Anonymous 05/12/2020 (Tue) 22:32:42 Id: 440354 No.79794 del
>>79788
(from above) Brain invasion is potentially this virus's role towards causing patients to have lung failure.
>>>/news/15854
>More recently, a study of 214 Covid‐19 patients further found that about 88% (78/88) of the severe patients displayed neurologic manifestations including acute cerebrovascular diseases and impaired consciousness.
They studied 214 patients with the virus. 78 of 88 had unnatural brain issues, including diseases of the brain and weakened awareness.
>the nicotinic acetylcholine receptor (nAChR) plays a key role in the pathophysiology of Covid-19 infection and might represent a target for the prevention and control of Covid-19 infection.
There are receptors in your central and peripheral nervous system which respond to drugs. Besides being important for your brain to communicate because they release certain neurotransmitters, nicotinic acetylcholine receptors are specifically what binds nicotine. These receptors play a key role in the function of the virus's invasion and may be studied to stop or control the virus.
>Based on an epidemiological survey on Covid‐19, the median time from the first symptom to dyspnea was 5.0 days, to hospital admission was 7.0 days, and to the intensive care was 8.0 days
Based on a medicine branch (this one of diseases) survey on the virus, the middle time from the first symptom (headaches, hives, nausea, dry cough, fever) to shortness of breath is 5 days. People are hospitalized 2 days later, and put in intensive care a day later.
>The nAChR pathway is hypothesized to be engaged in the Covid-19 inflammatory syndrome. The nervous system, through the vagus nerve, can significantly and rapidly inhibit the release of macrophage TNF, and attenuate systemic inflammatory responses
The pathway of nicotinic acetylcholine receptors engaging in the virus is a limited evidence based theory in what causes the cytokine release which results in inflammation. The nervous system through ten pairs of brain nerves that supply hearts, lungs, upper digestive tracts, and other organs of the chest and abdomen with communication to function - can stop the release of white blood cells' Tumor Necrosis Factor (pro-inflammatory cytokines) and reduce inflammation.
>This cytokine profile shows striking analogies with the cytokine storm syndrome, leading to the hyperinflammatory syndrome described in a subgroup of Covid-19 patients
^Should be understood by now.
>Interestingly, 𝛼7 agonists, including nicotine, have proven to be effective in reducing macrophage cytokine production and inflammation in animal models of pancreatitis and peritonitis
Drugs which activate receptors in your central and peripheral nervous system, like nicotine, are proven to reduce white blood cells' cytokine production and inflammation in animals with the above mentioned problems.
>In this setting, a nicotinic treatment that might possibly antagonize the blocking action of SARS-CoV-2 on the AChR through a possible modulation of the ACE2 – nAChR interaction, would act earlier than anti-cytokine therapies.
A treatment of a drug that controls the effects produced by nicotine might make the blocking action of Covid-19 hostile to a brain-transmitting binding protein through a possible controlled change of the biochemical catalyst that regulates blood pressure reaction to receptors in your central and peripheral nervous system which respond to drugs. Which may work before anti-inflammation drugs.

Message too long. Click here to view full text.