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Post by kritters on Apr 7, 2011 7:43:42 GMT -5
I hate to put a kink in your left brained equations...
but I'm sure we're dealing with 'unknowns' which could affect and influence all the 'known's we are discussing. When you're dealing with chemistry and organisms, I've learned there ARE no definitive answers you can base on logic, because of their ability to morph and adapt. The chemistry changes constantly.
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Post by katinka on Apr 7, 2011 9:48:23 GMT -5
but I'm sure we're dealing with 'unknowns' which could affect and influence all the 'known's we are discussing. When you're dealing with chemistry and organisms, I've learned there ARE no definitive answers you can base on logic, because of their ability to morph and adapt. The chemistry changes constantly. I certainly agree. The problem is there are too many x (variables).... Hope you're feeling better today
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Post by kammy on Apr 7, 2011 12:41:42 GMT -5
This isn't MY theory... I'm just trying to help Kritts with HER theory. You see how drawing a flowchart to this monster is not easy then, if it were - I'd already done it. If you want a flowchart - I da' woman - just give the variables and I can plug them in. First of all, we've got to find what A is?... lol
If you think the cause (A) is B and C... then you run a test to see if B and C respond to what is known to act on them to equal A. It's very simple.
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Post by skyship on Apr 7, 2011 13:53:45 GMT -5
Lil sissy, HERE is proof. It walks into 1q 42 and 1q21. Chromosome breaks in the above 2. Specific chromosome 1 breaks induced by human cytomegalovirus Human cytomegalovirus (HCMV) is the major viral cause of birth defects and a serious problem for immunocompromised individu- als. Here we show that infection of cells with HCMV during the S-phase of the cell cycle results in two specific chromosome 1 breaks at positions 1q42 and 1q21. www.pnas.org/content/97/2/853.full.pdf==================== The old way of changing genes was using viruses, and they have used many. In this one there is the SV40 from polio. This somehow affects the pancreas. skyship
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Post by kritters on Apr 7, 2011 14:04:57 GMT -5
Hey Katink! Thanks, I'm on the mend, finally. Still weak and shakey, but I lost weight, so all is good I think personally (I'm the ambi-brained with more strength on the right) that having a tri-organism like CMV enables it to slide in and out of it's mask whenever it needs to do damage and/or avoid kingdom specific medications/supplements. What can kill fungus might not kill bacteria, etc. so all it has to do is put it's bacteria alter ego in charge. I certainly don't know anything about proteins, viruses etc. and their specifics with regard to what can or cannot work, but I'd think with this tri-organism would be the scariest kind of stealth entity one can have in the body. How could you kill it unless you'd take all three or at least two of the known meds together? I feel like I'm having a discussion somewhere in the twilight zone! What happened to the gool ol' days when you only had to worry about coming home at dinner time before it got dark!!! ;D ;D Kritts
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Post by skyship on Apr 7, 2011 14:18:09 GMT -5
lil sis and all, ..."adenoviruses, there is no evidence for specific site-directed breakage. In the case of adenovirus type 12, infection of human cells at low multiplicity induces specific fragility at four distinct loci (5, 6). The three most common sites, 17q21–22, 1p36, and 1q12–22, coincide with the major small nuclear RNA loci, while the fourth site at 1q42–43, which is only observed at a low frequency in infected primary human cells, lies adjacent to the 5S rRNA locus (5–10)." so the locus is 5S rRNA? "Most of the damage appears to be random, and with the exception of the oncogenic adenoviruses, there is no evidence for specific site-directed breakage. In the case of adenovirus type 12, infection of human cells at low multiplicity induces specific fragility at four distinct loci (5, 6). The three most common sites, 17q21–22, 1p36, and 1q12–22, coincide with the major small nuclear RNA loci, while the fourth site at 1q42–43, which is only observed at a low frequency in infected primary human cells, lies adjacent to the 5S rRNA locus (5–10). The above observations raise key questions regarding the role of virus-mediated mutagenesis