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Posts posted by Txzen
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Having rented a few boats on local lakes recently, none of them came with an anchor. I can somewhat understand it as there can be a bit of an art to property anchoring a boat in wind and current, let alone accounting for what it may be sticking in (sounds like this lake/reservoir had lots of submerged foliage). I'm going to guess she was not a super experienced boater, and it is often surprising how much even a big pontoon boat can drift in the breeze. Agreed the whole scenario has some strange components to it, though.
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4 hours ago, ChiTownDoc said:
Sister in Law lives in Geneva. Switzerland is pretty badass. Starts to feel small but quick flight to some other amazing places.
Oh and it’s expensive af.Lovely place, but (and no offense to your SIL) unfortunately it's full of Swiss people.
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It will be interesting to see if the inhaled form has even greater benefit.
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That's probably a fair interpretation of the data, the question then is how many particles (and how unlucky) do you have to be to contract it. But it's measuring the actual number of viral particles (titer), and note that we're starting with a pretty large number, and that's a log scale graph.
These are all mechanically-generated aerosols, and there are other studies out there which say you've got measurable virus farther out to 16h : link
There's some additional consideration that aerosols are not always so easily generated in real life, and the dynamics of a normal room (like an OR) could be different: Link
Quote“These are only generated under very specific circumstances during certain hospital procedures,” she explains, such as bronchoscopy or intubation. That could actually mean these findings – which saw COVID-19 aerosols created using a nebulizer – hold some good news for ongoing coronavirus treatment.
“This data suggests that aerosolized virus half-life is measured in hours,” Dr. Rasmussen suggests, “and aerosols generated by these medical procedures will not persist for days, for example in the hospital procedure rooms.”
“Furthermore, both viruses also showed a 3-log decrease in infectious virus on stainless steel and plastic surfaces after 48-72 hours,” she added. “This suggests that, while viruses can stay on some surfaces for days, their infectious titer is greatly reduced (1000-fold).”
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On 6/22/2020 at 12:37 PM, jimmyjazz said:
I'm sure I could dig back and find this, but maybe someone can provide a quick answer informed by current science:
What is the expected "hang time" for aerosolized particles indoors? One of my wife's best friends owns a dance studio and her employee who did routine after-class cleaning quit. The owner can't do it all herself so she asked my wife to help out. I'm just wondering how long is a reasonable amount of time to wait after classes before entering the facility. All kids wear masks while in class . . . but, kids. All are screened for fever before class as well, but that's certainly not diagnostically robust.
We want to help her out, as she has always been super helpful to us, but I need to know the risks.
I think the issue (for me) would be an indoor area where a lot of exertion has occurred. The more and deeper you breathe, the more droplets you will generate
There's a fair amount of data out there on survival or aerosols of this coronovirus family. I think the time component of aerosol infectivity is still in the period of understanding, and it certainly depends on the size of the droplet, the temperature at least:
- "...airborne coronavirus MERS-CoV exhibited strong capability of surviving, with about 64% of microorganisms remaining infectious 60 min after atomization at 25 °C and 79% relative humidity (RH) (9). On the other hand, rapid virus decay occurred, with only 5% survival over a 60-min procedure at 38 °C and 24% RH, indicative of inactivation. Recent experimental studies have examined the stability of SARS-CoV-2, showing that the virus remains infectious in aerosols for hours (12) and on surfaces up to days". link
- "The SARS-CoV-2 virus has been found to remain viable in aerosols for 3 h, while it, in the form of droplets, is more stable on plastic and stainless steel, copper, cardboard, and glass with durations detected up to 72, 4, 24, and 84 h, respectively. In comparison, the SARS-CoV virus was also found to be airborne in the form of aerosols for 3 h, indicating that both SARS viruses behave more or less in the same manner in the air. Nevertheless, the SARS-CoV virus remains stable and viable in the form of droplets on plastic and stainless steel, copper, cardboard, and glass with durations (half-lives) lasting to 72, 8, 8, and 96 h, respectively." link, and the original NEJM paper which shows at least 3h of aerosol data: NEJM
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2 hours ago, Captainant said:
Even followed parliamentarian procedure. Nice lmao
"I yield my time, FUCK YOU"
Robert's Rules of Order, motherfucker.
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3 hours ago, Treefidy said:
Not just speculation, let me help out with this line of thinking.
here: https://www.nature.com/articles/nm.3985.pdf?origin=ppub
this is a scientific paper about how they were combining SHC014 which is the virus 96% similar to COV19 with SARS to create something that
And about SHC014
https://www.sciencedaily.com/releases/2015/11/151110115711.htm
i mean, it's not as good as YouTube for some people on here, but they were absolutely fucking around with bat corona viruses and making new ones that were both highly pathogenic, infects the airways through ACE2, transfers straight from bat to humans, and resistant to known treatments. We don't know for certain where this virus originated but all the coincidences surrounding the lab make it hard to think it instead came from the market a block away with no known intermediate host.
