This is the exact problem with our government's thinking & response- despite this strategy of 'tolerating deaths' and half-way measures having spectacularly failed, it's quite amazing that our govt still hasn't learned anything, & continues to promote a policy of death. Thread
U.K. needs to confront
— Esther McVey (@EstherMcVey1) January 2, 2021
\u2018The challenge that faces us is to decide - are we going to try to pursue the elimination of Covid-19 regardless of the costs or decide on a tolerable level of deaths (like we do with the flu) in order to return to a normal life?\u2019
https://t.co/9hWbHIPJUq
https://t.co/VPqJBbkFik
The govt has completely failed us & their continued pursuit of pseudoscience will cost many more lives.
More from Deepti Gurdasani
Brief thread to debunk the repeated claims we hear about transmission not happening 'within school walls', infection in school children being 'a reflection of infection from the community', and 'primary school children less likely to get infected and contribute to transmission'.
I've heard a lot of scientists claim these three - including most recently the chief advisor to the CDC, where the claim that most transmission doesn't happen within the walls of schools. There is strong evidence to rebut this claim. Let's look at
Let's look at the trends of infection in different age groups in England first- as reported by the ONS. Being a random survey of infection in the community, this doesn't suffer from the biases of symptom-based testing, particularly important in children who are often asymptomatic
A few things to note:
1. The infection rates among primary & secondary school children closely follow school openings, closures & levels of attendance. E.g. We see a dip in infections following Oct half-term, followed by a rise after school reopening.
We see steep drops in both primary & secondary school groups after end of term (18th December), but these drops plateau out in primary school children, where attendance has been >20% after re-opening in January (by contrast with 2ndary schools where this is ~5%).
I've heard a lot of scientists claim these three - including most recently the chief advisor to the CDC, where the claim that most transmission doesn't happen within the walls of schools. There is strong evidence to rebut this claim. Let's look at
The science shows us that most disease transmission does not happen in the walls of the school, but it comes in from the community. So, CDC is advocating to get our K-5 students back in school at least in a hybrid mode with universal mask wearing and 6 ft of distancing. https://t.co/dfvJ2nl2s4
— Rochelle Walensky, MD, MPH (@CDCDirector) February 14, 2021
Let's look at the trends of infection in different age groups in England first- as reported by the ONS. Being a random survey of infection in the community, this doesn't suffer from the biases of symptom-based testing, particularly important in children who are often asymptomatic
A few things to note:
1. The infection rates among primary & secondary school children closely follow school openings, closures & levels of attendance. E.g. We see a dip in infections following Oct half-term, followed by a rise after school reopening.
We see steep drops in both primary & secondary school groups after end of term (18th December), but these drops plateau out in primary school children, where attendance has been >20% after re-opening in January (by contrast with 2ndary schools where this is ~5%).
Thread on the recent report on the possible risk of increased death associated with the new UK variant (B117)- with a discussion of the evidence around this, and what this means.
First, there is strong evidence to support increased transmissibility of B117 - current estimates of increased transmissibility range between 30-70% - from epidemiological evidence examining the differential rate of growth of B117 with respect to other variants & increase in R
There is also evidence from PHE contact studies that the risk of transmission from those carrying the B117 variant is ~50% greater than with other non-B117 variants.
Increased transmissibility, even if a variant has the same fatality rate can increase deaths substantially, because the rate of growth of cases is higher- & more cases means more deaths.
Increased fatality rates also increase deaths- but do so
So how was risk of death with the variant studied?
We don't routinely sequence all samples for the virus. We've found that the variant has a particular deletion which means that some PCR tests on samples with the variant give a different read-out when the variant is present.
First, there is strong evidence to support increased transmissibility of B117 - current estimates of increased transmissibility range between 30-70% - from epidemiological evidence examining the differential rate of growth of B117 with respect to other variants & increase in R
There is also evidence from PHE contact studies that the risk of transmission from those carrying the B117 variant is ~50% greater than with other non-B117 variants.
Increased transmissibility, even if a variant has the same fatality rate can increase deaths substantially, because the rate of growth of cases is higher- & more cases means more deaths.
Increased fatality rates also increase deaths- but do so
How dangerous are the B.1.1.7 and 501Y.V2 hyper-transmissible strains?
— Eric Topol (@EricTopol) January 11, 2021
by @AdamJKucharski @CFR_orghttps://t.co/aycWMN3b5h
h/t @Karl_Lauterbach pic.twitter.com/JlaFzzP06t
So how was risk of death with the variant studied?