in human disease. In this paper, we focus on HCMV, a herpesvirus that is the major viral cause of birth defects. Each year, approximately 1% of all newborns are congen- itally infected, and of these infants, 5–10%manifest signs of serious neurological defects at birth, which can include deafness, mental retardation, blindness, microcephaly, and cerebral calcification (11–14). In addition, 10–15% of infected infants who are asymp- tomatic at birth subsequently develop varying levels of sensorineu- ral hearing loss andyor learning disabilities.HCMV infection is also a major medical problem in immunocompromised individuals (11). In the past few years, it has become apparent that HCMV markedly dysregulates host cell functions and can inhibit cell cycle transit (15–18). Initial entry ofHCMVinto the cell leads to a second messenger-type response similar to that which occurs during reg- ulation by means of hormones and growth factors (19). The productive HCMV infection stimulates the expression of genes encoding several proteins involved in preparing the cell for DNA replication, thereby leading to a fully ‘‘activated’’ state in the permissive cell (20–24). Although HCMV induces elevated steady state levels of p53 (15, 25, 26), there does not appear to be signaling to its downstream damage response targets, p21 and MDM2 (refs. 17 and 27, and E.A.F., unpublished results). Whether this block in signaling is because of viral protein binding and inhibition (25, 28, 29) or sequestration of p53 (30), it suggests a mechanism by which HCMV may fully ‘‘activate’’ the infected cell and precipitate genotoxic effects without triggering cell death. A major breakthrough here people..........that tells us that they are looking at this......... or have been in past, but, hands tied as well............ So, when the sequencing of genome began, is that when the alterations of genes began as a "great work" so to speak, bringing in the artificial right at chromosome 1 and proceeding to chromosome 23? If the chromosome in histones 3 and 4 are altered with the synthetic then that is how through HCMV and other viruses the mutations took place, in the the cytoskeleton, which finds its way to the amino substitutions, and the dna itself. If chromosomes are altered, that is where the dna breaks to allow the third (trisomy) strand in. So, the whole seq was meant to alter genes? =============================== And they began at the beginning, Gene Number 1. REVIEW ESSAY: HUMAN GENE THERAPY AND THE LAW: AN INTRODUCTION TO THE LITERATURE SUMMER, 1990 39 Emory L.J. 855 Author Edward J. Larson * Excerpt Early in the movie The Wizard of Oz, Dorothy faces the daunting task of deciding where to begin her quest for the great Wizard whom she though could solve all problems. At this point the good witch Glinda matter-of-factly advises her, "It's always best to start at the beginning." This simple advice helps Dorothy by altering her question from "Where to begin?" to "What is the beginning?" Glinda's advice also applies to the question of where to begin an introduction to the literature of human gene therapy. This question is a daunting one because the quantity of such literature continually expands with the increasing number of legal scholars, biomedical ethicists, geneticists, theologians, political scientists, historians, and other commentators drawn to this topic. 1 They are drawn by the topic's apparent significance to our future, in that human gene therapy offers the potential of doing significant (and perhaps unprecedented) good or bad through restructuring the genetic make-up of human beings. tinyurl.com/3jo8ffeThe great work involves changing the genes, the alchemy connection. They have done this before. Skyship
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Post by kritters on Apr 7, 2011 14:19:30 GMT -5
The( Morgellons ?) 1q42 insert is put in a break in our code caused by Cytomegalovirus and ahhh gezz, pertussin toxin..a.k.a whopping cough which my son and grandchildren had last winter. Whopping cough made a come back here in Michigan. Cytomegalovirus is a D.N.A. code breaker. Lil Sissy and Sky, Sounds like an evil little sucker from the git-go. How does an organism know to break codes and screw up DNA? Is that something a geneticist would orchestrate, or does it happen naturally? All over my head, but watching with interest all input! Kritts
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Post by skyship on Apr 7, 2011 14:21:54 GMT -5
Cytoskeletal restructuring begins in chromosomes. But the helical double strand has to be broken, and new chromosome put in.
