XPost: misc.news.internet.discuss   
   From: here@is.invalid   
      
   A Supercomputer Analyzed Covid-19 -- and an Interesting New Theory Has   
   Emerged   
      
   A closer look at the Bradykinin hypothesis   
      
   Earlier this summer, the Summit supercomputer at Oak Ridge National   
   Lab in Tennessee set about crunching data on more than 40,000 genes   
   from 17,000 genetic samples in an effort to better understand   
   Covid-19. Summit is the second-fastest computer in the world, but the   
   process -- which involved analyzing 2.5 billion genetic combinations   
   -- still took more than a week.   
      
   When Summit was done, researchers analyzed the results. It was, in the   
   words of Dr. Daniel Jacobson, lead researcher and chief scientist for   
   computational systems biology at Oak Ridge, a "eureka moment." The   
   computer had revealed a new theory about how Covid-19 impacts the   
   body: the bradykinin hypothesis. The hypothesis provides a model that   
   explains many aspects of Covid-19, including some of its most bizarre   
   symptoms. It also suggests 10-plus potential treatments, many of which   
   are already FDA approved. Jacobson's group published their results in   
   a paper in the journal eLife in early July.   
      
   According to the team's findings, a Covid-19 infection generally   
   begins when the virus enters the body through ACE2 receptors in the   
   nose, (The receptors, which the virus is known to target, are abundant   
   there.) The virus then proceeds through the body, entering cells in   
   other places where ACE2 is also present: the intestines, kidneys, and   
   heart. This likely accounts for at least some of the disease's cardiac   
   and GI symptoms.   
      
   But once Covid-19 has established itself in the body, things start to   
   get really interesting. According to Jacobson's group, the data Summit   
   analyzed shows that Covid-19 isn't content to simply infect cells that   
   already express lots of ACE2 receptors. Instead, it actively hijacks   
   the body's own systems, tricking it into upregulating ACE2 receptors   
   in places where they're usually expressed at low or medium levels,   
   including the lungs.   
      
   In this sense, Covid-19 is like a burglar who slips in your unlocked   
   second-floor window and starts to ransack your house. Once inside,   
   though, they don't just take your stuff -- they also throw open all   
   your doors and windows so their accomplices can rush in and help   
   pillage more efficiently.   
      
   The renin-angiotensin system (RAS) controls many aspects of the   
   circulatory system, including the body's levels of a chemical called   
   bradykinin, which normally helps to regulate blood pressure. According   
   to the team's analysis, when the virus tweaks the RAS, it causes the   
   body's mechanisms for regulating bradykinin to go haywire. Bradykinin   
   receptors are resensitized, and the body also stops effectively   
   breaking down bradykinin. (ACE normally degrades bradykinin, but when   
   the virus downregulates it, it can't do this as effectively.)   
      
      
   The end result, the researchers say, is to release a bradykinin storm   
   -- a massive, runaway buildup of bradykinin in the body. According to   
   the bradykinin hypothesis, it's this storm that is ultimately   
   responsible for many of Covid-19's deadly effects. Jacobson's team   
   says in their paper that "the pathology of Covid-19 is likely the   
   result of Bradykinin Storms rather than cytokine storms," which had   
   been previously identified in Covid-19 patients, but that "the two may   
   be intricately linked." Other papers had previously identified   
   bradykinin storms as a possible cause of Covid-19's pathologies.   
      
   As bradykinin builds up in the body, it dramatically increases   
   vascular permeability. In short, it makes your blood vessels leaky.   
   This aligns with recent clinical data, which increasingly views   
   Covid-19 primarily as a vascular disease, rather than a respiratory   
   one. But Covid-19 still has a massive effect on the lungs. As blood   
   vessels start to leak due to a bradykinin storm, the researchers say,   
   the lungs can fill with fluid. Immune cells also leak out into the   
   lungs, Jacobson's team found, causing inflammation.   
      
   And Covid-19 has another especially insidious trick. Through another   
   pathway, the team's data shows, it increases production of hyaluronic   
   acid (HLA) in the lungs. HLA is often used in soaps and lotions for   
   its ability to absorb more than 1,000 times its weight in fluid. When   
   it combines with fluid leaking into the lungs, the results are   
   disastrous: It forms a hydrogel, which can fill the lungs in some   
   patients. According to Jacobson, once this happens, "it's like trying   
   to breathe through Jell-O."   
      
   More....   
      
      
      
   --- SoupGate-Win32 v1.05   
    * Origin: you cannot sedate... all the things you hate (1:229/2)