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Pretty sure that hardline grizzled CCP general that gave the speech about “the America problem”
originally posted by: tonycodes
a reply to: Cobaltic1978
I feel more comfortable putting this here than doing anything else with it. So let me know bc I didnt post this as a joke and I feel confident what im reading is what I am claiming.
originally posted by: tonycodes
Like a cat on a hot tin roof to see what yall think. Just trying to do my part as not just an American, but also a human. Let me know. This would be the source of an antidote too. A real one.
originally posted by: tonycodes
Soon after, by 2017 the grease got pulled back from the worldwide elites running these programs. So in response they dropped a classic Spin, smoke N mirror, propaganda, alibi, misdirection, if we just warn about it first the dumb a$$ sheep don’t suspect us, works like a charm every time, corrupt, imperial, World Domination, Troy turned Roman Empire turned Catholic Church, Nazi Founding, Uboat Funding, cash broke Hitler backing to find the Holy Grail, Pedophile, Politician, children harvesting,
blue blood, cousin f#cker, msm,
press release
That's all I got. Probably easy to tie any individuals named in the PDFs to the final result we are experiencing today with a little bit of Google Research.
originally posted by: Cobaltic1978
Have you handed this information over to the appropriate law enforcement agencies?
Seriously, if this proves what you are claiming, then this is an act of war.
originally posted by: Wide-Eyes
Good thread Tony.
As I've said here a few times recently, the war has already started.
People think that because no shots have been fired, we're not at war. The thing is, we are.
We're at war with the NWO and they are winning...
originally posted by: smurfy
originally posted by: Cobaltic1978
Have you handed this information over to the appropriate law enforcement agencies?
Seriously, if this proves what you are claiming, then this is an act of war.
By whom? the experiment was an international team.
originally posted by: Cobaltic1978
originally posted by: smurfy
originally posted by: Cobaltic1978
Have you handed this information over to the appropriate law enforcement agencies?
Seriously, if this proves what you are claiming, then this is an act of war.
By whom? the experiment was an international team.
Whether it was an international team carrying out the experiment or not, it’s an act of war on humanity.
Intravascular crawling and signaling through RhoA induces actin, microfilament and microtubule reorganizations and the production of endothelial cell docking structures, which surround the inflammatory cell and span tight junctions [56]. Although controversial, myofibril contractile structures may also contribute in to the assembly of these structures. In any event, inflammatory cell transmigration requires the formation of actin-myosin II contractile structures which are attached to tight junction membranes by VE-cadherins, resulting in increased endothelial tension, and programmed separation and expansion of the tight junctions which allow for leukocyte/monocyte passage into the surrounding tissues [61]. It seems likely that Trim55, with its roles in myosin and myofibril maintenance and microtubule organization, contributes to the programmed formation of endothelial docking structures and regulation of inflammatory cell transmigration; key features associated with the formation of perivascular cuffs around vessels in the lung. Our data (Figs Figs55 and and66) demonstrate that Trim55 contributes to vascular cuffing following SARS-CoV infection. While the mechanism is not yet fully understood, the data strongly suggest that Trim55 is important for extravasation of inflammatory cells, and thus overall SARS-CoV pathogenesis, by altering intercellular junctions and chemotactic signals. Increased studies of Trim55 and Cdhr2 function within the CC population, either via specific crosses of lines with high and low alleles at the HrS1 and HrS4 loci, or via CRISPR-Cas9 modification of these loci will allow further insight into the role that these two genes play during SARS-CoV pathogenesis and recovery, as well as increasing understanding of the more general process of extravasation.
The Collaborative Cross was conceived of as a resource to drive insight into a variety of biomedically important diseases via the reassortment of genetic variants and expansion of phenotypic ranges [62]. Indeed, previous studies with various preCC subsets have demonstrated expanded phenotypes in preCC mice body weight and hematological parameters [23,63,64], response to Aspergillus [65] and susceptibility to Influenza A infection [27,66]. More recently it has been shown that novel combinations of alleles have also resulted in new models for human disease such a spontaneous colitis [67], and that F1 hybrids of CC mice were used to create an improved mouse model for Ebola virus disease [68] including hemorrhagic signs of disease previously not observed in a small animal model. Within our study of SARS-CoV infection within the preCC, we showed more extreme disease phenotypes than those seen within the eight founder strains of the CC. These disease phenotypes included virus titer, weight loss, pathology and lethality. Further, we saw the emergence of new phenotypes including ARDS and DAD not traditionally seen within young inbred strains [11]. Importantly, our results highlight another exciting aspect of the nature of CC genome: transgressive segregation, or the release of cryptic genetic variation [69,70]. As the three wild-derived CC founders all showed mortality early in the course of SARS-CoV infection, genetic variants within these three strains impacting later-stage SARS-CoV responses would normally not be seen. Only via the reassortment of these alleles into a variety of genetic backgrounds (some resistant to clinical disease, some susceptible) were we able to show that alleles from all three wild-derived founders impacted perivascular cuffing or viral titer levels independent of their effects on clinical disease or SARS-CoV mortality. Collectively, these data support the hypothesis that the CC population represents a robust platform for developing improved animal models that more readily replicate disease phenotypes seen in human populations. All told, our identification of multiple QTL related to SARS-CoV pathogenesis, identification of a novel function for Trim55, and the development of new models of acute lung injury, further solidify the utility of the CC as a valuable community resource for research of infectious diseases and other biological systems driven by complex host response networks.