#MadagascarFrogs
It's another stunning Malagasy #dartfrog/#poisonfrog for today's #FrogOfTheDay, #42 Mantella cowani Boulenger, 1882! A highly threatened, actively conserved and managed frog from the highlands of central #Madagascar
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📸D.Edmonds/CalPhotos
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https://t.co/dwaHMbrYbj
#MadagascarFrogs
📸B.Freiermuth/CalPhotos
#MadagascarFrogs
📸Mantella cowanii Action Plan, 2021–2025 (on which more below)
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https://t.co/VMFGZ7tP0Y
https://t.co/9uFZ7KBRzZ
https://t.co/gJXip5xMTv
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https://t.co/SAON3F2VqF
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https://t.co/ozm89CMSSR
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.
Ever since @JesseJenkins and colleagues work on a zero carbon US and this work by @DrChrisClack and colleagues on incorporating DER, I've been having the following set of thoughts about how to reduce the risk of failure in a US clean energy buildout. Bottom line is much more DER.
Typically, when we see zero-carbon electricity coupled to electrification of transport and buildings, implicitly standing behind that is totally unprecedented buildout of the transmission system. The team from Princeton's modeling work has this in spades for example.
But that, more even than the new generation required, runs straight into a thicket/woodchipper of environmental laws and public objections that currently (and for the last 50y) limit new transmission in the US. We built most transmission prior to the advent of environmental law.
So what these studies are really (implicitly) saying is that NEPA, CEQA, ESA, §404 permitting, eminent domain law, etc, - and the public and democratic objections that drive them - will have to change in order to accommodate the necessary transmission buildout.
I live in a D supermajority state that has, for at least the last 20 years, been in the midst of a housing crisis that creates punishing impacts for people's lives in the here-and-now and is arguably mostly caused by the same issues that create the transmission bottlenecks.
Rooftop solar can play a key role in a transition to 100% renewable energy - and it can help American's pocketbooks #GoSolarhttps://t.co/6p9jb62EGW
— Environment America (@EnvAm) January 14, 2021
Typically, when we see zero-carbon electricity coupled to electrification of transport and buildings, implicitly standing behind that is totally unprecedented buildout of the transmission system. The team from Princeton's modeling work has this in spades for example.
But that, more even than the new generation required, runs straight into a thicket/woodchipper of environmental laws and public objections that currently (and for the last 50y) limit new transmission in the US. We built most transmission prior to the advent of environmental law.
So what these studies are really (implicitly) saying is that NEPA, CEQA, ESA, §404 permitting, eminent domain law, etc, - and the public and democratic objections that drive them - will have to change in order to accommodate the necessary transmission buildout.
I live in a D supermajority state that has, for at least the last 20 years, been in the midst of a housing crisis that creates punishing impacts for people's lives in the here-and-now and is arguably mostly caused by the same issues that create the transmission bottlenecks.
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1/12
RT-PCR corona (test) scam
Symptomatic people are tested for one and only one respiratory virus. This means that other acute respiratory infections are reclassified as
2/12
It is tested exquisitely with a hypersensitive non-specific RT-PCR test / Ct >35 (>30 is nonsense, >35 is madness), without considering Ct and clinical context. This means that more acute respiratory infections are reclassified as
3/12
The Drosten RT-PCR test is fabricated in a way that each country and laboratory perform it differently at too high Ct and that the high rate of false positives increases massively due to cross-reaction with other (corona) viruses in the "flu
4/12
Even asymptomatic, previously called healthy, people are tested (en masse) in this way, although there is no epidemiologically relevant asymptomatic transmission. This means that even healthy people are declared as COVID
5/12
Deaths within 28 days after a positive RT-PCR test from whatever cause are designated as deaths WITH COVID. This means that other causes of death are reclassified as
RT-PCR corona (test) scam
Symptomatic people are tested for one and only one respiratory virus. This means that other acute respiratory infections are reclassified as
4/10
— Dr. Thomas Binder, MD (@Thomas_Binder) October 22, 2020
...indication, first of all that testing for a (single) respiratory virus is done outside of surveillance systems or need for specific therapy, but even so the lack of consideration of Ct, symptoms and clinical findings when interpreting its result. https://t.co/gHH6kwRdZG
2/12
It is tested exquisitely with a hypersensitive non-specific RT-PCR test / Ct >35 (>30 is nonsense, >35 is madness), without considering Ct and clinical context. This means that more acute respiratory infections are reclassified as
6/10
— Dr. Thomas Binder, MD (@Thomas_Binder) October 22, 2020
The neither validated nor standardised hypersensitive RT-PCR test / Ct 35-45 for SARS-CoV-2 is abused to mislabel (also) other diseases, especially influenza, as COVID-19.https://t.co/AkFIfTCTkS
3/12
The Drosten RT-PCR test is fabricated in a way that each country and laboratory perform it differently at too high Ct and that the high rate of false positives increases massively due to cross-reaction with other (corona) viruses in the "flu
External peer review of the RTPCR test to detect SARS-CoV-2 reveals 10 major scientific flaws at the molecular and methodological level: consequences for false positive results.https://t.co/mbNY8bdw1p pic.twitter.com/OQBD4grMth
— Dr. Thomas Binder, MD (@Thomas_Binder) November 29, 2020
4/12
Even asymptomatic, previously called healthy, people are tested (en masse) in this way, although there is no epidemiologically relevant asymptomatic transmission. This means that even healthy people are declared as COVID
Thread web\u2b06\ufe0f\u2b07\ufe0f
— Dr. Thomas Binder, MD (@Thomas_Binder) December 16, 2020
The fabrication of the "asymptomatic (super) spreader" is the coronation of the total nons(ci)ense in the belief system of #CoronasWitnesses.
Asymptomatic transmission 0.7%; 95% CI 0%-4.9% - could well be 0%!https://t.co/VeZTzxXfvT
5/12
Deaths within 28 days after a positive RT-PCR test from whatever cause are designated as deaths WITH COVID. This means that other causes of death are reclassified as
8/8
— Dr. Thomas Binder, MD (@Thomas_Binder) March 24, 2020
By the way, who the f*** created this obviously (almost) worldwide definition of #CoronaDeath?
This is not only medical malpractice, this is utterly insane!https://t.co/FFsTx4L2mw
