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Post by lilsissy on Jan 1, 2010 21:08:07 GMT -5
Is this the blue green stuff we are finding , it was found in the blood of %5 of heathy people but we are not so heathy. A co-infection possibly ? I saw someone's picture here the thread the other day that looked like this but I can't find the thread now but anyhow, www.sciencedaily.com/releases/2008/04/080423115917.htmjen The new cyanobacteria produce a relatively pure, gel-like form of cellulose that can be broken down easily into glucose A photosynthetic cyanobacterium with chlorophyll (red) and the cellulose material (blue) it produced. (Credit: Brown and Nobles, the University of Texas at Austin) Nobles made the new cyanobacteria (also known as blue-green algae) by giving them a set of cellulose-making genes from a non-photosynthetic "vinegar" bacterium, Acetobacter xylinum, well known as a prolific cellulose producer. « Last Edit: Dec 30, 2009, 11:42pm by lilsissy » Link to Post - Back to Top Logged tinyurl.com/ylkgh3s April 14, 2005 A Novel Bacterium Associated with Lymphadenitis in a Patient with Chronic Granulomatous Disease Chronic granulomatous disease (CGD) is a rare inherited disease of the phagocyte NADPH oxidase system causing defective production of toxic oxygen metabolites, impaired bacterial and fungal killing, and recurrent life-threatening infections. We identified a novel gram-negative rod in excised lymph nodes from a patient with CGD. Abstract Top Chronic granulomatous disease (CGD) is a rare inherited disease of the phagocyte NADPH oxidase system causing defective production of toxic oxygen metabolites, impaired bacterial and fungal killing, and recurrent life-threatening infections. We identified a novel gram-negative rod in excised lymph nodes from a patient with CGD. Gram-negative rods grew on charcoal-yeast extract, but conventional tests could not identify it. The best 50 matches of the 16S rRNA (using BLAST) were all members of the family Acetobacteraceae, with the closest match being Gluconobacter sacchari. . We identified a novel gram-negative rod from a patient with CGD. This is the first reported case of invasive human disease caused by any of the Acetobacteraceae. Polyphasic taxonomic analysis shows this organism to be a new genus and species for which we propose the name Granulobacter bethesdensis. Synopsis Top As new bacteria continue to be discovered every year, it is inevitable that some of them will be found to cause human disease. The authors describe the isolation and characterization of a new bacterium, grown from a patient with chronic granulomatous disease (CGD). In this genetic disease, one of the main lines of defense against infection, the neutrophil, has a discrete defect in the generation of superoxide, leading to recurrent infections with a narrow spectrum of bacteria and fungi. This new organism was cultured from lymph nodes that had been inflamed for several months. To prove that this new bacterium was indeed a pathogen, Greenberg and colleagues measured specific antibody response in the patient: they inoculated CGD mice with this organism and reproduced the appearance of the human infection; they recovered the organism in pure growth from infected mouse spleens. This new bacterium belongs to the family Acetobacteraceae, bacteria that are found widely in the environment. They have a variety of industrial uses, such as the production of vinegar, but have never been reported to cause invasive human disease. Disease-causing organisms remain to be discovered. The researchers outline some of the steps that can be taken to verify the pathogenicity of novel organisms. They found that the mystery bug was most closely related to a family called Acetobacteraceae, whose members were thought to be mostly harmless and are found in fruit, plants and soil. They can contaminate wine and beer fermentation, and are used industrially to make vinegar. Not so harmless To prove that the bacterium they had found was causing the problem, the team injected it into mice that had a version of CGD and found that the bacteria also infected the animals' lymph nodes. The researchers have published their results in PLoS Pathogens - and have since determined the bacterium's entire genetic sequence. The pressing question is whether G. bethesdensis infects other people with weak immune systems and whether it is a wider threat to human health, and Greenberg and his colleagues are starting to explore this. Worryingly, it seems to be resistant to most antibiotics. The patient who triggered the investigation still carries an infection. The investigators have found the bacterium in another two CGD patients with similar symptoms. They have also seen signs of infection in around 5% of healthy people, based on the presence of tell-tale antibodies in the blood. It is possible that the bug regularly invades healthy people, but that most fight it off with no ill effects.
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Post by lilsissy on Jan 2, 2010 0:53:45 GMT -5
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Post by aqt on Jan 2, 2010 7:08:31 GMT -5
how interesting...
I am a firm believer of the use of CYANOBACTERIA as part of the base architecture of morgellon's...it is fused with trypanosoma
now, we have a synthetic cyanobacteria capable of photosynthesis?
very interesting....
thanks lilsissy and sky...
you girls rock the house!!
aqt
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Post by skyship on Jan 2, 2010 14:45:36 GMT -5
It started with the blood changer, then the very nucleus in typan, and the gene cyanide.....
Brown is using to make fuel supply out of cyanobacteria.
But, the plan was to use organisms from plants, animals, to form capillaries, to replace nerves, to cause cytoskeleton rearrangements.
We have to look at this as bottom up, by using top down procedures.
top down, links us to the middle, bottom up tells us what they created.
How nano works.
I see the word kinase over and over. IF we look at what diseases besides Morgellons are showing up we are seeing the consequences of this great endeavor that is going on.
However, they began somewhere, the first was the blood.
Changing A and B to O. There is proof.
How did they do it?
beginning with a bacterial glycoside. BACTERIAL...........VIRAL is what gets it there.
We must start with bacteria and viral...............
Yet, at the same time consider the new diseaeses and emerging virals that are present.
this way we smash them in middle.
