sevenperforce

Let's look at the actual statistics. The most accurate way of assessing "How many people are really dying here" is not to ask what percentage of the population is dying, but how many people are dying compared to how many people usually die. The average annual death rate in the United States is 723.6 per 100,000, or 0.7%. In poor places like West Virginia, Kentucky, and Alabama it is higher: 0.9-1.0%. In places like California, Colorado, and Massachusetts it is lower: 0.6-0.7%. How many people have died from COVID this year compared to how many people usually die in a given state? In Georgia, COVID deaths are over 11% of the number of deaths in a normal year. In Arizona, COVID deaths are over 13% of the number of deaths in a normal year. In North Dakota, COVID deaths are over 16% of the number of deaths in a normal year. In Connecticut, COVID deaths are almost 21% of the number of deaths in a normal year. In New York, COVID deaths are over 28% of the number of deaths in a normal year. An average flu season in the United States is responsible for 1.4% of the number of deaths that year. Stop pretending this is normal. It isn't.

In one Texas prison, 6% of the inmates have died of COVID-19. Currently the COVID death rate in Texas prisons is approximately 30 per month and rising. More than half of those who have died in Texas jails were not even convicted of a crime; they were just awaiting trial and were too poor to post bail. And before you protest that it's "only old people" dying, 20% of dead Texas inmates were under 55. That's not negligible. Yes, primarily NL63. Since cold infections are regional, this tends to confound case-by-case evaluations of mitigation strategies. This is simply not true. I know your wife is a surgeon, but you are not accurately describing how cause of death is identified in the United States. If someone is COVID-positive and the attending physician finds that they died of pneumonia, acute respiratory distress syndrome, or another pathology related to epithelial or endothelial cell infection, the physician will assess whether the COVID infection was a contributing factor and mark the cause of death accordingly. If the infection was not a contributing factor, it will not be included on the death certificate. Love the comparison to the Kessler syndrome. Well, then, read this. https://www.nejm.org/doi/full/10.1056/NEJMoa2029717 They had 1848 Marine recruits under strict quarantine during basic training. They did regular qPCR testing. Whenever they received a positive test, they sequenced it in order to use phylogenetic analysis to locate the transmission events. The results? 16 asymptomatic carriers spread the virus to 61 more recruits. More than 90% of the cases were asymptomatic, and daily symptom monitoring did not help reveal asymptomatic cases. Phylogenetic nucleotide analysis showed that the virus spread in six clustered transmission events involving 18 people. Now, don't draw any big conclusions from the overall percentages here. These recruits were all carefully segregated and in lockdown. They are all also at the prime of their lives -- literally the most COVID-resistant group of people you could find anywhere. But this ABSOLUTELY shows that multiple stages of asymptomatic reinfections are real. Contact tracing underestimates asymptomatic transmission because it doesn't test a large enough population. With most infectious diseases, those resistant to the illness cannot effectively spread it. That is not true with COVID-19. That is why vulnerable people of all ages are dying. 100% right.

So you're telling me I'm **less** attracted to Uranus than I am to all the ones on Earth?