We don't routinely sequence all samples for the virus. We've found that the variant has a particular deletion which means that some PCR tests on samples with the variant give a different read-out when the variant is present.
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Keep dwelling on this:
Further Examination of the Motif near PRRA Reveals Close Structural Similarity to the SEB Superantigen as well as Sequence Similarities to Neurotoxins and a Viral SAg.
The insertion PRRA together with 7 sequentially preceding residues & succeeding R685 (conserved in β-CoVs) form a motif, Y674QTQTNSPRRAR685, homologous to those of neurotoxins from Ophiophagus (cobra) and Bungarus genera, as well as neurotoxin-like regions from three RABV strains
(20) (Fig. 2D). We further noticed that the same segment bears close similarity to the HIV-1 glycoprotein gp120 SAg motif F164 to V174.
https://t.co/EwwJOSa8RK
In (B), the segment S680PPRAR685 including the PRRA insert and highly conserved cleavage site *R685* is shown in van der Waals representation (black labels) and nearby CDR residues of the TCRVβ domain are labeled in blue/white
https://t.co/BsY8BAIzDa
Sequence Identity %
https://t.co/BsY8BAIzDa
Y674 - QTQTNSPRRA - R685
Similar to neurotoxins from Ophiophagus (cobra) & Bungarus genera & neurotoxin-like regions from three RABV strains
T678 - NSPRRA- R685
Superantigenic core, consistently aligned against bacterial or viral SAgs
Further Examination of the Motif near PRRA Reveals Close Structural Similarity to the SEB Superantigen as well as Sequence Similarities to Neurotoxins and a Viral SAg.
The insertion PRRA together with 7 sequentially preceding residues & succeeding R685 (conserved in β-CoVs) form a motif, Y674QTQTNSPRRAR685, homologous to those of neurotoxins from Ophiophagus (cobra) and Bungarus genera, as well as neurotoxin-like regions from three RABV strains
(20) (Fig. 2D). We further noticed that the same segment bears close similarity to the HIV-1 glycoprotein gp120 SAg motif F164 to V174.
https://t.co/EwwJOSa8RK
In (B), the segment S680PPRAR685 including the PRRA insert and highly conserved cleavage site *R685* is shown in van der Waals representation (black labels) and nearby CDR residues of the TCRVβ domain are labeled in blue/white
https://t.co/BsY8BAIzDa
Sequence Identity %
https://t.co/BsY8BAIzDa
Y674 - QTQTNSPRRA - R685
Similar to neurotoxins from Ophiophagus (cobra) & Bungarus genera & neurotoxin-like regions from three RABV strains
T678 - NSPRRA- R685
Superantigenic core, consistently aligned against bacterial or viral SAgs
"I really want to break into Product Management"
make products.
"If only someone would tell me how I can get a startup to notice me."
Make Products.
"I guess it's impossible and I'll never break into the industry."
MAKE PRODUCTS.
Courtesy of @edbrisson's wonderful thread on breaking into comics – https://t.co/TgNblNSCBj – here is why the same applies to Product Management, too.
There is no better way of learning the craft of product, or proving your potential to employers, than just doing it.
You do not need anybody's permission. We don't have diplomas, nor doctorates. We can barely agree on a single standard of what a Product Manager is supposed to do.
But – there is at least one blindingly obvious industry consensus – a Product Manager makes Products.
And they don't need to be kept at the exact right temperature, given endless resource, or carefully protected in order to do this.
They find their own way.
make products.
"If only someone would tell me how I can get a startup to notice me."
Make Products.
"I guess it's impossible and I'll never break into the industry."
MAKE PRODUCTS.
Courtesy of @edbrisson's wonderful thread on breaking into comics – https://t.co/TgNblNSCBj – here is why the same applies to Product Management, too.
"I really want to break into comics"
— Ed Brisson (@edbrisson) December 4, 2018
make comics.
"If only someone would tell me how I can get an editor to notice me."
Make Comics.
"I guess it's impossible and I'll never break into the industry."
MAKE COMICS.
There is no better way of learning the craft of product, or proving your potential to employers, than just doing it.
You do not need anybody's permission. We don't have diplomas, nor doctorates. We can barely agree on a single standard of what a Product Manager is supposed to do.
But – there is at least one blindingly obvious industry consensus – a Product Manager makes Products.
And they don't need to be kept at the exact right temperature, given endless resource, or carefully protected in order to do this.
They find their own way.