Genetically modified chimeric humans.....

[al]

This is just a teaser, I need to get my head around the concept, the mechanics, the gene sequencing, the terminology, the hows and wherefores.

Key concepts;
CYTOKININE STORM=> Where the immune system overreacts and attacks the body causing multiple organ system failure.

ACMPD3N7=>Family of genes controlling aminocarboxmuconate paraldehyde decarbolase.

ACMPD3N7 modifies responses of the amygdala and cingulate gyrus in th ebrain; potentiall link to neurodegenerative disease, thought that neurodegenerative disease were a result of disruptions to the maturational pathways in the brain.

COX-2 => gene produces enzyme which causes pain. Celebrex blocks COX-2 enzymes.

"Furthermore, transgenics was never a matter of inserting a single gene. Researchers also had to insert the associated genes neccessary for the primary gene to function. i.e. most genes have insulators and promoters. The promoters might make protiens that switched off the animals own genes to allow the new addittion to take over. Or, they might enhance the workings of the injected gene itself. The insulators keep the new gene seperated from the genes around it. This was to make sure the new genetic material remained available within the cell." "Next" Micheal Chrighton.
Marriage of nano-particles and genetically modified clostridium perfringens bacteria....
Vogelmans paresis....BRD7A.

D4DR "Risk taking Gene"

Guys, this is way over my head but I'm going to do it to death till I understand what they have done to us.
My gut feeling is that we have been innoculated with another Gene sequence, several in fact, creating in us chimeric attributes.
How does it fuul to be on the cutting edge.
It all makes sense, if we look at the term cytokinine storm, that is Us, our body is fighting itself.

Any how all of the above is from Chrightons book, and I personally believe that it is perhaps the most valuable reference to create the actual genomic sequencing we have been exposed to.

Christ, we need a lawyer, not a doctor.
But I'm going to search all th eterms I ve introduced and if I feel I can publish , I will.
If I can sue, well, hell I'm going to do that too.

[al]

http://www.australiagroup.net/en/con...bio_agents.htm

Im flying blind people, but we need to be informed, we will get better.

[al]

A cytokine storm is a potentially fatal immune reaction consisting of a positive feedback loop between cytokines and immune cells, with highly elevated levels of various cytokines.

Overview
When the immune system is fighting pathogens, cytokines signal immune cells such as T-cells and macrophages to travel to the site of infection. In addition, cytokines activate those cells, stimulating them to produce more cytokines. Normally this feedback loop is kept in check by the body. However, in some instances, the reaction becomes uncontrolled, and too many immune cells are activated in a single place. The precise reason for this is not entirely understood, but may be caused by an exaggerated response when the immune system encounters a new and highly pathogenic invader. Cytokine storms have potential to do significant damage to body tissues and organs. If a cytokine storm occurs in the lungs, for example, fluids and immune cells such as macrophages may accumulate and eventually block off the airways, potentially resulting in death.

The cytokine storm (hypercytokinemia) is the systemic expression of a healthy and vigorous immune system resulting in the release of more than 150 inflammatory mediators (cytokines, oxygen free radicals, and coagulation factors).
Both pro-inflammatory cytokines (such as Tumor necrosis factor-alpha, Interleukin-1, and Interleukin-6) and anti-inflammatory cytokines (such as interleukin 10, and interleukin 1 receptor antagonist) are elevated in the serum of patients experiencing a cytokine storm.

Cytokine storms can occur in a number of infectious and non-infectious diseases including graft versus host disease (GVHD), adult respiratory distress syndrome (ARDS), sepsis, avian influenza, smallpox, and systemic inflammatory response syndrome (SIRS).

The first reference to the term "cytokine storm" in the published medical literature appears to be by ''Ferrara et al'' in GVHD, in February 1993.

Role in pandemic deaths
It is believed that cytokine storms were responsible for many of the deaths during the 1918 influenza pandemic, which killed a disproportionate number of young adults (a phenomenon that could repeat itself in future flu pandemics). In this case, a healthy immune system may have been a liability rather than an asset. Preliminary research results from Hong Kong also indicated this as the probable reason of many deaths during the SARS epidemic in 2003. Human deaths from the bird flu H5N1 usually involve cytokine storms.

Clinical trials of TGN1412
In March 2006, all 6 men who had received the experimental drug TGN1412 suffered extremely serious symptoms 1 from what was likely the effects of a cytokine storm.Mystery over drug trial debacle deepens, New Scientist.com news service, 14 August 2006. Based on results from animal trials, the company claimed that TGN1412 could activate T-cells in a way that would not cause the cytokine storm one would expect based on results from other drugs with similar mechanisms of action. All 6 men had been participating in a Phase 1 trial.