It is called the changing Human Blueprint by lovely bio/chem/geo/phys Engineers
There is something called organic chemistry, organic geology, etc.
Particles first...............
then there is molecular. Morgellons in my opinion is a molecular disease, these are the new diseases, created by recombination of human genes with animal, insect, plant by way of peptides and enzymes.
the core of blood cells, the core of muscle cells, actin, fibronectin, axons, fibronectin is involved in over 100 cytoskeletal cells, the basis of the human body.
Kinesis, signaling from outside, from environment, homologous genes, found in human similar genes found in flies, tyrpanasoma, etc.
Tam Tam has it, but, does not have how the mitochondria is being changed.
We are walking through it.
skyship
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Post by aqt on Jan 2, 2010 15:42:28 GMT -5
Abstract Mitochondria are key organelles in conversion of energy, regulation of cellular signaling and amplification of programmed cell death. The anatomy of the organelle matches this functional versatility in complexity and is modulated by the concerted action of proteins that impinge on its fusion–fission equilibrium. A growing body of evidence implicates changes in mitochondrial shape in the progression of apoptosis and, therefore, proteins governing such changes are likely candidates for involvement in pathogenetic mechanisms in neurodegeneration and cancer. Here, we discuss the recent advancements in our knowledge about the machinery that regulates mitochondrial shape and on the role of molecular mechanisms controlling mitochondrial morphology during cell death.www.cell.com/trends/endocrinology-metabolism/abstract/S1043-2760(09)00076-9 In many organisms, ranging from yeast to humans, mitochondria fuse and divide to change their morphology in response to a multitude of ...
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Post by aqt on Jan 2, 2010 15:56:14 GMT -5
When cells become committed to apoptosis, they shatter their mitochondrial networks through the actions of the mitochondrial fission protein DRP1. Massive fragmentation of mitochondria facilitates simultaneous release of cytochrome c from all mitochondria within a cell, thus promoting further progression along the apoptotic pathway. In this issue, Tondera et al (2009) describe a new process with the opposite effect. When cells are subjected to modest levels of stress (well below levels needed to induce apoptosis), their mitochondria fuse to each other forming a closed network, similar to networks observed when mitochondrial fission is blocked. Stress-induced mitochondrial hyperfusion (SIMH), as this process was called, might counter stress by optimizing mitochondrial ATP production. www.nature.com/emboj/journal/v28/n11/full/emboj2009130a.htmlMitochondria of healthy cells continually divide and fuse with each .... These types of questions will inevitably change the course of future experiments
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Post by aqt on Jan 2, 2010 16:01:03 GMT -5
tiny.cc/VBhcn Mitochondrial electron transport generates the ATP that is essential for the excitability and survival of neurons, and the protein phosphorylation reactions that mediate synaptic signaling and related long-term changes in neuronal structure and function. Mitochondria are highly dynamic organelles that divide, fuse, and move purposefully within axons and dendrites. Major functions of mitochondria in neurons include the regulation of Ca2+ and redox signaling, developmental and synaptic plasticity, and the arbitration of cell survival and death. The importance of mitochondria in neurons is evident in the neurological phenotypes in rare diseases caused by mutations in mitochondrial genes. Mitochondria-mediated oxidative stress, perturbed Ca2+ homeostasis, and apoptosis may also contribute to the pathogenesis of prominent neurological diseases including Alzheimer’s, Parkinson’s, and Huntington’s diseases; stroke; amyotrophic lateral sclerosis; and psychiatric disorders. Advances in understanding the molecular and cell biology of mitochondria are leading to novel approaches for the prevention and treatment of neurological disorders.
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Post by skyship on Jan 2, 2010 16:21:47 GMT -5
Mitochondria-mediated oxidative stress, perturbed Ca2+ homeostasis, and apoptosis may also contribute to the pathogenesis of prominent neurological diseases including Alzheimer’s, Parkinson’s, and Huntington’s diseases; stroke; amyotrophic lateral sclerosis; and psychiatric disorders.
Mitochondria mediated, meaning something is interupting the mitochondria.
Tam Tam mentions this from the doctor he conversed with and she said "Did they not notice that mitochondria was present?" meaning in constuction of this transforming mitochondria, what genes from what organism was used that had mitochondria in it? used as mitochondria for humans?
If any mitochondria is in insect gene, peptide, enzyme, used for substitution in human, then it will change human mitochondria, or will recognize human mitochondria in itself, and relate it to human mitochondria. For a virus to mutate into human genes it has to recognize itself in the human.
This is what XMRV is. it recognizes the mitochondria so can translate its baggage.
Same for A and B blood being changed to Universal O.
skyship
How is it perturbed? Ca2+ homeostasis......through the calcium channel.
How is ca2+ homeostasis happen?
kinase change...........signal recognition.............recognizes mito in environment
particles.............. haarp increases voltage and electrochemical fields.
we cannot leave out the organic chemistry changes by way of temperature or voltage increase that can affect the mitochondria.
a signal has to take place first. I am going after that stinking signal.
I believe the signal involves the trypanasome nucleus.......
so we are looking into the nucleus itself. Deeper down the d......ang rabbit hole, We go!
In fact rabbit genes were used for something as well. Leaving nothing untouched are they?
skyship
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Post by aqt on Jan 2, 2010 18:40:01 GMT -5
We report that a trypanosome nuclear localiza tion signal is contained within the amino termi nus of ribosomal protein L25 tiny.cc/txsDnOverall, these data demonstrate that calcium moves into and out of the trypanosome nucleus in a manner which closely parallels changes in [Ca2+]cyt. A small calcium ion gradient between nucleus and cytoplasm was also observed aqt
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