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1. I find it remarkable that some medics and scientists aren’t raising their voices to make children as safe as possible. The comment about children being less infectious than adults is unsupported by evidence.
2. @c_drosten has talked about this extensively and @dgurdasani1 and @DrZoeHyde have repeatedly pointed out flaws in the studies which have purported to show this. Now for the other assertion: children are very rarely ill with COVID19.
3. Children seem to suffer less with acute illness, but we have no idea of the long-term impact of infection. We do know #LongCovid affects some children. @LongCovidKids now speaks for 1,500 children struggling with a wide range of long-term symptoms.
4. 1,500 children whose parents found a small campaign group. How many more are out there? We don’t know. ONS data suggests there might be many, but the issue hasn’t been studied sufficiently well or long enough for a definitive answer.
5. Some people have talked about #COVID19 being this generation’s Polio. According to US CDC, Polio resulted in inapparent infection in more than 99% of people. Severe disease occurred in a tiny fraction of those infected. Source:
I find it remarkable that a section of society not rejoicing that children very rarely ill with COVID compared to other viruses and much less infectious than adults
— Michael Absoud \U0001f499 (@MAbsoud) February 12, 2021
Instead trying prove the opposite!
Why??
2. @c_drosten has talked about this extensively and @dgurdasani1 and @DrZoeHyde have repeatedly pointed out flaws in the studies which have purported to show this. Now for the other assertion: children are very rarely ill with COVID19.
3. Children seem to suffer less with acute illness, but we have no idea of the long-term impact of infection. We do know #LongCovid affects some children. @LongCovidKids now speaks for 1,500 children struggling with a wide range of long-term symptoms.
4. 1,500 children whose parents found a small campaign group. How many more are out there? We don’t know. ONS data suggests there might be many, but the issue hasn’t been studied sufficiently well or long enough for a definitive answer.
5. Some people have talked about #COVID19 being this generation’s Polio. According to US CDC, Polio resulted in inapparent infection in more than 99% of people. Severe disease occurred in a tiny fraction of those infected. Source:
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.
#DDDD $LBPS $LOAC
A thread on the potential near term catalysts behind why I have increased my position in 4d Pharma @4dpharmaplc (LON: #DDDD):
1) NASDAQ listing. This is the most obvious.
The idea behind this is that the huge pool of capital and institutional interest in the NASDAQ will enable a higher per-share valuation for #DDDD than was achievable in the UK.
Comparators to @4dpharmaplc #DDDD (market capitalisation £150m) on the NASDAQ and their market capitalisation:
Seres Therapeutics: $2.33bn = £1.72bn (has had a successful phase 3 C. difficile trial); from my previous research (below) the chance of #DDDD achieving this at least once is at least
Kaleido Biosciences: $347m = £256m. 4 products under consideration, compared to #DDDD's potential 16. When you view @4dpharmaplc's 1000+ patents and AI-driven MicroRx platform (not to mention their end-to-end manufacturing capability), 4d's undervaluation is clear.
A thread on the potential near term catalysts behind why I have increased my position in 4d Pharma @4dpharmaplc (LON: #DDDD):
1) NASDAQ listing. This is the most obvious.
The idea behind this is that the huge pool of capital and institutional interest in the NASDAQ will enable a higher per-share valuation for #DDDD than was achievable in the UK.
Comparators to @4dpharmaplc #DDDD (market capitalisation £150m) on the NASDAQ and their market capitalisation:
Seres Therapeutics: $2.33bn = £1.72bn (has had a successful phase 3 C. difficile trial); from my previous research (below) the chance of #DDDD achieving this at least once is at least
While looking at speculative pharmaceutical stocks I am reminded of why I am averse to these risky picks.#DDDD was compelling enough, though, to break this rule. The 10+ treatments under trial, industry-leading IP portfolio, and comparable undervaluation are inescapable.
— Shrey Srivastava (@BlogShrey) December 16, 2020
Kaleido Biosciences: $347m = £256m. 4 products under consideration, compared to #DDDD's potential 16. When you view @4dpharmaplc's 1000+ patents and AI-driven MicroRx platform (not to mention their end-to-end manufacturing capability), 4d's undervaluation is clear.
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.
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.
https://t.co/a6yrWK5dqg
https://t.co/Xe5xFdtDfO
https://t.co/e3RBxj0ly3
https://t.co/cJlCMqyP2v
https://t.co/5n5TK67iKB
https://t.co/Xe5xFdtDfO
https://t.co/e3RBxj0ly3
1. Monkey Outrage!
— Billy Bostickson \U0001f3f4\U0001f441&\U0001f441 \U0001f193 (@BillyBostickson) August 17, 2020
The worst treatment was kept for the monkeys. The macaques breed of monkeys are small, relatively light primates, which are often used for animal experiments at LPT. \u2018They are kept in cramped conditions in small cages. https://t.co/6D0yisjd9B
https://t.co/cJlCMqyP2v
11. Max Planck Monkey Photos (2) pic.twitter.com/0yE9D6iswp
— Billy Bostickson \U0001f3f4\U0001f441&\U0001f441 \U0001f193 (@BillyBostickson) August 17, 2020
https://t.co/5n5TK67iKB
💥💥 Situation Update, Dec. 7th – DNI John Ratcliffe, the bogus science of PCR testing and China’s GMO super soldiers
✅ I cover the bogus science behind PCR testing, explaining from a lab science point of view why no PCR instrument can “quantify” anything,
[M. Adams]
1. whether it’s a coronavirus viral load or the percentage of a food that’s GMO. In fact, literally all the tests currently conducted with PCR equipment are scientifically invalid when it comes to diagnosing illness or determining infectiousness. The sample acquisition used for
2. PCR tests — nasal swabs — aren’t even standardized! (100% bogus junk science).
After covering PCR tests, today’s update then goes into detail about Director of National Intelligence (DNI) John Ratcliffe, pointing out that he will be issuing a report on foreign interference
3. in U.S. elections on or before Dec. 18th. If this report confirms the existence of foreign interference that was capable of altering the outcome of the election, it gives President Trump full justification to declare the election null and void and dispatch military troops
4. to seize all ballots and hold a new count under military authority.
👉 Podcast notes and sources:
The office of military commissions has cleared its calendar for December:
https://t.co/u4nFRiUj8m
US military STOCKPILED Pfizer’s mRNA vaccineBEFORE it was approved by theFDA
✅ I cover the bogus science behind PCR testing, explaining from a lab science point of view why no PCR instrument can “quantify” anything,
[M. Adams]
1. whether it’s a coronavirus viral load or the percentage of a food that’s GMO. In fact, literally all the tests currently conducted with PCR equipment are scientifically invalid when it comes to diagnosing illness or determining infectiousness. The sample acquisition used for
2. PCR tests — nasal swabs — aren’t even standardized! (100% bogus junk science).
After covering PCR tests, today’s update then goes into detail about Director of National Intelligence (DNI) John Ratcliffe, pointing out that he will be issuing a report on foreign interference
3. in U.S. elections on or before Dec. 18th. If this report confirms the existence of foreign interference that was capable of altering the outcome of the election, it gives President Trump full justification to declare the election null and void and dispatch military troops
4. to seize all ballots and hold a new count under military authority.
👉 Podcast notes and sources:
The office of military commissions has cleared its calendar for December:
https://t.co/u4nFRiUj8m
US military STOCKPILED Pfizer’s mRNA vaccineBEFORE it was approved by theFDA