Is hybridized in with existing chromosomes, but, a dna break has to occur.
Viruses are the way in.
However, now they know it can be done by signal outside the cell.
The artificial hybridizes with the existing native dna.
That artificial was used in the Influenza A virion which includes up to 8 antisense, non coding, dna. meaning can be inserted into dna without changing the hereditary dna.
But, is done like through the back door, like computer viruses, through the back door!
Kammy, there you are. So much like computers aren't we?
Skyship
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Post by skyship on Apr 7, 2011 14:24:45 GMT -5
Kritts,
No, not over your head, you got it!
That was the initiation, the virus. And it replicates, so the original replicator was the CMV, because it could connect to the viral vaccine from SV40. Polio. So, this keep the viral component there. replicating when immune system is down.
So the first replicator would have been right at chromosome 1. 1950s,,,,,, onward.......
Skyship
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Post by skyship on Apr 7, 2011 14:27:02 GMT -5
It carried to dna, because it was infectious, not dna hereditary.
so infections are used to hybridize the artificial or synthetic in.
In fact some hybrid probes were used as probes then became part of the dna replication.
the probe itself became the hybridizer.
Skyship
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Post by skyship on Apr 7, 2011 14:33:14 GMT -5
The changes are at locus, or junctions. Those junctions are N terminal and C terminals. ============ The N-terminus (also known as the amino-terminus, NH2-terminus, N-terminal end or amine-terminus) refers to the start of a protein or polypeptide terminated by an amino acid with a free amine group (-NH2). en.wikipedia.org/wiki/N-terminus=================== C-terminal The C-terminus (also known as the carboxyl-terminus, carboxy-terminus, C-terminal tail, C-terminal end, or COOH-terminus) of a protein or polypeptide is the end of the amino acid chain terminated by a free carboxyl group (-COOH). When the protein is translated from messenger RNA, it is created from N-terminus to C-terminus. The convention for writing peptide sequences is to put the C-terminal end on the right and write the sequence from N- to C-terminus. en.wikipedia.org/wiki/C-terminusRewriting the code by viral replicators: As told in this novel? ? en.wikipedia.org/wiki/Invasive_Procedures_%28novel%29sounds about right, doesn't it? Skyship
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Post by skyship on Apr 7, 2011 14:41:21 GMT -5
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Post by skyship on Apr 7, 2011 14:42:39 GMT -5
Virus initiator, then molecular molecules, then synthetic or artificial.
Morgellons is a process, we were hit right from the beginning of the genome.
At chromosome 1.
Skyship
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Post by skyship on Apr 7, 2011 14:45:09 GMT -5
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Post by skyship on Apr 7, 2011 15:33:31 GMT -5
I do wonder if the pseudovesicles come in here with late infection of CMV. Many articles here on CMV. The Tegument Protein UL71 of Human Cytomegalovirus Is Involved in Late Envelopment and Affects Multivesicular Bodies [Structure and Assembly] Morphogenesis of human cytomegalovirus (HCMV) is still only partially understood. We have characterized the role of HCMV tegument protein pUL71 in viral replication and morphogenesis. By using a rabbit antibody raised against the C terminus of pUL71, we could detect the protein in infected cells, as well as in virions showing a molecular mass of approximately 48 kDa. The expression of pUL71, detected as early as 48 h postinfection, was not blocked by the antiviral drug foscarnet, indicating an early expression. The role of pUL71 during virus replication was investigated by construction and analysis of a UL71 stop mutant (TBstop71). The mutant could be reconstituted on noncomplementing cells proving that pUL71 is nonessential for virus replication in human fibroblasts. However, the inhibition of pUL71 expression resulted in a severe growth defect, as reflected by an up to 16-fold reduced extracellular virus yield after a high-multiplicity infection and a small-plaque phenotype. Ultrastructural analysis of cells infected with TBstop71 virus revealed an increased number of nonenveloped nucleocapsids in the cytoplasm, many of them at different stages of envelopment, indicating that final envelopment of nucleocapsids in the cytoplasm was affected. In addition, enlarged multivesicular bodies (MVBs) were found in close proximity to the viral assembly compartment, suggesting that pUL71 affects MVBs during virus infection. The observation of numerous TBstop71 virus particles attached to MVB membranes and budding processes into MVBs indicated that these membranes can be used for final envelopment of HCMV. Virus study gateway: flavors.me/viruspt#e8a/feedskyship
