It’s come to this. The human body is being described as if it were a nation state (and it’s not an exaggeration, quite the opposite):
Inflammation can help to eliminate infection, but excessive inflammation can cause damage to the body. The sensor proteins that trigger an inflammatory immune response must therefore be carefully regulated. Some intracellular immune-sensor proteins detect components in a cell that become abnormal or altered during a cellular crisis. Signs of cellular crisis are sometimes produced in the absence of an infection, so mechanisms are needed to prevent the proteins from triggering an inappropriate inflammatory response. Writing in Nature, Sharif et al.1 report a structural study that investigates an immune-sensor protein called NLRP3, revealing that a protein called NEK7 acts as a ‘licence’ that enables this protein to cause inflammation. …
Proteins that are normally present in mammalian cells do not seem able to trigger the accidental formation of NLRC4-containing inflammasomes, given the lack of reports of such aberrant events. By contrast, inflammasomes that contain NLRP3 are activated when NLRP3 recognizes — by an as yet unknown mechanism — hallmarks of cellular catastrophe, such as extremely low concentrations of potassium in the cytoplasm, or signs of dysfunction in organelles called mitochondria2. Such events can arise from tissue damage that is unrelated to infection, and NLRP3 activation in such cases has been implicated as a possible cause of inflammatory diseases such as atherosclerosis. …
Finally, we still don’t know the answer to perhaps the most important question of all: what direct interaction between NLRP3 and an unknown cellular factor results in the formation of the inflammasome? Perhaps the evidence that the NEK7 licence is revoked during cell division provides a clue. If inappropriate activation of NLRP3 is likely to occur during cell division, then having an NEK7-licensing step would help to combat this potential problem. Thus, one could imagine that the type of cellular catastrophe detected by NLRP3 also occurs during cell division but in a controlled manner. Kengo Nozaki & Edward A. Miao[name], “A licence to kill during inflammation” at Nature
The crux we now face: If there is so much intelligent organization in nature that a body resembles a state with a complex government, if there is no design, consciousness itself must also be an evolved illusion., That is a view that many quietly hold. But then science has no defence against the raging Woke, demanding that their grievances be science. There is no way to escape the dilemma: design or chaos
See also: Researchers: Gene translation “much more complex than previously thought” We keep learning about a variety of life forms that they are “more complex than expected.” So why do we keep expecting them to be simpler? How be we turn it around and say: Such-and-so features layers on layers of complexity, as we expected. What would be the implications?
Materialism’s secret of success. Hint: It’s not evidence Materialism enables irrational ideas about ourselves to compete with rational ones on an equal basis. It won’t work
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