I agree that Ct data should be reported -- in fact, reporting Ct data along with positives could help to determine overall infection rate. Of course, Ct is not directly comparable between different manufacturers, so maybe that's why they don't. But it's simply not true that testing higher than 35 will only detect old infections. You can have positives at Ct = 38 or even higher when you are first infected and presymptomatic. If your PCR test trips positive at a Ct of 38 or 39, they shouldn't tell you you're negative. They should tell you that your test came back with a "marginal positive" and you should quarantine and retest in 2 days. If your Ct on the second test remains high, then you know it's a past infection. If your Ct has come down, then you know you caught it early and you were smart to quarantine right away. Elon's initial positive PCR test had a Ct in the mid-to-high 30s and he threw a big fit, but after Michael Mina calmed him down he admitted that subsequent PCRs had come back with Ct<20. If you stopped at 35 you would miss early infections. No it hasn't. http://91-divoc.com/pages/covid-visualization/?chart=countries-normalized&highlight=Sweden&show=25-lg&y=both&scale=linear&data=deaths&data-source=jhu&xaxis=right&extra=Netherlands%2CLuxembourg%2CUnited Kingdom%2CFrance%2CBelgium%2CItaly#countries-normalized If mitigations actually mattered, Sweden would have far worse mortality. They don't. These are cumulative deaths per capita, not deaths per day. So you have to look at the slope of the curve. 210 days ago, the death rate per capita (slope of the curve) in Sweden was approximately the same as the rates in France, Italy, and the Netherlands. It was higher than the death rate in Luxembourg. Luxembourg, France, Italy, and the Netherlands all successfully lowered the slope of their curves after that point, but Sweden didn't. Sweden's curve doesn't get close to flattening until 119 days ago. That's significantly later than Luxembourg, the Netherlands, Italy, France, or even the UK. (Belgium counts its cases differently, so the absolute number is off, but even it flattened its curve much earlier.) Immunoglobulin G and M tests are not reliable for differentiating between coronaviruses. The earliest positive PCR tests I've seen from Italian wastewater were in mid-December 2019, unless you have a different source. We know from genetic sequencing that the pandemic onset spread in China to Europe and then to the rest of the world in December and January. A handful of "conservatives" protesting is deeply concerning, but millions of "not conservatives" doing so in June was not? Because magic? Pretty sure the difference in such protest attendance is orders of magnitude. I didn't mean physically protesting; I meant that conservatives in blue states refused to follow the lockdown restrictions and thus continued to endanger everyone. Neither the anti-mask protests nor the anti-police protests were associated with any significant rise in cases, because the anti-mask protests weren't big enough and the anti-police protests typically involved masks and took place outside. Again, you have to look at the curvature of the slope. Northeastern states have much higher population density and had the earliest onset of spread, so of course they have had higher cumulative per capita deaths. But Florida, Texas, Mississippi, and other southern states have nearly monotonically-increasing rates because they're not actually mitigating. The average CFR for people under 65 is not the problem. The variance in the CFR for people under 65 is the problem. Along with the ease of transmissibility, rate of presymptomatic/asymptomatic transmission, and all the people who actually do have pre-existing conditions. Say what you will about people in nursing homes, but there are a lot of people over 65 who are NOT in nursing homes. And a lot of people with pre-existing conditions. And a lot of COVID-related complications with permanency, even in populations with low CFR. We do not have any data to suggest infection confers immunity anywhere close to what vaccination confers. Lockdown until a vaccine was never the plan. What we should have done was a serious, well-enforced, nationwide lockdown (with significant emergency federal assistance) for 3-4 weeks, to starve out the virus, then maintained reasonable containment measures (distancing, telework, N95s in public, no large-capacity events) until a vaccine. Instead we've been clawing our way forward against the wind. No, he should have been retested after a couple of days to find out whether it was an old infection that wouldn't risk the surgery team or a new infection that would.

Devastating.

So beautifully understated. Randall Munroe explains what it would be like to fly a plane on Venus: "But physics calculations give us an idea of what flight there would be like. The upshot is: Your plane would fly pretty well, except it would be on fire the whole time, and then it would stop flying, and then stop being a plane." And he has similar thoughts to you about Titan: "Humans on Titan could fly by muscle power. A human in a hang glider could comfortably take off and cruise around powered by oversized swim-flipper boots—or even take off by flapping artificial wings. The power requirements are minimal—it would probably take no more effort than walking." And let us never forget...

It should also be noted that because the F9B5 has a quadrilateral footprint, the overlay above actually exaggerates by about 41%. The critical tipover angle for F9B5 must be measured from a tipover on two legs, not a tipover on one leg. If you adjust for the actual tipover angle on F9B5 it gives you a better idea:

That terrific animation made me wonder what how the footprint of Starship compares to the footprint of the F9B5 first stage, so I did a quick overlay. This isn't to physical scale; rather, it is scaled such that it shows the relative fooprints of the two vehicles. You can see that F9B5 has a much bigger footprint relative to its height. However, it's not QUITE as bad as you might assume just by looking at Starship. Not knowing the exact distribution of mass inside a landed starship, it's hard to know the exact fatal tipover angle. But it's not too much worse than F9B5's.

This is mildly horrifying. https://covid19-projections.com/ Here's Nate Silver's discussion of it: Using statistical methods to estimate actual infections seems pretty smart.

So that's why we saw the sparks flying during the preceding test fire -- bits of martyte getting blasted to kingdom come and glowing white-hot. I love the euphemism -- "bad shutdown of Raptor." It melted. Or at least some part of its innards. If you think about it, it might not be that big of an issue on Mars. No repeated firing and no big shards of material to be weakened over time.

