So proud of my @UNGlobalPulse team and collaborators that step by step and over the years have managed to bring 🤖 science closer to humanitarian and development work. We now have a library!! 📚 📚📚 https://t.co/rOxXQRllo5 Some peer-reviewed highlights in this thread 👇
More from Science
JUST ONE PERSON—UK 🇬🇧 scientists think one immunocompromised person who cleared virus slowly & only partially wiped out an infection, leaving behind genetically-hardier viruses that rebound & learn how to survive better. That’s likely how #B117 started. 🧵 https://t.co/bMMjM8Hiuz
2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.
same thing happened in Boston in another immunocompromised person that was sick for 155 days.
3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117.
4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved.
5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.
2) The leading hypothesis is that the new variant evolved within just one person, chronically infected with the virus for so long it was able to evolve into a new, more infectious form.
same thing happened in Boston in another immunocompromised person that was sick for 155 days.
3) What happened in Boston with one 45 year old man who was highly infectious for 155 days straight before he died... is exactly what scientists think happened in Kent, England that gave rise to #B117.
Immunocompromised 45 year old suffered from #COVID19 for 155 days before he died. The virus was changing very quickly inside the man's body\u2014it acquired a big cluster of >20 mutations\u2014resembled the same ones seen in #B117 & #B1351. (NPR audio Part 1 of 2)\U0001f9f5https://t.co/7kWiBZ1xGk pic.twitter.com/ZJ7AExB78Y
— Eric Feigl-Ding (@DrEricDing) February 8, 2021
4) Doctors were shocked to find virus has evolved many different forms inside of this one immunocompromised man. 20 new mutations in one virus, akin to the #B117. This is possibly how #B1351 in South Africa 🇿🇦 and #P1 in Brazil 🇧🇷 also evolved.
2) NPR report audio part 2 of 2:
— Eric Feigl-Ding (@DrEricDing) February 8, 2021
Dr. Li couldn't believe what they found. "I was shocked," he says. "When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important." pic.twitter.com/HT3Yt6djFd
5) “On its own, the appearance of a new variant in genomic databases doesn’t tell us much. “That’s just one genome amongst thousands every week. It wouldn’t necessarily stick out,” says Oliver Pybus, a professor of evolution and infectious disease at Oxford.
@mugecevik is an excellent scientist and a responsible professional. She likely read the paper more carefully than most. She grasped some of its strengths and weaknesses that are not apparent from a cursory glance. Below, I will mention a few points some may have missed.
1/
The paper does NOT evaluate the effect of school closures. Instead it conflates all ‘educational settings' into a single category, which includes universities.
2/
The paper primarily evaluates data from March and April 2020. The article is not particularly clear about this limitation, but the information can be found in the hefty supplementary material.
3/
The authors applied four different regression methods (some fancier than others) to the same data. The outcomes of the different regression models are correlated (enough to reach statistical significance), but they vary a lot. (heat map on the right below).
4/
The effect of individual interventions is extremely difficult to disentangle as the authors stress themselves. There is a very large number of interventions considered and the model was run on 49 countries and 26 US States (and not >200 countries).
5/
1/
I've recently come across a disinformation around evidence relating to school closures and community transmission that's been platformed prominently. This arises from flawed understanding of the data that underlies this evidence, and the methodologies used in these studies. pic.twitter.com/VM7cVKghgj
— Deepti Gurdasani (@dgurdasani1) February 1, 2021
The paper does NOT evaluate the effect of school closures. Instead it conflates all ‘educational settings' into a single category, which includes universities.
2/
The paper primarily evaluates data from March and April 2020. The article is not particularly clear about this limitation, but the information can be found in the hefty supplementary material.
3/
The authors applied four different regression methods (some fancier than others) to the same data. The outcomes of the different regression models are correlated (enough to reach statistical significance), but they vary a lot. (heat map on the right below).
4/
The effect of individual interventions is extremely difficult to disentangle as the authors stress themselves. There is a very large number of interventions considered and the model was run on 49 countries and 26 US States (and not >200 countries).
5/
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
https://t.co/V3D1umHf04
Carp can switch over to an anaerobic metabolism and quietly exhale booze until the situation gets better.
They basically evolved the same metabolic pathway as yeast, independently.
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.
The really interesting thing about anaerobic carp, is that they can go 4-5 months without oxygen by relying on liver glycogen.
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.
In humans, glycogen is also burned for energy. This is where the marathon runner's bonk comes from: you only have about 2,000 calories worth, and running a marathon burns those 2,000 calories.
The waste ethanol is diffused out the gills
https://t.co/V3D1umHf04
Carp can switch over to an anaerobic metabolism and quietly exhale booze until the situation gets better.
They basically evolved the same metabolic pathway as yeast, independently.
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.
The really interesting thing about anaerobic carp, is that they can go 4-5 months without oxygen by relying on liver glycogen.
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.
In humans, glycogen is also burned for energy. This is where the marathon runner's bonk comes from: you only have about 2,000 calories worth, and running a marathon burns those 2,000 calories.
Recently I learned something about DNA that blew my mind, and in this thread, I'll attempt to blow your mind as well. Behold: Chargaff's 2nd Parity Rule for DNA N-Grams.
If you are into cryptography or reverse engineering, you should love this.
Thread:
DNA consists of four different 'bases', A, C, G and T. These bases have specific meaning within our biology. Specifically, within the 'coding part' of a gene, a triplet of bases encodes for an amino acid
Most DNA is stored redundantly, in two connected strands. Wherever there is an A on one strand, you'll find a T on the other one. And similarly for C and G:
T G T C A G T
A C A G T C A
(note how the other strand is upside down - this matters!)
If you take all the DNA of an organism (both strands), you will find equal numbers of A's and T's, as well as equal numbers of C's and G's. This is true by definition.
This is called Chargaff's 1st parity rule.
https://t.co/jD4cMt0PJ0
Strangely enough, this rule also holds per strand! So even if you take away the redundancy, there are 99% equal numbers of A/T and C/G * on each strand *. And we don't really know why.
This is called Chargaff's 2nd parity rule.
If you are into cryptography or reverse engineering, you should love this.
Thread:
DNA consists of four different 'bases', A, C, G and T. These bases have specific meaning within our biology. Specifically, within the 'coding part' of a gene, a triplet of bases encodes for an amino acid
Most DNA is stored redundantly, in two connected strands. Wherever there is an A on one strand, you'll find a T on the other one. And similarly for C and G:
T G T C A G T
A C A G T C A
(note how the other strand is upside down - this matters!)
If you take all the DNA of an organism (both strands), you will find equal numbers of A's and T's, as well as equal numbers of C's and G's. This is true by definition.
This is called Chargaff's 1st parity rule.
https://t.co/jD4cMt0PJ0
Strangely enough, this rule also holds per strand! So even if you take away the redundancy, there are 99% equal numbers of A/T and C/G * on each strand *. And we don't really know why.
This is called Chargaff's 2nd parity rule.