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Post by skyship on Apr 7, 2011 15:37:46 GMT -5
enlarged multivesicular bodies (MVBs) were found in close proximity to the viral assembly compartment, suggesting that pUL71 affects MVBs during virus infection. The observation of numerous TBstop71 virus particles attached to MVB membranes and budding processes into MVBs indicated that these membranes can be used for final envelopment of HCMV. flavors.me/viruspt#e8a/feedCytomegalovirus protein pUL71 works like a microscopic UPS Store tinyurl.com/3dowozgThese articles help explain the virulence of CMV or HCMV Skyship
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Post by kritters on Apr 7, 2011 17:03:03 GMT -5
Kritts, No, not over your head, you got it! That was the initiation, the virus. And it replicates, so the original replicator was the CMV, because it could connect to the viral vaccine from SV40. Polio. So, this keep the viral component there. replicating when immune system is down. So the first replicator would have been right at chromosome 1. 1950s,,,,,, onward....... Skyship Sky, are you saying I got CMV from my polio shot (born in 1948) and it has pre-disposed me to getting Morgellons? (I should just be quiet now before you realize just how clueless I really am! )
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Post by skyship on Apr 7, 2011 19:43:21 GMT -5
This is what most of us, including me, did not recognize, I born in 1951. No, the CMV localizes to it, we are the SV40 acceptor, the CMV has the Sv40 in it, so recognizes it in us. We had the original vaccines for polio. They were tainted. We got the original live virus, I am thinking, it sure fits. viewzone2.com/sv40x.html I hope this is not true. skyship
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Post by skyship on Apr 7, 2011 19:54:02 GMT -5
Origin of CMV
all of this in CMV "Cytomegalovirus (from the Greek cyto-, "cell", and -megalo-, "large") is a viral genus of the viral group known as Herpesviridae or herpesviruses. It is typically abbreviated as CMV: The species that infects humans it is commonly known as human CMV (HCMV) or human herpesvirus-5 (HHV-5), and is the best studied of all cytomegoloviruses. Within Herpesviridae, CMV belongs to the Betaherpesvirinae subfamily, which also includes the genera Muromegalovirus and Roseolovirus.[2] It is related to other herpesviruses within the subfamilies of Alphaherpesvirinae that includes herpes simplex viruses (HSV)-1 and -2 and varicella-zoster virus (VZV), and the Gammaherpesvirinae subfamily that includes Epstein-Barr virus.[1] All herpesviruses share a characteristic ability to remain latent within the body over long periods. Although they may be found throughout the body, CMV infections are frequently associated with the salivary glands in humans and other mammals.[2] Other CMV viruses are found in several mammal species, but species isolated from animals differ from HCMV in terms of genomic structure, and have not been reported to cause human disease." .."HCMV Main article: HCMV (human cytomegalovirus) Human cytomegalovirus is a species of virus the belongs to the viral family known as Herpesviridae or herpesviruses. It is typically abbreviated as HCMV and is alternatively known as human herpesvirus-5 (HHV-5).[1] Within Herpesviridae, HCMV belongs to the Betaherpesvirinae subfamily, which also includes cytomegaloviruses from other mammals.[2]"............. en.wikipedia.org/wiki/CytomegalovirusSo, the base of polio would accept any and all of this. It could take on some strange forms. And yes it is herpes related. image: tinyurl.com/3qmhe79skyship
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Post by skyship on Apr 7, 2011 19:59:48 GMT -5
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Post by skyship on Apr 7, 2011 20:06:48 GMT -5