Seems a lot more likely it came out of the lab and the market turned out to be an early place for it to spread easily.
You cracked it, man - the virus came from UNC Chapel Hill (where most of the authors of those papers were from).
No credible evidence supporting claims of the laboratory engineering of SARS-CoV-2
QuoteSome people have alleged that the human SARS-CoV-2 was leaked directly from a laboratory in Wuhan where a bat CoV (RaTG13) was recently reported, which shared ∼96% homology with the SARS-CoV-2 [4]. However, as we know, the human SARS-CoV and intermediate host palm civet SARS-like CoV shared 99.8% homology, with a total of 202 single-nucleotide (nt) variations (SNVs) identified across the genome [6]. Given that there are greater than 1,100 nt differences between the human SARS-CoV-2 and the bat RaTG13-CoV [4], which are distributed throughout the genome in a naturally occurring pattern following the evolutionary characteristics typical of CoVs, it is highly unlikely that RaTG13 CoV is the immediate source of SARS-CoV-2. The absence of a logical targeted pattern in the new viral sequences and a close relative in a wildlife species (bats) are the most revealing signs that SARS-CoV-2 evolved by natural evolution.
QuoteAnother claim in Chinese social media points to a Nature Medicine paper published in 2015 [7], which reports the construction of a chimeric CoV with a bat CoV S gene (SHC014) in the backbone of a SARS CoV that has adapted to infect mice (MA15) and is capable of infecting human cells [8]. However, this claim lacks any scientific basis and must be discounted because of significant divergence in the genetic sequence of this construct with the new SARS-CoV-2 (>5,000 nucleotides).
QuoteRegardless, upon careful phylogenetic analyses by multiple international groups [5,14], the SARS-CoV-2 is undoubtedly distinct from SL-SHC014-MA15, with >6,000 nucleotide differences across the whole genome. Therefore, once again there is no credible evidence to support the claim that the SARS-CoV-2 is derived from the chimeric SL-SHC014-MA15 virus.
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56 minutes ago, ChiTownDoc said:
Definitely next level shit.
It is, but this same approach for MERS and SARS didn't really get far as previously mentioned, though that may be more business driven than science driven.
I see early safety reports from this approach from Oxford for SARS and MERS, with similar findings that it appears that neutralizing antibodies were produced, and cellular immunity induced. Don't know if it actually provides immunity, yet. It sure needs to work.
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1 hour ago, XYZ said:
The common cold is also a coronavirus, there there ain’t no vaccine for that, either.
Amongst the viruses that make up the common cold are such diverse elements as the coronovirus...I'll come in again.
Ain't no vaccine because there's no pressing medical need.
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1 minute ago, BabaYaga said:
You willing to bet your entire life's savings on that? Your house? Your car? Your job? Your family? All I'm saying is this can't continue. Big pharma is not the light at the end of the tunnel. If they are, we should all be scared. Destroying generational wealth for a virus with a mortality rate of less than 1% isn't going to cut it for much longer.
Clearly I won't waste my time talking science with you. Carry on.
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16 minutes ago, BabaYaga said:
We can "hope", but hope is not a plan. Nor does the economy or people's livelihood have 18 months to gamble on this. In 18 months if maintaining our current SOP of being locked up, would make the Great Depression look like a wet fart in a windstorm.
There are way more resources being thrown at COVID-19 than SARS across the entire pharma industry right now. There is a plan, and hope.
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23 minutes ago, BabaYaga said:
We are a decade removed from the earlier Coronavirus (SARS) and still without a vaccine. I have little faith 18 months from now this will change. I hope it will, but pinning the removal of SIP on a vaccine seems incredibly dangerous.
That gives me pause as well, though I'm still hopeful. In the end, SARS didn't have nearly the long-lasting or global impact, and so I think there was less motivation to continue with the research. The paucity of infectious disease research in large pharma I think also contributed to this - in the last 10 years so many have gotten out of the business all together. So perhaps there are some economical and business factors driving this (as well as some potential scientific hurdles posed by the coronovirus itself).
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2 hours ago, Newdoc said:
Also, the protocols are all borked from a surface glance. The drug is given to various people at various stages in their illness. End points appear to discharge or death. You’re going to need a LARGE sample size to get good data out of that.