The virulence, spread, transmission characteristics, and mortality of SARS-CoV-2 can be pretty well-modeled by a couple of hypotheses which account for a handful of variables. The high-affinity (S) spike glycoprotein. The spike protein on the SARS-CoV-2 has an extremely high affinity for the human ACES2 receptor. Its affinity is 10-20 times higher than that of SARS-CoV-1, the coronavirus which caused SARS. So the necessary viral load for COVID-19 is very low. It doesn't take many virions to infect someone, so they can be infected readily by indirect transmission. Common human coronaviruses. 229E, NL63, OC43, and HKU1 are all prevalent coronaviruses which produce mild cold symptoms. While HKU1 and OC43 bind to the Neu5Ac receptor and 229E binds to the APN receptor, NL63 binds to ACES2 just like SARS-CoV-1 and SARS-CoV-2. NL63 is a recombinant virus which evolved from 229E about 1,000 years ago. Serological surveys in 2007 and 2008 found that depending on age, between 43% and 75% of children under age 4 had antibodies related to one of these four coronaviruses, with the highest number (75%) being NL63. In one study of older people with obstructive pulmonary disease, 98% had antibodies for NL63. Human neutralizing antibodies. The dependence of coronaviruses on their spike proteins to invade human endothelial cells means that the human immune system is quite good at dealing with them. Human neutralizing antibodies bind to one of the four domains on S1 subunit of coronavirus spike proteins, inhibiting their ability to interact with hACES2 or other receptor proteins. This doesn't directly reduce the viral population, but it reduces the ability of the virions to reproduce. Additional studies show that human neutralizing antibodies for NL63 convey short-term protective immunity against 229E despite their different spike proteins, and that SARS patients had a rise in antibodies to both 229E and NL63. Our hypothesis, then, is pretty simple. Prior infection by hCoV-229E conveys some degree of protection against SARS-CoV-2, while prior infection by hCoV-NL63 conveys a different but also-important degree of protection against SARS-CoV-2. Antibodies derived from 229E infection probably allow the human immune system to directly attack and suppress the SARS-CoV-2 population, while antibodies derived from NL63 infection probably reduce the severity of symptoms by blocking the spike proteins and inhibiting viral spread. The longer it has been since you were infected with NL63, the less available those antibodies are and thus the more serious your symptoms can be. Because SARS-CoV-2 has such a high hACES2 affinity, your chances of becoming infected is pretty high as long as you were initially exposed to a sufficient viral load. However, once you are infected, your resistance and the course of the illness depends on how recently you were exposed to NL63 and 229E. Those with high levels of 229E antibodies are not as contagious but can suffer from COVID-19 for a long time and have numerous other complications. Those with high levels of NL63 antibodies remain very contagious but have very few symptoms. If you have both antibodies, you're likely to be asymptomatic and not very contagious at all; you'll recover quickly, but you may not build up enough SARS-CoV-2 antibodies to be fully immune. Healthy people without significant antibodies from NL63 or 229E can quickly succumb because they have no natural resistance, just like people with pre-existing conditions. That hypothesis would explain the high variance in contagiousness and morbidity, as well as reports of reinfection.

LOL! Some minks in Denmark caught it, and it mutated, and now the minks are giving it back to people. No indication that it's any different (in terms of virulence or transmissibility) than the D-Strain or G-strain, but it seems to be vaccine-resistant, so that sucks. They are working hard to keep it contained. The biggest risk right now would be a zoonotic mutation that increases the deadliness of the virus without reducing how rapidly it spreads. MERS, for example, is fatal in 35% of diagnosed cases. The good news is that the relatively low CFR in most of the population is probably part of why COVID-19 spreads so rapidly. It is contagious in carriers who are asymptomatic, presymptomatic, or mild-symptomatic, which encourages transmission. But if people got sicker, then there would be fewer asymptomatic/presymptomatic transmission events. The scary scenario would be a mutation that increases the lethality of serious infections without decreasing the percentage of asymptomatic/mild-symptomatic cases. Which could mean that parents could be protected against COVID-19 by their kids. By having endured lots of infections in the previous years that their kids "brought home" from day care or school. (As I mentioned earlier in this thread.) P.S. Yes, I'm aware, it's a theory. And it could also be the other way around. But I like the idea that parents may have a benefit from being sick all the time. I mean it certainly fits that data. Children trade common colds all year long and their parents are exposed as well, so children can be carriers but typically have good disease outcomes.

The metal itself probably ignited.

Research to date shows that the mutation rate of SARS-CoV-2 does not adversely impact vaccine efficacy. https://www.newswise.com/coronavirus/potential-covid-19-vaccines-not-affected-by-dominant-g-strain There are two major strains, D-strain and G-strain. The initial vaccines were developed on D-strain but are still effective against G-strain. The cluster-5 variant could be a problem, though.

Looks like we now know where the drippy slag from SN8 originated. Melty.

The very first rocket designed for a moon mission would have used a heat shield for ascent but not for re-entry. It would not have gone well.