seems this one may be related? Dermatitis repens (also known as "Acrodermatitis continua,"[1]:1026 "Acrodermatitis perstans," "Pustular acrodermatitis," "Acrodermatitis continua of Hallopeau," "Acrodermatitis continua suppurativa Hallopeau," "Hallopeau's acrodermatitis,",[1] "Hallopeau's acrodermatitis continua," and "Dermatitis repens Crocker") is a rare, sterile, pustular eruption of the fingers and toes that slowly extends proximally. en.wikipedia.org/wiki/Dermatitis_repens=================== Cutaneous conditions There are many conditions of or affecting the human integumentary system—the organ system that comprises the entire surface of the body and includes skin, hair, nails, and related muscle and glands.[1] History In 1572, Geronimo Mercuriali of Forlì, Italy, completed De morbis cutaneis (translated "On the diseases of the skin"). It is considered the first scientific work dedicated to dermatology. [edit] Epidemiology In World War I, over two million days of service are estimated to have been lost by reason of skin diseases alone.[2] en.wikipedia.org/wiki/Skin_lesion```````````````` skyship
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Post by skyship on Apr 7, 2011 20:11:53 GMT -5
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Post by skyship on Apr 7, 2011 20:16:47 GMT -5
quoted from previous link: "TBstop71 virus particles attached to MVB membranes and budding processes into MVBs indicated that these membranes can be used for final envelopment of HCMV." TBstop71 virus particles It seems this is considered an extracellular virus, floating in and around organs, etc. just like what attached to Karen's pancreas....Human Cytomegalovirus pUS27 G Protein-Coupled Receptor Homologue Is Required for Efficient Spread by the Extracellular Route but Not for Direct Cell-to-Cell Spread Received 22 November 2010/ Accepted 31 January 2011 Human cytomegalovirus (HCMV) encodes multiple G protein-coupled receptor (GPCR) homologues, including pUS27, pUS28, pUL33, and pUL78. To explore the function of pUS27, we constructed pUS27-deficient derivates of two clinical isolates of HCMV. BFX-GFPstopUS27 is a FIX variant with a single base pair change in the US27 open reading frame, generating a stop codon that ablates accumulation of the GPCR homologue, and TB40/E-mCherrydlUS27 lacks the entire US27 coding region. BFX-GFPstopUS27 generated 10-fold less extracellular progeny in fibroblasts, and TB40/E-mCherrydlUS27 exhibited a similar defect in endothelial cells. The pUS27-deficient FIX derivative produced normal quantities of viral DNA and viral proteins tested, and a late virion protein was appropriately localized to the cytoplasmic assembly zone. After infection at a low multiplicity with wild-type FIX virus, neutralizing antibody reduced the accumulation of intracellular viral DNA and intracellular virions, as would be expected if the virus is limited to direct cell-to-cell spread by neutralization of extracellular virus. In contrast, the antibody had little effect on the spread of the BFX-GFPstopUS27 virus. Further, after infection at a low multiplicity, the pUS27-deficient TB40/E virus exhibited a growth defect in endothelial cells, where the clinical isolate normally generates extracellular virus, but the TB40/E derivative exhibited little defect in epithelial cells, where the wild-type virus does not produce extracellular virus. Thus, mutants lacking pUS27 rely primarily on direct cell-to-cell spread, and we conclude that the viral GCPR homologue acts at a late stage of the HCMV replication cycle to support spread of virus by the extracellular route.jvi.asm.org/cgi/content/short/85/8/3700?rss=1So, this means is in fluid, serum, mucus, the flowing fluids.? extra cell u lar......... Extracellular? that means is in the plasma membranes. In cell biology, molecular biology and related fields, the word extracellular (or sometimes extracellular space) means "outside the cell". This space is usually taken to be outside the plasma membranes, and occupied by fluiden.wikipedia.org/wiki/Extracellularskyship
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Post by skyship on Apr 7, 2011 20:23:42 GMT -5