It's kind of important to understand when in the patient management cycle the drug will be effective. Obviously if you are in the middle of CRS and multi-organ failure, the clinical situation is more complicated. But that's why you run the study with wide inclusion criteria.
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2 hours ago, Anastasis said:
Posted this on the #stonk thread, because I am inclined to short GILD each time they pull one of these bullshit announcements.
I believe that this is the right study. https://clinicaltrials.gov/ct2/show/NCT04280705 The primary endpoint they are touting is time to recovery. They are quiet on the secondary mortality endpoints in the releases that I read. I be interested to hear @ChiTownDoc @Newdoc and others chime in, I would be more interested if it actually reduces mortality, time to discharge, hospitalization days, etc. A time to recovery outcome could represent a very modest benefit, similar to antivirals for treatment of flu. They also bloated the release up with some open label results that don't provide any real insight into effectiveness.
Aways easy to slam big pharma, but this is a good first trial with additional data coming. Details of the trial:
- Two, randomized multi-center Phase 3 trials in countries with high COVID prevalence
- 397 patients received 200mg on the first day, followed by 100mg until day 5 or day 10 in addition to standard of care
- Patients had severe COVID manifestations: pneumonia but not under mechanical ventilation
- An additional expansion phase of the study will enroll and additional 5,600 patients including those on mechanical ventilation, conducted at 180 trial sites (US, China, France, Germany, Hong Kong, Italy, Japan, Korea, Netherlands, Singapore, Spain, Sweden Switzerland, Taiwan, UK)
- A second trial will read out in May, comparing safety and efficacy of 5 and 10-day durations compared to standard of care. The first data from 600 patients will be available at the end of May.
Data from the trial:
- Study sought to see if 5-day was as effective as the shorter 5-day course (10-day is currently being used world-wide)
- 10-day treatment course as effected in achieving clinical status as 5-day
- No new safety signals seen
- Benefit as measured by improvement in clinical score as determined by a seven point scale including hospital discharge, increasing levels of oxygen support, and death
- Patients achieved clinical recovery if they no longer required oxygen support and medical care or were discharged from the hospital.
- Time for clinical improvement for 50% of patients was 10 days in the 5-day treatment, and 11 days in the 10-day treatment
- Clinical outcomes varied by geography - Outside of Italy, the overall morality rate at day 14 was 7% across both groups
- 61-64% of patients were discharged from the hospital on the 5 and 10 day regimens, respectively
- Patients who received the drug within 10 days of symptom onset had improved outcomes compare to those treated after 10 days
- Worst tox I see is Grade 3 ALT in 7% of patients, with 3% discontinuing due to liver tox.
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For those who don't want to sit through 4 minutes of Tucker talking before you get to the the actual guest (and if you don't think Tucker's preamble that 'fear is hurting people' isn't political, well...) : Jay Bhattacharya, Stanford. He also authored an article in the WSJ recently.
I'm not saying that we shouldn't look at the death rate with some skepticism until we know more. But there's something at the center of his argument that 'what if it's only 1/1000 who die, we've overreacted' that misses the point.
I think it is likely true that the extent of people exposed, infected and asymptomatic is higher than we'll ever know, given the paucity of testing. The fact that the first evidence of Covid infections and deaths in California were in the Vacaville-Sacramento corridor, and not SF, LA or SD, and from people with no association of foreign travel suggests community spreading. It was, and likely has been, very widespread. That certainly means that the death rate is lower than initially thought, certainly lower than some of the dire estimates in the early days.
Right now, the deaths per capita in the Netherlands, Belgium, Spain, Italy, UK and France already eclipse the ~0.01% per capita deaths from the common flu. If you assume everyone got infected in those countries, the death rate of 0.02 - 0.04% is higher than the flu, happened in a short time, and has proved to be disastrous for some areas in that resources were totally overwhelmed.
But not everyone has been exposed to it, and we ensured that (and the low death rate) by cratering the world economy and telling everyone to stay home. Also, unlike the flu, this is more contagious, widespread, and deadly (even Bhattacharya agreed with that) and there's no vaccine.
Spoiler -
19 hours ago, Shaddie said:
Pete confirmed he was bisexual in an interview around 2001.
...or in 1980, for those that were paying attention to 'Rough Boys' on Empty Glass.
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Per capita deaths, Daily vs. total : Link. Belgium not looking very good, slope for UK worrying.
Spoiler -
It's pretty dubious - basically, someone did some molecular modeling and said that Covid could bind heme in red blood cells, and that would be a major mechanism for the clinical outcome. It hasn't been proven that this is occurring, it's not very likely based on current understanding of the mechanism of coronoviruses, and the research is a bit shite.