Treatment
OX40 IG
A 2003 report in the Journal of Experimental Medicine and published by researchers at Imperial College in London demonstrates the possibility of preventing a cytokine storm by inhibiting or disabling T-cell response. A few days after T cells are activated, they produce a biologic molecule called OX40, a ?survival signal? that keeps activated T-cells working at the site of inflammation during infection with influenza or other pathogens. OX40 binds to receptors on T-cells, preventing them from dying and subsequently increasing cytokine production. A combined protein, OX40-immunoglobulin (OX40-Ig), a man-made fusion protein, prevents OX40 from reaching the T-cell receptors, thus reducing the T-cell response. Experiments in mice have demonstrated that OX40-Ig can reduce the symptoms associated with an immune overreaction while allowing the immune system to fight off the virus successfully. By blocking the OX40 receptor on T-cells, researchers were able to prevent the development of the most serious flu symptoms in these experimental mice (paper in J. of Experimental Medicine and reported in New Scientist). The drug, to be made by a company called Xenova Research, was supposed to be in phase I clinical trial in 2004, but we have no further information of its status (this link will update the reader when a clinical trial appears on OX-40 Ig).

ACE inhibitors and Angiotensin II Receptor Blockers
The Renin Angiotensin system (RAS) has been implicated in the mediation of the cytokine storm, suggesting a potential benefit for Angiotensin Converting Enzyme (ACE) inhibitors and Angiotensin II Receptor Blockers (ARBs), and ACE has been implicated in inflammatory lung pathologies, and Shigehara et all published research confirming that serum angiotensin-converting enzyme (ACE) is a useful marker for disease activity in cytokine-mediated inflammatory lung disease.

Marshall and co-workers found that angiotensin II was associated with cytokine-mediated lung injury and suggested a role for ACE inhibitors.

Wang and co-workers published data linking cytokine-mediated pulmonary damage (apoptosis of lung epithelial cells) in response to the pro-inflammatory cytokine TNF-alpha (implicated in the cytokine storm) requires the presence of angiotensin II, suggesting that ARBs might have clinical utility in this setting.

Das published a review of ACE inhibitor and angiotensin-II receptor blocker use in a number of cytokine-mediated inflammatory pathologies and suggested that ACE inhibitors and Angiotensin receptor blockers have theoretical benefit in downregulation of the cytokine storm.

Corticosteroids
Although frequently employed to treat patients experiencing the cytokine storm associated with ARDS, corticosteroids and NSAIDs have been evaluated in clinical trials and have shown no effect on lung mechanics, gas exchange or beneficial outcome in early established ARDS.

Free Radical Scavengers
Preliminary data from clinical trials involving patients with sepsis-induced ARDS have shown a reduction in organ damage and a trend toward improvement in survival (survival in ARDS is approximately 60%) after administering or upregulating a variety of free radical scavengers.

External links
* A Critical Role for OX40 in T Cell?mediated Immunopathology during Lung Viral Infection
* Pub Med data on OX-40
* Cytokine Storm and the Influenza Pandemic

References
Category:Cytokines

Cytokine storm Wikipedia RSS Feed Preview
Cytokinin >> << Cytokine secretion assay







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[al]

New Drug Beats Flu
UK scientists think that they may have found a way to beat flu and possibly even SARS. Dr Tracy Hussell and colleagues at Imperial College London have found a way of controlling the way in which the immune system responds to flu. Research suggests that the immune system can react too strongly if we are infected with certain strains of flu, and that this immune react to infection can sometimes prove fatal. When flu infects the body it triggers the immune system into action and cells called T-cells begin to produce high levels of inflammatory molecules called cytokines. These cells are needed to help the body to destroy invading cells, however when levels get too high they can block the airways and prevent efficient transfer of oxygen into the bloodstream. Hussell found that blocking a molecule called OX40 prevents these immune system cells from clogging up airways. OX40’s job is to instruct activated T-cells to remain in the lungs for longer than normal in order to help fight infection, however when there is an excessive immune response there are so many cells entering the lungs that there is no need for the cells to hang around. Tests on mice infected with influenza A, the strain responsible for the 1919 flu pandemic that killed roughly 20 million people, revealed that blocking OX40 with an experimental drug called OX40:Ig effectively halted the excessive immune response and relieved the animals’ symptoms. Hussell says that the findings suggest that OX40:Ig could be used to treat any disease caused by an excessive T-cell inflammatory response, for example asthma, pneumonia, bronchitis, or possibly even SARS.

SOURCE/REFERENCE: Reported by www.bbc.co.uk on the 20th October 2003.

[al]

Ok guys I'm off to work, I'm a carpenter and as I hammer I think, thats what we must all be doing; think.
Peace to you all, and lets hope that the blinkers come off those who could really help us.

[al]

http://www.aussmc.org/pdf/Genetics_in_a_Nutshell_UK.pdf

[al]

http://www.staningerreport.com/welcome.php