According to the Gene Ontology database the Extracellular Space is a Cellular Component defined as: "That part of a multicellular organism outside the cells proper, usually taken to be outside the plasma membranes, and occupied by fluid. Note that for multicellular organisms, the extracellular space refers to everything outside a cell, but still within the organism (excluding the extracellular matrix). Gene products from a multi-cellular organism are secreted from a cell into the interstitial fluid or blood can therefore be annotated to this term".[1]The composition of the extracellular space includes metabolites, ions, various proteins and non-protein substances (i.e. DNA, RNA, lipids, microbial products etc) that might affect cellular function. For example, hormones, growth factors, cytokines and chemokines act by travelling the extracellular space towards biochemical receptors on cells. Other proteins that are active outside the cell are various enzymes, including digestive enzymes (Trypsin, Pepsin), extracellular proteinases (Matrix metalloproteinases, ADAMTSs, Cathepsins) and antioxidant enzymes (e xtracellular superoxide dismutase). Often, proteins present in the extracellular space are stored outside the cells by attaching to various Extracellular matrix components (Collagens, Proteoglycans, etc).[2] In addition, Extracellular matrix proteolytic products are also present in the extracellular space, especially in tissues undergoing remodelling [2]. The term 'extracellular' is often used in reference to the extracellular fluid (ECF) compartment which composes about 15 litres of an average adult 70 kg human body which is assumed to contain a total of about 50 litres of water (thus, about 30% of the body's water is in the ECF compartment). en.wikipedia.org/wiki/Extracellulargene products for multicellular organism
One we may not have thought ofl between prokaryotes and eukaryotes and could live in the extracellular spaces.
==================== Giardia: A Missing Link between Prokaryotes and Eukaryotes janus.ucc.nau.edu/gaud/bio372/class/readings/giard.htm========================= a proposed secondary structure?
Did some one say"woods hole" at one time?janus.ucc.nau.edu/gaud/bio372/images/giard9.jpg========================== Long before multicellular organisms appeared on Earth, unicellular organisms had developed mechanisms for responding to physical and chemical changes in their environment. These almost certainly included mechanisms for response to the presence of other cells. Evidence comes from studies of present-day unicellular organisms such as bacteria and yeasts. Although these cells largely lead independent lives, they can communicate and influence one another’s behavior. Many bacteria, for example, respond to chemical signals that are secreted by their neighbors and increase in concentration with increasing population density. This process, called quorum sensing, allows bacteria to coordinate their behavior, including their motility, antibiotic production, spore formation, and sexual conjugation.www.garlandscience.com/textbooks/0815341059/pdfs/ch15.pdfSo whatever extracellullar multicellular organism that was created, is what is in our plasma, or fluids, or extra cellular matrix. skyship
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Post by skyship on Apr 7, 2011 20:48:36 GMT -5
It seems CMV was way into cell, causes the dna breaks, and then this multicellular organism moved in. or the multicellular organism signals to the CMV? over and over I have seen issues with Cytosol here it shows cytosol in the plasma membrane? This covers a lot, but, the signals outside cell plasma, signals inside cell plasma and cell. Very long chapter, but, has a lot in it. Mechanisms of Cell Communication www.garlandscience.com/textbooks/0815341059/pdfs/ch15.pdfskyship
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Post by lilsissy on Apr 8, 2011 0:59:26 GMT -5
I hate to put a kink in your left brained equations... but I'm sure we're dealing with 'unknowns' which could affect and influence all the 'known's we are discussing. When you're dealing with chemistry and organisms, I've learned there ARE no definitive answers you can base on logic, because of their ability to morph and adapt. The chemistry changes constantly. I have just been learning that as well!
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Post by lilsissy on Apr 8, 2011 1:23:13 GMT -5
I have some catching up to do here but lil at a time
Sky said
If chromosomes are altered, that is where the DNA breaks to allow the third (trisomy) strand in.