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Compassionate use of Remdesivir for Patients with Severe Covid-19 : New England Journal of Medicine, April 10
Details :
- 53 patients with severe complications, international cohort
- 34/53 (64%) were on mechanical ventilation
- Treatment resulted in an improvement in oxygen support class for 68% or patients over a median of 18 days following the first dose
- More than half were extubated
- 47% were discharged following treatment
- Clinical improvement less frequent among patients on severe ventilation versus noninvasive ventilation, and among patients at least 70 years of age
SpoilerSpoiler-
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9 hours ago, SydneyCarton said:
Well this seems like good news, and I don’t remember it being posted yet.
Perhaps for a few who are very ill, but it's a placental-derived stem cell therapy, and not likely to be mainstream therapy any time soon.
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5 minutes ago, Skipper said:
I don't think you necessarily need a 'cure'. You just need something that significantly limits the severity. If you could reduce hospital admissions/ICU admissions to a point that it would be extremely unlikely to overrun the increased infrastructure and reduce death rates to something that looks like a really bad flu season, that would drastically change policy and may be a risk most could live with then you continue to isolate those (elderly) that would continue to be most as risk. I don't know how likely we are to find that, determine it's safe, and mass produce it before a vaccine, but that's probably our best bet.
Perhaps, but it's also the scale of production for whatever that treatment is. We know already that there are shortages of hydroxycholoroquine (and that's due to some minor hoarding and its expanded used in trials), and while Gilead is spooling up production of rendemisvir, right now the supply is only 1.5 million doses. It's possible that the production and rollout of a vaccine may be the only way to really 'control' this. I'm not sure there's enough supply of drugs worldwide for everyone to be prescribed these meds, and certainly not for prophylactic use.
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Daily reported deaths per capita (7 day average) vs. total reported cases:
Spoiler-
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Study to test if COVID was in California earlier than previously thought
Will be interesting to see the data from this.
QuoteResearchers at Stanford Medicine are working to find out what proportion of Californians have already had COVID-19. The new study could help policymakers make more informed decisions during the coronavirus pandemic.
The team tested 3,200 people at three Bay Area locations on Saturday using an antibody test for COVID-19 and expect to release results in the coming weeks. The data could help to prove COVID-19 arrived undetected in California much earlier than previously thought.
The hypothesis that COVID-19 first started spreading in California in the fall of 2019 is one explanation for the state's lower than expected case numbers.
[snip]
Hanson said he thinks it is possible COVID-19 has been spreading among Californians since the fall when doctors reported an early flu season in the state. During that same time, California was welcoming as many as 8,000 Chinese nationals daily into our airports. Some of those visitors even arriving on direct flights from Wuhan, the epicenter of the coronavirus outbreak in China.
"When you add it all up it would be naïve to think that California did not have some exposure," said Hanson.
For years California has been the No. 1 travel destination for Chinese tourists in the United States. Even after the U.S. halted flights from China this winter Chinese travelers were still able to come to California on flights from Europe and Canada.
Hanson said through all of this the Chinese have been disingenuous about the timing of the initial outbreak of COVID-19.
"They originally said it was in early January, then it got backdated to December and then early December and now they are saying as early as November 17," said Hanson.
If Californians were exposed earlier than the rest of the country to COVID-19 we may have had a chance to build up some herd immunity to the disease. We won't know if that is the case until results from the Stanford Medicine study come back.
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1 hour ago, Captainant said:
Haven't seen much discussion here yet on some early challenges with HCQ treatments. Medical professionals, have y'all seen or heard much on this yet?
Yes, cardiac issues are a potential side effect of both hydroxychloroquine and azithromycin for a population of patientis even when given individually, which is why co-administration is potentially tricky.
American College of Cardiology
Quote- Hydroxychloroquine or chloroquine therapy should occur in the context of a clinical trial or registry, until sufficient evidence is available for use in clinical practice.
- Hydroxychloroquine or chloroquine use outside of a clinical trial should occur at the direction of an infectious disease or COVID-19 expert, with cardiology input regarding QT monitoring.
- The intensity of QT and arrhythmia monitoring should be considered in the context of potential drug benefit, drug safety, resource availability and quarantine considerations.
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COVID-19 medical discussion
in Daily Texan
Posted
I'm hopeful as anyone else, mostly because mRNA vaccines may be the best approach from a scalability standpoint for a global pandemic. It's great to see there's a titer raised, but we don't yet know if it is effective (or protective). The adverse events with the 250ug injection mirror some of the moderate to severe reactions seen in previous trials with this approach in a cancer setting. Still a lot to understand with this system.