Here's more on the new mitigation scenario for 1.5C. How does it work? What would society look like? Are we willing to do what's required to stop climate breakdown? See thread.
•a shift from private cars to public transportation
•reduction in flights
•smaller average house size
Meanwhile, consumption in the global South (non-Annex 1 countries) rises to converge.
•Meat consumption in high-income nations falls by about two-thirds (with specific focus on beef).
•Significant reduction in food waste.
•Global transition from industrial farming to regenerative agricultural methods to restore soils and biodiversity.
•Universal public services
•Shorter working hours
•Basic income and maximum wage
•Radical reduction in inequality
These measures ensure that all people have access to the resources they need to live flourishing lives even as aggregate economic output declines.
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.
https://t.co/hXlo8qgkD0
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get
A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from
The Taq. https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals
Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.
The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get
A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from
The Taq. https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals
Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.
The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process
@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/