Exactly my view but some breakpoints are called historic breakpoints or A.K.A. ....historic gaps I took it to mean commonly occur or are known often to occur at ( something like 8 frequent points in out whole genome) at the same locations frequently but especially in those ofcertain races, 1q42 was near the top of the list. So if we have a gap point it allows for another gene to fit in...Trisomy... Is it that Cytomeglovirus fits in their neatly? Or is it that Cytomeglovirusis what broke that area historically? Not sure..need to look into that.
Antonietta Gatti from Lifeboat and W.H.O. had done much of the pioneer research into D.U.and nano infections along with pics showing inserts in the code. She had some great science pages illustrating this. She also has great stuff on bio-nano-warfare.
Small matter slipping right in along with graphs analyzing what the inserts where made of all nano level.
I recommend reading her material, very enlightening.
You can also silence a code by writing that same code backwards over it... ATCG...GCTA, I found that interesting.
ATCG are chemicals you can buy at you local hardware store, these chemicals have molecular makeups that we could call shapes. These shapes have frequenicies that repel or attract, cytomeglovirus is made up of these chemicals codes...shapes...nano and frequenices. Whopping cough too.
It was a matter of looking at what nature did, where natural attractions deposited and repeating it.
The radiation breaks our D.N.A. and at a time when the Army is issuing Cipro to all members?
D.N.A. breaks in those who survive.... + ....D.N.A.virsus issued = Takeover of the survivors of what is left of the human race?
Just wondering out loud here, then it would not be our Army doing it, hey?
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Post by lilsissy on Apr 8, 2011 1:35:07 GMT -5
www.youris.com/Nano/Interviews/Dr_Antonietta_Gatti_IM_Convinced_That_Nanopollution_Is_Mainly_Responsible_For_CancerS_Increase.klDr. Antonietta Gatti: “I'm convinced that nanopollution is mainly responsible for cancer's increase” How common are diseases developed by micro – and nanoparticles? So far I have studied about 1,400 patients with micro- and nanoparticles in their tissues. All patients were affected by cancer and I’m convinced that there is a correlation between the particles trapped in the tissues and diseases. My in-vitro tests showed nanoparticles in contact with DNA strands during the replication phase. This means there is a real possibility to induce DNA damage. Nanoparticles are not toxic in the classic sense; they do not induce cell death as their concentration increases. An uptake of nanoparticles can change the cell function and, since they can be persistent, they can be transmitted through generations. If nanoparticles are biodegradable, they don’t cause a lot of damage once trapped in human or animal tissues. If they are not biodegradable they remain in the tissues or in the cells for the patient’s life and are perceived as foreign bodies. Once nanoparticles are dispersed in the environment there is a high probability they can be inhaled or ingested with the vegetables grown under this pollution
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Post by kritters on Apr 8, 2011 9:15:05 GMT -5
I have some catching up to do here but lil at a time The radiation breaks our D.N.A. and at a time when the Army is issuing Cipro to all members? D.N.A. breaks in those who survive.... + ....D.N.A.virsus issued = Takeover of the survivors of what is left of the human race? Just wondering out loud here, then it would not be our Army doing it, hey? Lilsissy, what an amazing amount of relative material and more! I have to put this all aside to explore! my thought: the army is issued Cipro, so they could be doing it. IMO most definitely are carrying out duty from higher ups.... Kritts
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Post by kritters on Apr 8, 2011 9:21:43 GMT -5
This is fitting so snugly with what I'm researching today...for different reasons I'll tell you about later. (still freaking sick, do you believe it?) Yeah, it's called sick by nano. that nano is being dispursed from the chemtrails above. I told you, I think, that I got sick 2 weeks ago at the same time as my grandchild who said her eyes were burning. She now has conjunctivitis (and of course her doc is clueless) but he said in the last two weeks he's had an amazing amount of kids in with same thing. this is really pissing me off. And people don't even notice anything different in the sky. No WONDER they're so blatant about the chemtrails when there are such oblivious people on the ground! One way for sure nanopollution is responsible is because it's putting foreign metals undetected into our bodies. We breathe them from the trails and we eat them and drink them from our food, as you say. Kritts
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