is not confined to its local telomeric environment but it migrates to the sites of DNA breakage following exposure of cells to ionizing radiation." ================= Ionizing radiation such as that created by radioactive decay or in cosmic rays causes breaks in DNA strands. radioactive decay............ uranium? =============== cosmic rays............ tinyurl.com/y8jdxd4wonder where the aerosol operations fit in? skyship
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