Well /sci/ explain yourselves
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(20 replies)
(5 replies)
Can science explain fainting goats? What is the evolutionary purpose??
(8 replies)
do mathematicians masturbate or they do semen retention? what are some famous mathematician coomers?
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Computer science is a legit fields of study and research, but software engineering as a career seems like a joke.
I know tons of non-software engineers who can code just as well as software engineers.
For example I'm a mechanical engineer who has tons of custom machine learning software on my GitHub.
That's the problem - ANYONE can do software engineering.
Being a software engineer is like being an air breather.
All impactful things in society are a mix of hardware and software - it seems like if you don't do both then you're just gonna be a nobody.
I know tons of non-software engineers who can code just as well as software engineers.
For example I'm a mechanical engineer who has tons of custom machine learning software on my GitHub.
That's the problem - ANYONE can do software engineering.
Being a software engineer is like being an air breather.
All impactful things in society are a mix of hardware and software - it seems like if you don't do both then you're just gonna be a nobody.
(15 replies)
Why do teachers insist on being called "Professor?" I'm currently in an online school degree mill targeted at military. My barely literate entry level English teacher insists she be called professor. She doesn't have a postgraduate degree. She doesn't develop her own course material, she receives the same curriculum. She doesn't do research. She doesn't lecture.
She grades assignments, she responds to discussion posts with "Sounds great!" and that's about it.
Also I made my profile picture a black guy and started receiving higher marks on my assignments.
Is this a professor?
She grades assignments, she responds to discussion posts with "Sounds great!" and that's about it.
Also I made my profile picture a black guy and started receiving higher marks on my assignments.
Is this a professor?
(17 replies)
https://pubmed.ncbi.nlm.nih.gov/20015551/
Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies
Yi-Ting Fang 1 , Chiou-Feng Lin, Pao-Chi Liao, Yu-Min Kuo, Shuying Wang, Trai-Ming Yeh, Chi-Chang K Shieh, Ih-Jen Su, Huan-Yao Lei, Yee-Shin Lin
>The target of this autoimmune attack is Annexin A2, a phospholipid-binding protein, which acts as a cofactor for tPA, ensuring integrity of the pulmonary vasculature and promoting lung elasticity. Antagonism of Annexin A2 would cause lung blood clots, pulmonary edema, and ARDS.
>n essence, anti-Annexin A2 would cause all the hallmark pulmonary pathology already identified on autopsy among severe cases of acute COVID-19. Autoantibodies to this lung protective protein were already identified among hospitalized SARS patients.
>Furthermore, Annexin A2 is also expressed in the vasculature of the brain. Therefore, antagonism of Annexin A2 can cause microvascular stroke and damage to the blood-brain barrier, which would result in neuro-inflammation and long-term neurological injury.
>The implications for acute COVID-19 are enormous. Not only would it explain why steroids work in this disease, but it would suggest that we should be treating the disease more like other autoimmune diseases of the lung.
>We have misdiagnosed severe cases of acute COVID-19 as a viral pneumonia, which disregards the established evidence that shows viral load of SARS-CoV-2 is markedly diminished by the time patients develop the respiratory distress that only occurs in second stage of the disease.
>We are also misdiagnosing Long COVID, which is also characterized by lung perfusion deficits, pulmonary fibrosis, and various neurologic sequelae. Our next studies will establish whether these autoantibodies are also present among patients with persistent post-COVID symptoms.
Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies
Yi-Ting Fang 1 , Chiou-Feng Lin, Pao-Chi Liao, Yu-Min Kuo, Shuying Wang, Trai-Ming Yeh, Chi-Chang K Shieh, Ih-Jen Su, Huan-Yao Lei, Yee-Shin Lin
>The target of this autoimmune attack is Annexin A2, a phospholipid-binding protein, which acts as a cofactor for tPA, ensuring integrity of the pulmonary vasculature and promoting lung elasticity. Antagonism of Annexin A2 would cause lung blood clots, pulmonary edema, and ARDS.
>n essence, anti-Annexin A2 would cause all the hallmark pulmonary pathology already identified on autopsy among severe cases of acute COVID-19. Autoantibodies to this lung protective protein were already identified among hospitalized SARS patients.
>Furthermore, Annexin A2 is also expressed in the vasculature of the brain. Therefore, antagonism of Annexin A2 can cause microvascular stroke and damage to the blood-brain barrier, which would result in neuro-inflammation and long-term neurological injury.
>The implications for acute COVID-19 are enormous. Not only would it explain why steroids work in this disease, but it would suggest that we should be treating the disease more like other autoimmune diseases of the lung.
>We have misdiagnosed severe cases of acute COVID-19 as a viral pneumonia, which disregards the established evidence that shows viral load of SARS-CoV-2 is markedly diminished by the time patients develop the respiratory distress that only occurs in second stage of the disease.
>We are also misdiagnosing Long COVID, which is also characterized by lung perfusion deficits, pulmonary fibrosis, and various neurologic sequelae. Our next studies will establish whether these autoantibodies are also present among patients with persistent post-COVID symptoms.
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What's the next step of your master plan?
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>The data say
>These data show
>These data show
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Today is the day, anons.
You guy's ready?
You guy's ready?
(12 replies)
It gets proven that the concept of superposition is totally incorrect? Is it likely that this will happen?
