He's a scientist; I'm in computer support.
Let's talk about Avi Loeb and his theory about alien
He's a scientist; I'm in computer support.
The interview above is worth a read, and a lot of serious thought, because there's an idea there that's really critical to science, and it isn't whether or not aliens have visited (exactly).
In particular he compares his theory on alien visitation with the multiverse theory.
Which of these is more deserving of ridicule?
So bizarre that there's no really good theory for what it might be. Except maybe for Dr. Loeb's theory.
The hypotheses we form can and should help guide us in how we look.
And because "Aliens!" is based on observable phenomena: us.
The competing theories are all about phenomena with NO prior observations.
Why is it unsafe to talk about "Aliens!" but safe to talk about the "multiverse"?
Yet the notion has always (to me) been utterly absurd.
But this isn't the scientific theory of the multiverse at all.
But under this theory, there'd be an infinite number of "adjacent" universes spinning off of that one single particle at the tip of my pinky toe.
In such a multiverse system, the "nearest" (by measure of similarity) million, trillion... heck the nearest googol of alternate universes would be utterly identical to ours.
And really, an utterly pointless one.
https://t.co/XiHA9cRwjR
So THAT'S why we never saw Oumuamua leaving the solar system. https://t.co/pSlwmRMctU
— Thomas A. Fine \U0001f1fa\U0001f1f8 (@thomasafine) February 27, 2020
https://t.co/hj1ytCbFDH
But the thought that's been running around in the back of my mind for the last two years is... if all of a sudden something shows up in orbit around the Earth, I'd be very suspicious of that something.
— Thomas A. Fine \U0001f1fa\U0001f1f8 (@thomasafine) February 27, 2020
More from Science
Hugh Everett's birthday! Pioneer of the Many-Worlds Interpretation of quantum mechanics. Let us celebrate by thinking about ontological extravagance. I will do so by way of analogy, because I have found that everyone loves analogies and nobody ever willfully misconstrues them.
We look at the night sky and see photons arriving to us, emitted by distant stars. Let's contrast two different theories about how stars emit photons.
One theory says, we know how stars shine, and our equations predict that they emit photons roughly uniformly in all directions. Call this the "Many-Photons Interpretation" (MPI).
But! Others object. That is *so many photons*. Most of which we don't observe, and can't observe, since they're moving away at the speed of light. It's too ontologically extravagant to posit a huge number of unobservable things!
So they suggest a "Photon Collapse Interpretation." According to this theory, the photons emitted toward us actually exist. But photons that would be emitted in directions we will never observe simply collapse into utter non-existence.
The physicist Hugh Everett III was born #OTD in 1930. His \u201crelative state\u201d formulation of quantum mechanics, which we now call the \u201cMany Worlds Interpretation,\u201d was published in 1957. pic.twitter.com/ZqMsZcPJDG
— Robert McNees, the bastegod (@mcnees) November 11, 2020
We look at the night sky and see photons arriving to us, emitted by distant stars. Let's contrast two different theories about how stars emit photons.
One theory says, we know how stars shine, and our equations predict that they emit photons roughly uniformly in all directions. Call this the "Many-Photons Interpretation" (MPI).
But! Others object. That is *so many photons*. Most of which we don't observe, and can't observe, since they're moving away at the speed of light. It's too ontologically extravagant to posit a huge number of unobservable things!
So they suggest a "Photon Collapse Interpretation." According to this theory, the photons emitted toward us actually exist. But photons that would be emitted in directions we will never observe simply collapse into utter non-existence.
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.