We don't know yet what sort of natural immunity is conferred by infection. We also don't know the dependency of mutagenic rate on immunity. There are certain things like strep that most people will never be immune to. Strep is a very hardy bacteria that must be beaten down with antibiotics before the immune system can really deal with it. As a result, even if you have strep antibodies, your immune system cannot defeat it faster than it duplicates and so you can be reinfected. Before the invention of antibiotics, strep throat could be fatal or could progress to scarlet fever. My ex actually ignored her strep throat (at age 26!!) long enough that it became scarlet fever...one of the first scarlet fever cases her doctor had ever seen in an adult. If you beat scarlet fever without antibiotics, you are immune to strep for life. You're probably also scarred for life, but that's another matter. Flu antibodies last a lifetime. However, flu mutates so fast (and each flu season contains multiple flu strains) that immunity does not last longer than a single flu season, because your antibodies are only useful against a single strain. The flu vaccine is effective because it stimulates antibody production for a wide variety of strains at once, although it is still not 100% effective. So what about COVID? A SARS-CoV-2 infection certainly produces antibodies, but will the antibodies for one strain work against other strains? SARS-CoV-2 mutates fairly quickly but none of the mutations have been shown to be very significant, so it's possible that the antibodies protect you against other strains. Alternately, they may provide partial protection...meaning you will still contract a new strain, but your symptoms will be minor, just like how the flu vaccine can reduce the severity of influenza even if you catch it. Unfortunately, with something as virulent as this virus, an asymptomatic or mild-symptom case increases your risk of spreading it to other people. One of my early theories (which I still think seems probable) is that people with past exposure to mild coronaviruses (like the common cold) had partial protection against SARS-CoV-2. As a result, they had mild symptoms or no symptoms, and recovered quickly but spread the virus rapidly. This explains the huge variance in symptomaticity and why resistance seemed to be "clustered" in certain groups. An effective vaccine would confer broad protection against all known strains, so you should still get the vaccine even if you have recently had COVID and recovered.

The flame creep up the sides of stage 1 just past Max-Q was spectacular. Looked like a Saturn V.

I don’t see anything in the trunk.

I can’t believe I missed the launch. Nice to see the rest of it though.

According to official sources out of Ontario, the CDC has been able to culture live SARS-CoV-2 from Ct over 35, but only very rarely. One issue is the variability between tests. Each manufacturer tests its assays against negative controls so one assay’s positivity cutoff could be 37 while another could be 42. This may be where we are going to disagree strongly. I have seen no evidence beyond speculation that tests at Ct > 32 constitute a majority of positive tests, let alone a vast majority. Are you in NM then? Sweden’s mortality has skyrocketed in comparison to most of Europe. I agree that the United States did a terrible job. Blue states had restrictive lockdowns that didn’t do much good because red states refused to follow suit and conservatives in blue states kept protesting. There was no national leadership and so we have had draconian restrictions for little or no reason. If we had done the right thing and gone to a national lockdown early, we could have brought transmission low enough at the beginning. I’m glad Elon has a mild case. The problem is that the variance in case severity is ridiculously high. Some people are contagious and asymptomatic. Some people are contagious but their symptoms are so mild that they think it’s just allergies and they’re spreading it like crazy. Some people are dead in under a week with no pre-existing conditions.

It was as much info as I could fit into the medium -- I didn't have time to go into the impact of Ct and doubling via amplification. True FP for COVID PCR is roughly 0.01% based on the Ontario guidelines. Anything under Ct 25 means you're contagious. From 25-35 you're looking at a low risk of contagiousness; it's more probable that you've recovered. At 35-38 you're definitely not contagious but you still definitely had the virus recently. Above 38-40 cycles you get into the possibility of amplifying incomplete viral material. They shouldn't stop cycling at 30; that's a bad idea. But they should report cycle threshold on positives so that physicians can make recommendations.

It was pointed out to me that discussion of Elon's poor decision-making w/r/t COVID would be better suited for this thread, so....

Remember the ideal gas equation: PV = nRT. Recall, also, that the boiling point of a liquid scales with changes in the temperature of the liquid. Pumping hot, pressurized GOX into the top of the header tank will not significantly increase the temperature of the LOX itself, because the heat transfer coefficient between gas and liquid is very low. However, the heat transfer coefficient between liquid and solid is higher and so the LOX will warm up a lot while flowing down the feed line; that LOX in the feed line will be significantly warmer than the LOX in the header tank or in the main tank because it has more surface area exposure. Adding insulation to the feed line might help matters. Another question I'm not sure about -- is there a phase transition in the LOX or the CH4 between the feed lines and the preburners? The schematics I've seen have both propellants remaining liquid all the way through until they enter the preburners, but if there is a phase transition, then the enthalpy of vaporization would be the primary source of cooling and the entry temperature wouldn't matter. The more I think about it, the more convinced I am that adding gas accumulators to Starship is going to be necessary. Just posted about Elon:

Pure trivia here, but coal is so bad that it kills more people per kilowatt-hour than nuclear power even if you include Hiroshima and Nagasaki as part of "nuclear power".