Carp can switch over to an anaerobic metabolism and quietly exhale booze until the situation gets better.
An interesting thing about carp is that they can go into anoxic hibernation and switch to an anaerobic metabolism based on converting glycogen to ethanol.
The waste ethanol is diffused out the gills
Carp can switch over to an anaerobic metabolism and quietly exhale booze until the situation gets better.
In theory, if you spent a few thousand years breeding carp for it, you could use them to make booze.
They'd be enormous, almost entirely glycogen deposits with a fish added as an afterthought.
You, a human, have only about 100 grams of glycogen in your liver, about 400 more grams in your skeletal muscles. Call it 500 grams total.
Carp can be 12% glycogen by weight.
A 75kg human would need to have 9kg of glycogen to match their carp friend.
https://t.co/Bt29kS7pO5
Call it 18 days worth. You'd need a lot more if you wanted to beat your carp friend at holding your breaths.
You currently do this in the liver, by further metabolizing ethanol into acetaldehyde.
You do this completely differently depending on whether you're a fetus or not.
https://t.co/gsnliVwr3G
You're gonna need a bigger liver or a better way
You're gonna scare your carp friends by pissing vinegar at them.
More from Anosognosiogenesis
Look at some historical examples of mass psychogenic illnesses: dancing plagues, laughing plagues, meowing nuns,
Here's a video on them:
They are interesting, but what is more interesting to me is Culture Bound Syndrome. https://t.co/hMKaApUMZn
Basically: mass psychogenic illness, and presentation of various mental illnesses, do not occur in a vacuum. Cultures shape them.
For instance, Koro.
There have been several mass outbreaks of men completely convinced their penises are shrinking, anchoring them with string at night so they don't get sucked back inside.
Almost all in Southeast
Here's a description of one outbreak in Hainan in 1984:
Here's a video on them:
They are interesting, but what is more interesting to me is Culture Bound Syndrome. https://t.co/hMKaApUMZn
Basically: mass psychogenic illness, and presentation of various mental illnesses, do not occur in a vacuum. Cultures shape them.
For instance, Koro.
There have been several mass outbreaks of men completely convinced their penises are shrinking, anchoring them with string at night so they don't get sucked back inside.
Almost all in Southeast
Here's a description of one outbreak in Hainan in 1984:
More from Science
Hard agree. And if this is useful, let me share something that often gets omitted (not by @kakape).
Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.
You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.
The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.
In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.
The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.
Variants always emerge, & are not good or bad, but expected. The challenge is figuring out which variants are bad, and that can't be done with sequence alone.
Feels like the next thing we're going to need is a ranking system for how concerning "variants of concern\u201d actually are.
— Kai Kupferschmidt (@kakape) January 15, 2021
A lot of constellations of mutations are concerning, but people are lumping together variants with vastly different levels of evidence that we need to worry.
You can't just look at a sequence and say, "Aha! A mutation in spike. This must be more transmissible or can evade antibody neutralization." Sure, we can use computational models to try and predict the functional consequence of a given mutation, but models are often wrong.
The virus acquires mutations randomly every time it replicates. Many mutations don't change the virus at all. Others may change it in a way that have no consequences for human transmission or disease. But you can't tell just looking at sequence alone.
In order to determine the functional impact of a mutation, you need to actually do experiments. You can look at some effects in cell culture, but to address questions relating to transmission or disease, you have to use animal models.
The reason people were concerned initially about B.1.1.7 is because of epidemiological evidence showing that it rapidly became dominant in one area. More rapidly that could be explained unless it had some kind of advantage that allowed it to outcompete other circulating variants.
